From the Editor

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

This implies early senescence, segmental aging, and, in young adult patients, premature onset of multi-system medical illnesses associated with aging, including cardiovascular disease, cancer, brain atrophy, and cognitive decline. This might be the real reason why persons with schizophrenia die 25 to 30 years too early, not only because of an unhealthy lifestyle and iatrogenic cardio-metabolic adverse effects.

One of the most consistent observations pointing to accelerated aging in schizophrenia is shortened telomeres.^2,3 Telomeres are the terminal part of chromosomes (similar to the plastic aglets of shoelaces), which are known to shorten with each cell division because of “end replication losses.” Telomeres are measured in lymphocytes, which researchers regard as “windows to the brain” because they reflect brain aging.⁴ One study of lymphocytes in patients with schizophrenia found that they appear to be approximately 25 years older than the lymphocytes of healthy individuals!⁴

Possible causes of accelerated aging

Inflammation. The leading hypothesis for accelerated aging in schizophrenia is based on the inflammatory theory of aging. Schizophrenia has been strongly linked to immune dysregulation and neuroinflammation.⁵ Other components of the accelerated aging hypothesis include oxidative and nitrosative stress, which is associated with high levels of free radicals, and, importantly, mitochondrial dysfunction that fails to generate antioxidants (glutathione peroxidase, superoxide dismutase, and catalase) that can neutralize free radicals and reverse oxidative stress, as numerous studies have shown.

Clinically, and at a relatively young age, persons with schizophrenia show many physical features consistent with aging,⁶ including the following system changes:

• CNS: dilated ventricles, reduced brain volume and gray matter volume; hypofrontality, neurocognitive deficits such as executive functioning, working memory, and attention; neurophysiologic (low amplitudes on evoked potentials)
• Musculoskeletal system: abnormalities in muscle fibers; altered nerve conduction velocity; reduced bone density
• Skin: aging skin
• Eyes: increased rate of cataracts (not caused by medications); degradation in motion discrimination
• Endocrine system: abnormal gonadal hormones; low estrogen; low androgen; thyroid dysfunction, elevated cortisol
• Metabolism: increased rates of obesity; glucose dysregulation even before antipsychotic treatment; increased insulin resistance; abnormal glucose tolerance; reduced insulin-like growth factor-1 levels
• Immune system: increased pro-inflammatory cytokines (interleukin [IL]-1B, IL-6, IL-3, IL-4, IL-10, IL-13, tumor necrosis factor-Symbol Stdα) and decrease in anti-inflammatory cytokines (IL-2, interferon [INF]-Symbol Stdα, INF-Symbol Stdγ) and vitamin D
• Cardiovascular: systolic hypertension, increased pulse pressure
• Oxidative stress and mitochondrial dysfunction: increase in reactive oxygen species in brain tissue and increased DNA and RNA oxidation markers
• Telomere dynamics: significantly higher rates of telomere loss.

The mitochondrial theory of aging.⁷ The origin of this theory dates back to the landmark work of Denham Harman more than 2 decades ago in which he proposed a connection between free radicals and aging, which is associated with cell mutations and cancer.⁸ He suggested that because mitochondrial DNA is not protected by histones as DNA in the nucleus is, it might be the main target for free radicals, making the mitochondria more susceptible to oxidative damage. Therefore, it is possible that the high oxidative stress of schizophrenia could contribute to mitochondrial dysfunction, which leads to further telomere erosion.⁹ Perhaps reducing oxidative stress in schizophrenia with a powerful antioxidant, such as the supplement N-acetylcysteine,¹⁰ could help repair the dysfunctional mitochondria found in patients with schizophrenia and might mitigate accelerated aging.

I would like to propose a bolder, even radical, “out-of-the-box” therapeutic strategy for accelerated aging: mitochondrial transplantation. In fact, “mitochondrial donation” and transplant has been performed on fetuses with genetically defective mitochondria, which has prevented rapid death after birth.¹¹

Similarities with progeria. The accumulating evidence for accelerated aging in schizophrenia has promoted some researchers to consider it a form of progeria¹² because of the accelerated aging features that patients with schizophrenia manifest. Patients with schizophrenia share some risk factors with patients with progeria, including high paternal age, prenatal stress, prenatal famine, low birth weight, and premature cognitive decline. Both progeria and schizophrenia are associated with increased apoptosis and cell senescence, which could reduce the risk of cancer but result in premature aging along with age-related medical disorders that lead to mortality in the elderly.

This is why collaborative care between psychiatrists and primary care providers is so vital for patients with schizophrenia from the onset of the illness during the teens and young adulthood, not after years of treatment and unhealthy lifestyle habits (smoking, sedentary living, high-fat and high-calorie diet), which add insult to injury, culminating in loss of 25 to 30 years of potential life. Preventative medical care starting when schizophrenia is first diagnosed is vital, in addition to comprehensive psychiatric care, because premature mortality is the worst outcome in medicine.

Henry A. Nasrallah, MD

Editor-in-Chief

This implies early senescence, segmental aging, and, in young adult patients, premature onset of multi-system medical illnesses associated with aging, including cardiovascular disease, cancer, brain atrophy, and cognitive decline. This might be the real reason why persons with schizophrenia die 25 to 30 years too early, not only because of an unhealthy lifestyle and iatrogenic cardio-metabolic adverse effects.

One of the most consistent observations pointing to accelerated aging in schizophrenia is shortened telomeres.^2,3 Telomeres are the terminal part of chromosomes (similar to the plastic aglets of shoelaces), which are known to shorten with each cell division because of “end replication losses.” Telomeres are measured in lymphocytes, which researchers regard as “windows to the brain” because they reflect brain aging.⁴ One study of lymphocytes in patients with schizophrenia found that they appear to be approximately 25 years older than the lymphocytes of healthy individuals!⁴

Possible causes of accelerated aging

Inflammation. The leading hypothesis for accelerated aging in schizophrenia is based on the inflammatory theory of aging. Schizophrenia has been strongly linked to immune dysregulation and neuroinflammation.⁵ Other components of the accelerated aging hypothesis include oxidative and nitrosative stress, which is associated with high levels of free radicals, and, importantly, mitochondrial dysfunction that fails to generate antioxidants (glutathione peroxidase, superoxide dismutase, and catalase) that can neutralize free radicals and reverse oxidative stress, as numerous studies have shown.

Clinically, and at a relatively young age, persons with schizophrenia show many physical features consistent with aging,⁶ including the following system changes:

• CNS: dilated ventricles, reduced brain volume and gray matter volume; hypofrontality, neurocognitive deficits such as executive functioning, working memory, and attention; neurophysiologic (low amplitudes on evoked potentials)
• Musculoskeletal system: abnormalities in muscle fibers; altered nerve conduction velocity; reduced bone density
• Skin: aging skin
• Eyes: increased rate of cataracts (not caused by medications); degradation in motion discrimination
• Endocrine system: abnormal gonadal hormones; low estrogen; low androgen; thyroid dysfunction, elevated cortisol
• Metabolism: increased rates of obesity; glucose dysregulation even before antipsychotic treatment; increased insulin resistance; abnormal glucose tolerance; reduced insulin-like growth factor-1 levels
• Immune system: increased pro-inflammatory cytokines (interleukin [IL]-1B, IL-6, IL-3, IL-4, IL-10, IL-13, tumor necrosis factor-Symbol Stdα) and decrease in anti-inflammatory cytokines (IL-2, interferon [INF]-Symbol Stdα, INF-Symbol Stdγ) and vitamin D
• Cardiovascular: systolic hypertension, increased pulse pressure
• Oxidative stress and mitochondrial dysfunction: increase in reactive oxygen species in brain tissue and increased DNA and RNA oxidation markers
• Telomere dynamics: significantly higher rates of telomere loss.

The mitochondrial theory of aging.⁷ The origin of this theory dates back to the landmark work of Denham Harman more than 2 decades ago in which he proposed a connection between free radicals and aging, which is associated with cell mutations and cancer.⁸ He suggested that because mitochondrial DNA is not protected by histones as DNA in the nucleus is, it might be the main target for free radicals, making the mitochondria more susceptible to oxidative damage. Therefore, it is possible that the high oxidative stress of schizophrenia could contribute to mitochondrial dysfunction, which leads to further telomere erosion.⁹ Perhaps reducing oxidative stress in schizophrenia with a powerful antioxidant, such as the supplement N-acetylcysteine,¹⁰ could help repair the dysfunctional mitochondria found in patients with schizophrenia and might mitigate accelerated aging.

I would like to propose a bolder, even radical, “out-of-the-box” therapeutic strategy for accelerated aging: mitochondrial transplantation. In fact, “mitochondrial donation” and transplant has been performed on fetuses with genetically defective mitochondria, which has prevented rapid death after birth.¹¹

Similarities with progeria. The accumulating evidence for accelerated aging in schizophrenia has promoted some researchers to consider it a form of progeria¹² because of the accelerated aging features that patients with schizophrenia manifest. Patients with schizophrenia share some risk factors with patients with progeria, including high paternal age, prenatal stress, prenatal famine, low birth weight, and premature cognitive decline. Both progeria and schizophrenia are associated with increased apoptosis and cell senescence, which could reduce the risk of cancer but result in premature aging along with age-related medical disorders that lead to mortality in the elderly.

This is why collaborative care between psychiatrists and primary care providers is so vital for patients with schizophrenia from the onset of the illness during the teens and young adulthood, not after years of treatment and unhealthy lifestyle habits (smoking, sedentary living, high-fat and high-calorie diet), which add insult to injury, culminating in loss of 25 to 30 years of potential life. Preventative medical care starting when schizophrenia is first diagnosed is vital, in addition to comprehensive psychiatric care, because premature mortality is the worst outcome in medicine.

Henry A. Nasrallah, MD

Editor-in-Chief

This implies early senescence, segmental aging, and, in young adult patients, premature onset of multi-system medical illnesses associated with aging, including cardiovascular disease, cancer, brain atrophy, and cognitive decline. This might be the real reason why persons with schizophrenia die 25 to 30 years too early, not only because of an unhealthy lifestyle and iatrogenic cardio-metabolic adverse effects.

One of the most consistent observations pointing to accelerated aging in schizophrenia is shortened telomeres.^2,3 Telomeres are the terminal part of chromosomes (similar to the plastic aglets of shoelaces), which are known to shorten with each cell division because of “end replication losses.” Telomeres are measured in lymphocytes, which researchers regard as “windows to the brain” because they reflect brain aging.⁴ One study of lymphocytes in patients with schizophrenia found that they appear to be approximately 25 years older than the lymphocytes of healthy individuals!⁴

Possible causes of accelerated aging

Inflammation. The leading hypothesis for accelerated aging in schizophrenia is based on the inflammatory theory of aging. Schizophrenia has been strongly linked to immune dysregulation and neuroinflammation.⁵ Other components of the accelerated aging hypothesis include oxidative and nitrosative stress, which is associated with high levels of free radicals, and, importantly, mitochondrial dysfunction that fails to generate antioxidants (glutathione peroxidase, superoxide dismutase, and catalase) that can neutralize free radicals and reverse oxidative stress, as numerous studies have shown.

Clinically, and at a relatively young age, persons with schizophrenia show many physical features consistent with aging,⁶ including the following system changes:

• CNS: dilated ventricles, reduced brain volume and gray matter volume; hypofrontality, neurocognitive deficits such as executive functioning, working memory, and attention; neurophysiologic (low amplitudes on evoked potentials)
• Musculoskeletal system: abnormalities in muscle fibers; altered nerve conduction velocity; reduced bone density
• Skin: aging skin
• Eyes: increased rate of cataracts (not caused by medications); degradation in motion discrimination
• Endocrine system: abnormal gonadal hormones; low estrogen; low androgen; thyroid dysfunction, elevated cortisol
• Metabolism: increased rates of obesity; glucose dysregulation even before antipsychotic treatment; increased insulin resistance; abnormal glucose tolerance; reduced insulin-like growth factor-1 levels
• Immune system: increased pro-inflammatory cytokines (interleukin [IL]-1B, IL-6, IL-3, IL-4, IL-10, IL-13, tumor necrosis factor-Symbol Stdα) and decrease in anti-inflammatory cytokines (IL-2, interferon [INF]-Symbol Stdα, INF-Symbol Stdγ) and vitamin D
• Cardiovascular: systolic hypertension, increased pulse pressure
• Oxidative stress and mitochondrial dysfunction: increase in reactive oxygen species in brain tissue and increased DNA and RNA oxidation markers
• Telomere dynamics: significantly higher rates of telomere loss.

The mitochondrial theory of aging.⁷ The origin of this theory dates back to the landmark work of Denham Harman more than 2 decades ago in which he proposed a connection between free radicals and aging, which is associated with cell mutations and cancer.⁸ He suggested that because mitochondrial DNA is not protected by histones as DNA in the nucleus is, it might be the main target for free radicals, making the mitochondria more susceptible to oxidative damage. Therefore, it is possible that the high oxidative stress of schizophrenia could contribute to mitochondrial dysfunction, which leads to further telomere erosion.⁹ Perhaps reducing oxidative stress in schizophrenia with a powerful antioxidant, such as the supplement N-acetylcysteine,¹⁰ could help repair the dysfunctional mitochondria found in patients with schizophrenia and might mitigate accelerated aging.

I would like to propose a bolder, even radical, “out-of-the-box” therapeutic strategy for accelerated aging: mitochondrial transplantation. In fact, “mitochondrial donation” and transplant has been performed on fetuses with genetically defective mitochondria, which has prevented rapid death after birth.¹¹

Similarities with progeria. The accumulating evidence for accelerated aging in schizophrenia has promoted some researchers to consider it a form of progeria¹² because of the accelerated aging features that patients with schizophrenia manifest. Patients with schizophrenia share some risk factors with patients with progeria, including high paternal age, prenatal stress, prenatal famine, low birth weight, and premature cognitive decline. Both progeria and schizophrenia are associated with increased apoptosis and cell senescence, which could reduce the risk of cancer but result in premature aging along with age-related medical disorders that lead to mortality in the elderly.

This is why collaborative care between psychiatrists and primary care providers is so vital for patients with schizophrenia from the onset of the illness during the teens and young adulthood, not after years of treatment and unhealthy lifestyle habits (smoking, sedentary living, high-fat and high-calorie diet), which add insult to injury, culminating in loss of 25 to 30 years of potential life. Preventative medical care starting when schizophrenia is first diagnosed is vital, in addition to comprehensive psychiatric care, because premature mortality is the worst outcome in medicine.

Henry A. Nasrallah, MD

Editor-in-Chief

Lately, I’ve been thinking a lot about you and me. No, not being creepy.  I meant all of us, vascular surgeons. Something might be wrong. I credit my concern to Dawn Coleman. Last spring, I was attending a session at the SVS and Dr. Coleman’s presentation was running over. The red light signal began to flash and she quickly covered the content of her last few slides. As she finished her talk I thought I heard her say, almost under her breath, that vascular surgeons lead all medical specialists in suicidal ideation. “Did she just say suicidal ideation?”, I asked the person next to me. It was an odd statement and certainly a fact I had never heard.

For the next few weeks, the thought stuck with me. Why us? It turns out the study she was quoting from ¹ was an American College of Surgeons survey that found that suicidal ideation (SI) was 6.4% among American surgeons, compared with 3.3% of the general population. And yes, the highest incidence of suicidal ideation was found in vascular surgeons (7.7%). The study also found that 50% of those with SI will make an attempt but only 26% will seek psychiatric treatment. The most commonly stated deterrent to seeking professional help was fear of a negative impact on their licensure. While SI and suicide rates are disproportionately higher in physicians, clinical depression is not. Therefore there are other factors in play. So we must look at burnout and quality of life (QOL) issues.

None of this is to disparage the validity of surveys.  Vascular surgeons face real health risks related to radiation exposure, repetitive movements, and long surgical times. Spine issues and cataracts have been closely correlated to our vocation, and I do look forward to the results of this study from the SCVS.

So what do we do? Michael Sosin, MD, and his colleagues recently published an extensive review of quality of life and burnout rates across surgical specialties.⁴

I’ll paraphrase some of their recommendations here:

• Streamline specialty training.

• Optimize reimbursement.

• Reevaluate training paradigms.

• Examine department cultures.

• Look carefully at tort reform.

• Examine the medical education dept.

The good news is that the ACS survey was performed 8 years ago and the work hours report from the Community Tracking Survey is nearly 12 years old. Looking at the recommendations from Dr. Sosin, we have made a massive move to streamline our training with the advent of the 0+5 integrated vascular residencies. Work hours correlate closely to caring for acutely ill patients who require intensive monitoring. The widespread adoption of endovascular options has likely had a positive impact on our work hours with shorter lengths of stay and fewer ICU patients.

Nevertheless, being the lead specialty in several of these surveys should be eye opening, to say the least. We need to take a closer look at burnout, depression, and suicidal ideation in our field. We need to fight with the SVS for serious reform in reimbursements and malpractice legislation. We need to identify and transform malignant department cultures where they exist. Finally, removing the stigma of psychiatric assistance may be the most important goal of all.
 

References

1. Arch Surg. 2011;146(1):54-62.

2. Ann Surg. 2011;254:558-68.

3. Arch Intern Med. 2011;171(13):1211-3.

4. JAMA Surg. 2016;151(10):970-8.

Dr. Malachi Sheahan III, from the Louisiana State University Health Sciences Center, New Orleans, is the Associate Medical Editor of Vascular Specialist.

Lately, I’ve been thinking a lot about you and me. No, not being creepy.  I meant all of us, vascular surgeons. Something might be wrong. I credit my concern to Dawn Coleman. Last spring, I was attending a session at the SVS and Dr. Coleman’s presentation was running over. The red light signal began to flash and she quickly covered the content of her last few slides. As she finished her talk I thought I heard her say, almost under her breath, that vascular surgeons lead all medical specialists in suicidal ideation. “Did she just say suicidal ideation?”, I asked the person next to me. It was an odd statement and certainly a fact I had never heard.

For the next few weeks, the thought stuck with me. Why us? It turns out the study she was quoting from ¹ was an American College of Surgeons survey that found that suicidal ideation (SI) was 6.4% among American surgeons, compared with 3.3% of the general population. And yes, the highest incidence of suicidal ideation was found in vascular surgeons (7.7%). The study also found that 50% of those with SI will make an attempt but only 26% will seek psychiatric treatment. The most commonly stated deterrent to seeking professional help was fear of a negative impact on their licensure. While SI and suicide rates are disproportionately higher in physicians, clinical depression is not. Therefore there are other factors in play. So we must look at burnout and quality of life (QOL) issues.

None of this is to disparage the validity of surveys.  Vascular surgeons face real health risks related to radiation exposure, repetitive movements, and long surgical times. Spine issues and cataracts have been closely correlated to our vocation, and I do look forward to the results of this study from the SCVS.

So what do we do? Michael Sosin, MD, and his colleagues recently published an extensive review of quality of life and burnout rates across surgical specialties.⁴

I’ll paraphrase some of their recommendations here:

• Streamline specialty training.

• Optimize reimbursement.

• Reevaluate training paradigms.

• Examine department cultures.

• Look carefully at tort reform.

• Examine the medical education dept.

The good news is that the ACS survey was performed 8 years ago and the work hours report from the Community Tracking Survey is nearly 12 years old. Looking at the recommendations from Dr. Sosin, we have made a massive move to streamline our training with the advent of the 0+5 integrated vascular residencies. Work hours correlate closely to caring for acutely ill patients who require intensive monitoring. The widespread adoption of endovascular options has likely had a positive impact on our work hours with shorter lengths of stay and fewer ICU patients.

Nevertheless, being the lead specialty in several of these surveys should be eye opening, to say the least. We need to take a closer look at burnout, depression, and suicidal ideation in our field. We need to fight with the SVS for serious reform in reimbursements and malpractice legislation. We need to identify and transform malignant department cultures where they exist. Finally, removing the stigma of psychiatric assistance may be the most important goal of all.
 

References

1. Arch Surg. 2011;146(1):54-62.

2. Ann Surg. 2011;254:558-68.

3. Arch Intern Med. 2011;171(13):1211-3.

4. JAMA Surg. 2016;151(10):970-8.

Dr. Malachi Sheahan III, from the Louisiana State University Health Sciences Center, New Orleans, is the Associate Medical Editor of Vascular Specialist.

Lately, I’ve been thinking a lot about you and me. No, not being creepy.  I meant all of us, vascular surgeons. Something might be wrong. I credit my concern to Dawn Coleman. Last spring, I was attending a session at the SVS and Dr. Coleman’s presentation was running over. The red light signal began to flash and she quickly covered the content of her last few slides. As she finished her talk I thought I heard her say, almost under her breath, that vascular surgeons lead all medical specialists in suicidal ideation. “Did she just say suicidal ideation?”, I asked the person next to me. It was an odd statement and certainly a fact I had never heard.

For the next few weeks, the thought stuck with me. Why us? It turns out the study she was quoting from ¹ was an American College of Surgeons survey that found that suicidal ideation (SI) was 6.4% among American surgeons, compared with 3.3% of the general population. And yes, the highest incidence of suicidal ideation was found in vascular surgeons (7.7%). The study also found that 50% of those with SI will make an attempt but only 26% will seek psychiatric treatment. The most commonly stated deterrent to seeking professional help was fear of a negative impact on their licensure. While SI and suicide rates are disproportionately higher in physicians, clinical depression is not. Therefore there are other factors in play. So we must look at burnout and quality of life (QOL) issues.

None of this is to disparage the validity of surveys.  Vascular surgeons face real health risks related to radiation exposure, repetitive movements, and long surgical times. Spine issues and cataracts have been closely correlated to our vocation, and I do look forward to the results of this study from the SCVS.

So what do we do? Michael Sosin, MD, and his colleagues recently published an extensive review of quality of life and burnout rates across surgical specialties.⁴

I’ll paraphrase some of their recommendations here:

• Streamline specialty training.

• Optimize reimbursement.

• Reevaluate training paradigms.

• Examine department cultures.

• Look carefully at tort reform.

• Examine the medical education dept.

The good news is that the ACS survey was performed 8 years ago and the work hours report from the Community Tracking Survey is nearly 12 years old. Looking at the recommendations from Dr. Sosin, we have made a massive move to streamline our training with the advent of the 0+5 integrated vascular residencies. Work hours correlate closely to caring for acutely ill patients who require intensive monitoring. The widespread adoption of endovascular options has likely had a positive impact on our work hours with shorter lengths of stay and fewer ICU patients.

Nevertheless, being the lead specialty in several of these surveys should be eye opening, to say the least. We need to take a closer look at burnout, depression, and suicidal ideation in our field. We need to fight with the SVS for serious reform in reimbursements and malpractice legislation. We need to identify and transform malignant department cultures where they exist. Finally, removing the stigma of psychiatric assistance may be the most important goal of all.
 

References

1. Arch Surg. 2011;146(1):54-62.

2. Ann Surg. 2011;254:558-68.

3. Arch Intern Med. 2011;171(13):1211-3.

4. JAMA Surg. 2016;151(10):970-8.

Dr. Malachi Sheahan III, from the Louisiana State University Health Sciences Center, New Orleans, is the Associate Medical Editor of Vascular Specialist.

The email came with the words, “It is with sadness we report that Frank Moody died. …” I was instantly transported to the last time I saw the man and a flood of emotions swept over me. The name Frank Moody will ring a distant bell or none at all to some in our profession. Like many of the greats of surgery, he belongs to the ages.

I remember the first time I asked a student, “Who is Michael DeBakey?” I was dumbfounded to be greeted with a blank stare. How could a student of medicine not know of Dr. DeBakey? A few years later, the same question prompted a smart aleck reply that he was the man who invented DeBakey forceps. Well, of course he did invent the forceps, but to know nothing further of the man who was the world’s expert on ulcer disease in the 1940s, the progenitor of the National Medical Library, and among the foremost pioneers of heart surgery seemed beyond belief.

Photo credit: Dwight Andrews/UTHealth

My mentor, Ernest Poulos, has long since left the active surgical scene. At times he would note the passing of one of his heroes like Carl Moyer (look it up!) and say, “Sic transit gloria mundi.” At 27 and anxious to get the right to cut into my fellow human beings, I would cock my head like a confounded puppy and wonder what that meant. I looked up the translation and meaning long ago, but now with age I understand the phrase in my bones.

I have long been a hanger-on at surgical meetings, hoping to meet those mighty figures that shaped surgical history. I saw W. Dean Warren once and had a very long hour with the great Mark Ravitch. Oliver Beahrs once performed magic tricks at a dinner I attended. At every surgical meeting there is an old guy (and now occasionally with the change in our profession, an elderly lady) getting on the bus to go to the reception or dinner dance. Often they are alone, their spouses having departed before them. As a young man, I wondered why the heck they came to the meetings. Just like every generation before, ours was eager to grab the reins, and in our ardor for future glory, we were polite but also restless for them to move aside. I hadn’t yet learned the importance of history and of listening.

What I missed while carousing with my young colleagues was an opportunity to hear history first hand and to learn that, what we thought was so cutting edge, these men and women had long ago considered. Many of our living legends imagined some of today’s innovations but they lacked the technology to bring their dreams to fruition, or time and age defeated them before they reached the final chapter of their research. It was when I was about 50 that I wised up and began seeking out living legends like Frank Moody and Frank Spencer.

In the case of Frank Moody, he was quite elderly when I first met him. For some reason, he knew who I was and shook my hand softly. I didn’t recognize him initially, but at the sound of his name, I knew I was in the presence of a major figure in 20th century gastrointestinal surgery. He had been at the University of California, San Francisco, during an historic time when George Sheldon, Donald Trunkey and other great surgeons trained there with J. Englebert Dunphy as their chief. Dr. Moody’s CV lists 141 articles in basic and clinical science that have had a profound impact on how we view the gastrointestinal tract. He was Chief at the University of Utah and the University of Alabama and finished his career as professor at the University of Texas-Houston. His awards and achievements were legion.

Parkinson’s had only recently really begun to affect him when I met him, and as the years went by his voice became so very faint that I had to lean in to hear him. We would sit together at the back of the dinner dance room so that we could hear each other. And while the other guests entertained themselves, Dr. Moody and I would discuss his life, scientific method and philosophy as well as his insights into his own case of Parkinsonism. I would see him at meetings, making his way slowly but steadily along a corridor while others briskly walked by, unaware that the man they just passed was among the most important surgical pioneers of our time. It was not sad that Dr. Moody was elderly and unrecognized, but that we younger surgeons missed knowing a great man in our tendency to rush past history.

History is not facts and dates, but rather, it is people and their lives. Yes, the history of our profession is embodied by pioneers like Frank Moody and the others I’ve mentioned.

We have many Fellows among us who are living history, still contributing – maybe not at the dais but at the dinner table, speaking softly and walking a bit slower than their juniors. Thanks to LaMar McGinnis who started it and Don Nakayama who continues it, the College has a History Community on the ACS Communities, an active Surgical History Group, and a will to acknowledge the history that lives and breathes among us. The Surgical History Group has organized a full program of events at the Clinical Congress and I hope many attendees take the opportunity to attend.

Take a moment at your next meeting or at the Clinical Congress and look for those historic surgeons still with us. Be smarter than I was at a young age and get to know them. You may learn something from them you can’t learn anyplace else.

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

The email came with the words, “It is with sadness we report that Frank Moody died. …” I was instantly transported to the last time I saw the man and a flood of emotions swept over me. The name Frank Moody will ring a distant bell or none at all to some in our profession. Like many of the greats of surgery, he belongs to the ages.

I remember the first time I asked a student, “Who is Michael DeBakey?” I was dumbfounded to be greeted with a blank stare. How could a student of medicine not know of Dr. DeBakey? A few years later, the same question prompted a smart aleck reply that he was the man who invented DeBakey forceps. Well, of course he did invent the forceps, but to know nothing further of the man who was the world’s expert on ulcer disease in the 1940s, the progenitor of the National Medical Library, and among the foremost pioneers of heart surgery seemed beyond belief.

Photo credit: Dwight Andrews/UTHealth

My mentor, Ernest Poulos, has long since left the active surgical scene. At times he would note the passing of one of his heroes like Carl Moyer (look it up!) and say, “Sic transit gloria mundi.” At 27 and anxious to get the right to cut into my fellow human beings, I would cock my head like a confounded puppy and wonder what that meant. I looked up the translation and meaning long ago, but now with age I understand the phrase in my bones.

I have long been a hanger-on at surgical meetings, hoping to meet those mighty figures that shaped surgical history. I saw W. Dean Warren once and had a very long hour with the great Mark Ravitch. Oliver Beahrs once performed magic tricks at a dinner I attended. At every surgical meeting there is an old guy (and now occasionally with the change in our profession, an elderly lady) getting on the bus to go to the reception or dinner dance. Often they are alone, their spouses having departed before them. As a young man, I wondered why the heck they came to the meetings. Just like every generation before, ours was eager to grab the reins, and in our ardor for future glory, we were polite but also restless for them to move aside. I hadn’t yet learned the importance of history and of listening.

What I missed while carousing with my young colleagues was an opportunity to hear history first hand and to learn that, what we thought was so cutting edge, these men and women had long ago considered. Many of our living legends imagined some of today’s innovations but they lacked the technology to bring their dreams to fruition, or time and age defeated them before they reached the final chapter of their research. It was when I was about 50 that I wised up and began seeking out living legends like Frank Moody and Frank Spencer.

In the case of Frank Moody, he was quite elderly when I first met him. For some reason, he knew who I was and shook my hand softly. I didn’t recognize him initially, but at the sound of his name, I knew I was in the presence of a major figure in 20th century gastrointestinal surgery. He had been at the University of California, San Francisco, during an historic time when George Sheldon, Donald Trunkey and other great surgeons trained there with J. Englebert Dunphy as their chief. Dr. Moody’s CV lists 141 articles in basic and clinical science that have had a profound impact on how we view the gastrointestinal tract. He was Chief at the University of Utah and the University of Alabama and finished his career as professor at the University of Texas-Houston. His awards and achievements were legion.

Parkinson’s had only recently really begun to affect him when I met him, and as the years went by his voice became so very faint that I had to lean in to hear him. We would sit together at the back of the dinner dance room so that we could hear each other. And while the other guests entertained themselves, Dr. Moody and I would discuss his life, scientific method and philosophy as well as his insights into his own case of Parkinsonism. I would see him at meetings, making his way slowly but steadily along a corridor while others briskly walked by, unaware that the man they just passed was among the most important surgical pioneers of our time. It was not sad that Dr. Moody was elderly and unrecognized, but that we younger surgeons missed knowing a great man in our tendency to rush past history.

History is not facts and dates, but rather, it is people and their lives. Yes, the history of our profession is embodied by pioneers like Frank Moody and the others I’ve mentioned.

We have many Fellows among us who are living history, still contributing – maybe not at the dais but at the dinner table, speaking softly and walking a bit slower than their juniors. Thanks to LaMar McGinnis who started it and Don Nakayama who continues it, the College has a History Community on the ACS Communities, an active Surgical History Group, and a will to acknowledge the history that lives and breathes among us. The Surgical History Group has organized a full program of events at the Clinical Congress and I hope many attendees take the opportunity to attend.

Take a moment at your next meeting or at the Clinical Congress and look for those historic surgeons still with us. Be smarter than I was at a young age and get to know them. You may learn something from them you can’t learn anyplace else.

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

The email came with the words, “It is with sadness we report that Frank Moody died. …” I was instantly transported to the last time I saw the man and a flood of emotions swept over me. The name Frank Moody will ring a distant bell or none at all to some in our profession. Like many of the greats of surgery, he belongs to the ages.

I remember the first time I asked a student, “Who is Michael DeBakey?” I was dumbfounded to be greeted with a blank stare. How could a student of medicine not know of Dr. DeBakey? A few years later, the same question prompted a smart aleck reply that he was the man who invented DeBakey forceps. Well, of course he did invent the forceps, but to know nothing further of the man who was the world’s expert on ulcer disease in the 1940s, the progenitor of the National Medical Library, and among the foremost pioneers of heart surgery seemed beyond belief.

Photo credit: Dwight Andrews/UTHealth

My mentor, Ernest Poulos, has long since left the active surgical scene. At times he would note the passing of one of his heroes like Carl Moyer (look it up!) and say, “Sic transit gloria mundi.” At 27 and anxious to get the right to cut into my fellow human beings, I would cock my head like a confounded puppy and wonder what that meant. I looked up the translation and meaning long ago, but now with age I understand the phrase in my bones.

I have long been a hanger-on at surgical meetings, hoping to meet those mighty figures that shaped surgical history. I saw W. Dean Warren once and had a very long hour with the great Mark Ravitch. Oliver Beahrs once performed magic tricks at a dinner I attended. At every surgical meeting there is an old guy (and now occasionally with the change in our profession, an elderly lady) getting on the bus to go to the reception or dinner dance. Often they are alone, their spouses having departed before them. As a young man, I wondered why the heck they came to the meetings. Just like every generation before, ours was eager to grab the reins, and in our ardor for future glory, we were polite but also restless for them to move aside. I hadn’t yet learned the importance of history and of listening.

What I missed while carousing with my young colleagues was an opportunity to hear history first hand and to learn that, what we thought was so cutting edge, these men and women had long ago considered. Many of our living legends imagined some of today’s innovations but they lacked the technology to bring their dreams to fruition, or time and age defeated them before they reached the final chapter of their research. It was when I was about 50 that I wised up and began seeking out living legends like Frank Moody and Frank Spencer.

In the case of Frank Moody, he was quite elderly when I first met him. For some reason, he knew who I was and shook my hand softly. I didn’t recognize him initially, but at the sound of his name, I knew I was in the presence of a major figure in 20th century gastrointestinal surgery. He had been at the University of California, San Francisco, during an historic time when George Sheldon, Donald Trunkey and other great surgeons trained there with J. Englebert Dunphy as their chief. Dr. Moody’s CV lists 141 articles in basic and clinical science that have had a profound impact on how we view the gastrointestinal tract. He was Chief at the University of Utah and the University of Alabama and finished his career as professor at the University of Texas-Houston. His awards and achievements were legion.

Parkinson’s had only recently really begun to affect him when I met him, and as the years went by his voice became so very faint that I had to lean in to hear him. We would sit together at the back of the dinner dance room so that we could hear each other. And while the other guests entertained themselves, Dr. Moody and I would discuss his life, scientific method and philosophy as well as his insights into his own case of Parkinsonism. I would see him at meetings, making his way slowly but steadily along a corridor while others briskly walked by, unaware that the man they just passed was among the most important surgical pioneers of our time. It was not sad that Dr. Moody was elderly and unrecognized, but that we younger surgeons missed knowing a great man in our tendency to rush past history.

History is not facts and dates, but rather, it is people and their lives. Yes, the history of our profession is embodied by pioneers like Frank Moody and the others I’ve mentioned.

We have many Fellows among us who are living history, still contributing – maybe not at the dais but at the dinner table, speaking softly and walking a bit slower than their juniors. Thanks to LaMar McGinnis who started it and Don Nakayama who continues it, the College has a History Community on the ACS Communities, an active Surgical History Group, and a will to acknowledge the history that lives and breathes among us. The Surgical History Group has organized a full program of events at the Clinical Congress and I hope many attendees take the opportunity to attend.

Take a moment at your next meeting or at the Clinical Congress and look for those historic surgeons still with us. Be smarter than I was at a young age and get to know them. You may learn something from them you can’t learn anyplace else.

Dr. Hughes is clinical professor in the department of surgery and director of medical education at the Kansas University School of Medicine, Salina Campus, and Co-Editor of ACS Surgery News.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Lactate measurement is widely used in emergency departments (EDs) and intensive care units (ICUs) to facilitate the early diagnosis and management of sepsis, severe trauma, ischemic bowel, and necrotizing fasciitis. Measuring lactate levels is much less commonly utilized in the practice of obstetrics and gynecology; increasing measurement in our practices may improve our early recognition and treatment of women with severe sepsis and other serious diseases.

Lactate physiology

The metabolism of glucose in the Embden-Meyerhof pathway results in the production of pyruvate and the high-energy compounds ATP and NADH. Pyruvate can enter 3 alternative metabolic pathways: 1) the mitochondrial Krebs cycle, 2) conversion to lactate in the cell cytosol, or 3) conversion back to glucose in the process of gluconeogenesis.

Under aerobic conditions, most pyruvate enters the Krebs cycle and little is converted to lactate. Molecular oxygen is an absolute requirement for Krebs cycle activity. Under anaerobic conditions, pyruvate cannot enter the Krebs cycle and is preferentially converted to lactate.¹

An elevated lactate level is a sensitive marker for tissue hypoxia caused by a variety of diseases, including sepsis, trauma, ischemic bowel, and necrotizing fasciitis. With sepsis, additional mechanisms also contribute to the increase in lactate, including increased glycolysis, impaired lactate clearance, and activation of inflammatory cells that shift cellular metabolism toward lactate production.^2,3

The normal range for venous plasma lactate in adults is 0.5 to 2.2 mM, although the normal range may vary because of differences in local laboratory methods. Arterial, capillary, and venous lactate are all highly positively correlated.⁴ Venous lactate concentrations between 2.3 and 3.9 mM are suggestive of mild physiologic dysfunction, and values ≥4.0 mM are consistent with severe physiologic dysfunction. In hospitalized patients, sepsis is one of the most common causes of a lactate level ≥4 mM.⁵

In many patients with an elevated lactate concentration the anion gap is also increased—but this is not always the case. In fact, in one large observational study, among patients with sepsis and a lactate concentration ≥4 mM, approximately 25% had a normal bicarbonate level and normal anion gap.⁶

Elevated lactate levels applied in obstetric and gynecologic practice

CASE 1. Obstetric practice: Hernia identified during labor

A 30-year-old woman (G1P0) presents in early labor at 37 weeks’ gestation. Two years prior to the pregnancy she had a Roux-en-Y gastric bypass and lost more than 100 lb. In addition to reporting lower abdominal pain occurring during contractions, she reports the new onset of mid-epigastric pain. A surgical consult is requested. The initial white blood cell count is 6,290 per uL, and the lactate level is 1.0 mM.

The surgeon consulted orders a computed tomography (CT) scan with oral contrast, but the patient has difficulty retaining the oral contrast due to her nausea, delaying the performance of the CT scan. Three hours following admission a follow-up lactate measurement is 3.3 mM, and an emergency CT scan is performed.

The CT scan shows an internal hernia with swirling of the mesenteric vessels and twisting of the small bowel mesentery. An urgent cesarean delivery and repair of the internal hernia is performed.

The patient and her newborn do well postoperatively. The postoperative lactate level is 0.8 mM.

In pregnant women with a past history of a Roux-en-Y gastric bypass and abdominal discomfort who are in labor it is challenging to rapidly diagnose internal hernias and other bowel problems.⁷⁻⁹ In this case, the increased lactate level from 1.0 mM to 3.3 mM raised concern for ischemic bowel and triggered the emergency CT and urgent exploratory laparotomy and cesarean delivery.

Up to 14% of maternal deaths in the United States are due to infection.¹⁰ In many of these cases, there is a delay in sepsis recognition because previously healthy pregnant women with sepsis may not manifest classic signs such as fever, hypotension, or mental status changes until late in the disease course. Measurement of lactate can facilitate the early recognition of severe sepsis in pregnant women, thereby accelerating and focusing their treatment.¹¹

To reduce mortality due to sepsis, aggressive intervention needs to occur within the first 6 hours following the onset of the infection.

CASE 2. Gynecologic practice: Bacterial infection identified in the presence of abdominal pain and vomiting

A 40-year-old woman presents to the ED 5 days following a myomectomy, with nausea, vomiting, and abdominal pain. Her vital signs reveal: temperature, 98.4°F (36.9°C); heart rate, 122 bpm; blood pressure, 115/70 mm Hg; and white blood cell count, 6,270 per uL. Her lactate level is 4.0 mM. She is admitted to the ICU with a presumptive diagnosis of severe sepsis and treatment with broad-spectrum antibiotics is initiated. Twenty-four hours following admission, gram-negative rods are identified in blood cultures that are later identified to be Bacteroides fragilis.

For the past 2 decades there has been a concerted national effort to reduce mortality caused by sepsis through early diagnosis and aggressive treatment of sepsis in an ICU setting. Observational studies have reported that an elevated lactate level is an excellent early biomarker for sepsis and may be observed prior to the onset of fever, elevated white blood cell count, or hypotension.⁶ For example, in one large study of patients with sepsis and a lactate measurement ≥4 mM, only 50% of patients had a systolic blood pressure <90 mm Hg.

Elevated lactate levels also are associated with an increased risk of death. Among 13,932 consecutive patients admitted to an ICU in Alberta, Canada, the mortality rate among patients with a venous or arterial lactate >2 mM was 20%, compared with a mortality rate of 5% for patients with a lactate level ≤2 mM.¹² In a study of 1,278 patients with infection admitted to the hospital from the ED, mortality increased as baseline lactate concentration rose. For lactate concentrations of 0 to 2.4, 2.5 to 3.9, and ≥4.0 mM, mortality rates were 5%, 9%, and 28%, respectively.¹³

In patients with sepsis, serial measurement of lactate can help to guide treatment. In a randomized trial, 348 patients admitted to an ICU with a lactate ≥3 mM were randomly assigned to standard treatment, in which the clinicians had no knowledge of patients’ lactate levels, or to an experimental group, in which the clinicians were provided lactate measurement results every 2 hours. Compared with clinicians in the control group, the clinicians with access to frequent lactate measurements administered more fluids and vasodilators to their patients. Compared with patients in the control group, the hospital mortality rate was lower when the clinicians had access to frequent lactate measurements (34% vs 44%, respectively; adjusted hazard ratio, 0.61; 95% confidence interval, 0.43−0.87; P = .0006).¹⁴

Elevated lactate levels in the fetus and newborn

The physiologic status of the newborn is routinely assessed with the Apgar score. Umbilical artery and venous blood gases, including measurement of pH, are often used as a corroborating biomarker. Most studies report that umbilical artery or vein lactate measurement is as useful as a pH measurement in assessing newborn physiologic status. The normal range of lactate in fetuses and newborns is not precisely defined, with values between 3.5 and 7 mM being cited as the upper limit of normal.¹⁵⁻¹⁸

In many countries (but not the United States), in utero fetal status during labor is assessed by fetal scalp sampling of blood and measurement of either pH or lactate. Fetal scalp sampling is difficult and often very little blood is obtained, making it difficult to measure pH. A Cochrane review reported that in 2 randomized trials, fetal scalp sampling produced a successful measurement of lactate in 99% of attempts, while a pH result could only be obtained in 79% of cases due to an inadequate volume of blood or clotted blood.¹⁹

Increased lactate measurement can help our patients

Measuring lactate in order to rapidly identify patients with major physiologic derangements is practiced widely in EDs and ICUs. There is significant opportunity to increase the use of lactate measurement in obstetrics and gynecology. Increasing this use will help to rapidly identify women with severe sepsis and other diseases, leading to more rapid intervention and improved outcomes.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Lactate measurement is widely used in emergency departments (EDs) and intensive care units (ICUs) to facilitate the early diagnosis and management of sepsis, severe trauma, ischemic bowel, and necrotizing fasciitis. Measuring lactate levels is much less commonly utilized in the practice of obstetrics and gynecology; increasing measurement in our practices may improve our early recognition and treatment of women with severe sepsis and other serious diseases.

Lactate physiology

The metabolism of glucose in the Embden-Meyerhof pathway results in the production of pyruvate and the high-energy compounds ATP and NADH. Pyruvate can enter 3 alternative metabolic pathways: 1) the mitochondrial Krebs cycle, 2) conversion to lactate in the cell cytosol, or 3) conversion back to glucose in the process of gluconeogenesis.

Under aerobic conditions, most pyruvate enters the Krebs cycle and little is converted to lactate. Molecular oxygen is an absolute requirement for Krebs cycle activity. Under anaerobic conditions, pyruvate cannot enter the Krebs cycle and is preferentially converted to lactate.¹

An elevated lactate level is a sensitive marker for tissue hypoxia caused by a variety of diseases, including sepsis, trauma, ischemic bowel, and necrotizing fasciitis. With sepsis, additional mechanisms also contribute to the increase in lactate, including increased glycolysis, impaired lactate clearance, and activation of inflammatory cells that shift cellular metabolism toward lactate production.^2,3

The normal range for venous plasma lactate in adults is 0.5 to 2.2 mM, although the normal range may vary because of differences in local laboratory methods. Arterial, capillary, and venous lactate are all highly positively correlated.⁴ Venous lactate concentrations between 2.3 and 3.9 mM are suggestive of mild physiologic dysfunction, and values ≥4.0 mM are consistent with severe physiologic dysfunction. In hospitalized patients, sepsis is one of the most common causes of a lactate level ≥4 mM.⁵

In many patients with an elevated lactate concentration the anion gap is also increased—but this is not always the case. In fact, in one large observational study, among patients with sepsis and a lactate concentration ≥4 mM, approximately 25% had a normal bicarbonate level and normal anion gap.⁶

Elevated lactate levels applied in obstetric and gynecologic practice

CASE 1. Obstetric practice: Hernia identified during labor

A 30-year-old woman (G1P0) presents in early labor at 37 weeks’ gestation. Two years prior to the pregnancy she had a Roux-en-Y gastric bypass and lost more than 100 lb. In addition to reporting lower abdominal pain occurring during contractions, she reports the new onset of mid-epigastric pain. A surgical consult is requested. The initial white blood cell count is 6,290 per uL, and the lactate level is 1.0 mM.

The surgeon consulted orders a computed tomography (CT) scan with oral contrast, but the patient has difficulty retaining the oral contrast due to her nausea, delaying the performance of the CT scan. Three hours following admission a follow-up lactate measurement is 3.3 mM, and an emergency CT scan is performed.

The CT scan shows an internal hernia with swirling of the mesenteric vessels and twisting of the small bowel mesentery. An urgent cesarean delivery and repair of the internal hernia is performed.

The patient and her newborn do well postoperatively. The postoperative lactate level is 0.8 mM.

In pregnant women with a past history of a Roux-en-Y gastric bypass and abdominal discomfort who are in labor it is challenging to rapidly diagnose internal hernias and other bowel problems.⁷⁻⁹ In this case, the increased lactate level from 1.0 mM to 3.3 mM raised concern for ischemic bowel and triggered the emergency CT and urgent exploratory laparotomy and cesarean delivery.

Up to 14% of maternal deaths in the United States are due to infection.¹⁰ In many of these cases, there is a delay in sepsis recognition because previously healthy pregnant women with sepsis may not manifest classic signs such as fever, hypotension, or mental status changes until late in the disease course. Measurement of lactate can facilitate the early recognition of severe sepsis in pregnant women, thereby accelerating and focusing their treatment.¹¹

To reduce mortality due to sepsis, aggressive intervention needs to occur within the first 6 hours following the onset of the infection.

CASE 2. Gynecologic practice: Bacterial infection identified in the presence of abdominal pain and vomiting

A 40-year-old woman presents to the ED 5 days following a myomectomy, with nausea, vomiting, and abdominal pain. Her vital signs reveal: temperature, 98.4°F (36.9°C); heart rate, 122 bpm; blood pressure, 115/70 mm Hg; and white blood cell count, 6,270 per uL. Her lactate level is 4.0 mM. She is admitted to the ICU with a presumptive diagnosis of severe sepsis and treatment with broad-spectrum antibiotics is initiated. Twenty-four hours following admission, gram-negative rods are identified in blood cultures that are later identified to be Bacteroides fragilis.

For the past 2 decades there has been a concerted national effort to reduce mortality caused by sepsis through early diagnosis and aggressive treatment of sepsis in an ICU setting. Observational studies have reported that an elevated lactate level is an excellent early biomarker for sepsis and may be observed prior to the onset of fever, elevated white blood cell count, or hypotension.⁶ For example, in one large study of patients with sepsis and a lactate measurement ≥4 mM, only 50% of patients had a systolic blood pressure <90 mm Hg.

Elevated lactate levels also are associated with an increased risk of death. Among 13,932 consecutive patients admitted to an ICU in Alberta, Canada, the mortality rate among patients with a venous or arterial lactate >2 mM was 20%, compared with a mortality rate of 5% for patients with a lactate level ≤2 mM.¹² In a study of 1,278 patients with infection admitted to the hospital from the ED, mortality increased as baseline lactate concentration rose. For lactate concentrations of 0 to 2.4, 2.5 to 3.9, and ≥4.0 mM, mortality rates were 5%, 9%, and 28%, respectively.¹³

In patients with sepsis, serial measurement of lactate can help to guide treatment. In a randomized trial, 348 patients admitted to an ICU with a lactate ≥3 mM were randomly assigned to standard treatment, in which the clinicians had no knowledge of patients’ lactate levels, or to an experimental group, in which the clinicians were provided lactate measurement results every 2 hours. Compared with clinicians in the control group, the clinicians with access to frequent lactate measurements administered more fluids and vasodilators to their patients. Compared with patients in the control group, the hospital mortality rate was lower when the clinicians had access to frequent lactate measurements (34% vs 44%, respectively; adjusted hazard ratio, 0.61; 95% confidence interval, 0.43−0.87; P = .0006).¹⁴

Elevated lactate levels in the fetus and newborn

The physiologic status of the newborn is routinely assessed with the Apgar score. Umbilical artery and venous blood gases, including measurement of pH, are often used as a corroborating biomarker. Most studies report that umbilical artery or vein lactate measurement is as useful as a pH measurement in assessing newborn physiologic status. The normal range of lactate in fetuses and newborns is not precisely defined, with values between 3.5 and 7 mM being cited as the upper limit of normal.¹⁵⁻¹⁸

In many countries (but not the United States), in utero fetal status during labor is assessed by fetal scalp sampling of blood and measurement of either pH or lactate. Fetal scalp sampling is difficult and often very little blood is obtained, making it difficult to measure pH. A Cochrane review reported that in 2 randomized trials, fetal scalp sampling produced a successful measurement of lactate in 99% of attempts, while a pH result could only be obtained in 79% of cases due to an inadequate volume of blood or clotted blood.¹⁹

Increased lactate measurement can help our patients

Measuring lactate in order to rapidly identify patients with major physiologic derangements is practiced widely in EDs and ICUs. There is significant opportunity to increase the use of lactate measurement in obstetrics and gynecology. Increasing this use will help to rapidly identify women with severe sepsis and other diseases, leading to more rapid intervention and improved outcomes.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Lactate measurement is widely used in emergency departments (EDs) and intensive care units (ICUs) to facilitate the early diagnosis and management of sepsis, severe trauma, ischemic bowel, and necrotizing fasciitis. Measuring lactate levels is much less commonly utilized in the practice of obstetrics and gynecology; increasing measurement in our practices may improve our early recognition and treatment of women with severe sepsis and other serious diseases.

Lactate physiology

The metabolism of glucose in the Embden-Meyerhof pathway results in the production of pyruvate and the high-energy compounds ATP and NADH. Pyruvate can enter 3 alternative metabolic pathways: 1) the mitochondrial Krebs cycle, 2) conversion to lactate in the cell cytosol, or 3) conversion back to glucose in the process of gluconeogenesis.

Under aerobic conditions, most pyruvate enters the Krebs cycle and little is converted to lactate. Molecular oxygen is an absolute requirement for Krebs cycle activity. Under anaerobic conditions, pyruvate cannot enter the Krebs cycle and is preferentially converted to lactate.¹

An elevated lactate level is a sensitive marker for tissue hypoxia caused by a variety of diseases, including sepsis, trauma, ischemic bowel, and necrotizing fasciitis. With sepsis, additional mechanisms also contribute to the increase in lactate, including increased glycolysis, impaired lactate clearance, and activation of inflammatory cells that shift cellular metabolism toward lactate production.^2,3

The normal range for venous plasma lactate in adults is 0.5 to 2.2 mM, although the normal range may vary because of differences in local laboratory methods. Arterial, capillary, and venous lactate are all highly positively correlated.⁴ Venous lactate concentrations between 2.3 and 3.9 mM are suggestive of mild physiologic dysfunction, and values ≥4.0 mM are consistent with severe physiologic dysfunction. In hospitalized patients, sepsis is one of the most common causes of a lactate level ≥4 mM.⁵

In many patients with an elevated lactate concentration the anion gap is also increased—but this is not always the case. In fact, in one large observational study, among patients with sepsis and a lactate concentration ≥4 mM, approximately 25% had a normal bicarbonate level and normal anion gap.⁶

Elevated lactate levels applied in obstetric and gynecologic practice

CASE 1. Obstetric practice: Hernia identified during labor

A 30-year-old woman (G1P0) presents in early labor at 37 weeks’ gestation. Two years prior to the pregnancy she had a Roux-en-Y gastric bypass and lost more than 100 lb. In addition to reporting lower abdominal pain occurring during contractions, she reports the new onset of mid-epigastric pain. A surgical consult is requested. The initial white blood cell count is 6,290 per uL, and the lactate level is 1.0 mM.

The surgeon consulted orders a computed tomography (CT) scan with oral contrast, but the patient has difficulty retaining the oral contrast due to her nausea, delaying the performance of the CT scan. Three hours following admission a follow-up lactate measurement is 3.3 mM, and an emergency CT scan is performed.

The CT scan shows an internal hernia with swirling of the mesenteric vessels and twisting of the small bowel mesentery. An urgent cesarean delivery and repair of the internal hernia is performed.

The patient and her newborn do well postoperatively. The postoperative lactate level is 0.8 mM.

In pregnant women with a past history of a Roux-en-Y gastric bypass and abdominal discomfort who are in labor it is challenging to rapidly diagnose internal hernias and other bowel problems.⁷⁻⁹ In this case, the increased lactate level from 1.0 mM to 3.3 mM raised concern for ischemic bowel and triggered the emergency CT and urgent exploratory laparotomy and cesarean delivery.

Up to 14% of maternal deaths in the United States are due to infection.¹⁰ In many of these cases, there is a delay in sepsis recognition because previously healthy pregnant women with sepsis may not manifest classic signs such as fever, hypotension, or mental status changes until late in the disease course. Measurement of lactate can facilitate the early recognition of severe sepsis in pregnant women, thereby accelerating and focusing their treatment.¹¹

To reduce mortality due to sepsis, aggressive intervention needs to occur within the first 6 hours following the onset of the infection.

CASE 2. Gynecologic practice: Bacterial infection identified in the presence of abdominal pain and vomiting

A 40-year-old woman presents to the ED 5 days following a myomectomy, with nausea, vomiting, and abdominal pain. Her vital signs reveal: temperature, 98.4°F (36.9°C); heart rate, 122 bpm; blood pressure, 115/70 mm Hg; and white blood cell count, 6,270 per uL. Her lactate level is 4.0 mM. She is admitted to the ICU with a presumptive diagnosis of severe sepsis and treatment with broad-spectrum antibiotics is initiated. Twenty-four hours following admission, gram-negative rods are identified in blood cultures that are later identified to be Bacteroides fragilis.

For the past 2 decades there has been a concerted national effort to reduce mortality caused by sepsis through early diagnosis and aggressive treatment of sepsis in an ICU setting. Observational studies have reported that an elevated lactate level is an excellent early biomarker for sepsis and may be observed prior to the onset of fever, elevated white blood cell count, or hypotension.⁶ For example, in one large study of patients with sepsis and a lactate measurement ≥4 mM, only 50% of patients had a systolic blood pressure <90 mm Hg.

Elevated lactate levels also are associated with an increased risk of death. Among 13,932 consecutive patients admitted to an ICU in Alberta, Canada, the mortality rate among patients with a venous or arterial lactate >2 mM was 20%, compared with a mortality rate of 5% for patients with a lactate level ≤2 mM.¹² In a study of 1,278 patients with infection admitted to the hospital from the ED, mortality increased as baseline lactate concentration rose. For lactate concentrations of 0 to 2.4, 2.5 to 3.9, and ≥4.0 mM, mortality rates were 5%, 9%, and 28%, respectively.¹³

In patients with sepsis, serial measurement of lactate can help to guide treatment. In a randomized trial, 348 patients admitted to an ICU with a lactate ≥3 mM were randomly assigned to standard treatment, in which the clinicians had no knowledge of patients’ lactate levels, or to an experimental group, in which the clinicians were provided lactate measurement results every 2 hours. Compared with clinicians in the control group, the clinicians with access to frequent lactate measurements administered more fluids and vasodilators to their patients. Compared with patients in the control group, the hospital mortality rate was lower when the clinicians had access to frequent lactate measurements (34% vs 44%, respectively; adjusted hazard ratio, 0.61; 95% confidence interval, 0.43−0.87; P = .0006).¹⁴

Elevated lactate levels in the fetus and newborn

The physiologic status of the newborn is routinely assessed with the Apgar score. Umbilical artery and venous blood gases, including measurement of pH, are often used as a corroborating biomarker. Most studies report that umbilical artery or vein lactate measurement is as useful as a pH measurement in assessing newborn physiologic status. The normal range of lactate in fetuses and newborns is not precisely defined, with values between 3.5 and 7 mM being cited as the upper limit of normal.¹⁵⁻¹⁸

In many countries (but not the United States), in utero fetal status during labor is assessed by fetal scalp sampling of blood and measurement of either pH or lactate. Fetal scalp sampling is difficult and often very little blood is obtained, making it difficult to measure pH. A Cochrane review reported that in 2 randomized trials, fetal scalp sampling produced a successful measurement of lactate in 99% of attempts, while a pH result could only be obtained in 79% of cases due to an inadequate volume of blood or clotted blood.¹⁹

Increased lactate measurement can help our patients

Measuring lactate in order to rapidly identify patients with major physiologic derangements is practiced widely in EDs and ICUs. There is significant opportunity to increase the use of lactate measurement in obstetrics and gynecology. Increasing this use will help to rapidly identify women with severe sepsis and other diseases, leading to more rapid intervention and improved outcomes.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

As 2016 winds down, we are already gearing up for the 2019 implementation of the Medicare Access and CHIP Reauthorization Act, or MACRA. The bipartisan 2015 legislation will replace the current sustainable growth rate as well as streamline the existing quality reporting programs and redirect us from the current volume-based Medicare payments to value- and performance-based payments. On page 394 of this issue, two community- based colleagues, JCSO Editor Dr Linda Bosserman and Dr Robin Zon, a community oncologist and chair of the American Society of Clinical Oncology’s Task Force on Clinical Pathways, discuss the ins and outs of MACRA – what it is, what it replaces, how it will work, and what we need to be doing to prepare for its implementation in 2019.

Click on the PDF icon at the top of this introduction to read the full article.

As 2016 winds down, we are already gearing up for the 2019 implementation of the Medicare Access and CHIP Reauthorization Act, or MACRA. The bipartisan 2015 legislation will replace the current sustainable growth rate as well as streamline the existing quality reporting programs and redirect us from the current volume-based Medicare payments to value- and performance-based payments. On page 394 of this issue, two community- based colleagues, JCSO Editor Dr Linda Bosserman and Dr Robin Zon, a community oncologist and chair of the American Society of Clinical Oncology’s Task Force on Clinical Pathways, discuss the ins and outs of MACRA – what it is, what it replaces, how it will work, and what we need to be doing to prepare for its implementation in 2019.

Click on the PDF icon at the top of this introduction to read the full article.

As 2016 winds down, we are already gearing up for the 2019 implementation of the Medicare Access and CHIP Reauthorization Act, or MACRA. The bipartisan 2015 legislation will replace the current sustainable growth rate as well as streamline the existing quality reporting programs and redirect us from the current volume-based Medicare payments to value- and performance-based payments. On page 394 of this issue, two community- based colleagues, JCSO Editor Dr Linda Bosserman and Dr Robin Zon, a community oncologist and chair of the American Society of Clinical Oncology’s Task Force on Clinical Pathways, discuss the ins and outs of MACRA – what it is, what it replaces, how it will work, and what we need to be doing to prepare for its implementation in 2019.

Click on the PDF icon at the top of this introduction to read the full article.

Predicting the future has been a favorite topic of surgeons through the ages for addresses to august surgical societies.

Confident predictions of the future of surgery, however, have not always stood the test of time. Speaking at the University of Manchester’s Centenary celebration in 1973 at an international symposium on “Medicine in the 21st Century,” the noted surgeon J. Englebert Dunphy correctly predicted the prominence of joint-replacement procedures, but incorrectly asserted that medical advances would virtually eliminate the need for cholecystectomy through dissolution of gallstones and the need for surgical approaches to atherosclerosis through plaque prevention and dissolution. He accurately predicted that infections and sepsis would remain serious problems. But he missed the mark when he predicted that surgical pain would be eliminated by a pill that would block somatic nerve impulses without any respiratory or circulatory effects (Surgery. 1974 Mar;75:332-7). Technologic advances such as laparoscopic cholecystectomy, which emerged less than 20 years into the future, were not on his radar screen.

Change and disruptive technology

To be sure, the surgical procedures and methods have changed markedly since the time I trained in surgery in the 1970s. The most obvious change is the shift from large incisions to small ones, with the commensurate quick recovery and short hospital stays. This change is primarily because of the emergence of disruptive technology, a concept that has pervaded every avenue of our current lives, not just surgery: Think Uber, robotics in industry, the Internet, smartphones, and the miniaturization of just about every communication means. In medicine, these disruptive technologies have led to the emergence of the electronic health record, new imaging modalities, percutaneous interventional techniques, fiber optic endoscopy, laparoscopy, and endovascular surgery.

Maintaining capacity to do infrequent operations

During my training, H₂ receptor antagonists and Helicobacter pylori came on the scene, with the result that ulcer operations almost disappeared from our surgical armamentarium; one of my most frequent operations as a senior and chief resident has become a rarity 40 years later for our trainees. And yet, a general surgeon must know how to perform an ulcer operation and which type is the best for a given circumstance, since perforated and bleeding ulcers are still seen, if infrequently. The perforated ulcer is seen most often in patients with multiple comorbidities who can least tolerate a complication and need one effective and well-executed operation if they are going to survive. How do we continue to teach residents these procedures when they have become infrequent?

There is perhaps some utility in keeping some aging surgeons around to teach residents on fresh cadavers, or to call them out of their assisted living facilities when needed for consultation! Now that the majority of operations in most places are being performed by minimally invasive surgical (MIS) methods, we may not need MIS fellowships or training much longer for trainees to become proficient in these skills, because it is the open operations that are less frequent. Our chief residents are much less secure about performing an open cholecystectomy, of which they have performed perhaps 5, than they are about performing laparoscopic cholecystectomy, of which they have performed 105.

Technologies on the verge of disrupting

Mark Aeder, MD, FACS, recently asked an important question in the ACS Communities thread on the future of surgery: What will the future disruptive innovations be? Which areas of surgery will bloom next?

There are many game-changing emerging technologies that could well turn out to be future “disruptors” of surgery as we know it. Cancer surgery is on track to be transformed by the development of genomics and personalized medicine and immunotherapy for melanoma and lung cancer.

The areas most likely to remain in the surgical realm are trauma, infections, and inflammation. Though safer cars, seatbelt laws, and helmet laws for motorcyclists have already decreased motor vehicle accidents and injury severity, we have still not produced a cure for stupidity or bad luck. Traumatic injuries will always be with us, and surgeons well trained in trauma management will continue to be needed. Appendicitis, cholecystitis, and diverticulitis will continue to require operations, even though inroads have begun with the studies showing success of antibiotic treatment for appendicitis and diverticulitis.

Keep current, avoid bandwagons

The key lesson, not only for our young surgeons-in-training but also for our seasoned surgeons, is to keep learning, keep networking, and keep adopting new techniques as soon as they show true evidence of success.

The best way for surgeons to remain prepared for whatever the future will bring is to stay current with innovations coming on the scene but not jump on the bandwagon too early and adopt new fads without substantial evidence of their soundness. A few retrospective case series reporting success with a new operation is insufficient evidence to try it out on the unsuspecting public. Although the completion of well-designed randomized trials with adequate follow-up takes time, it is better to stick with well-established and evidence-based techniques than rush to embrace an inadequately vetted procedure that may end up harming a patient.

Not all innovative devices or procedures rise to the level of being so truly “experimental” that they would require an institutional review board, and this ought to prompt an extra measure of caution by surgeons. Some “innovations,” such as the endobariatric devices reported elsewhere in this issue, represent novel variations of previous procedures but are as yet unvalidated by long-term studies. Responsible adoption of these novel procedures requires a full disclosure to the patient that the procedure or device is novel, without long-term evidence of success, and may entail unknown risks. Don’t let your enthusiasm to be an early adopter overcome your scientific and historic obligation to prevent harm to the patient.

Dr. Deveney is professor of surgery and vice chair of education in the department of surgery, Oregon Health & Science University, Portland. She is the co-Editor of ACS Surgery News.

Predicting the future has been a favorite topic of surgeons through the ages for addresses to august surgical societies.

Confident predictions of the future of surgery, however, have not always stood the test of time. Speaking at the University of Manchester’s Centenary celebration in 1973 at an international symposium on “Medicine in the 21st Century,” the noted surgeon J. Englebert Dunphy correctly predicted the prominence of joint-replacement procedures, but incorrectly asserted that medical advances would virtually eliminate the need for cholecystectomy through dissolution of gallstones and the need for surgical approaches to atherosclerosis through plaque prevention and dissolution. He accurately predicted that infections and sepsis would remain serious problems. But he missed the mark when he predicted that surgical pain would be eliminated by a pill that would block somatic nerve impulses without any respiratory or circulatory effects (Surgery. 1974 Mar;75:332-7). Technologic advances such as laparoscopic cholecystectomy, which emerged less than 20 years into the future, were not on his radar screen.

Change and disruptive technology

To be sure, the surgical procedures and methods have changed markedly since the time I trained in surgery in the 1970s. The most obvious change is the shift from large incisions to small ones, with the commensurate quick recovery and short hospital stays. This change is primarily because of the emergence of disruptive technology, a concept that has pervaded every avenue of our current lives, not just surgery: Think Uber, robotics in industry, the Internet, smartphones, and the miniaturization of just about every communication means. In medicine, these disruptive technologies have led to the emergence of the electronic health record, new imaging modalities, percutaneous interventional techniques, fiber optic endoscopy, laparoscopy, and endovascular surgery.

Maintaining capacity to do infrequent operations

During my training, H₂ receptor antagonists and Helicobacter pylori came on the scene, with the result that ulcer operations almost disappeared from our surgical armamentarium; one of my most frequent operations as a senior and chief resident has become a rarity 40 years later for our trainees. And yet, a general surgeon must know how to perform an ulcer operation and which type is the best for a given circumstance, since perforated and bleeding ulcers are still seen, if infrequently. The perforated ulcer is seen most often in patients with multiple comorbidities who can least tolerate a complication and need one effective and well-executed operation if they are going to survive. How do we continue to teach residents these procedures when they have become infrequent?

There is perhaps some utility in keeping some aging surgeons around to teach residents on fresh cadavers, or to call them out of their assisted living facilities when needed for consultation! Now that the majority of operations in most places are being performed by minimally invasive surgical (MIS) methods, we may not need MIS fellowships or training much longer for trainees to become proficient in these skills, because it is the open operations that are less frequent. Our chief residents are much less secure about performing an open cholecystectomy, of which they have performed perhaps 5, than they are about performing laparoscopic cholecystectomy, of which they have performed 105.

Technologies on the verge of disrupting

Mark Aeder, MD, FACS, recently asked an important question in the ACS Communities thread on the future of surgery: What will the future disruptive innovations be? Which areas of surgery will bloom next?

There are many game-changing emerging technologies that could well turn out to be future “disruptors” of surgery as we know it. Cancer surgery is on track to be transformed by the development of genomics and personalized medicine and immunotherapy for melanoma and lung cancer.

The areas most likely to remain in the surgical realm are trauma, infections, and inflammation. Though safer cars, seatbelt laws, and helmet laws for motorcyclists have already decreased motor vehicle accidents and injury severity, we have still not produced a cure for stupidity or bad luck. Traumatic injuries will always be with us, and surgeons well trained in trauma management will continue to be needed. Appendicitis, cholecystitis, and diverticulitis will continue to require operations, even though inroads have begun with the studies showing success of antibiotic treatment for appendicitis and diverticulitis.

Keep current, avoid bandwagons

The key lesson, not only for our young surgeons-in-training but also for our seasoned surgeons, is to keep learning, keep networking, and keep adopting new techniques as soon as they show true evidence of success.

The best way for surgeons to remain prepared for whatever the future will bring is to stay current with innovations coming on the scene but not jump on the bandwagon too early and adopt new fads without substantial evidence of their soundness. A few retrospective case series reporting success with a new operation is insufficient evidence to try it out on the unsuspecting public. Although the completion of well-designed randomized trials with adequate follow-up takes time, it is better to stick with well-established and evidence-based techniques than rush to embrace an inadequately vetted procedure that may end up harming a patient.

Not all innovative devices or procedures rise to the level of being so truly “experimental” that they would require an institutional review board, and this ought to prompt an extra measure of caution by surgeons. Some “innovations,” such as the endobariatric devices reported elsewhere in this issue, represent novel variations of previous procedures but are as yet unvalidated by long-term studies. Responsible adoption of these novel procedures requires a full disclosure to the patient that the procedure or device is novel, without long-term evidence of success, and may entail unknown risks. Don’t let your enthusiasm to be an early adopter overcome your scientific and historic obligation to prevent harm to the patient.

Dr. Deveney is professor of surgery and vice chair of education in the department of surgery, Oregon Health & Science University, Portland. She is the co-Editor of ACS Surgery News.

Predicting the future has been a favorite topic of surgeons through the ages for addresses to august surgical societies.

Confident predictions of the future of surgery, however, have not always stood the test of time. Speaking at the University of Manchester’s Centenary celebration in 1973 at an international symposium on “Medicine in the 21st Century,” the noted surgeon J. Englebert Dunphy correctly predicted the prominence of joint-replacement procedures, but incorrectly asserted that medical advances would virtually eliminate the need for cholecystectomy through dissolution of gallstones and the need for surgical approaches to atherosclerosis through plaque prevention and dissolution. He accurately predicted that infections and sepsis would remain serious problems. But he missed the mark when he predicted that surgical pain would be eliminated by a pill that would block somatic nerve impulses without any respiratory or circulatory effects (Surgery. 1974 Mar;75:332-7). Technologic advances such as laparoscopic cholecystectomy, which emerged less than 20 years into the future, were not on his radar screen.

Change and disruptive technology

To be sure, the surgical procedures and methods have changed markedly since the time I trained in surgery in the 1970s. The most obvious change is the shift from large incisions to small ones, with the commensurate quick recovery and short hospital stays. This change is primarily because of the emergence of disruptive technology, a concept that has pervaded every avenue of our current lives, not just surgery: Think Uber, robotics in industry, the Internet, smartphones, and the miniaturization of just about every communication means. In medicine, these disruptive technologies have led to the emergence of the electronic health record, new imaging modalities, percutaneous interventional techniques, fiber optic endoscopy, laparoscopy, and endovascular surgery.

Maintaining capacity to do infrequent operations

During my training, H₂ receptor antagonists and Helicobacter pylori came on the scene, with the result that ulcer operations almost disappeared from our surgical armamentarium; one of my most frequent operations as a senior and chief resident has become a rarity 40 years later for our trainees. And yet, a general surgeon must know how to perform an ulcer operation and which type is the best for a given circumstance, since perforated and bleeding ulcers are still seen, if infrequently. The perforated ulcer is seen most often in patients with multiple comorbidities who can least tolerate a complication and need one effective and well-executed operation if they are going to survive. How do we continue to teach residents these procedures when they have become infrequent?

There is perhaps some utility in keeping some aging surgeons around to teach residents on fresh cadavers, or to call them out of their assisted living facilities when needed for consultation! Now that the majority of operations in most places are being performed by minimally invasive surgical (MIS) methods, we may not need MIS fellowships or training much longer for trainees to become proficient in these skills, because it is the open operations that are less frequent. Our chief residents are much less secure about performing an open cholecystectomy, of which they have performed perhaps 5, than they are about performing laparoscopic cholecystectomy, of which they have performed 105.

Technologies on the verge of disrupting

Mark Aeder, MD, FACS, recently asked an important question in the ACS Communities thread on the future of surgery: What will the future disruptive innovations be? Which areas of surgery will bloom next?

There are many game-changing emerging technologies that could well turn out to be future “disruptors” of surgery as we know it. Cancer surgery is on track to be transformed by the development of genomics and personalized medicine and immunotherapy for melanoma and lung cancer.

The areas most likely to remain in the surgical realm are trauma, infections, and inflammation. Though safer cars, seatbelt laws, and helmet laws for motorcyclists have already decreased motor vehicle accidents and injury severity, we have still not produced a cure for stupidity or bad luck. Traumatic injuries will always be with us, and surgeons well trained in trauma management will continue to be needed. Appendicitis, cholecystitis, and diverticulitis will continue to require operations, even though inroads have begun with the studies showing success of antibiotic treatment for appendicitis and diverticulitis.

Keep current, avoid bandwagons

The key lesson, not only for our young surgeons-in-training but also for our seasoned surgeons, is to keep learning, keep networking, and keep adopting new techniques as soon as they show true evidence of success.

The best way for surgeons to remain prepared for whatever the future will bring is to stay current with innovations coming on the scene but not jump on the bandwagon too early and adopt new fads without substantial evidence of their soundness. A few retrospective case series reporting success with a new operation is insufficient evidence to try it out on the unsuspecting public. Although the completion of well-designed randomized trials with adequate follow-up takes time, it is better to stick with well-established and evidence-based techniques than rush to embrace an inadequately vetted procedure that may end up harming a patient.

Not all innovative devices or procedures rise to the level of being so truly “experimental” that they would require an institutional review board, and this ought to prompt an extra measure of caution by surgeons. Some “innovations,” such as the endobariatric devices reported elsewhere in this issue, represent novel variations of previous procedures but are as yet unvalidated by long-term studies. Responsible adoption of these novel procedures requires a full disclosure to the patient that the procedure or device is novel, without long-term evidence of success, and may entail unknown risks. Don’t let your enthusiasm to be an early adopter overcome your scientific and historic obligation to prevent harm to the patient.

Dr. Deveney is professor of surgery and vice chair of education in the department of surgery, Oregon Health & Science University, Portland. She is the co-Editor of ACS Surgery News.

The dilemma of a diminishing workforce pool might seem more the province of medical school deans, psychiatry department chairs, and psychiatry residency training directors, but our ability to recruit and retain psychiatrists is, in reality, everyone’s concern—including hospitals, clinics, and, especially, patients and their families. Even without knowledge of the specialty or any numerical appraisal, for example, it is common knowledge that we have a dire shortage of child and adolescent and geriatric psychiatrists—a topic of widespread interest and great consequence for access to mental health care.

Tracking a decline

The very title of a recent provocative paper¹ in Health Affairs says it all: “Population of US practicing psychiatrists declined 2003-13, which may help explain poor access to mental health care.” In an elegant analysis, the authors expose (1) a 10% decline in the number of psychiatrists for every 100,000 people and (2) wide regional variability in the availability of psychiatrists. In stark contrast, the number of neurologists increased by >15% and the primary care workforce remained stable, with a 1.3% increase in the number of physicians, over the same 10 years.

At the beginning of the psychiatry workforce pipeline, the number of medical students who choose psychiatry remains both small (typically, slightly more than 4% of graduating students) and remarkably stable over time. Wilbanks et al,² in a thoughtful analysis of the 2011 to 2013 Medical School Graduation Questionnaire of the Association of American Medical Colleges, affirm and, in part, explain this consistent pattern. They note that the 4 most important considerations among students who select psychiatry are:

• personality fit
• specialty content
• work–life balance
• role model influences.

Some of these considerations also overlap with those of students in other specialties; the authors also note that older medical students and women are more likely to choose psychiatry.

Here is what we must do to erase the shortage

It does appear that, despite scientific advances in brain and behavior, expanding therapeutic options, and unique patient interactions that, taken together, should make a career in psychiatry exciting and appealing, there are simply not enough of us to meet the population’s mental health needs. This is a serious problem. It is our professional obligation—all of us—that we take on this shortage and develop solutions to it.

At its zenith, only about 7% of medical students chose psychiatry. We need to proactively prime the pump for our specialty by encouraging more observerships and promoting mental health careers through community outreach to high school students.

We must be diligent and effective mentors to medical students; mentorship is a powerful catalyst for career decision-making.

We need to make psychiatry clerkships exciting, to show off the best of what our specialty has to offer, and to cultivate sustained interest among our students in the brain and its psychiatric disorders.

We need to highlight the momentous advances in knowledge, biology, and treatments that now characterize our psychiatric profession. We need to advocate for more of these accomplishments.

We must be public stigma-busters! (Our patients need us to do this, too.)

And there is more to do:

Collaborate. In delivering psychiatric health care, we need to expand our effectiveness to achieve more collaboration, greater extension of effect, and broader outreach. Collaborative care has come of age as a delivery model; it should be embraced more broadly. We need to continue our efforts to bridge the many sister mental health disciplines—psychology, nursing, social work, counseling—that collectively provide mental health care.

Unite. Given the inadequate workforce numbers and enormous need, we will diminish ourselves by “guild infighting” and, consequently, weaken our legislative advocacy and leverage. We need to embrace and support all medical specialties and have them support us as well. We need to grow closer to primary care and support this specialty as the true front line of mental health. We also need to bridge the gap between addiction medicine and psychiatry, especially given the high level of addiction comorbidity in many psychiatric disorders.

Foster innovation. The deficit of psychiatric workers might be buffered by innovations in how we leverage our expertise. Telepsychiatry, for example, is clearly advancing, and brings psychiatry to remote areas where psychiatrists are scarce. Mobile health also has great potential for mental health. As one of us (H.A.N.) highlighted recently,³ as genetics become more molecular, what has been the potential of clinically applicable pharmacogenomics might become reality. Psychiatry needs to make progress toward personalized medicine because the disorders we treat are extremely heterogeneous in their etiology, phenomenology, treatment response, and outcomes.

The appeal of working with mind and brain

The extent to which we can convey unfettered optimism about the role of psychiatry in medicine and the relentless progress in neurobiological research, together, will go a long way toward attracting the best and brightest newly minted physicians to our specialty. The brain is the last frontier in medicine; psychiatry is intimately tethered to its unfolding complexity. With millennials placing a higher premium on work–life issues, the enviable balance and quality of life of a psychiatric career might now be particularly opportune, enhancing the quantity and quality of professionals that we can attract to psychiatry.
 

The dilemma of a diminishing workforce pool might seem more the province of medical school deans, psychiatry department chairs, and psychiatry residency training directors, but our ability to recruit and retain psychiatrists is, in reality, everyone’s concern—including hospitals, clinics, and, especially, patients and their families. Even without knowledge of the specialty or any numerical appraisal, for example, it is common knowledge that we have a dire shortage of child and adolescent and geriatric psychiatrists—a topic of widespread interest and great consequence for access to mental health care.

Tracking a decline

The very title of a recent provocative paper¹ in Health Affairs says it all: “Population of US practicing psychiatrists declined 2003-13, which may help explain poor access to mental health care.” In an elegant analysis, the authors expose (1) a 10% decline in the number of psychiatrists for every 100,000 people and (2) wide regional variability in the availability of psychiatrists. In stark contrast, the number of neurologists increased by >15% and the primary care workforce remained stable, with a 1.3% increase in the number of physicians, over the same 10 years.

At the beginning of the psychiatry workforce pipeline, the number of medical students who choose psychiatry remains both small (typically, slightly more than 4% of graduating students) and remarkably stable over time. Wilbanks et al,² in a thoughtful analysis of the 2011 to 2013 Medical School Graduation Questionnaire of the Association of American Medical Colleges, affirm and, in part, explain this consistent pattern. They note that the 4 most important considerations among students who select psychiatry are:

• personality fit
• specialty content
• work–life balance
• role model influences.

Some of these considerations also overlap with those of students in other specialties; the authors also note that older medical students and women are more likely to choose psychiatry.

Here is what we must do to erase the shortage

It does appear that, despite scientific advances in brain and behavior, expanding therapeutic options, and unique patient interactions that, taken together, should make a career in psychiatry exciting and appealing, there are simply not enough of us to meet the population’s mental health needs. This is a serious problem. It is our professional obligation—all of us—that we take on this shortage and develop solutions to it.

At its zenith, only about 7% of medical students chose psychiatry. We need to proactively prime the pump for our specialty by encouraging more observerships and promoting mental health careers through community outreach to high school students.

We must be diligent and effective mentors to medical students; mentorship is a powerful catalyst for career decision-making.

We need to make psychiatry clerkships exciting, to show off the best of what our specialty has to offer, and to cultivate sustained interest among our students in the brain and its psychiatric disorders.

We need to highlight the momentous advances in knowledge, biology, and treatments that now characterize our psychiatric profession. We need to advocate for more of these accomplishments.

We must be public stigma-busters! (Our patients need us to do this, too.)

And there is more to do:

Collaborate. In delivering psychiatric health care, we need to expand our effectiveness to achieve more collaboration, greater extension of effect, and broader outreach. Collaborative care has come of age as a delivery model; it should be embraced more broadly. We need to continue our efforts to bridge the many sister mental health disciplines—psychology, nursing, social work, counseling—that collectively provide mental health care.

Unite. Given the inadequate workforce numbers and enormous need, we will diminish ourselves by “guild infighting” and, consequently, weaken our legislative advocacy and leverage. We need to embrace and support all medical specialties and have them support us as well. We need to grow closer to primary care and support this specialty as the true front line of mental health. We also need to bridge the gap between addiction medicine and psychiatry, especially given the high level of addiction comorbidity in many psychiatric disorders.

Foster innovation. The deficit of psychiatric workers might be buffered by innovations in how we leverage our expertise. Telepsychiatry, for example, is clearly advancing, and brings psychiatry to remote areas where psychiatrists are scarce. Mobile health also has great potential for mental health. As one of us (H.A.N.) highlighted recently,³ as genetics become more molecular, what has been the potential of clinically applicable pharmacogenomics might become reality. Psychiatry needs to make progress toward personalized medicine because the disorders we treat are extremely heterogeneous in their etiology, phenomenology, treatment response, and outcomes.

The appeal of working with mind and brain

The extent to which we can convey unfettered optimism about the role of psychiatry in medicine and the relentless progress in neurobiological research, together, will go a long way toward attracting the best and brightest newly minted physicians to our specialty. The brain is the last frontier in medicine; psychiatry is intimately tethered to its unfolding complexity. With millennials placing a higher premium on work–life issues, the enviable balance and quality of life of a psychiatric career might now be particularly opportune, enhancing the quantity and quality of professionals that we can attract to psychiatry.
 

The dilemma of a diminishing workforce pool might seem more the province of medical school deans, psychiatry department chairs, and psychiatry residency training directors, but our ability to recruit and retain psychiatrists is, in reality, everyone’s concern—including hospitals, clinics, and, especially, patients and their families. Even without knowledge of the specialty or any numerical appraisal, for example, it is common knowledge that we have a dire shortage of child and adolescent and geriatric psychiatrists—a topic of widespread interest and great consequence for access to mental health care.

Tracking a decline

The very title of a recent provocative paper¹ in Health Affairs says it all: “Population of US practicing psychiatrists declined 2003-13, which may help explain poor access to mental health care.” In an elegant analysis, the authors expose (1) a 10% decline in the number of psychiatrists for every 100,000 people and (2) wide regional variability in the availability of psychiatrists. In stark contrast, the number of neurologists increased by >15% and the primary care workforce remained stable, with a 1.3% increase in the number of physicians, over the same 10 years.

At the beginning of the psychiatry workforce pipeline, the number of medical students who choose psychiatry remains both small (typically, slightly more than 4% of graduating students) and remarkably stable over time. Wilbanks et al,² in a thoughtful analysis of the 2011 to 2013 Medical School Graduation Questionnaire of the Association of American Medical Colleges, affirm and, in part, explain this consistent pattern. They note that the 4 most important considerations among students who select psychiatry are:

• personality fit
• specialty content
• work–life balance
• role model influences.

Some of these considerations also overlap with those of students in other specialties; the authors also note that older medical students and women are more likely to choose psychiatry.

Here is what we must do to erase the shortage

It does appear that, despite scientific advances in brain and behavior, expanding therapeutic options, and unique patient interactions that, taken together, should make a career in psychiatry exciting and appealing, there are simply not enough of us to meet the population’s mental health needs. This is a serious problem. It is our professional obligation—all of us—that we take on this shortage and develop solutions to it.

At its zenith, only about 7% of medical students chose psychiatry. We need to proactively prime the pump for our specialty by encouraging more observerships and promoting mental health careers through community outreach to high school students.

We must be diligent and effective mentors to medical students; mentorship is a powerful catalyst for career decision-making.

We need to make psychiatry clerkships exciting, to show off the best of what our specialty has to offer, and to cultivate sustained interest among our students in the brain and its psychiatric disorders.

We need to highlight the momentous advances in knowledge, biology, and treatments that now characterize our psychiatric profession. We need to advocate for more of these accomplishments.

We must be public stigma-busters! (Our patients need us to do this, too.)

And there is more to do:

Collaborate. In delivering psychiatric health care, we need to expand our effectiveness to achieve more collaboration, greater extension of effect, and broader outreach. Collaborative care has come of age as a delivery model; it should be embraced more broadly. We need to continue our efforts to bridge the many sister mental health disciplines—psychology, nursing, social work, counseling—that collectively provide mental health care.

Unite. Given the inadequate workforce numbers and enormous need, we will diminish ourselves by “guild infighting” and, consequently, weaken our legislative advocacy and leverage. We need to embrace and support all medical specialties and have them support us as well. We need to grow closer to primary care and support this specialty as the true front line of mental health. We also need to bridge the gap between addiction medicine and psychiatry, especially given the high level of addiction comorbidity in many psychiatric disorders.

Foster innovation. The deficit of psychiatric workers might be buffered by innovations in how we leverage our expertise. Telepsychiatry, for example, is clearly advancing, and brings psychiatry to remote areas where psychiatrists are scarce. Mobile health also has great potential for mental health. As one of us (H.A.N.) highlighted recently,³ as genetics become more molecular, what has been the potential of clinically applicable pharmacogenomics might become reality. Psychiatry needs to make progress toward personalized medicine because the disorders we treat are extremely heterogeneous in their etiology, phenomenology, treatment response, and outcomes.

The appeal of working with mind and brain

The extent to which we can convey unfettered optimism about the role of psychiatry in medicine and the relentless progress in neurobiological research, together, will go a long way toward attracting the best and brightest newly minted physicians to our specialty. The brain is the last frontier in medicine; psychiatry is intimately tethered to its unfolding complexity. With millennials placing a higher premium on work–life issues, the enviable balance and quality of life of a psychiatric career might now be particularly opportune, enhancing the quantity and quality of professionals that we can attract to psychiatry.