Patients with spastic arm paralysis who received a contralateral C7 nerve graft from their nonparalyzed side to their paralyzed side led to greater improvement in arm function and reduction in spasticity after a year, compared with rehabilitation alone, investigators from Huashan Hospital in China reported online Jan. 3 in the New England Journal of Medicine.

The researchers randomly assigned 36 patients who had unilateral arm paralysis for at least 5 years to either surgical C7 nerve transfer plus rehabilitation or rehabilitation only. Results of the trial’s primary outcome – arm function using the Fugl-Meyer score – showed that those in the surgery group had an average increase of 17.7, while those in the rehabilitation-only group had an average increase of 2.6 (P less than .001). This 15.1-point difference had a 95% confidence interval ranging from 12.2 to 17.9.

To evaluate spasticity, the researchers used the Modified Ashworth Scale, which is a 0-5 scale to score spasticity; a higher score means more spasticity. Surgery patients saw improvement from baseline in all five areas measured across the board, and none saw worsening in scores. The smallest difference between the two groups was in thumb extension, with 15 surgery patients having a 1- and 2-unit improvement and 3 having no change, while 7 controls showed a 1- or 2-unit improvement, another 7 showed no improvement, and 4 had a 1-unit worsening in score (P less than .001). At 1 year, 16 (89%) of surgery patients could accomplish three or more of the functional tasks researchers gave them, whereas none of the controls could.

“The majority of clinical improvements coincided with physiological evidence of connectivity between the hemisphere on the side of the donor nerve and the paralyzed arm,” said lead author Mou-Xiong Zheng, MD, PhD, of the department of hand surgery at Huashan Hospital at Fudan University in Shanghai, and colleagues.

The research by Dr. Zheng and coauthors arises from what is known about hand paralysis after stroke, that damage to the contralateral cerebral hemisphere arises from interruption of the inhibitory activity of upper motor neurons, which causes spasticity, along with hand weakness and loss of fractionated fine motor control. Other studies have noted activity in the cerebral hemisphere on the same side of paralysis during recovery (Neuroimage. 2004;22:1775-83; J Neurophysiol. 2005;93:1209-22; J Neurosci. 2006;26:6096-102; Front Neurol. 2015;6:214), but Dr. Zheng and coauthors noted “sparse” connections between the hand and that part of the brain limit the body’s ability to compensate for spasticity and functional loss.

The latest study followed earlier studies, including one by Dr. Zheng’s coauthors (J Hand Surg Br. 1992;17:518-21), that reported the paralyzed hand could be connected to the unaffected hemisphere by transferring a cervical spine nerve from the nonparalyzed side, a treatment previously reported for injuries of the brachial plexus. Of the five nerves of the brachial plexus, Dr. Zheng and coauthors chose the C7 nerve because it accounts for about 20% of the nerve fibers in the brachial bundle and severing the nerve typically results in transient weakness and numbness in the arm or leg on the same side. Hence, when evaluating the hand on the side of the donor graft, the researchers found no significant changes in power, tactile threshold, or two-point discrimination as a result of surgery.

Their surgical approach was a modification of the C7 nerve transfer method that Dr. Zheng and coauthors had previously reported (Microsurgery. 2011;31:404-8; Neurosurgery. 2015;76:187-95). The operation involved making an incision at the superior aspect of the sternum, mobilizing the donor C7 nerve on the nonparalyzed side, and routing it between the spinal column and esophagus. Then, an anastomosis was performed directly with the C7 nerve on the paralyzed side.

Rehabilitation therapy for both the surgery group and controls was identical, administered four times weekly for 12 months at a single facility, although surgery patients wore an immobilizing cast after their operations.

The nature of the study population – men of varying ages with varying causes of the underlying cerebral lesions – makes it difficult to generalize the findings, Dr. Zheng and coauthors noted. “A larger cohort, followed for a longer period, would be necessary to determine whether cervical nerve transfer results in safe, consistent, and long-term improvements in the function of an arm that is chronically paralyzed as a result of a cerebral lesion,” the authors concluded.

Grants from the following supported the study: National Natural Science Foundation of China; Science and Technology Commission of Shanghai Municipality; Health and Family Planning Commission of Shanghai; and Shanghai Shen-Kang Hospital Development Center. 

SOURCE: Zheng M et al. N Engl J Med. 2018;378:22-34

Patients with spastic arm paralysis who received a contralateral C7 nerve graft from their nonparalyzed side to their paralyzed side led to greater improvement in arm function and reduction in spasticity after a year, compared with rehabilitation alone, investigators from Huashan Hospital in China reported online Jan. 3 in the New England Journal of Medicine.

The researchers randomly assigned 36 patients who had unilateral arm paralysis for at least 5 years to either surgical C7 nerve transfer plus rehabilitation or rehabilitation only. Results of the trial’s primary outcome – arm function using the Fugl-Meyer score – showed that those in the surgery group had an average increase of 17.7, while those in the rehabilitation-only group had an average increase of 2.6 (P less than .001). This 15.1-point difference had a 95% confidence interval ranging from 12.2 to 17.9.

To evaluate spasticity, the researchers used the Modified Ashworth Scale, which is a 0-5 scale to score spasticity; a higher score means more spasticity. Surgery patients saw improvement from baseline in all five areas measured across the board, and none saw worsening in scores. The smallest difference between the two groups was in thumb extension, with 15 surgery patients having a 1- and 2-unit improvement and 3 having no change, while 7 controls showed a 1- or 2-unit improvement, another 7 showed no improvement, and 4 had a 1-unit worsening in score (P less than .001). At 1 year, 16 (89%) of surgery patients could accomplish three or more of the functional tasks researchers gave them, whereas none of the controls could.

“The majority of clinical improvements coincided with physiological evidence of connectivity between the hemisphere on the side of the donor nerve and the paralyzed arm,” said lead author Mou-Xiong Zheng, MD, PhD, of the department of hand surgery at Huashan Hospital at Fudan University in Shanghai, and colleagues.

The research by Dr. Zheng and coauthors arises from what is known about hand paralysis after stroke, that damage to the contralateral cerebral hemisphere arises from interruption of the inhibitory activity of upper motor neurons, which causes spasticity, along with hand weakness and loss of fractionated fine motor control. Other studies have noted activity in the cerebral hemisphere on the same side of paralysis during recovery (Neuroimage. 2004;22:1775-83; J Neurophysiol. 2005;93:1209-22; J Neurosci. 2006;26:6096-102; Front Neurol. 2015;6:214), but Dr. Zheng and coauthors noted “sparse” connections between the hand and that part of the brain limit the body’s ability to compensate for spasticity and functional loss.

The latest study followed earlier studies, including one by Dr. Zheng’s coauthors (J Hand Surg Br. 1992;17:518-21), that reported the paralyzed hand could be connected to the unaffected hemisphere by transferring a cervical spine nerve from the nonparalyzed side, a treatment previously reported for injuries of the brachial plexus. Of the five nerves of the brachial plexus, Dr. Zheng and coauthors chose the C7 nerve because it accounts for about 20% of the nerve fibers in the brachial bundle and severing the nerve typically results in transient weakness and numbness in the arm or leg on the same side. Hence, when evaluating the hand on the side of the donor graft, the researchers found no significant changes in power, tactile threshold, or two-point discrimination as a result of surgery.

Their surgical approach was a modification of the C7 nerve transfer method that Dr. Zheng and coauthors had previously reported (Microsurgery. 2011;31:404-8; Neurosurgery. 2015;76:187-95). The operation involved making an incision at the superior aspect of the sternum, mobilizing the donor C7 nerve on the nonparalyzed side, and routing it between the spinal column and esophagus. Then, an anastomosis was performed directly with the C7 nerve on the paralyzed side.

Rehabilitation therapy for both the surgery group and controls was identical, administered four times weekly for 12 months at a single facility, although surgery patients wore an immobilizing cast after their operations.

The nature of the study population – men of varying ages with varying causes of the underlying cerebral lesions – makes it difficult to generalize the findings, Dr. Zheng and coauthors noted. “A larger cohort, followed for a longer period, would be necessary to determine whether cervical nerve transfer results in safe, consistent, and long-term improvements in the function of an arm that is chronically paralyzed as a result of a cerebral lesion,” the authors concluded.

Grants from the following supported the study: National Natural Science Foundation of China; Science and Technology Commission of Shanghai Municipality; Health and Family Planning Commission of Shanghai; and Shanghai Shen-Kang Hospital Development Center. 

SOURCE: Zheng M et al. N Engl J Med. 2018;378:22-34

Patients with spastic arm paralysis who received a contralateral C7 nerve graft from their nonparalyzed side to their paralyzed side led to greater improvement in arm function and reduction in spasticity after a year, compared with rehabilitation alone, investigators from Huashan Hospital in China reported online Jan. 3 in the New England Journal of Medicine.

The researchers randomly assigned 36 patients who had unilateral arm paralysis for at least 5 years to either surgical C7 nerve transfer plus rehabilitation or rehabilitation only. Results of the trial’s primary outcome – arm function using the Fugl-Meyer score – showed that those in the surgery group had an average increase of 17.7, while those in the rehabilitation-only group had an average increase of 2.6 (P less than .001). This 15.1-point difference had a 95% confidence interval ranging from 12.2 to 17.9.

To evaluate spasticity, the researchers used the Modified Ashworth Scale, which is a 0-5 scale to score spasticity; a higher score means more spasticity. Surgery patients saw improvement from baseline in all five areas measured across the board, and none saw worsening in scores. The smallest difference between the two groups was in thumb extension, with 15 surgery patients having a 1- and 2-unit improvement and 3 having no change, while 7 controls showed a 1- or 2-unit improvement, another 7 showed no improvement, and 4 had a 1-unit worsening in score (P less than .001). At 1 year, 16 (89%) of surgery patients could accomplish three or more of the functional tasks researchers gave them, whereas none of the controls could.

“The majority of clinical improvements coincided with physiological evidence of connectivity between the hemisphere on the side of the donor nerve and the paralyzed arm,” said lead author Mou-Xiong Zheng, MD, PhD, of the department of hand surgery at Huashan Hospital at Fudan University in Shanghai, and colleagues.

The research by Dr. Zheng and coauthors arises from what is known about hand paralysis after stroke, that damage to the contralateral cerebral hemisphere arises from interruption of the inhibitory activity of upper motor neurons, which causes spasticity, along with hand weakness and loss of fractionated fine motor control. Other studies have noted activity in the cerebral hemisphere on the same side of paralysis during recovery (Neuroimage. 2004;22:1775-83; J Neurophysiol. 2005;93:1209-22; J Neurosci. 2006;26:6096-102; Front Neurol. 2015;6:214), but Dr. Zheng and coauthors noted “sparse” connections between the hand and that part of the brain limit the body’s ability to compensate for spasticity and functional loss.

The latest study followed earlier studies, including one by Dr. Zheng’s coauthors (J Hand Surg Br. 1992;17:518-21), that reported the paralyzed hand could be connected to the unaffected hemisphere by transferring a cervical spine nerve from the nonparalyzed side, a treatment previously reported for injuries of the brachial plexus. Of the five nerves of the brachial plexus, Dr. Zheng and coauthors chose the C7 nerve because it accounts for about 20% of the nerve fibers in the brachial bundle and severing the nerve typically results in transient weakness and numbness in the arm or leg on the same side. Hence, when evaluating the hand on the side of the donor graft, the researchers found no significant changes in power, tactile threshold, or two-point discrimination as a result of surgery.

Their surgical approach was a modification of the C7 nerve transfer method that Dr. Zheng and coauthors had previously reported (Microsurgery. 2011;31:404-8; Neurosurgery. 2015;76:187-95). The operation involved making an incision at the superior aspect of the sternum, mobilizing the donor C7 nerve on the nonparalyzed side, and routing it between the spinal column and esophagus. Then, an anastomosis was performed directly with the C7 nerve on the paralyzed side.

Rehabilitation therapy for both the surgery group and controls was identical, administered four times weekly for 12 months at a single facility, although surgery patients wore an immobilizing cast after their operations.

The nature of the study population – men of varying ages with varying causes of the underlying cerebral lesions – makes it difficult to generalize the findings, Dr. Zheng and coauthors noted. “A larger cohort, followed for a longer period, would be necessary to determine whether cervical nerve transfer results in safe, consistent, and long-term improvements in the function of an arm that is chronically paralyzed as a result of a cerebral lesion,” the authors concluded.

Grants from the following supported the study: National Natural Science Foundation of China; Science and Technology Commission of Shanghai Municipality; Health and Family Planning Commission of Shanghai; and Shanghai Shen-Kang Hospital Development Center. 

SOURCE: Zheng M et al. N Engl J Med. 2018;378:22-34

Pathological changes in the brain’s white matter may contribute to focal epilepsy, suggests a recent review of the scientific research.

• Investigators have uncovered pathological changes in white matter myelination, axonal integrity, and cellular composition among patients with epilepsy, based on ex vivo and postmortem studies.
• Microstructural changes in several areas of the brain’s white matter near and at a distance from the epileptic focus have been discovered with the help of diffusion-weighted magnetic resonance imaging (MRI), including diffusion tensor imaging.
• MRI of the brain’s white matter may also be helpful in predicting patients’ cognitive functioning and how they respond to drug and surgical treatment.
• The literature review focuses on temporal lobe epilepsy and focal cortical dysplasia and the white matter anomalies detected in these disorders.

Histological and MRI markers of white matter damage in focal epilepsy. Epilepsy Res. 2018;140:29-38.

Pathological changes in the brain’s white matter may contribute to focal epilepsy, suggests a recent review of the scientific research.

• Investigators have uncovered pathological changes in white matter myelination, axonal integrity, and cellular composition among patients with epilepsy, based on ex vivo and postmortem studies.
• Microstructural changes in several areas of the brain’s white matter near and at a distance from the epileptic focus have been discovered with the help of diffusion-weighted magnetic resonance imaging (MRI), including diffusion tensor imaging.
• MRI of the brain’s white matter may also be helpful in predicting patients’ cognitive functioning and how they respond to drug and surgical treatment.
• The literature review focuses on temporal lobe epilepsy and focal cortical dysplasia and the white matter anomalies detected in these disorders.

Histological and MRI markers of white matter damage in focal epilepsy. Epilepsy Res. 2018;140:29-38.

Pathological changes in the brain’s white matter may contribute to focal epilepsy, suggests a recent review of the scientific research.

• Investigators have uncovered pathological changes in white matter myelination, axonal integrity, and cellular composition among patients with epilepsy, based on ex vivo and postmortem studies.
• Microstructural changes in several areas of the brain’s white matter near and at a distance from the epileptic focus have been discovered with the help of diffusion-weighted magnetic resonance imaging (MRI), including diffusion tensor imaging.
• MRI of the brain’s white matter may also be helpful in predicting patients’ cognitive functioning and how they respond to drug and surgical treatment.
• The literature review focuses on temporal lobe epilepsy and focal cortical dysplasia and the white matter anomalies detected in these disorders.

Histological and MRI markers of white matter damage in focal epilepsy. Epilepsy Res. 2018;140:29-38.

Myeloablative autologous hematopoietic stem-cell transplantation shows long-term benefits for patients with severe scleroderma, with improved event-free and overall survival over intravenous cyclophosphamide, according to Keith M. Sullivan, MD, and his associates.

A total of 75 patients with severe scleroderma (diffuse cutaneous systemic sclerosis) underwent randomization to open-label treatment with either transplantation or intravenous cyclophosphamide at an initial dose of 500 mg/m² of body-surface area, followed by 11 monthly infusions of 750 mg/m² with mesna prophylaxis.

Fnaq / Wikimedia Commons / CC BY-SA 4.0

llaubach@frontlinemedcom.com

SOURCE: Sullivan K et al. N Engl J Med. 2018;378;35-47.

Myeloablative autologous hematopoietic stem-cell transplantation shows long-term benefits for patients with severe scleroderma, with improved event-free and overall survival over intravenous cyclophosphamide, according to Keith M. Sullivan, MD, and his associates.

A total of 75 patients with severe scleroderma (diffuse cutaneous systemic sclerosis) underwent randomization to open-label treatment with either transplantation or intravenous cyclophosphamide at an initial dose of 500 mg/m² of body-surface area, followed by 11 monthly infusions of 750 mg/m² with mesna prophylaxis.

Fnaq / Wikimedia Commons / CC BY-SA 4.0

llaubach@frontlinemedcom.com

SOURCE: Sullivan K et al. N Engl J Med. 2018;378;35-47.

Myeloablative autologous hematopoietic stem-cell transplantation shows long-term benefits for patients with severe scleroderma, with improved event-free and overall survival over intravenous cyclophosphamide, according to Keith M. Sullivan, MD, and his associates.

A total of 75 patients with severe scleroderma (diffuse cutaneous systemic sclerosis) underwent randomization to open-label treatment with either transplantation or intravenous cyclophosphamide at an initial dose of 500 mg/m² of body-surface area, followed by 11 monthly infusions of 750 mg/m² with mesna prophylaxis.

Fnaq / Wikimedia Commons / CC BY-SA 4.0

llaubach@frontlinemedcom.com

SOURCE: Sullivan K et al. N Engl J Med. 2018;378;35-47.

Thrombectomy plus standard care was superior to standard care alone in patients who had experienced an acute ischemic stroke 6-24 hours earlier and who had a mismatch between clinical deficit and infarct, according to Raul G. Nogueira, MD, and his DAWN trial coinvestigators.

A total of 206 patients who had experienced occlusion of the intracranial internal carotid artery or proximal middle cerebral artery in the past 6-24 hours were included in the study – 107 receiving thrombectomy with the Trevo device plus standard care and 99 receiving standard care alone. After 90 days of treatment, the mean utility-weighted modified Rankin scale score for patients who received thrombectomy was 5.5, compared with 3.4 in the control group. The rate of functional independence was 49% in the thrombectomy group and 13% in the control group.

lfranki@frontlinemedcom.com

SOURCE: Nogueira R et al. N Engl J Med. 2018;378:11-21

Thrombectomy plus standard care was superior to standard care alone in patients who had experienced an acute ischemic stroke 6-24 hours earlier and who had a mismatch between clinical deficit and infarct, according to Raul G. Nogueira, MD, and his DAWN trial coinvestigators.

A total of 206 patients who had experienced occlusion of the intracranial internal carotid artery or proximal middle cerebral artery in the past 6-24 hours were included in the study – 107 receiving thrombectomy with the Trevo device plus standard care and 99 receiving standard care alone. After 90 days of treatment, the mean utility-weighted modified Rankin scale score for patients who received thrombectomy was 5.5, compared with 3.4 in the control group. The rate of functional independence was 49% in the thrombectomy group and 13% in the control group.

lfranki@frontlinemedcom.com

SOURCE: Nogueira R et al. N Engl J Med. 2018;378:11-21

Thrombectomy plus standard care was superior to standard care alone in patients who had experienced an acute ischemic stroke 6-24 hours earlier and who had a mismatch between clinical deficit and infarct, according to Raul G. Nogueira, MD, and his DAWN trial coinvestigators.

A total of 206 patients who had experienced occlusion of the intracranial internal carotid artery or proximal middle cerebral artery in the past 6-24 hours were included in the study – 107 receiving thrombectomy with the Trevo device plus standard care and 99 receiving standard care alone. After 90 days of treatment, the mean utility-weighted modified Rankin scale score for patients who received thrombectomy was 5.5, compared with 3.4 in the control group. The rate of functional independence was 49% in the thrombectomy group and 13% in the control group.

lfranki@frontlinemedcom.com

SOURCE: Nogueira R et al. N Engl J Med. 2018;378:11-21

I wrote about physician burnout and well-being in the July 2017 version of this column, and am still thinking a great deal about those issues. In the past 6 months, I can’t identify anything that strikes me as a real breakthrough in addressing these issues. However, the ever-increasing attention and resources directed at physician burnout and wellness, on both a local and national level, strike me as reason for cautious optimism.

A chief wellness officer

In summer 2017, Stanford University created a new physician executive role called chief wellness officer (CWO). As far as I am aware, this is the first such position connected with a hospital or medical school. It will be interesting to see if other organizations create similar positions, although I suspect that in places where it is explicitly recognized as a priority, responsibility for this work will be one of the many duties of a chief medical officer or other such executive, and not a position devoted solely to wellness. Interestingly, an Internet search revealed that some non–health care businesses have executive positions with that title, though the role seems focused more on physical health – as in exercise and smoking cessation – than emotional well-being and burnout.

According to a statement on the Stanford Medicine website, the new CWO will work with colleagues to continue “building on its innovative WellMD Center , which was established in 2016. The center has engaged more than 200 physicians through programs focusing on peer support, stress reduction, and ways to cultivate compassion and resilience, as well as a literature and a dinner series in which physicians explore the challenges and rewards of being a doctor. The center also aims to relieve some of the burden on physicians by improving efficiency and simplifying workplace systems, such as electronic medical records.”

A national conference

Over the last 2 or 3 years many, if not most, physician conferences, including the SHM annual conference, have added some content around physician burnout and well-being. But for the first time I’m aware of, an entire conference, the American Conference on Physician Health, addressed these topics in San Francisco in October 2017, and attracted 425 attendees along with an all-star faculty. I couldn’t attend myself, but found a reporter’s summary informative and I recommend it.

While the summary didn’t suggest the conference provided a cure or simple path to improvement, I’m encouraged that the topic has attracted the attention of some pretty smart people. If there is a second edition of this conference, I’ll try hard to attend.

Worthwhile web resources

The home page of Stanford’s WellMD Center provides a continuously updated list of recent research publications on physician health and links to many other resources, and is worth bookmarking.

Another great educational resource for physician wellness is the AMA’s STEPS Forward, a site devoted to practice improvement that provides guidance on patient care, work flow and process, leading change, technology and finance, as well as professional well-being. Of the five separate education modules in the latter category, I found the one on “Preventing Physician Burnout” especially informative. The site is free, doesn’t require an AMA membership, and can provide CME credit.

Making a difference locally: Individuals

Surveys, research, and the experience of experts available via the above resources and others are very valuable, but may be hard to translate into action for you and your fellow local caregivers. My sense is that many hospitalists address their own work-related distress by simply working less in total – reducing their full-time equivalents. That may be the most tangible and accessible intervention, and undeniably the right thing to do in some cases. But it isn’t an ideal approach for our field, which faces chronic staffing shortages. And it doesn’t do anything to change the average level of distress of a day of work. I worry that many people will find disappointment if working fewer shifts is their only burnout mitigation strategy.

Ensuring that you have some work-related interest outside of direct patient care, such as being the local electronic health record expert, or even the person leading formation of a support committee, can be really valuable. I first addressed this topic in the June 2011 issue of The Hospitalist, and there is a long list of things to consider: mindfulness, practicing “ self-compassion ,” cultivating deeper social connections in and out of the workplace, etc. Ultimately, each of us will have to choose our own path, and for some that should include professional help, e.g., from a mental health care provider.

But as a colleague once put it, a focus on changing ourselves is akin to just learning to take a punch better. A worthwhile endeavor, but it’s also necessary to try to decrease the number of punches thrown our way.

Making a difference locally: Medical staff

I’m part of the Provider Support Committee at my hospital, and I have concluded that nearly every hospital should have a group like this. Our own committee was modeled after the support committee at a hospital five miles away, and both groups see value in collaborating in our efforts. In fact, a person from each hospital’s committee serves on the committee at the other hospital.

These committees have popped up in other institutions, and many have been at it longer than at my hospital. But they all seem to share a mission of developing and implementing programs to position caregivers to thrive in their work, increase resilience, and reduce their risk of burnout. Some interventions are focused on making changes to an EHR, work schedules, work flows, or even staffing levels (i.e., reducing the “number of punches”). Other efforts are directed toward establishing groups that support personal reflection and/or social connections among providers.

A review of activities undertaken by seven different organizations is available at the AMA STEPS forward Preventing Physician Burnout website (click on “STEPS in practice.”)

Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Contact him at john.nelson@nelsonflores.com

I wrote about physician burnout and well-being in the July 2017 version of this column, and am still thinking a great deal about those issues. In the past 6 months, I can’t identify anything that strikes me as a real breakthrough in addressing these issues. However, the ever-increasing attention and resources directed at physician burnout and wellness, on both a local and national level, strike me as reason for cautious optimism.

A chief wellness officer

In summer 2017, Stanford University created a new physician executive role called chief wellness officer (CWO). As far as I am aware, this is the first such position connected with a hospital or medical school. It will be interesting to see if other organizations create similar positions, although I suspect that in places where it is explicitly recognized as a priority, responsibility for this work will be one of the many duties of a chief medical officer or other such executive, and not a position devoted solely to wellness. Interestingly, an Internet search revealed that some non–health care businesses have executive positions with that title, though the role seems focused more on physical health – as in exercise and smoking cessation – than emotional well-being and burnout.

According to a statement on the Stanford Medicine website, the new CWO will work with colleagues to continue “building on its innovative WellMD Center , which was established in 2016. The center has engaged more than 200 physicians through programs focusing on peer support, stress reduction, and ways to cultivate compassion and resilience, as well as a literature and a dinner series in which physicians explore the challenges and rewards of being a doctor. The center also aims to relieve some of the burden on physicians by improving efficiency and simplifying workplace systems, such as electronic medical records.”

A national conference

Over the last 2 or 3 years many, if not most, physician conferences, including the SHM annual conference, have added some content around physician burnout and well-being. But for the first time I’m aware of, an entire conference, the American Conference on Physician Health, addressed these topics in San Francisco in October 2017, and attracted 425 attendees along with an all-star faculty. I couldn’t attend myself, but found a reporter’s summary informative and I recommend it.

While the summary didn’t suggest the conference provided a cure or simple path to improvement, I’m encouraged that the topic has attracted the attention of some pretty smart people. If there is a second edition of this conference, I’ll try hard to attend.

Worthwhile web resources

The home page of Stanford’s WellMD Center provides a continuously updated list of recent research publications on physician health and links to many other resources, and is worth bookmarking.

Another great educational resource for physician wellness is the AMA’s STEPS Forward, a site devoted to practice improvement that provides guidance on patient care, work flow and process, leading change, technology and finance, as well as professional well-being. Of the five separate education modules in the latter category, I found the one on “Preventing Physician Burnout” especially informative. The site is free, doesn’t require an AMA membership, and can provide CME credit.

Making a difference locally: Individuals

Surveys, research, and the experience of experts available via the above resources and others are very valuable, but may be hard to translate into action for you and your fellow local caregivers. My sense is that many hospitalists address their own work-related distress by simply working less in total – reducing their full-time equivalents. That may be the most tangible and accessible intervention, and undeniably the right thing to do in some cases. But it isn’t an ideal approach for our field, which faces chronic staffing shortages. And it doesn’t do anything to change the average level of distress of a day of work. I worry that many people will find disappointment if working fewer shifts is their only burnout mitigation strategy.

Ensuring that you have some work-related interest outside of direct patient care, such as being the local electronic health record expert, or even the person leading formation of a support committee, can be really valuable. I first addressed this topic in the June 2011 issue of The Hospitalist, and there is a long list of things to consider: mindfulness, practicing “ self-compassion ,” cultivating deeper social connections in and out of the workplace, etc. Ultimately, each of us will have to choose our own path, and for some that should include professional help, e.g., from a mental health care provider.

But as a colleague once put it, a focus on changing ourselves is akin to just learning to take a punch better. A worthwhile endeavor, but it’s also necessary to try to decrease the number of punches thrown our way.

Making a difference locally: Medical staff

I’m part of the Provider Support Committee at my hospital, and I have concluded that nearly every hospital should have a group like this. Our own committee was modeled after the support committee at a hospital five miles away, and both groups see value in collaborating in our efforts. In fact, a person from each hospital’s committee serves on the committee at the other hospital.

These committees have popped up in other institutions, and many have been at it longer than at my hospital. But they all seem to share a mission of developing and implementing programs to position caregivers to thrive in their work, increase resilience, and reduce their risk of burnout. Some interventions are focused on making changes to an EHR, work schedules, work flows, or even staffing levels (i.e., reducing the “number of punches”). Other efforts are directed toward establishing groups that support personal reflection and/or social connections among providers.

A review of activities undertaken by seven different organizations is available at the AMA STEPS forward Preventing Physician Burnout website (click on “STEPS in practice.”)

Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Contact him at john.nelson@nelsonflores.com

I wrote about physician burnout and well-being in the July 2017 version of this column, and am still thinking a great deal about those issues. In the past 6 months, I can’t identify anything that strikes me as a real breakthrough in addressing these issues. However, the ever-increasing attention and resources directed at physician burnout and wellness, on both a local and national level, strike me as reason for cautious optimism.

A chief wellness officer

In summer 2017, Stanford University created a new physician executive role called chief wellness officer (CWO). As far as I am aware, this is the first such position connected with a hospital or medical school. It will be interesting to see if other organizations create similar positions, although I suspect that in places where it is explicitly recognized as a priority, responsibility for this work will be one of the many duties of a chief medical officer or other such executive, and not a position devoted solely to wellness. Interestingly, an Internet search revealed that some non–health care businesses have executive positions with that title, though the role seems focused more on physical health – as in exercise and smoking cessation – than emotional well-being and burnout.

According to a statement on the Stanford Medicine website, the new CWO will work with colleagues to continue “building on its innovative WellMD Center , which was established in 2016. The center has engaged more than 200 physicians through programs focusing on peer support, stress reduction, and ways to cultivate compassion and resilience, as well as a literature and a dinner series in which physicians explore the challenges and rewards of being a doctor. The center also aims to relieve some of the burden on physicians by improving efficiency and simplifying workplace systems, such as electronic medical records.”

A national conference

Over the last 2 or 3 years many, if not most, physician conferences, including the SHM annual conference, have added some content around physician burnout and well-being. But for the first time I’m aware of, an entire conference, the American Conference on Physician Health, addressed these topics in San Francisco in October 2017, and attracted 425 attendees along with an all-star faculty. I couldn’t attend myself, but found a reporter’s summary informative and I recommend it.

While the summary didn’t suggest the conference provided a cure or simple path to improvement, I’m encouraged that the topic has attracted the attention of some pretty smart people. If there is a second edition of this conference, I’ll try hard to attend.

Worthwhile web resources

The home page of Stanford’s WellMD Center provides a continuously updated list of recent research publications on physician health and links to many other resources, and is worth bookmarking.

Another great educational resource for physician wellness is the AMA’s STEPS Forward, a site devoted to practice improvement that provides guidance on patient care, work flow and process, leading change, technology and finance, as well as professional well-being. Of the five separate education modules in the latter category, I found the one on “Preventing Physician Burnout” especially informative. The site is free, doesn’t require an AMA membership, and can provide CME credit.

Making a difference locally: Individuals

Surveys, research, and the experience of experts available via the above resources and others are very valuable, but may be hard to translate into action for you and your fellow local caregivers. My sense is that many hospitalists address their own work-related distress by simply working less in total – reducing their full-time equivalents. That may be the most tangible and accessible intervention, and undeniably the right thing to do in some cases. But it isn’t an ideal approach for our field, which faces chronic staffing shortages. And it doesn’t do anything to change the average level of distress of a day of work. I worry that many people will find disappointment if working fewer shifts is their only burnout mitigation strategy.

Ensuring that you have some work-related interest outside of direct patient care, such as being the local electronic health record expert, or even the person leading formation of a support committee, can be really valuable. I first addressed this topic in the June 2011 issue of The Hospitalist, and there is a long list of things to consider: mindfulness, practicing “ self-compassion ,” cultivating deeper social connections in and out of the workplace, etc. Ultimately, each of us will have to choose our own path, and for some that should include professional help, e.g., from a mental health care provider.

But as a colleague once put it, a focus on changing ourselves is akin to just learning to take a punch better. A worthwhile endeavor, but it’s also necessary to try to decrease the number of punches thrown our way.

Making a difference locally: Medical staff

I’m part of the Provider Support Committee at my hospital, and I have concluded that nearly every hospital should have a group like this. Our own committee was modeled after the support committee at a hospital five miles away, and both groups see value in collaborating in our efforts. In fact, a person from each hospital’s committee serves on the committee at the other hospital.

These committees have popped up in other institutions, and many have been at it longer than at my hospital. But they all seem to share a mission of developing and implementing programs to position caregivers to thrive in their work, increase resilience, and reduce their risk of burnout. Some interventions are focused on making changes to an EHR, work schedules, work flows, or even staffing levels (i.e., reducing the “number of punches”). Other efforts are directed toward establishing groups that support personal reflection and/or social connections among providers.

A review of activities undertaken by seven different organizations is available at the AMA STEPS forward Preventing Physician Burnout website (click on “STEPS in practice.”)

Dr. Nelson has had a career in clinical practice as a hospitalist starting in 1988. He is cofounder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is codirector for SHM’s practice management courses. Contact him at john.nelson@nelsonflores.com

• Ovarian cancer: Risk assessment and patient management in the prevention of morbidity and mortality
• Ovarian cancer epidemiology for the practicing gynecologist
• Roundtable: Optimal risk assessment and management of the potential ovarian cancer case

• Ovarian cancer: Risk assessment and patient management in the prevention of morbidity and mortality
• Ovarian cancer epidemiology for the practicing gynecologist
• Roundtable: Optimal risk assessment and management of the potential ovarian cancer case

• Ovarian cancer: Risk assessment and patient management in the prevention of morbidity and mortality
• Ovarian cancer epidemiology for the practicing gynecologist
• Roundtable: Optimal risk assessment and management of the potential ovarian cancer case

BOSTON—Changes in the retina seem to mirror changes that begin to reshape the brain in preclinical Alzheimer’s disease.

Manifested as a reduction in volume in the retinal nerve fiber layer, these changes appear to track the aggregation of beta-amyloid brain plaques well before cognitive problems arise. The changes can be measured with equipment present already in many optometry offices, Peter J. Snyder, PhD, said at the Clinical Trials in Alzheimer’s Disease conference.

A Potential Window to the Brain

The retina begins to form in the third week of embryologic life, arising from the neural tube cells that also form the brain and spinal cord. It makes sense, then, that early neuronal changes in Alzheimer’s disease could occur in the retina as well, said Dr. Snyder, Professor of Neurology and Surgery (Ophthalmology) at Rhode Island Hospital and Brown University in Providence.

“The retina is really a protrusion of the brain, and it is part and parcel of the CNS,” Dr. Snyder said. “In terms of the neuronal structure, the retina develops in layers with specific cell types that are neurochemically and physiologically the same as the nervous tissue in the brain. That is why it is, potentially, literally a window that could let us see what is happening in the brain in early Alzheimer’s disease.”

Prior studies have examined the retina as a predictive marker for Alzheimer’s disease. At the 2016 Alzheimer’s Association International Conference, Fang Sarah Ko, MD, an ophthalmologist in Tallahassee, Florida, presented three-year data associating retinal nerve fiber layer thinning to cognitive decline in the UK Biobank, an ongoing prospective health outcomes study.

Other researchers have explored amyloid in the lens and retina as a possible early Alzheimer’s identification tool. But Dr. Snyder’s study is the first to demonstrate a longitudinal association between neuronal changes in the eye and amyloid burden in the brain among clinically normal subjects.

Patients Had Subjective Memory Complaints

For 27 months, he followed 56 people who had normal cognition but were beginning to experience subjective memory complaints. All subjects had at least one parent with Alzheimer’s disease. Everyone underwent an amyloid PET scan at baseline. Of the cohort, 15 had PET imaging evidence of abnormal beta-amyloid protein aggregation in the neocortex. This group was deemed to have preclinical Alzheimer’s disease, while the remainder served as a control group.

Dr. Snyder imaged each subject’s retinas at baseline and at 27 months, when everyone underwent a second amyloid PET scan. He examined the retina with spectral domain optical coherence tomography, a relatively new method of imaging the retina that typically is used to detect retinal and ocular changes associated with diabetes, macular degeneration, glaucoma, and multiple sclerosis.

Dr. Snyder examined the optic nerve head and macula at both time points and assessed volumetric changes in the peripapillary retinal nerve fiber layer, the macular retinal nerve fiber layer, the ganglion cell layer, the inner plexiform layer, the outer nuclear layer, the outer plexiform layer, and the inner nuclear layer. He also computed changes in total retinal volume.

Between-Group Differences

At baseline assessment, Dr. Snyder found a significant difference between the groups. Among the amyloid-positive subjects, the inner plexiform layer was slightly larger in volume. “This seems a bit counterintuitive, but … it suggests that there may be inflammatory processes going on in this early stage and that we are catching that inflammation.” An independent research group has replicated this finding with a larger sample of participants and plans to report its results later this year, Dr. Snyder noted.

At 27 months, the total retinal volume and the macular retinal nerve fiber layer volume were significantly lower in the preclinical Alzheimer’s disease group than in the control group. There was also a volume reduction in the peripapillary retinal nerve fiber layer, although the between-group difference was not statistically significant.

In a multivariate linear regression model that controlled for age and total amyloid burden, the mean volume change in the macular retinal nerve fiber layer accounted for about 10% of the variation in PET binding to brain amyloid by 27 months. Volume reductions in all the other layers appeared to be associated only with age, representing normal age-related changes in the eye.

Using Advances in Imaging

This volume loss in the retinal nerve fiber layer probably represents early demyelination or degeneration of axons, Dr. Snyder said. “This finding in the retina appears analogous, and possibly directly related, to a similar loss of white matter that is readily observable in the early stages of Alzheimer’s disease,” he said. “At the same time, patients are beginning to experience cholinergic changes in the basal forebrain and the abnormal aggregation of fibrillar beta-amyloid plaques. I do not know to what extent these changes are mechanistically dependent on each other, but they appear to also be happening, in the earliest stages of the disease course, in the retina.”

More research is needed before retinal scanning can be employed as a risk-assessment tool, however. “Every time we have a major advance in imaging, the technical engineering breakthroughs precede our detailed understanding of what we are looking at and what to measure,” Dr. Snyder said. “This is where we are right now with retinal imaging. Biologically, it makes sense to be looking at this as a marker of risk in those who are clinically healthy, and maybe later as a marker of disease progression. But there is a lot of work to be done here yet.”

Dr. Snyder’s project was supported by a research award from Pfizer and a grant from Avid Radiopharmaceuticals.

—Michele G. Sullivan

BOSTON—Changes in the retina seem to mirror changes that begin to reshape the brain in preclinical Alzheimer’s disease.

Manifested as a reduction in volume in the retinal nerve fiber layer, these changes appear to track the aggregation of beta-amyloid brain plaques well before cognitive problems arise. The changes can be measured with equipment present already in many optometry offices, Peter J. Snyder, PhD, said at the Clinical Trials in Alzheimer’s Disease conference.

A Potential Window to the Brain

The retina begins to form in the third week of embryologic life, arising from the neural tube cells that also form the brain and spinal cord. It makes sense, then, that early neuronal changes in Alzheimer’s disease could occur in the retina as well, said Dr. Snyder, Professor of Neurology and Surgery (Ophthalmology) at Rhode Island Hospital and Brown University in Providence.

“The retina is really a protrusion of the brain, and it is part and parcel of the CNS,” Dr. Snyder said. “In terms of the neuronal structure, the retina develops in layers with specific cell types that are neurochemically and physiologically the same as the nervous tissue in the brain. That is why it is, potentially, literally a window that could let us see what is happening in the brain in early Alzheimer’s disease.”

Prior studies have examined the retina as a predictive marker for Alzheimer’s disease. At the 2016 Alzheimer’s Association International Conference, Fang Sarah Ko, MD, an ophthalmologist in Tallahassee, Florida, presented three-year data associating retinal nerve fiber layer thinning to cognitive decline in the UK Biobank, an ongoing prospective health outcomes study.

Other researchers have explored amyloid in the lens and retina as a possible early Alzheimer’s identification tool. But Dr. Snyder’s study is the first to demonstrate a longitudinal association between neuronal changes in the eye and amyloid burden in the brain among clinically normal subjects.

Patients Had Subjective Memory Complaints

For 27 months, he followed 56 people who had normal cognition but were beginning to experience subjective memory complaints. All subjects had at least one parent with Alzheimer’s disease. Everyone underwent an amyloid PET scan at baseline. Of the cohort, 15 had PET imaging evidence of abnormal beta-amyloid protein aggregation in the neocortex. This group was deemed to have preclinical Alzheimer’s disease, while the remainder served as a control group.

Dr. Snyder imaged each subject’s retinas at baseline and at 27 months, when everyone underwent a second amyloid PET scan. He examined the retina with spectral domain optical coherence tomography, a relatively new method of imaging the retina that typically is used to detect retinal and ocular changes associated with diabetes, macular degeneration, glaucoma, and multiple sclerosis.

Dr. Snyder examined the optic nerve head and macula at both time points and assessed volumetric changes in the peripapillary retinal nerve fiber layer, the macular retinal nerve fiber layer, the ganglion cell layer, the inner plexiform layer, the outer nuclear layer, the outer plexiform layer, and the inner nuclear layer. He also computed changes in total retinal volume.

Between-Group Differences

At baseline assessment, Dr. Snyder found a significant difference between the groups. Among the amyloid-positive subjects, the inner plexiform layer was slightly larger in volume. “This seems a bit counterintuitive, but … it suggests that there may be inflammatory processes going on in this early stage and that we are catching that inflammation.” An independent research group has replicated this finding with a larger sample of participants and plans to report its results later this year, Dr. Snyder noted.

At 27 months, the total retinal volume and the macular retinal nerve fiber layer volume were significantly lower in the preclinical Alzheimer’s disease group than in the control group. There was also a volume reduction in the peripapillary retinal nerve fiber layer, although the between-group difference was not statistically significant.

In a multivariate linear regression model that controlled for age and total amyloid burden, the mean volume change in the macular retinal nerve fiber layer accounted for about 10% of the variation in PET binding to brain amyloid by 27 months. Volume reductions in all the other layers appeared to be associated only with age, representing normal age-related changes in the eye.

Using Advances in Imaging

This volume loss in the retinal nerve fiber layer probably represents early demyelination or degeneration of axons, Dr. Snyder said. “This finding in the retina appears analogous, and possibly directly related, to a similar loss of white matter that is readily observable in the early stages of Alzheimer’s disease,” he said. “At the same time, patients are beginning to experience cholinergic changes in the basal forebrain and the abnormal aggregation of fibrillar beta-amyloid plaques. I do not know to what extent these changes are mechanistically dependent on each other, but they appear to also be happening, in the earliest stages of the disease course, in the retina.”

More research is needed before retinal scanning can be employed as a risk-assessment tool, however. “Every time we have a major advance in imaging, the technical engineering breakthroughs precede our detailed understanding of what we are looking at and what to measure,” Dr. Snyder said. “This is where we are right now with retinal imaging. Biologically, it makes sense to be looking at this as a marker of risk in those who are clinically healthy, and maybe later as a marker of disease progression. But there is a lot of work to be done here yet.”

Dr. Snyder’s project was supported by a research award from Pfizer and a grant from Avid Radiopharmaceuticals.

—Michele G. Sullivan

BOSTON—Changes in the retina seem to mirror changes that begin to reshape the brain in preclinical Alzheimer’s disease.

Manifested as a reduction in volume in the retinal nerve fiber layer, these changes appear to track the aggregation of beta-amyloid brain plaques well before cognitive problems arise. The changes can be measured with equipment present already in many optometry offices, Peter J. Snyder, PhD, said at the Clinical Trials in Alzheimer’s Disease conference.

A Potential Window to the Brain

The retina begins to form in the third week of embryologic life, arising from the neural tube cells that also form the brain and spinal cord. It makes sense, then, that early neuronal changes in Alzheimer’s disease could occur in the retina as well, said Dr. Snyder, Professor of Neurology and Surgery (Ophthalmology) at Rhode Island Hospital and Brown University in Providence.

“The retina is really a protrusion of the brain, and it is part and parcel of the CNS,” Dr. Snyder said. “In terms of the neuronal structure, the retina develops in layers with specific cell types that are neurochemically and physiologically the same as the nervous tissue in the brain. That is why it is, potentially, literally a window that could let us see what is happening in the brain in early Alzheimer’s disease.”

Prior studies have examined the retina as a predictive marker for Alzheimer’s disease. At the 2016 Alzheimer’s Association International Conference, Fang Sarah Ko, MD, an ophthalmologist in Tallahassee, Florida, presented three-year data associating retinal nerve fiber layer thinning to cognitive decline in the UK Biobank, an ongoing prospective health outcomes study.

Other researchers have explored amyloid in the lens and retina as a possible early Alzheimer’s identification tool. But Dr. Snyder’s study is the first to demonstrate a longitudinal association between neuronal changes in the eye and amyloid burden in the brain among clinically normal subjects.

Patients Had Subjective Memory Complaints

For 27 months, he followed 56 people who had normal cognition but were beginning to experience subjective memory complaints. All subjects had at least one parent with Alzheimer’s disease. Everyone underwent an amyloid PET scan at baseline. Of the cohort, 15 had PET imaging evidence of abnormal beta-amyloid protein aggregation in the neocortex. This group was deemed to have preclinical Alzheimer’s disease, while the remainder served as a control group.

Dr. Snyder imaged each subject’s retinas at baseline and at 27 months, when everyone underwent a second amyloid PET scan. He examined the retina with spectral domain optical coherence tomography, a relatively new method of imaging the retina that typically is used to detect retinal and ocular changes associated with diabetes, macular degeneration, glaucoma, and multiple sclerosis.

Dr. Snyder examined the optic nerve head and macula at both time points and assessed volumetric changes in the peripapillary retinal nerve fiber layer, the macular retinal nerve fiber layer, the ganglion cell layer, the inner plexiform layer, the outer nuclear layer, the outer plexiform layer, and the inner nuclear layer. He also computed changes in total retinal volume.

Between-Group Differences

At baseline assessment, Dr. Snyder found a significant difference between the groups. Among the amyloid-positive subjects, the inner plexiform layer was slightly larger in volume. “This seems a bit counterintuitive, but … it suggests that there may be inflammatory processes going on in this early stage and that we are catching that inflammation.” An independent research group has replicated this finding with a larger sample of participants and plans to report its results later this year, Dr. Snyder noted.

At 27 months, the total retinal volume and the macular retinal nerve fiber layer volume were significantly lower in the preclinical Alzheimer’s disease group than in the control group. There was also a volume reduction in the peripapillary retinal nerve fiber layer, although the between-group difference was not statistically significant.

In a multivariate linear regression model that controlled for age and total amyloid burden, the mean volume change in the macular retinal nerve fiber layer accounted for about 10% of the variation in PET binding to brain amyloid by 27 months. Volume reductions in all the other layers appeared to be associated only with age, representing normal age-related changes in the eye.

Using Advances in Imaging

This volume loss in the retinal nerve fiber layer probably represents early demyelination or degeneration of axons, Dr. Snyder said. “This finding in the retina appears analogous, and possibly directly related, to a similar loss of white matter that is readily observable in the early stages of Alzheimer’s disease,” he said. “At the same time, patients are beginning to experience cholinergic changes in the basal forebrain and the abnormal aggregation of fibrillar beta-amyloid plaques. I do not know to what extent these changes are mechanistically dependent on each other, but they appear to also be happening, in the earliest stages of the disease course, in the retina.”

More research is needed before retinal scanning can be employed as a risk-assessment tool, however. “Every time we have a major advance in imaging, the technical engineering breakthroughs precede our detailed understanding of what we are looking at and what to measure,” Dr. Snyder said. “This is where we are right now with retinal imaging. Biologically, it makes sense to be looking at this as a marker of risk in those who are clinically healthy, and maybe later as a marker of disease progression. But there is a lot of work to be done here yet.”

Dr. Snyder’s project was supported by a research award from Pfizer and a grant from Avid Radiopharmaceuticals.

—Michele G. Sullivan

Influenza vaccine needs some help with its image.

I suspect most health care providers have heard the complaint, “The vaccine doesn’t work. One year I got the vaccine, and I still came down with the flu.”

Over the years, I’ve polished my responses to vaccine naysayers.

Influenza vaccine doesn’t protect you against every virus that can cause cold and flu symptoms. It only prevents influenza. It’s possible you had a different virus, such as adenovirus, coronavirus, parainfluenza virus, or respiratory syncytial virus.

KatarzynaBialasiewicz/Thinkstock

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital in Louisville. She said she had no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

Influenza vaccine needs some help with its image.

I suspect most health care providers have heard the complaint, “The vaccine doesn’t work. One year I got the vaccine, and I still came down with the flu.”

Over the years, I’ve polished my responses to vaccine naysayers.

Influenza vaccine doesn’t protect you against every virus that can cause cold and flu symptoms. It only prevents influenza. It’s possible you had a different virus, such as adenovirus, coronavirus, parainfluenza virus, or respiratory syncytial virus.

KatarzynaBialasiewicz/Thinkstock

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital in Louisville. She said she had no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

Influenza vaccine needs some help with its image.

I suspect most health care providers have heard the complaint, “The vaccine doesn’t work. One year I got the vaccine, and I still came down with the flu.”

Over the years, I’ve polished my responses to vaccine naysayers.

Influenza vaccine doesn’t protect you against every virus that can cause cold and flu symptoms. It only prevents influenza. It’s possible you had a different virus, such as adenovirus, coronavirus, parainfluenza virus, or respiratory syncytial virus.

KatarzynaBialasiewicz/Thinkstock

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital in Louisville. She said she had no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

The past year brought new information and guidance from the American College of Obstetricians and Gynecologists (ACOG) on many relevant obstetric topics, making it difficult to choose just a few for this Update. Opioid use in pregnancy was an obvious choice given the national media attention and the potential opportunity for intervention in pregnancy for both the mother and the fetus/newborn. Postpartum hemorrhage, an “oldie but goodie,” was chosen for several reasons: It got a new definition, a new focus on multidisciplinary care, and an exciting novel tool for the treatment toolbox. Finally, given the rapidly changing technology, new screening recommendations, and the complexity of counseling, carrier screening was chosen as a genetic hot topic for this year.

Opioids, obstetrics, and opportunities

Reddy UM, Davis JM, Ren Z, Greene MF; Opioid Use in Pregnancy, Neonatal Abstinence Syndrome, and Childhood Outcomes Workshop Invited Speakers. Opioid use in pregnancy, neonatal abstinence syndrome, and childhood outcomes: Executive summary of a joint workshop. Obstet Gynecol. 2017;130(1):10-28.

ACOG Committee on Obstetric Practice. ACOG committee opinion No. 711: Opioid use and opioid use disorder in pregnancy. Obstet Gynecol. 2017;130(2):e81-e94.

The term "opioid epidemic" is omnipresent in both the lay media and the medical literature. In the past decade, the United States has had a huge increase in the number of opioid prescriptions, the rate of admissions and deaths due to prescription opioid misuse and abuse, and an increased rate of heroin use attributed to prior prescription opioid use.

Obstetrics is unique in that opioid use and abuse disorders affect 2 patients simultaneously (the mother and fetus), and the treatment options are somewhat at odds in that they need to balance a stable maternal status and intrauterine environment with the risk of neonatal abstinence syndrome (NAS). Additionally, pregnancy is an opportunity for a woman with opioid use disorder to have access to medical care (possibly for the first time) leading to the diagnosis and treatment of her disease. As the clinicians on the front line, obstetricians therefore require education and guidance on best practice for management of opioid use in pregnancy.

In 2017, Reddy and colleagues, as part of a joint workshop on opioid use in pregnancy, and a committee opinion from ACOG provided the following recommendations.

Screening

Universally screen for substance use, starting at the first prenatal visit; this is recommended over risk factor-based screening.

Use a validated screening tool. A tool such as a questionnaire is recommended as the first-line screening test (for example, the 4Ps screen, the National Institute on Drug Abuse Quick Screen, and the CRAFFT Screening Interview).

Do not universally screen urine and hair for drugs. This type of screening has many limitations, such as the limited number of substances tested, false-positive results, and inaccurate determination of the frequency or timing of drug use. Information regarding the consequences of the test must be provided, and patient consent must be obtained prior to performing the test.

Treatment

Use medication-assisted treatment with buprenorphine or methadone, which is preferred to medically supervised withdrawal. Medication-assisted treatment prevents withdrawal symptoms and cravings, decreases the risk of relapse, improves compliance with prenatal care and addiction treatment programs, and leads to better obstetric outcomes (higher birth weight, lower rate of preterm birth, lower perinatal mortality).

Know that buprenorphine has several advantages over methadone, including the convenience of an outpatient prescription, a lower risk of overdose, and improved neonatal outcomes (higher birth weight, lower doses of morphine to treat NAS, shorter treatment duration).

Prioritize methadone as the preferred option for pregnant women who are already receiving methadone treatment (changing to buprenorphine may precipitate withdrawal), those with a long-standing history of or multi-substance abuse, and those who have failed other treatment programs.

Prenatal care

Screen for comorbid conditions such as sexually transmitted infections, other medications or substance use, social conditions, and mental health disorders.

Perform ultrasonography serially to monitor fetal growth because of the increased risk of fetal growth restriction.

Consult with anesthesiology for pain control recommendations for labor and delivery and with neonatalogy/pediatrics for NAS counseling.

Intrapartum/postpartum care

Recognize heightened pain. Women with opioid use disorder have increased sensitivity to painful stimuli.

Continue the maintenance dose of methadone or buprenorphine throughout hospitalization, with short-acting opioids added for a brief period for postoperative pain.

Prioritize regional anesthesia for pain control in labor or for cesarean delivery.

Consider alternative therapies such as regional blocks, nonopioid medications (nonsteroidal anti-inflammatory drugs, acetaminophen), or relaxation/mindfulness training.

Avoid mixed antagonist and agonist narcotics (butorphanol, nalbuphine, pentazocine) as they may cause acute withdrawal.

Encourage breastfeeding to decrease the severity of NAS and maternal stress and increase maternal-child bonding and maternal confidence.

Offer contraceptive counseling and services immediately postpartum in the hospital, with strong consideration for long-acting reversible contraception.

Opioid prescribing practices

Opioids are prescribed in excess post–cesarean delivery. Several recent studies have demonstrated that most women are prescribed opioids post–cesarean delivery in excess of the amount they use (median 30–40 tablets prescribed, median 20 tablets used).^1,2 The leftover opioid medication usually is not discarded and therefore is at risk for diversion or misuse. A small subset of patients will use all the opioids prescribed and feel as though they have not received enough medication.

Prescribe post–cesarean delivery opioids more appropriately by considering individual inpatient opioid requirements or a shared decision-making model.³

Prioritize acetaminophen and ibuprofen during breastfeeding. In a recent editorial in OBG Management, Robert L. Barbieri, MD, recommended that whenever possible, acetaminophen and ibuprofen should be the first-line treatment for breastfeeding women, and narcotics that are metabolized by CYP2D6 should be avoided to reduce the risk to the newborn.⁴

Read about new strategies for postpartum hemorrhage.

Postpartum hemorrhage: New definitions and new strategies for stemming the flow

ACOG Committee on Practice Bulletins—Obstetrics. ACOG practice bulletin No. 183: Postpartum hemorrhage. Obstet Gynecol. 2017;130(4):e168-e186.

From the very first sentence of the new ACOG practice bulletin, postpartum hemorrhage (PPH) is redefined as "cumulative blood loss greater than or equal to 1,000 mL or blood loss accompanied by signs or symptoms of hypovolemia within 24 hours after the birth process (includes intrapartum loss) regardless of route of delivery." Although this does not seem to be a huge change from the traditional teaching of a 500-mL blood loss at vaginal delivery and a 1,000-mL loss at cesarean delivery, it reflects a shift in focus from simply responding to a certain amount of bleeding to using a multidisciplinary action plan for treating this leading cause of maternal mortality worldwide.

Focus on developing a PPH action plan

As part of the shift toward a multidisciplinary action plan for PPH, all obstetric team members should be aware of the following:  

• For most postpartum women, by the time they begin to show signs of hemodynamic compromise, the amount of blood loss approaches 25% of their total blood volume (1,500 mL). Lactic acidosis, systemic inflammation, and a consumptive coagulopathy result.  
• Risk stratification prior to delivery, recognition and identification of the source of bleeding, and aggressive early resuscitation to prevent hypovolemia are paramount. Experience gleaned from trauma massive transfusion protocols suggests that judicious transfusion of packed red blood cells, fresh frozen plasma, and platelets in a 1:1:1 ratio is appropriate for obstetric patients. Additionally, patients with low fibrinogen levels should be treated with cryoprecipitate.  
• The use of fixed transfusion ratios and standardized protocols for recognition and management of PPH has been demonstrated to increase earlier intervention and resolution of hemorrhage at an earlier stage, although the maternal outcomes results have been mixed.  
• Multidisciplinary team drills and simulation exercises also should be considered to help solidify training of an institution's teams responsible for PPH response.

Novel management option: Tranexamic acid

In addition to these strategies, there is a new recommendation for managing refractory PPH: tranexamic acid, which works by binding to lysine receptors on plasminogen and plasmin, inhibiting plasmin-mediated fibrin degradation.5 Previously, tranexamic acid was known to be effective in trauma, heart surgery, and in patients with thrombophilias. Pacheco and colleagues recently demonstrated reduced mortality from obstetric bleeding if tranexamic acid was given within 3 hours of delivery, without increased thrombotic complications.⁵ ACOG recommends its use if initial medical therapy fails, while the World Health Organization strongly recommends that tranexamic acid be part of a standard PPH package for all cases of PPH (TABLE).⁶

Read about new ACOG guidance on prepregnancy and prenatal screening.

ACOG Committee on Genetics. Committee opinion No. 690: Carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129(3):e35-e40.

ACOG Committee on Genetics. Committee opinion No. 691: Carrier screening for genetic conditions. Obstet Gynecol. 2017;129(3):e41-e55.

Ideally, carrier screening should be offered prior to pregnancy to fully inform couples of their reproductive risks and options for pregnancy. If not performed in the preconception period, carrier screening should be offered to all pregnant women. If a patient chooses screening and screens positive for a particular disorder, her reproductive partner should then be offered screening so that the risk of having an affected child can be determined.

New ACOG guidance on prepregnancy and prenatal screening

Carrier screening recommendations have evolved as the technology available has expanded. All 3 of the following strategies now are considered "acceptable" according to 2 recently published ACOG committee opinions.

Traditional ethnic-specific carrier screening, previously ACOG's sole recommendation, involves offering specific genetic screening to patients from populations with a high prevalence for certain conditions. One such example is Tay-Sachs disease screening in Ashkenazi Jewish patients.

Panethnic screening, which takes into account mixed or uncertain backgrounds, involves screening for a certain panel of disorders and is available to all patients regardless of their background (for example, cystic fibrosis screening offered to all pregnant patients).

Expanded carrier screening is when a large number of disorders can be screened for simultaneously for a lower cost than previous testing strategies. Expanded carrier screening panels vary in number and which conditions are tested by the laboratory. An ideal expanded carrier screening panel has been debated in the literature but not agreed on.⁷

ObGyns and practices therefore are encouraged to develop a standard counseling and screening protocol to offer to all their patients while being flexible to make available any patient-requested screening that is outside their protocol. Pretest and posttest counseling, including a thorough family history, is essential (as with any genetic testing) and should include residual risk after testing, potential need for specific familial mutation testing instead of general carrier screening, and issues with consanguinity.

Three essential screens

Regardless of the screening strategy chosen from the above options, 3 screening tests should be offered to all pregnant women or couples considering pregnancy (either individually or in the context of an expanded screening panel):

• Cystic fibrosis. At the least, a panel of the 23 most common mutations should be used. More expanded panels, which include hundreds of mutations, increase detection in non-Caucasian populations and for milder forms of the disease or infertility-related mutations.
• Hemoglobinopathies (sickle cell, α- and β-thalassemia). Complete blood count and red blood indices are recommended for all, with hemoglobin electrophoresis recommended for patients of African, Middle Eastern, Mediterranean, or West Indian descent or if mean corpuscular volume is low.
• Spinal muscular atrophy (SMA). The most recent addition to ACOG's recommendations for general carrier screening due to the relatively high carrier frequency (1-in-40 to 1-in-60) and the severity of the disease, SMA causes degeneration of the spinal cord neurons, skeletal muscular atrophy, and overall weakness. Screening is via polymerase chain reaction for SMN1 copy number: 2 copies are normal, and 1 copy indicates a carrier of the SMN1 deletion. About 3% to 4% of patients will screen negative but still will be "carriers" due to having 2 copies of the SMN1 gene on 1 chromosome and no copies on the other chromosome.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

The past year brought new information and guidance from the American College of Obstetricians and Gynecologists (ACOG) on many relevant obstetric topics, making it difficult to choose just a few for this Update. Opioid use in pregnancy was an obvious choice given the national media attention and the potential opportunity for intervention in pregnancy for both the mother and the fetus/newborn. Postpartum hemorrhage, an “oldie but goodie,” was chosen for several reasons: It got a new definition, a new focus on multidisciplinary care, and an exciting novel tool for the treatment toolbox. Finally, given the rapidly changing technology, new screening recommendations, and the complexity of counseling, carrier screening was chosen as a genetic hot topic for this year.

Opioids, obstetrics, and opportunities

Reddy UM, Davis JM, Ren Z, Greene MF; Opioid Use in Pregnancy, Neonatal Abstinence Syndrome, and Childhood Outcomes Workshop Invited Speakers. Opioid use in pregnancy, neonatal abstinence syndrome, and childhood outcomes: Executive summary of a joint workshop. Obstet Gynecol. 2017;130(1):10-28.

ACOG Committee on Obstetric Practice. ACOG committee opinion No. 711: Opioid use and opioid use disorder in pregnancy. Obstet Gynecol. 2017;130(2):e81-e94.

The term "opioid epidemic" is omnipresent in both the lay media and the medical literature. In the past decade, the United States has had a huge increase in the number of opioid prescriptions, the rate of admissions and deaths due to prescription opioid misuse and abuse, and an increased rate of heroin use attributed to prior prescription opioid use.

Obstetrics is unique in that opioid use and abuse disorders affect 2 patients simultaneously (the mother and fetus), and the treatment options are somewhat at odds in that they need to balance a stable maternal status and intrauterine environment with the risk of neonatal abstinence syndrome (NAS). Additionally, pregnancy is an opportunity for a woman with opioid use disorder to have access to medical care (possibly for the first time) leading to the diagnosis and treatment of her disease. As the clinicians on the front line, obstetricians therefore require education and guidance on best practice for management of opioid use in pregnancy.

In 2017, Reddy and colleagues, as part of a joint workshop on opioid use in pregnancy, and a committee opinion from ACOG provided the following recommendations.

Screening

Universally screen for substance use, starting at the first prenatal visit; this is recommended over risk factor-based screening.

Use a validated screening tool. A tool such as a questionnaire is recommended as the first-line screening test (for example, the 4Ps screen, the National Institute on Drug Abuse Quick Screen, and the CRAFFT Screening Interview).

Do not universally screen urine and hair for drugs. This type of screening has many limitations, such as the limited number of substances tested, false-positive results, and inaccurate determination of the frequency or timing of drug use. Information regarding the consequences of the test must be provided, and patient consent must be obtained prior to performing the test.

Treatment

Use medication-assisted treatment with buprenorphine or methadone, which is preferred to medically supervised withdrawal. Medication-assisted treatment prevents withdrawal symptoms and cravings, decreases the risk of relapse, improves compliance with prenatal care and addiction treatment programs, and leads to better obstetric outcomes (higher birth weight, lower rate of preterm birth, lower perinatal mortality).

Know that buprenorphine has several advantages over methadone, including the convenience of an outpatient prescription, a lower risk of overdose, and improved neonatal outcomes (higher birth weight, lower doses of morphine to treat NAS, shorter treatment duration).

Prioritize methadone as the preferred option for pregnant women who are already receiving methadone treatment (changing to buprenorphine may precipitate withdrawal), those with a long-standing history of or multi-substance abuse, and those who have failed other treatment programs.

Prenatal care

Screen for comorbid conditions such as sexually transmitted infections, other medications or substance use, social conditions, and mental health disorders.

Perform ultrasonography serially to monitor fetal growth because of the increased risk of fetal growth restriction.

Consult with anesthesiology for pain control recommendations for labor and delivery and with neonatalogy/pediatrics for NAS counseling.

Intrapartum/postpartum care

Recognize heightened pain. Women with opioid use disorder have increased sensitivity to painful stimuli.

Continue the maintenance dose of methadone or buprenorphine throughout hospitalization, with short-acting opioids added for a brief period for postoperative pain.

Prioritize regional anesthesia for pain control in labor or for cesarean delivery.

Consider alternative therapies such as regional blocks, nonopioid medications (nonsteroidal anti-inflammatory drugs, acetaminophen), or relaxation/mindfulness training.

Avoid mixed antagonist and agonist narcotics (butorphanol, nalbuphine, pentazocine) as they may cause acute withdrawal.

Encourage breastfeeding to decrease the severity of NAS and maternal stress and increase maternal-child bonding and maternal confidence.

Offer contraceptive counseling and services immediately postpartum in the hospital, with strong consideration for long-acting reversible contraception.

Opioid prescribing practices

Opioids are prescribed in excess post–cesarean delivery. Several recent studies have demonstrated that most women are prescribed opioids post–cesarean delivery in excess of the amount they use (median 30–40 tablets prescribed, median 20 tablets used).^1,2 The leftover opioid medication usually is not discarded and therefore is at risk for diversion or misuse. A small subset of patients will use all the opioids prescribed and feel as though they have not received enough medication.

Prescribe post–cesarean delivery opioids more appropriately by considering individual inpatient opioid requirements or a shared decision-making model.³

Prioritize acetaminophen and ibuprofen during breastfeeding. In a recent editorial in OBG Management, Robert L. Barbieri, MD, recommended that whenever possible, acetaminophen and ibuprofen should be the first-line treatment for breastfeeding women, and narcotics that are metabolized by CYP2D6 should be avoided to reduce the risk to the newborn.⁴

Read about new strategies for postpartum hemorrhage.

Postpartum hemorrhage: New definitions and new strategies for stemming the flow

ACOG Committee on Practice Bulletins—Obstetrics. ACOG practice bulletin No. 183: Postpartum hemorrhage. Obstet Gynecol. 2017;130(4):e168-e186.

From the very first sentence of the new ACOG practice bulletin, postpartum hemorrhage (PPH) is redefined as "cumulative blood loss greater than or equal to 1,000 mL or blood loss accompanied by signs or symptoms of hypovolemia within 24 hours after the birth process (includes intrapartum loss) regardless of route of delivery." Although this does not seem to be a huge change from the traditional teaching of a 500-mL blood loss at vaginal delivery and a 1,000-mL loss at cesarean delivery, it reflects a shift in focus from simply responding to a certain amount of bleeding to using a multidisciplinary action plan for treating this leading cause of maternal mortality worldwide.

Focus on developing a PPH action plan

As part of the shift toward a multidisciplinary action plan for PPH, all obstetric team members should be aware of the following:  

• For most postpartum women, by the time they begin to show signs of hemodynamic compromise, the amount of blood loss approaches 25% of their total blood volume (1,500 mL). Lactic acidosis, systemic inflammation, and a consumptive coagulopathy result.  
• Risk stratification prior to delivery, recognition and identification of the source of bleeding, and aggressive early resuscitation to prevent hypovolemia are paramount. Experience gleaned from trauma massive transfusion protocols suggests that judicious transfusion of packed red blood cells, fresh frozen plasma, and platelets in a 1:1:1 ratio is appropriate for obstetric patients. Additionally, patients with low fibrinogen levels should be treated with cryoprecipitate.  
• The use of fixed transfusion ratios and standardized protocols for recognition and management of PPH has been demonstrated to increase earlier intervention and resolution of hemorrhage at an earlier stage, although the maternal outcomes results have been mixed.  
• Multidisciplinary team drills and simulation exercises also should be considered to help solidify training of an institution's teams responsible for PPH response.

Novel management option: Tranexamic acid

In addition to these strategies, there is a new recommendation for managing refractory PPH: tranexamic acid, which works by binding to lysine receptors on plasminogen and plasmin, inhibiting plasmin-mediated fibrin degradation.5 Previously, tranexamic acid was known to be effective in trauma, heart surgery, and in patients with thrombophilias. Pacheco and colleagues recently demonstrated reduced mortality from obstetric bleeding if tranexamic acid was given within 3 hours of delivery, without increased thrombotic complications.⁵ ACOG recommends its use if initial medical therapy fails, while the World Health Organization strongly recommends that tranexamic acid be part of a standard PPH package for all cases of PPH (TABLE).⁶

Read about new ACOG guidance on prepregnancy and prenatal screening.

ACOG Committee on Genetics. Committee opinion No. 690: Carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129(3):e35-e40.

ACOG Committee on Genetics. Committee opinion No. 691: Carrier screening for genetic conditions. Obstet Gynecol. 2017;129(3):e41-e55.

Ideally, carrier screening should be offered prior to pregnancy to fully inform couples of their reproductive risks and options for pregnancy. If not performed in the preconception period, carrier screening should be offered to all pregnant women. If a patient chooses screening and screens positive for a particular disorder, her reproductive partner should then be offered screening so that the risk of having an affected child can be determined.

New ACOG guidance on prepregnancy and prenatal screening

Carrier screening recommendations have evolved as the technology available has expanded. All 3 of the following strategies now are considered "acceptable" according to 2 recently published ACOG committee opinions.

Traditional ethnic-specific carrier screening, previously ACOG's sole recommendation, involves offering specific genetic screening to patients from populations with a high prevalence for certain conditions. One such example is Tay-Sachs disease screening in Ashkenazi Jewish patients.

Panethnic screening, which takes into account mixed or uncertain backgrounds, involves screening for a certain panel of disorders and is available to all patients regardless of their background (for example, cystic fibrosis screening offered to all pregnant patients).

Expanded carrier screening is when a large number of disorders can be screened for simultaneously for a lower cost than previous testing strategies. Expanded carrier screening panels vary in number and which conditions are tested by the laboratory. An ideal expanded carrier screening panel has been debated in the literature but not agreed on.⁷

ObGyns and practices therefore are encouraged to develop a standard counseling and screening protocol to offer to all their patients while being flexible to make available any patient-requested screening that is outside their protocol. Pretest and posttest counseling, including a thorough family history, is essential (as with any genetic testing) and should include residual risk after testing, potential need for specific familial mutation testing instead of general carrier screening, and issues with consanguinity.

Three essential screens

Regardless of the screening strategy chosen from the above options, 3 screening tests should be offered to all pregnant women or couples considering pregnancy (either individually or in the context of an expanded screening panel):

• Cystic fibrosis. At the least, a panel of the 23 most common mutations should be used. More expanded panels, which include hundreds of mutations, increase detection in non-Caucasian populations and for milder forms of the disease or infertility-related mutations.
• Hemoglobinopathies (sickle cell, α- and β-thalassemia). Complete blood count and red blood indices are recommended for all, with hemoglobin electrophoresis recommended for patients of African, Middle Eastern, Mediterranean, or West Indian descent or if mean corpuscular volume is low.
• Spinal muscular atrophy (SMA). The most recent addition to ACOG's recommendations for general carrier screening due to the relatively high carrier frequency (1-in-40 to 1-in-60) and the severity of the disease, SMA causes degeneration of the spinal cord neurons, skeletal muscular atrophy, and overall weakness. Screening is via polymerase chain reaction for SMN1 copy number: 2 copies are normal, and 1 copy indicates a carrier of the SMN1 deletion. About 3% to 4% of patients will screen negative but still will be "carriers" due to having 2 copies of the SMN1 gene on 1 chromosome and no copies on the other chromosome.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

The past year brought new information and guidance from the American College of Obstetricians and Gynecologists (ACOG) on many relevant obstetric topics, making it difficult to choose just a few for this Update. Opioid use in pregnancy was an obvious choice given the national media attention and the potential opportunity for intervention in pregnancy for both the mother and the fetus/newborn. Postpartum hemorrhage, an “oldie but goodie,” was chosen for several reasons: It got a new definition, a new focus on multidisciplinary care, and an exciting novel tool for the treatment toolbox. Finally, given the rapidly changing technology, new screening recommendations, and the complexity of counseling, carrier screening was chosen as a genetic hot topic for this year.

Opioids, obstetrics, and opportunities

Reddy UM, Davis JM, Ren Z, Greene MF; Opioid Use in Pregnancy, Neonatal Abstinence Syndrome, and Childhood Outcomes Workshop Invited Speakers. Opioid use in pregnancy, neonatal abstinence syndrome, and childhood outcomes: Executive summary of a joint workshop. Obstet Gynecol. 2017;130(1):10-28.

ACOG Committee on Obstetric Practice. ACOG committee opinion No. 711: Opioid use and opioid use disorder in pregnancy. Obstet Gynecol. 2017;130(2):e81-e94.

The term "opioid epidemic" is omnipresent in both the lay media and the medical literature. In the past decade, the United States has had a huge increase in the number of opioid prescriptions, the rate of admissions and deaths due to prescription opioid misuse and abuse, and an increased rate of heroin use attributed to prior prescription opioid use.

Obstetrics is unique in that opioid use and abuse disorders affect 2 patients simultaneously (the mother and fetus), and the treatment options are somewhat at odds in that they need to balance a stable maternal status and intrauterine environment with the risk of neonatal abstinence syndrome (NAS). Additionally, pregnancy is an opportunity for a woman with opioid use disorder to have access to medical care (possibly for the first time) leading to the diagnosis and treatment of her disease. As the clinicians on the front line, obstetricians therefore require education and guidance on best practice for management of opioid use in pregnancy.

In 2017, Reddy and colleagues, as part of a joint workshop on opioid use in pregnancy, and a committee opinion from ACOG provided the following recommendations.

Screening

Universally screen for substance use, starting at the first prenatal visit; this is recommended over risk factor-based screening.

Use a validated screening tool. A tool such as a questionnaire is recommended as the first-line screening test (for example, the 4Ps screen, the National Institute on Drug Abuse Quick Screen, and the CRAFFT Screening Interview).

Do not universally screen urine and hair for drugs. This type of screening has many limitations, such as the limited number of substances tested, false-positive results, and inaccurate determination of the frequency or timing of drug use. Information regarding the consequences of the test must be provided, and patient consent must be obtained prior to performing the test.

Treatment

Use medication-assisted treatment with buprenorphine or methadone, which is preferred to medically supervised withdrawal. Medication-assisted treatment prevents withdrawal symptoms and cravings, decreases the risk of relapse, improves compliance with prenatal care and addiction treatment programs, and leads to better obstetric outcomes (higher birth weight, lower rate of preterm birth, lower perinatal mortality).

Know that buprenorphine has several advantages over methadone, including the convenience of an outpatient prescription, a lower risk of overdose, and improved neonatal outcomes (higher birth weight, lower doses of morphine to treat NAS, shorter treatment duration).

Prioritize methadone as the preferred option for pregnant women who are already receiving methadone treatment (changing to buprenorphine may precipitate withdrawal), those with a long-standing history of or multi-substance abuse, and those who have failed other treatment programs.

Prenatal care

Screen for comorbid conditions such as sexually transmitted infections, other medications or substance use, social conditions, and mental health disorders.

Perform ultrasonography serially to monitor fetal growth because of the increased risk of fetal growth restriction.

Consult with anesthesiology for pain control recommendations for labor and delivery and with neonatalogy/pediatrics for NAS counseling.

Intrapartum/postpartum care

Recognize heightened pain. Women with opioid use disorder have increased sensitivity to painful stimuli.

Continue the maintenance dose of methadone or buprenorphine throughout hospitalization, with short-acting opioids added for a brief period for postoperative pain.

Prioritize regional anesthesia for pain control in labor or for cesarean delivery.

Consider alternative therapies such as regional blocks, nonopioid medications (nonsteroidal anti-inflammatory drugs, acetaminophen), or relaxation/mindfulness training.

Avoid mixed antagonist and agonist narcotics (butorphanol, nalbuphine, pentazocine) as they may cause acute withdrawal.

Encourage breastfeeding to decrease the severity of NAS and maternal stress and increase maternal-child bonding and maternal confidence.

Offer contraceptive counseling and services immediately postpartum in the hospital, with strong consideration for long-acting reversible contraception.

Opioid prescribing practices

Opioids are prescribed in excess post–cesarean delivery. Several recent studies have demonstrated that most women are prescribed opioids post–cesarean delivery in excess of the amount they use (median 30–40 tablets prescribed, median 20 tablets used).^1,2 The leftover opioid medication usually is not discarded and therefore is at risk for diversion or misuse. A small subset of patients will use all the opioids prescribed and feel as though they have not received enough medication.

Prescribe post–cesarean delivery opioids more appropriately by considering individual inpatient opioid requirements or a shared decision-making model.³

Prioritize acetaminophen and ibuprofen during breastfeeding. In a recent editorial in OBG Management, Robert L. Barbieri, MD, recommended that whenever possible, acetaminophen and ibuprofen should be the first-line treatment for breastfeeding women, and narcotics that are metabolized by CYP2D6 should be avoided to reduce the risk to the newborn.⁴

Read about new strategies for postpartum hemorrhage.

Postpartum hemorrhage: New definitions and new strategies for stemming the flow

ACOG Committee on Practice Bulletins—Obstetrics. ACOG practice bulletin No. 183: Postpartum hemorrhage. Obstet Gynecol. 2017;130(4):e168-e186.

From the very first sentence of the new ACOG practice bulletin, postpartum hemorrhage (PPH) is redefined as "cumulative blood loss greater than or equal to 1,000 mL or blood loss accompanied by signs or symptoms of hypovolemia within 24 hours after the birth process (includes intrapartum loss) regardless of route of delivery." Although this does not seem to be a huge change from the traditional teaching of a 500-mL blood loss at vaginal delivery and a 1,000-mL loss at cesarean delivery, it reflects a shift in focus from simply responding to a certain amount of bleeding to using a multidisciplinary action plan for treating this leading cause of maternal mortality worldwide.

Focus on developing a PPH action plan

As part of the shift toward a multidisciplinary action plan for PPH, all obstetric team members should be aware of the following:  

• For most postpartum women, by the time they begin to show signs of hemodynamic compromise, the amount of blood loss approaches 25% of their total blood volume (1,500 mL). Lactic acidosis, systemic inflammation, and a consumptive coagulopathy result.  
• Risk stratification prior to delivery, recognition and identification of the source of bleeding, and aggressive early resuscitation to prevent hypovolemia are paramount. Experience gleaned from trauma massive transfusion protocols suggests that judicious transfusion of packed red blood cells, fresh frozen plasma, and platelets in a 1:1:1 ratio is appropriate for obstetric patients. Additionally, patients with low fibrinogen levels should be treated with cryoprecipitate.  
• The use of fixed transfusion ratios and standardized protocols for recognition and management of PPH has been demonstrated to increase earlier intervention and resolution of hemorrhage at an earlier stage, although the maternal outcomes results have been mixed.  
• Multidisciplinary team drills and simulation exercises also should be considered to help solidify training of an institution's teams responsible for PPH response.

Novel management option: Tranexamic acid

In addition to these strategies, there is a new recommendation for managing refractory PPH: tranexamic acid, which works by binding to lysine receptors on plasminogen and plasmin, inhibiting plasmin-mediated fibrin degradation.5 Previously, tranexamic acid was known to be effective in trauma, heart surgery, and in patients with thrombophilias. Pacheco and colleagues recently demonstrated reduced mortality from obstetric bleeding if tranexamic acid was given within 3 hours of delivery, without increased thrombotic complications.⁵ ACOG recommends its use if initial medical therapy fails, while the World Health Organization strongly recommends that tranexamic acid be part of a standard PPH package for all cases of PPH (TABLE).⁶

Read about new ACOG guidance on prepregnancy and prenatal screening.

ACOG Committee on Genetics. Committee opinion No. 690: Carrier screening in the age of genomic medicine. Obstet Gynecol. 2017;129(3):e35-e40.

ACOG Committee on Genetics. Committee opinion No. 691: Carrier screening for genetic conditions. Obstet Gynecol. 2017;129(3):e41-e55.

Ideally, carrier screening should be offered prior to pregnancy to fully inform couples of their reproductive risks and options for pregnancy. If not performed in the preconception period, carrier screening should be offered to all pregnant women. If a patient chooses screening and screens positive for a particular disorder, her reproductive partner should then be offered screening so that the risk of having an affected child can be determined.

New ACOG guidance on prepregnancy and prenatal screening

Carrier screening recommendations have evolved as the technology available has expanded. All 3 of the following strategies now are considered "acceptable" according to 2 recently published ACOG committee opinions.

Traditional ethnic-specific carrier screening, previously ACOG's sole recommendation, involves offering specific genetic screening to patients from populations with a high prevalence for certain conditions. One such example is Tay-Sachs disease screening in Ashkenazi Jewish patients.

Panethnic screening, which takes into account mixed or uncertain backgrounds, involves screening for a certain panel of disorders and is available to all patients regardless of their background (for example, cystic fibrosis screening offered to all pregnant patients).

Expanded carrier screening is when a large number of disorders can be screened for simultaneously for a lower cost than previous testing strategies. Expanded carrier screening panels vary in number and which conditions are tested by the laboratory. An ideal expanded carrier screening panel has been debated in the literature but not agreed on.⁷

ObGyns and practices therefore are encouraged to develop a standard counseling and screening protocol to offer to all their patients while being flexible to make available any patient-requested screening that is outside their protocol. Pretest and posttest counseling, including a thorough family history, is essential (as with any genetic testing) and should include residual risk after testing, potential need for specific familial mutation testing instead of general carrier screening, and issues with consanguinity.

Three essential screens

Regardless of the screening strategy chosen from the above options, 3 screening tests should be offered to all pregnant women or couples considering pregnancy (either individually or in the context of an expanded screening panel):

• Cystic fibrosis. At the least, a panel of the 23 most common mutations should be used. More expanded panels, which include hundreds of mutations, increase detection in non-Caucasian populations and for milder forms of the disease or infertility-related mutations.
• Hemoglobinopathies (sickle cell, α- and β-thalassemia). Complete blood count and red blood indices are recommended for all, with hemoglobin electrophoresis recommended for patients of African, Middle Eastern, Mediterranean, or West Indian descent or if mean corpuscular volume is low.
• Spinal muscular atrophy (SMA). The most recent addition to ACOG's recommendations for general carrier screening due to the relatively high carrier frequency (1-in-40 to 1-in-60) and the severity of the disease, SMA causes degeneration of the spinal cord neurons, skeletal muscular atrophy, and overall weakness. Screening is via polymerase chain reaction for SMN1 copy number: 2 copies are normal, and 1 copy indicates a carrier of the SMN1 deletion. About 3% to 4% of patients will screen negative but still will be "carriers" due to having 2 copies of the SMN1 gene on 1 chromosome and no copies on the other chromosome.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

A one-two combination consisting of a drug to deplete amyloid fibrils from circulation and a monoclonal antibody to mop up residual amyloid protein appears to be safe and shows promising activity against systemic amyloidosis in an early clinical trial.

Pairing the investigational small molecule agent miridesap and the experimental monoclonal antibody dezamizumab resulted in clearance or reductions in amyloid deposits in the livers, spleens, and kidneys of adults with systemic amyloidosis, reported Prof. Sir Mark B. Pepys of University College, London, and his colleagues.

©Nephron/Wikimedia Commons/CC BY SA 3.0

Source: Richards D et al. Sci. Transl. Med. 2018. doi: 10.1126/scitranslmed.aan3128.

A one-two combination consisting of a drug to deplete amyloid fibrils from circulation and a monoclonal antibody to mop up residual amyloid protein appears to be safe and shows promising activity against systemic amyloidosis in an early clinical trial.

Pairing the investigational small molecule agent miridesap and the experimental monoclonal antibody dezamizumab resulted in clearance or reductions in amyloid deposits in the livers, spleens, and kidneys of adults with systemic amyloidosis, reported Prof. Sir Mark B. Pepys of University College, London, and his colleagues.

©Nephron/Wikimedia Commons/CC BY SA 3.0

Source: Richards D et al. Sci. Transl. Med. 2018. doi: 10.1126/scitranslmed.aan3128.

A one-two combination consisting of a drug to deplete amyloid fibrils from circulation and a monoclonal antibody to mop up residual amyloid protein appears to be safe and shows promising activity against systemic amyloidosis in an early clinical trial.

Pairing the investigational small molecule agent miridesap and the experimental monoclonal antibody dezamizumab resulted in clearance or reductions in amyloid deposits in the livers, spleens, and kidneys of adults with systemic amyloidosis, reported Prof. Sir Mark B. Pepys of University College, London, and his colleagues.

©Nephron/Wikimedia Commons/CC BY SA 3.0

Source: Richards D et al. Sci. Transl. Med. 2018. doi: 10.1126/scitranslmed.aan3128.