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The team and I
As a physician or a patient, you probably have noticed that the quality of health care is better when there is a continuous relationship between the physician and the patient. Discontinuity can make doctor-patient communication less fluid, but familiarity can breed comfort and confidence. Patients often complain when they see a different physician at every visit. And physicians know they are less efficient when they are seeing a patient they have never seen before.
They discovered that less continuity was associated with more ambulatory sick visits and more ambulatory sensitive hospitalizations, particularly for children with chronic conditions. Interestingly, they could find no association between continuity measured at well visits and patients’ health outcomes.
With only a gut level and personal relationship with the subject, I wondered how the researchers measured something as nebulous as continuity. It turns out there are several ways to measure continuity, of which the investigators focused on two. The Usual Provider of Care is calculated by dividing the number of visits with the most common provider by the total number of primary care visits. The Bice and Boxerman Continuity of Care Index is more difficult to calculate because, rather than using a single provider, it lumps a small core of providers together (such as a team) as the most the common provider.
As a curmudgeonly, old school, egotistical kind of guy, I was surprised and disappointed to learn from this paper’s references of another study that found, in at least one scenario, the individual-based (Usual Provider of Care) and team-based (Bice and Boxerman Continuity of Care Index) methods of defining continuity yielded comparable results (Med Care. 2016 May;54[5]:e30-4). I always have assumed that, regardless of how well it had been crafted, that I could provide better continuity than a team of providers.
I know what you are thinking: This guy hasn’t bought into the maxim that “There is no I in team.” No, no, I do believe in it, but in the context of continuity of care, it seemed to me that sometimes the more links there are in the chain, the more chances there are for miscommunication. And we all know that primary care is 90% communication.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
As a physician or a patient, you probably have noticed that the quality of health care is better when there is a continuous relationship between the physician and the patient. Discontinuity can make doctor-patient communication less fluid, but familiarity can breed comfort and confidence. Patients often complain when they see a different physician at every visit. And physicians know they are less efficient when they are seeing a patient they have never seen before.
They discovered that less continuity was associated with more ambulatory sick visits and more ambulatory sensitive hospitalizations, particularly for children with chronic conditions. Interestingly, they could find no association between continuity measured at well visits and patients’ health outcomes.
With only a gut level and personal relationship with the subject, I wondered how the researchers measured something as nebulous as continuity. It turns out there are several ways to measure continuity, of which the investigators focused on two. The Usual Provider of Care is calculated by dividing the number of visits with the most common provider by the total number of primary care visits. The Bice and Boxerman Continuity of Care Index is more difficult to calculate because, rather than using a single provider, it lumps a small core of providers together (such as a team) as the most the common provider.
As a curmudgeonly, old school, egotistical kind of guy, I was surprised and disappointed to learn from this paper’s references of another study that found, in at least one scenario, the individual-based (Usual Provider of Care) and team-based (Bice and Boxerman Continuity of Care Index) methods of defining continuity yielded comparable results (Med Care. 2016 May;54[5]:e30-4). I always have assumed that, regardless of how well it had been crafted, that I could provide better continuity than a team of providers.
I know what you are thinking: This guy hasn’t bought into the maxim that “There is no I in team.” No, no, I do believe in it, but in the context of continuity of care, it seemed to me that sometimes the more links there are in the chain, the more chances there are for miscommunication. And we all know that primary care is 90% communication.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
As a physician or a patient, you probably have noticed that the quality of health care is better when there is a continuous relationship between the physician and the patient. Discontinuity can make doctor-patient communication less fluid, but familiarity can breed comfort and confidence. Patients often complain when they see a different physician at every visit. And physicians know they are less efficient when they are seeing a patient they have never seen before.
They discovered that less continuity was associated with more ambulatory sick visits and more ambulatory sensitive hospitalizations, particularly for children with chronic conditions. Interestingly, they could find no association between continuity measured at well visits and patients’ health outcomes.
With only a gut level and personal relationship with the subject, I wondered how the researchers measured something as nebulous as continuity. It turns out there are several ways to measure continuity, of which the investigators focused on two. The Usual Provider of Care is calculated by dividing the number of visits with the most common provider by the total number of primary care visits. The Bice and Boxerman Continuity of Care Index is more difficult to calculate because, rather than using a single provider, it lumps a small core of providers together (such as a team) as the most the common provider.
As a curmudgeonly, old school, egotistical kind of guy, I was surprised and disappointed to learn from this paper’s references of another study that found, in at least one scenario, the individual-based (Usual Provider of Care) and team-based (Bice and Boxerman Continuity of Care Index) methods of defining continuity yielded comparable results (Med Care. 2016 May;54[5]:e30-4). I always have assumed that, regardless of how well it had been crafted, that I could provide better continuity than a team of providers.
I know what you are thinking: This guy hasn’t bought into the maxim that “There is no I in team.” No, no, I do believe in it, but in the context of continuity of care, it seemed to me that sometimes the more links there are in the chain, the more chances there are for miscommunication. And we all know that primary care is 90% communication.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
Successful teams
As physicians, we know, and have been taught, that success comes from being smart and answering questions correctly. By doing so, we excelled in school, scored high on standardized tests, and confidently raised our hands in class. As a result, we were chosen for plum assignments like class officer, yearbook editor, and team captain. Success bred success and we were initiated into honor societies, accepted into prestigious internships, and allowed to work on important research projects.
These achievements guaranteed further success in medical school where the tradition of competition continued as we positioned for the attention of those who would someday write our letters of recommendation. This model of individual success served us very well until we joined a hematology group to begin our practice.
When we join a group of physicians, we join a team. The team might organize around diagnoses, laboratories, or geographic location, but it is a team nonetheless. The team, of course, includes more than just physicians. As a team member, we are expected to fulfill a role that advances the mission of the team and the larger organization. That mission may include some combination of academic, educational, and clinical productivity.
As physicians trained to compete with other individuals, teamwork does not come naturally. We might think that so long as the team consists of more and mor
As Margaret Heffernan brilliantly points out in “Margaret Heffernan: Why it’s time to forget the pecking order at work,” a TED talk video posted on YouTube, teams consisting of those skilled in interpersonal relationships are much more effective, efficient, and productive than are teams consisting of those skilled in problem-solving with superior IQs. The teams that function most successfully are those that create a culture of trust and helpfulness no matter the individual talents of those on the team.
As a department chair, I try to see past the thickness of the CV to ensure that I see into the person’s ability to relate with other people. If the CV is thick and the emotional intelligence high, then that is the person I want on my team, but I would rather have the latter than the former, and so would teammates and patients.
Research has shown repeatedly that no individuals can hope to achieve on their own what a good, functional team can achieve as a group. Yet, the academic hierarchy rewards individuals, not teams. Hopefully, the rewarded individual will recognize the support and effort of the team, but that is not always the case and not always done adequately.
How can academic departments develop social capital in their teams and reward them, in addition to individuals, for their successes? Social capital grows when the relationships between people become stronger. Those bonds develop though informal interaction outside the work environment. The more the team knows each other, the more they trust each other, the more they are willing to help each other, and the more they are likely to be civil to one another. Teams of friends are much more likely to solve problems quickly for less cost than teams of strangers.
Reward and recognition for a team is not as easy as it sounds. Everyone wants individual recognition for their work, not just as an integral member of a team. The world loves All-Stars and MVPs as much as they love their teams. We do not need to change the way we reward individuals, but we do need to also include teams for reward and recognition. How can a leader determine which teams are most deserving of the highest reward? Many institutions measure employee engagement through surveys. High-functioning teams are likely to be highly engaged and high scores on surveys should be recognized and rewarded. Teams with low employee turnover help reduce training costs and should be appreciated.
Successful implementation of continuous improvement projects are an often overlooked opportunity for an expression of gratitude. I am sure there are other ways to acknowledge a team’s efforts and I hope readers will write to us with their ideas for all to share. Perhaps by doing so, we can accelerate the cultural transformation of academic medicine from one of personal achievement to one of team success.
Dr. Kalaycio is editor in chief of Hematology News. He chairs the department of hematologic oncology and blood disorders at Cleveland Clinic Taussig Cancer Institute. Contact him at [email protected].
As physicians, we know, and have been taught, that success comes from being smart and answering questions correctly. By doing so, we excelled in school, scored high on standardized tests, and confidently raised our hands in class. As a result, we were chosen for plum assignments like class officer, yearbook editor, and team captain. Success bred success and we were initiated into honor societies, accepted into prestigious internships, and allowed to work on important research projects.
These achievements guaranteed further success in medical school where the tradition of competition continued as we positioned for the attention of those who would someday write our letters of recommendation. This model of individual success served us very well until we joined a hematology group to begin our practice.
When we join a group of physicians, we join a team. The team might organize around diagnoses, laboratories, or geographic location, but it is a team nonetheless. The team, of course, includes more than just physicians. As a team member, we are expected to fulfill a role that advances the mission of the team and the larger organization. That mission may include some combination of academic, educational, and clinical productivity.
As physicians trained to compete with other individuals, teamwork does not come naturally. We might think that so long as the team consists of more and mor
As Margaret Heffernan brilliantly points out in “Margaret Heffernan: Why it’s time to forget the pecking order at work,” a TED talk video posted on YouTube, teams consisting of those skilled in interpersonal relationships are much more effective, efficient, and productive than are teams consisting of those skilled in problem-solving with superior IQs. The teams that function most successfully are those that create a culture of trust and helpfulness no matter the individual talents of those on the team.
As a department chair, I try to see past the thickness of the CV to ensure that I see into the person’s ability to relate with other people. If the CV is thick and the emotional intelligence high, then that is the person I want on my team, but I would rather have the latter than the former, and so would teammates and patients.
Research has shown repeatedly that no individuals can hope to achieve on their own what a good, functional team can achieve as a group. Yet, the academic hierarchy rewards individuals, not teams. Hopefully, the rewarded individual will recognize the support and effort of the team, but that is not always the case and not always done adequately.
How can academic departments develop social capital in their teams and reward them, in addition to individuals, for their successes? Social capital grows when the relationships between people become stronger. Those bonds develop though informal interaction outside the work environment. The more the team knows each other, the more they trust each other, the more they are willing to help each other, and the more they are likely to be civil to one another. Teams of friends are much more likely to solve problems quickly for less cost than teams of strangers.
Reward and recognition for a team is not as easy as it sounds. Everyone wants individual recognition for their work, not just as an integral member of a team. The world loves All-Stars and MVPs as much as they love their teams. We do not need to change the way we reward individuals, but we do need to also include teams for reward and recognition. How can a leader determine which teams are most deserving of the highest reward? Many institutions measure employee engagement through surveys. High-functioning teams are likely to be highly engaged and high scores on surveys should be recognized and rewarded. Teams with low employee turnover help reduce training costs and should be appreciated.
Successful implementation of continuous improvement projects are an often overlooked opportunity for an expression of gratitude. I am sure there are other ways to acknowledge a team’s efforts and I hope readers will write to us with their ideas for all to share. Perhaps by doing so, we can accelerate the cultural transformation of academic medicine from one of personal achievement to one of team success.
Dr. Kalaycio is editor in chief of Hematology News. He chairs the department of hematologic oncology and blood disorders at Cleveland Clinic Taussig Cancer Institute. Contact him at [email protected].
As physicians, we know, and have been taught, that success comes from being smart and answering questions correctly. By doing so, we excelled in school, scored high on standardized tests, and confidently raised our hands in class. As a result, we were chosen for plum assignments like class officer, yearbook editor, and team captain. Success bred success and we were initiated into honor societies, accepted into prestigious internships, and allowed to work on important research projects.
These achievements guaranteed further success in medical school where the tradition of competition continued as we positioned for the attention of those who would someday write our letters of recommendation. This model of individual success served us very well until we joined a hematology group to begin our practice.
When we join a group of physicians, we join a team. The team might organize around diagnoses, laboratories, or geographic location, but it is a team nonetheless. The team, of course, includes more than just physicians. As a team member, we are expected to fulfill a role that advances the mission of the team and the larger organization. That mission may include some combination of academic, educational, and clinical productivity.
As physicians trained to compete with other individuals, teamwork does not come naturally. We might think that so long as the team consists of more and mor
As Margaret Heffernan brilliantly points out in “Margaret Heffernan: Why it’s time to forget the pecking order at work,” a TED talk video posted on YouTube, teams consisting of those skilled in interpersonal relationships are much more effective, efficient, and productive than are teams consisting of those skilled in problem-solving with superior IQs. The teams that function most successfully are those that create a culture of trust and helpfulness no matter the individual talents of those on the team.
As a department chair, I try to see past the thickness of the CV to ensure that I see into the person’s ability to relate with other people. If the CV is thick and the emotional intelligence high, then that is the person I want on my team, but I would rather have the latter than the former, and so would teammates and patients.
Research has shown repeatedly that no individuals can hope to achieve on their own what a good, functional team can achieve as a group. Yet, the academic hierarchy rewards individuals, not teams. Hopefully, the rewarded individual will recognize the support and effort of the team, but that is not always the case and not always done adequately.
How can academic departments develop social capital in their teams and reward them, in addition to individuals, for their successes? Social capital grows when the relationships between people become stronger. Those bonds develop though informal interaction outside the work environment. The more the team knows each other, the more they trust each other, the more they are willing to help each other, and the more they are likely to be civil to one another. Teams of friends are much more likely to solve problems quickly for less cost than teams of strangers.
Reward and recognition for a team is not as easy as it sounds. Everyone wants individual recognition for their work, not just as an integral member of a team. The world loves All-Stars and MVPs as much as they love their teams. We do not need to change the way we reward individuals, but we do need to also include teams for reward and recognition. How can a leader determine which teams are most deserving of the highest reward? Many institutions measure employee engagement through surveys. High-functioning teams are likely to be highly engaged and high scores on surveys should be recognized and rewarded. Teams with low employee turnover help reduce training costs and should be appreciated.
Successful implementation of continuous improvement projects are an often overlooked opportunity for an expression of gratitude. I am sure there are other ways to acknowledge a team’s efforts and I hope readers will write to us with their ideas for all to share. Perhaps by doing so, we can accelerate the cultural transformation of academic medicine from one of personal achievement to one of team success.
Dr. Kalaycio is editor in chief of Hematology News. He chairs the department of hematologic oncology and blood disorders at Cleveland Clinic Taussig Cancer Institute. Contact him at [email protected].
Spinal Cord Stimulation May Improve Gait in Patients With Advanced Parkinson’s Disease
VANCOUVER—Spinal cord stimulation improves gait in patients with advanced Parkinson’s disease, according to a pilot study described at the 21st International Congress of Parkinson’s Disease and Movement Disorders. The technique allows neurologists to determine which stimulation parameters provide the greatest benefit for each patient, said Mandar Jog, MD, Professor of Neurology and Engineering and Director of the Movement Disorders Center at Western University in London, Ontario. 
“Each participant demonstrated unique gait c
Treatment-Resistant Symptoms
Gait dysfunction and freezing of gait are common in advanced Parkinson’s disease, and gait symptoms are largely resistant to dopamine replacement therapy. Studies have suggested that epidural spinal cord stimulation, which is an approved therapy for pain, may help treat levodopa-resistant motor symptoms in Parkinson’s disease.
Dr. Jog and colleagues analyzed objective gait measurements to understand which spinal cord stimulation settings most improved gait. They tested combinations of pulse widths and frequencies that induced paresthesia in patients’ lower limbs.
The six-month study included five men with Parkinson’s disease who had significant gait disturbances on levodopa therapy. The patients were not eligible for deep brain stimulation. Mean age was 71, and mean disease duration was 14 years. The patients underwent mid-thoracic spinal cord stimulation surgery, and a dorsal spinal cord stimulator was implanted in the epidural space (T7–10). The researchers evaluated patients before the operation and at weeks 2, 4, 6, 8, 10, 12, 16, and 24 after surgery.
The investigators conducted randomized testing of different spinal cord stimulation settings at weeks 2, 4, 6, 8, 10, 12, and 16. At week 24, researchers evaluated patients when they had been off stimulation for 48 hours and then with stimulation.
Patients completed walking tasks on a 20-foot walkway with sensors that relayed each footfall to a computer with gait analysis software. The researchers grouped gait variables according to whether they were expected to increase with improvement (eg, step length and stride velocity) or decrease with improvement (eg, stride width and step time).
Determining Optimal Settings
For two of the patients, the most effective spinal cord stimulation setting was a pulse width of 400 µs and a frequency of 60 Hz. The optimal settings for the remaining three patients were 300 µs and 30 Hz, 300 µs and 130 Hz, and 300 or 400 µs and 130 Hz.
Key gait variables improved with spinal cord stimulation. For instance, stride velocity significantly improved by 54% with the optimal settings, compared with baseline. Mean number of freezing of gait episodes significantly decreased. Unified Parkinson’s Disease Rating Scale motor scores and patients’ confidence in performing activities of daily living also significantly improved, compared with baseline.
Patients achieved a greater degree of independence after receiving spinal cord stimulation, Dr. Jog said. For example, one patient no longer had to rely on a wheelchair or scooter to get around, and one patient no longer needed help getting out of a chair. One patient was able to resume working in fields, and one patient was able to walk on a beach. “Everybody improved to different levels. The improvement occurred immediately in the laboratory,” he said.
No adverse events were reported. The researchers plan to conduct further studies. Because spinal cord stimulation already is available for the treatment of pain, it may be feasible to pair a spinal cord stimulation device with a sensor system that allows physicians to optimize the stimulator’s settings for the treatment of gait dysfunction in Parkinson’s disease, Dr. Jog said.
—Jake Remaly
Suggested Reading
de Andrade EM, Ghilardi MG, Cury RG, et al. Spinal cord stimulation for Parkinson’s disease: a systematic review. Neurosurg Rev. 2016;39(1):27-35.
Pinto de Souza C, Hamani C, Oliveira Souza C, et al. Spinal cord stimulation improves gait in patients with Parkinson’s disease previously treated with deep brain stimulation. Mov Disord. 2017;32(2):278-282.
VANCOUVER—Spinal cord stimulation improves gait in patients with advanced Parkinson’s disease, according to a pilot study described at the 21st International Congress of Parkinson’s Disease and Movement Disorders. The technique allows neurologists to determine which stimulation parameters provide the greatest benefit for each patient, said Mandar Jog, MD, Professor of Neurology and Engineering and Director of the Movement Disorders Center at Western University in London, Ontario.
“Each participant demonstrated unique gait c
Treatment-Resistant Symptoms
Gait dysfunction and freezing of gait are common in advanced Parkinson’s disease, and gait symptoms are largely resistant to dopamine replacement therapy. Studies have suggested that epidural spinal cord stimulation, which is an approved therapy for pain, may help treat levodopa-resistant motor symptoms in Parkinson’s disease.
Dr. Jog and colleagues analyzed objective gait measurements to understand which spinal cord stimulation settings most improved gait. They tested combinations of pulse widths and frequencies that induced paresthesia in patients’ lower limbs.
The six-month study included five men with Parkinson’s disease who had significant gait disturbances on levodopa therapy. The patients were not eligible for deep brain stimulation. Mean age was 71, and mean disease duration was 14 years. The patients underwent mid-thoracic spinal cord stimulation surgery, and a dorsal spinal cord stimulator was implanted in the epidural space (T7–10). The researchers evaluated patients before the operation and at weeks 2, 4, 6, 8, 10, 12, 16, and 24 after surgery.
The investigators conducted randomized testing of different spinal cord stimulation settings at weeks 2, 4, 6, 8, 10, 12, and 16. At week 24, researchers evaluated patients when they had been off stimulation for 48 hours and then with stimulation.
Patients completed walking tasks on a 20-foot walkway with sensors that relayed each footfall to a computer with gait analysis software. The researchers grouped gait variables according to whether they were expected to increase with improvement (eg, step length and stride velocity) or decrease with improvement (eg, stride width and step time).
Determining Optimal Settings
For two of the patients, the most effective spinal cord stimulation setting was a pulse width of 400 µs and a frequency of 60 Hz. The optimal settings for the remaining three patients were 300 µs and 30 Hz, 300 µs and 130 Hz, and 300 or 400 µs and 130 Hz.
Key gait variables improved with spinal cord stimulation. For instance, stride velocity significantly improved by 54% with the optimal settings, compared with baseline. Mean number of freezing of gait episodes significantly decreased. Unified Parkinson’s Disease Rating Scale motor scores and patients’ confidence in performing activities of daily living also significantly improved, compared with baseline.
Patients achieved a greater degree of independence after receiving spinal cord stimulation, Dr. Jog said. For example, one patient no longer had to rely on a wheelchair or scooter to get around, and one patient no longer needed help getting out of a chair. One patient was able to resume working in fields, and one patient was able to walk on a beach. “Everybody improved to different levels. The improvement occurred immediately in the laboratory,” he said.
No adverse events were reported. The researchers plan to conduct further studies. Because spinal cord stimulation already is available for the treatment of pain, it may be feasible to pair a spinal cord stimulation device with a sensor system that allows physicians to optimize the stimulator’s settings for the treatment of gait dysfunction in Parkinson’s disease, Dr. Jog said.
—Jake Remaly
Suggested Reading
de Andrade EM, Ghilardi MG, Cury RG, et al. Spinal cord stimulation for Parkinson’s disease: a systematic review. Neurosurg Rev. 2016;39(1):27-35.
Pinto de Souza C, Hamani C, Oliveira Souza C, et al. Spinal cord stimulation improves gait in patients with Parkinson’s disease previously treated with deep brain stimulation. Mov Disord. 2017;32(2):278-282.
VANCOUVER—Spinal cord stimulation improves gait in patients with advanced Parkinson’s disease, according to a pilot study described at the 21st International Congress of Parkinson’s Disease and Movement Disorders. The technique allows neurologists to determine which stimulation parameters provide the greatest benefit for each patient, said Mandar Jog, MD, Professor of Neurology and Engineering and Director of the Movement Disorders Center at Western University in London, Ontario.
“Each participant demonstrated unique gait c
Treatment-Resistant Symptoms
Gait dysfunction and freezing of gait are common in advanced Parkinson’s disease, and gait symptoms are largely resistant to dopamine replacement therapy. Studies have suggested that epidural spinal cord stimulation, which is an approved therapy for pain, may help treat levodopa-resistant motor symptoms in Parkinson’s disease.
Dr. Jog and colleagues analyzed objective gait measurements to understand which spinal cord stimulation settings most improved gait. They tested combinations of pulse widths and frequencies that induced paresthesia in patients’ lower limbs.
The six-month study included five men with Parkinson’s disease who had significant gait disturbances on levodopa therapy. The patients were not eligible for deep brain stimulation. Mean age was 71, and mean disease duration was 14 years. The patients underwent mid-thoracic spinal cord stimulation surgery, and a dorsal spinal cord stimulator was implanted in the epidural space (T7–10). The researchers evaluated patients before the operation and at weeks 2, 4, 6, 8, 10, 12, 16, and 24 after surgery.
The investigators conducted randomized testing of different spinal cord stimulation settings at weeks 2, 4, 6, 8, 10, 12, and 16. At week 24, researchers evaluated patients when they had been off stimulation for 48 hours and then with stimulation.
Patients completed walking tasks on a 20-foot walkway with sensors that relayed each footfall to a computer with gait analysis software. The researchers grouped gait variables according to whether they were expected to increase with improvement (eg, step length and stride velocity) or decrease with improvement (eg, stride width and step time).
Determining Optimal Settings
For two of the patients, the most effective spinal cord stimulation setting was a pulse width of 400 µs and a frequency of 60 Hz. The optimal settings for the remaining three patients were 300 µs and 30 Hz, 300 µs and 130 Hz, and 300 or 400 µs and 130 Hz.
Key gait variables improved with spinal cord stimulation. For instance, stride velocity significantly improved by 54% with the optimal settings, compared with baseline. Mean number of freezing of gait episodes significantly decreased. Unified Parkinson’s Disease Rating Scale motor scores and patients’ confidence in performing activities of daily living also significantly improved, compared with baseline.
Patients achieved a greater degree of independence after receiving spinal cord stimulation, Dr. Jog said. For example, one patient no longer had to rely on a wheelchair or scooter to get around, and one patient no longer needed help getting out of a chair. One patient was able to resume working in fields, and one patient was able to walk on a beach. “Everybody improved to different levels. The improvement occurred immediately in the laboratory,” he said.
No adverse events were reported. The researchers plan to conduct further studies. Because spinal cord stimulation already is available for the treatment of pain, it may be feasible to pair a spinal cord stimulation device with a sensor system that allows physicians to optimize the stimulator’s settings for the treatment of gait dysfunction in Parkinson’s disease, Dr. Jog said.
—Jake Remaly
Suggested Reading
de Andrade EM, Ghilardi MG, Cury RG, et al. Spinal cord stimulation for Parkinson’s disease: a systematic review. Neurosurg Rev. 2016;39(1):27-35.
Pinto de Souza C, Hamani C, Oliveira Souza C, et al. Spinal cord stimulation improves gait in patients with Parkinson’s disease previously treated with deep brain stimulation. Mov Disord. 2017;32(2):278-282.
The impact of Election 2016
Because of the health care policy work I have done over the years, I often get asked about what to expect from Capitol Hill and from federal policy makers in D.C. Since the surprise election results in November, the most common questions revolve around what impact the Trump administration is likely to have on the delivery system reform work done since the passage of the Affordable Care Act (ACA).
While much uncertainty remains, events since the election have given us some clues to answer these and other questions.
Let’s address the ACA. It’s important to recognize that the ACA cannot be repealed completely for at least two reasons. First, it does not even exist as it was passed, having undergone several changes, including adjustments and exemptions. Second, parts of the bill would require 60 votes in the Senate to repeal, and those votes are not available to the party seeking repeal.
Yes, parts of the bill could be changed significantly with only Republican votes. However, the reality is that many changes would have occurred even if Hillary Clinton had won the election; there are elements of the current law that are not working and that both sides acknowledge need to be fixed, such as state individual insurance exchanges.
There also are parts of the ACA that neither party would like to see rescinded, which are unlikely to be removed in a new law – for example, losing insurance for preexisting conditions.
From the standpoint of providers, the most notable aspect of the current discussion is that proposed changes have largely been limited to addressing areas of insurance reform. This has potential impact on who is covered under a revised plan. In the meantime, the important work of delivery system reform – the elements of the ACA that providers care the most about (and that will have the most impact on their careers) – have been left untouched. There are strong signs that this will remain the case and that this important work will continue.
What are those signs? First of all, neither the “repeal” bill passed by the House nor any of the bills considered by the Senate made any mention of interrupting any of the important work being done by the Center for Medicare & Medicaid Innovation (CMMI), the part of the Centers for Medicare & Medicaid Services created by the ACA to develop and test alternative payment models (APMs), like accountable care organizations, bundled payments, etc. If successful, this work will improve quality while lowering the growth of health care costs and may save a health care system that, if unchecked, will create a crushing financial burden that threatens the Medicare Trust Fund. It also is a strong and clear sign that the CMMI continues its work today under the same effective leadership that first created excitement about its potential to improve the delivery system.
But probably the clearest sign that delivery system reform will continue was the strong bipartisan support shown in the passage of the Medicare Access and CHIP Reauthorization Act (MACRA) in April of 2015. This landmark piece of legislation creates a pathway that moves the entire health care system away from fee for service and toward payment models that will reward providers for innovations that will lower the cost of care, eliminate waste, improve safety, and achieve better outcomes. It puts in place a plan that will use APMs to offer providers the incentives to create care models that may be the salvation of our health care system. In the long run, isn’t this what matters the most?
Politicians in Washington can’t save our system. They can create or remove entitlements or support one segment of the population at the expense of another. But, in the end, they are only moving dollars around from one pocket to another, rearranging deck chairs on the Titanic of the American health care system.
The reality is that the only thing that can save our health care system is to lower the cost of care. And we all know that, as providers, only we can do that. SHM will be helping its members lead the way, providing educational content, training, advocacy, and policy leadership.
It will be up to the nation’s caregivers to reform the delivery system in a way that is sustainable for our generation and generations to come. We continue that work today, and I see no evidence that anyone on Capitol Hill wants us to stop.
Dr. Greeno is president of the Society of Hospital Medicine and senior adviser for medical affairs at TeamHealth.
Because of the health care policy work I have done over the years, I often get asked about what to expect from Capitol Hill and from federal policy makers in D.C. Since the surprise election results in November, the most common questions revolve around what impact the Trump administration is likely to have on the delivery system reform work done since the passage of the Affordable Care Act (ACA).
While much uncertainty remains, events since the election have given us some clues to answer these and other questions.
Let’s address the ACA. It’s important to recognize that the ACA cannot be repealed completely for at least two reasons. First, it does not even exist as it was passed, having undergone several changes, including adjustments and exemptions. Second, parts of the bill would require 60 votes in the Senate to repeal, and those votes are not available to the party seeking repeal.
Yes, parts of the bill could be changed significantly with only Republican votes. However, the reality is that many changes would have occurred even if Hillary Clinton had won the election; there are elements of the current law that are not working and that both sides acknowledge need to be fixed, such as state individual insurance exchanges.
There also are parts of the ACA that neither party would like to see rescinded, which are unlikely to be removed in a new law – for example, losing insurance for preexisting conditions.
From the standpoint of providers, the most notable aspect of the current discussion is that proposed changes have largely been limited to addressing areas of insurance reform. This has potential impact on who is covered under a revised plan. In the meantime, the important work of delivery system reform – the elements of the ACA that providers care the most about (and that will have the most impact on their careers) – have been left untouched. There are strong signs that this will remain the case and that this important work will continue.
What are those signs? First of all, neither the “repeal” bill passed by the House nor any of the bills considered by the Senate made any mention of interrupting any of the important work being done by the Center for Medicare & Medicaid Innovation (CMMI), the part of the Centers for Medicare & Medicaid Services created by the ACA to develop and test alternative payment models (APMs), like accountable care organizations, bundled payments, etc. If successful, this work will improve quality while lowering the growth of health care costs and may save a health care system that, if unchecked, will create a crushing financial burden that threatens the Medicare Trust Fund. It also is a strong and clear sign that the CMMI continues its work today under the same effective leadership that first created excitement about its potential to improve the delivery system.
But probably the clearest sign that delivery system reform will continue was the strong bipartisan support shown in the passage of the Medicare Access and CHIP Reauthorization Act (MACRA) in April of 2015. This landmark piece of legislation creates a pathway that moves the entire health care system away from fee for service and toward payment models that will reward providers for innovations that will lower the cost of care, eliminate waste, improve safety, and achieve better outcomes. It puts in place a plan that will use APMs to offer providers the incentives to create care models that may be the salvation of our health care system. In the long run, isn’t this what matters the most?
Politicians in Washington can’t save our system. They can create or remove entitlements or support one segment of the population at the expense of another. But, in the end, they are only moving dollars around from one pocket to another, rearranging deck chairs on the Titanic of the American health care system.
The reality is that the only thing that can save our health care system is to lower the cost of care. And we all know that, as providers, only we can do that. SHM will be helping its members lead the way, providing educational content, training, advocacy, and policy leadership.
It will be up to the nation’s caregivers to reform the delivery system in a way that is sustainable for our generation and generations to come. We continue that work today, and I see no evidence that anyone on Capitol Hill wants us to stop.
Dr. Greeno is president of the Society of Hospital Medicine and senior adviser for medical affairs at TeamHealth.
Because of the health care policy work I have done over the years, I often get asked about what to expect from Capitol Hill and from federal policy makers in D.C. Since the surprise election results in November, the most common questions revolve around what impact the Trump administration is likely to have on the delivery system reform work done since the passage of the Affordable Care Act (ACA).
While much uncertainty remains, events since the election have given us some clues to answer these and other questions.
Let’s address the ACA. It’s important to recognize that the ACA cannot be repealed completely for at least two reasons. First, it does not even exist as it was passed, having undergone several changes, including adjustments and exemptions. Second, parts of the bill would require 60 votes in the Senate to repeal, and those votes are not available to the party seeking repeal.
Yes, parts of the bill could be changed significantly with only Republican votes. However, the reality is that many changes would have occurred even if Hillary Clinton had won the election; there are elements of the current law that are not working and that both sides acknowledge need to be fixed, such as state individual insurance exchanges.
There also are parts of the ACA that neither party would like to see rescinded, which are unlikely to be removed in a new law – for example, losing insurance for preexisting conditions.
From the standpoint of providers, the most notable aspect of the current discussion is that proposed changes have largely been limited to addressing areas of insurance reform. This has potential impact on who is covered under a revised plan. In the meantime, the important work of delivery system reform – the elements of the ACA that providers care the most about (and that will have the most impact on their careers) – have been left untouched. There are strong signs that this will remain the case and that this important work will continue.
What are those signs? First of all, neither the “repeal” bill passed by the House nor any of the bills considered by the Senate made any mention of interrupting any of the important work being done by the Center for Medicare & Medicaid Innovation (CMMI), the part of the Centers for Medicare & Medicaid Services created by the ACA to develop and test alternative payment models (APMs), like accountable care organizations, bundled payments, etc. If successful, this work will improve quality while lowering the growth of health care costs and may save a health care system that, if unchecked, will create a crushing financial burden that threatens the Medicare Trust Fund. It also is a strong and clear sign that the CMMI continues its work today under the same effective leadership that first created excitement about its potential to improve the delivery system.
But probably the clearest sign that delivery system reform will continue was the strong bipartisan support shown in the passage of the Medicare Access and CHIP Reauthorization Act (MACRA) in April of 2015. This landmark piece of legislation creates a pathway that moves the entire health care system away from fee for service and toward payment models that will reward providers for innovations that will lower the cost of care, eliminate waste, improve safety, and achieve better outcomes. It puts in place a plan that will use APMs to offer providers the incentives to create care models that may be the salvation of our health care system. In the long run, isn’t this what matters the most?
Politicians in Washington can’t save our system. They can create or remove entitlements or support one segment of the population at the expense of another. But, in the end, they are only moving dollars around from one pocket to another, rearranging deck chairs on the Titanic of the American health care system.
The reality is that the only thing that can save our health care system is to lower the cost of care. And we all know that, as providers, only we can do that. SHM will be helping its members lead the way, providing educational content, training, advocacy, and policy leadership.
It will be up to the nation’s caregivers to reform the delivery system in a way that is sustainable for our generation and generations to come. We continue that work today, and I see no evidence that anyone on Capitol Hill wants us to stop.
Dr. Greeno is president of the Society of Hospital Medicine and senior adviser for medical affairs at TeamHealth.
VIDEO: How to discharge new pediatric diabetes cases in 2 days
NASHVILLE, TENN. – Pediatric endocrinologist Cassandra Brady, MD, caught the attention of her audience at Pediatric Hospital Medicine when she mentioned that children presenting with new-onset diabetes rarely spend more than 2 days at Vanderbilt University’s children’s hospital, even if they present in diabetic ketoacidosis.
In many places, children with new-onset diabetes spend quite a bit longer in the hospital – even if they are medically stable and feeling fine – for diabetes education.
That’s not the case at Vanderbilt, where Dr. Brady is an assistant professor. Once kids are stabilized, they and their parents undergo a 3-hour crash course – sometimes even in the PICU – on diabetes survival skills, and then they’re sent home with insulin. They learn the finer points about carbohydrate counting and tight glucose control at subsequent outpatient visits.
More and more payers are probably going to push for that model, Dr. Brady noted at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
For those interested in making the transition to outpatient eduction, she explained in an interview exactly how Vanderbilt’s been doing it safely for years.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN. – Pediatric endocrinologist Cassandra Brady, MD, caught the attention of her audience at Pediatric Hospital Medicine when she mentioned that children presenting with new-onset diabetes rarely spend more than 2 days at Vanderbilt University’s children’s hospital, even if they present in diabetic ketoacidosis.
In many places, children with new-onset diabetes spend quite a bit longer in the hospital – even if they are medically stable and feeling fine – for diabetes education.
That’s not the case at Vanderbilt, where Dr. Brady is an assistant professor. Once kids are stabilized, they and their parents undergo a 3-hour crash course – sometimes even in the PICU – on diabetes survival skills, and then they’re sent home with insulin. They learn the finer points about carbohydrate counting and tight glucose control at subsequent outpatient visits.
More and more payers are probably going to push for that model, Dr. Brady noted at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
For those interested in making the transition to outpatient eduction, she explained in an interview exactly how Vanderbilt’s been doing it safely for years.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN. – Pediatric endocrinologist Cassandra Brady, MD, caught the attention of her audience at Pediatric Hospital Medicine when she mentioned that children presenting with new-onset diabetes rarely spend more than 2 days at Vanderbilt University’s children’s hospital, even if they present in diabetic ketoacidosis.
In many places, children with new-onset diabetes spend quite a bit longer in the hospital – even if they are medically stable and feeling fine – for diabetes education.
That’s not the case at Vanderbilt, where Dr. Brady is an assistant professor. Once kids are stabilized, they and their parents undergo a 3-hour crash course – sometimes even in the PICU – on diabetes survival skills, and then they’re sent home with insulin. They learn the finer points about carbohydrate counting and tight glucose control at subsequent outpatient visits.
More and more payers are probably going to push for that model, Dr. Brady noted at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.
For those interested in making the transition to outpatient eduction, she explained in an interview exactly how Vanderbilt’s been doing it safely for years.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT PHM 2017
Treating RLS With Dopamine Agonists May Increase Risk for New-Onset Mental Disorders
BOSTON—Among patients with primary restless legs syndrome (RLS) and without a history of psychiatric disorders, patients who receive de novo dopamine agonist treatment are approximately twice as likely to subsequently develop a mental disorder as those who do not receive dopamine agonist treatment, according to a large-scale retrospective study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies.
Previous research has demonstrated an increased risk of mental disorders among patients with Parkinson’s disease who are treated with dopamine agonists. Many patients with RLS are also treated with dopamine agonists, although at lower doses than patients with Parkinson’s disease. Given these lower doses, clinicians assumed that the risk of dopamine agonist-induced mental disorders in RLS would be small. Clinical case studies suggest a higher-than-anticipated risk, however.
An Examination of Claims Data
To investigate whether dopamine agonists increase the risk of developing mental disorders in patients with RLS, Cheryl Hankin, PhD, President and Chief Scientific Officer of BioMedEcon, a health economics and outcomes research firm in Moss Beach, California, and colleagues examined Truven MarketScan Commercial and Medicare Supplemental databases of claims filed between July 1, 2008, and December 31, 2014. From a pool of 539,399 patients with a diagnosis of RLS, investigators identified adults with two or more years of claims data preceding and following their index RLS diagnosis dates. 
Patients were excluded from the analysis if, in the two or more years preceding RLS diagnosis, they received a diagnosis of mental disorder or filled a prescription for an antidepressant or antipsychotic. Also excluded were patients who filled a prescription for a dopamine agonist in the two or more years preceding RLS diagnosis. Patients who were ever diagnosed with Parkinson’s disease, kidney disease, iron deficiency, or pregnancy were assumed to have secondary RLS and were also excluded.
The investigators identified 5,419 eligible participants. Of this group, 1,649 patients received dopamine agonists after RLS diagnosis. Specifically, 571 participants received pramipexole, 915 received ropinirole, and 163 received both. Approximately 65% of patients were female. Patients residing in the Northeast were significantly less likely to receive dopamine agonists, compared with patients residing in the Midwest or the South. The investigators found no significant differences in treatment status by comorbid illness burden or by sex. The investigators also found no significant differences in demographic characteristics between patients receiving pramipexole and those receiving ropinirole.
Risk Was Significantly Greater in Patients Receiving Dopamine Agonist
Next, from this pool of eligible subjects, the researchers matched 1,080 patients treated with dopamine agonists with 1,080 dopamine agonist-naïve patients on sex, age at RLS diagnosis, region, employment, and illness burden. Dr. Hankin and colleagues found a significant increase in mental disorder diagnoses (eg, bipolar disorder, anxiety, depression, and substance abuse) among patients treated with dopamine agonists, compared with dopamine agonist-naïve patients. Among patients receiving dopamine agonists, the odds ratio for severe mental disorder (eg, psychoses and bipolar disorder) was 2.2, the odds ratio for moderate to severe mental disorder (eg, posttraumatic stress disorder and major depression) was 1.8, and the odds ratio for mild mental disorder (eg, anxiety disorders) was 1.9, compared with dopamine agonist-naïve patients.
“This is the first large-scale, real-world, claims-based study to examine the association between treatment of RLS with dopamine agonists and the development of psychiatric adverse events. Our findings are compelling, but need to be replicated in other patient populations,” said Dr. Hankin.
“Our retrospective analysis required careful consideration of matching,” said Daniel On-Fai Lee, MD, Clinical Professor of Neurology at the University of Kentucky College of Medicine in Lexington, who collaborated on the study. Although the investigators took care to match participants and to remove cases of secondary RLS from the analysis, they may have inadvertently overlooked one or more important matching variables that could affect the outcome, he added.
Arbor Pharmaceuticals provided funding for the study, but did not influence its methodology, analysis, results, or conclusion, said Dr. Lee.
—Erik Greb
Suggested Reading
Sierra M, Carnicella S, Strafella AP, et al. Apathy and impulse control disorders: yin & yang of dopamine dependent behaviors. J Parkinsons Dis. 2015;5(3):625-636.
Wilt TJ, MacDonald R, Ouellette J, et al. Pharmacologic therapy for primary restless legs syndrome: a systematic review and meta-analysis. JAMA Intern Med. 2013;173(7):496-505.
BOSTON—Among patients with primary restless legs syndrome (RLS) and without a history of psychiatric disorders, patients who receive de novo dopamine agonist treatment are approximately twice as likely to subsequently develop a mental disorder as those who do not receive dopamine agonist treatment, according to a large-scale retrospective study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies.
Previous research has demonstrated an increased risk of mental disorders among patients with Parkinson’s disease who are treated with dopamine agonists. Many patients with RLS are also treated with dopamine agonists, although at lower doses than patients with Parkinson’s disease. Given these lower doses, clinicians assumed that the risk of dopamine agonist-induced mental disorders in RLS would be small. Clinical case studies suggest a higher-than-anticipated risk, however.
An Examination of Claims Data
To investigate whether dopamine agonists increase the risk of developing mental disorders in patients with RLS, Cheryl Hankin, PhD, President and Chief Scientific Officer of BioMedEcon, a health economics and outcomes research firm in Moss Beach, California, and colleagues examined Truven MarketScan Commercial and Medicare Supplemental databases of claims filed between July 1, 2008, and December 31, 2014. From a pool of 539,399 patients with a diagnosis of RLS, investigators identified adults with two or more years of claims data preceding and following their index RLS diagnosis dates.
Patients were excluded from the analysis if, in the two or more years preceding RLS diagnosis, they received a diagnosis of mental disorder or filled a prescription for an antidepressant or antipsychotic. Also excluded were patients who filled a prescription for a dopamine agonist in the two or more years preceding RLS diagnosis. Patients who were ever diagnosed with Parkinson’s disease, kidney disease, iron deficiency, or pregnancy were assumed to have secondary RLS and were also excluded.
The investigators identified 5,419 eligible participants. Of this group, 1,649 patients received dopamine agonists after RLS diagnosis. Specifically, 571 participants received pramipexole, 915 received ropinirole, and 163 received both. Approximately 65% of patients were female. Patients residing in the Northeast were significantly less likely to receive dopamine agonists, compared with patients residing in the Midwest or the South. The investigators found no significant differences in treatment status by comorbid illness burden or by sex. The investigators also found no significant differences in demographic characteristics between patients receiving pramipexole and those receiving ropinirole.
Risk Was Significantly Greater in Patients Receiving Dopamine Agonist
Next, from this pool of eligible subjects, the researchers matched 1,080 patients treated with dopamine agonists with 1,080 dopamine agonist-naïve patients on sex, age at RLS diagnosis, region, employment, and illness burden. Dr. Hankin and colleagues found a significant increase in mental disorder diagnoses (eg, bipolar disorder, anxiety, depression, and substance abuse) among patients treated with dopamine agonists, compared with dopamine agonist-naïve patients. Among patients receiving dopamine agonists, the odds ratio for severe mental disorder (eg, psychoses and bipolar disorder) was 2.2, the odds ratio for moderate to severe mental disorder (eg, posttraumatic stress disorder and major depression) was 1.8, and the odds ratio for mild mental disorder (eg, anxiety disorders) was 1.9, compared with dopamine agonist-naïve patients.
“This is the first large-scale, real-world, claims-based study to examine the association between treatment of RLS with dopamine agonists and the development of psychiatric adverse events. Our findings are compelling, but need to be replicated in other patient populations,” said Dr. Hankin.
“Our retrospective analysis required careful consideration of matching,” said Daniel On-Fai Lee, MD, Clinical Professor of Neurology at the University of Kentucky College of Medicine in Lexington, who collaborated on the study. Although the investigators took care to match participants and to remove cases of secondary RLS from the analysis, they may have inadvertently overlooked one or more important matching variables that could affect the outcome, he added.
Arbor Pharmaceuticals provided funding for the study, but did not influence its methodology, analysis, results, or conclusion, said Dr. Lee.
—Erik Greb
Suggested Reading
Sierra M, Carnicella S, Strafella AP, et al. Apathy and impulse control disorders: yin & yang of dopamine dependent behaviors. J Parkinsons Dis. 2015;5(3):625-636.
Wilt TJ, MacDonald R, Ouellette J, et al. Pharmacologic therapy for primary restless legs syndrome: a systematic review and meta-analysis. JAMA Intern Med. 2013;173(7):496-505.
BOSTON—Among patients with primary restless legs syndrome (RLS) and without a history of psychiatric disorders, patients who receive de novo dopamine agonist treatment are approximately twice as likely to subsequently develop a mental disorder as those who do not receive dopamine agonist treatment, according to a large-scale retrospective study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies.
Previous research has demonstrated an increased risk of mental disorders among patients with Parkinson’s disease who are treated with dopamine agonists. Many patients with RLS are also treated with dopamine agonists, although at lower doses than patients with Parkinson’s disease. Given these lower doses, clinicians assumed that the risk of dopamine agonist-induced mental disorders in RLS would be small. Clinical case studies suggest a higher-than-anticipated risk, however.
An Examination of Claims Data
To investigate whether dopamine agonists increase the risk of developing mental disorders in patients with RLS, Cheryl Hankin, PhD, President and Chief Scientific Officer of BioMedEcon, a health economics and outcomes research firm in Moss Beach, California, and colleagues examined Truven MarketScan Commercial and Medicare Supplemental databases of claims filed between July 1, 2008, and December 31, 2014. From a pool of 539,399 patients with a diagnosis of RLS, investigators identified adults with two or more years of claims data preceding and following their index RLS diagnosis dates.
Patients were excluded from the analysis if, in the two or more years preceding RLS diagnosis, they received a diagnosis of mental disorder or filled a prescription for an antidepressant or antipsychotic. Also excluded were patients who filled a prescription for a dopamine agonist in the two or more years preceding RLS diagnosis. Patients who were ever diagnosed with Parkinson’s disease, kidney disease, iron deficiency, or pregnancy were assumed to have secondary RLS and were also excluded.
The investigators identified 5,419 eligible participants. Of this group, 1,649 patients received dopamine agonists after RLS diagnosis. Specifically, 571 participants received pramipexole, 915 received ropinirole, and 163 received both. Approximately 65% of patients were female. Patients residing in the Northeast were significantly less likely to receive dopamine agonists, compared with patients residing in the Midwest or the South. The investigators found no significant differences in treatment status by comorbid illness burden or by sex. The investigators also found no significant differences in demographic characteristics between patients receiving pramipexole and those receiving ropinirole.
Risk Was Significantly Greater in Patients Receiving Dopamine Agonist
Next, from this pool of eligible subjects, the researchers matched 1,080 patients treated with dopamine agonists with 1,080 dopamine agonist-naïve patients on sex, age at RLS diagnosis, region, employment, and illness burden. Dr. Hankin and colleagues found a significant increase in mental disorder diagnoses (eg, bipolar disorder, anxiety, depression, and substance abuse) among patients treated with dopamine agonists, compared with dopamine agonist-naïve patients. Among patients receiving dopamine agonists, the odds ratio for severe mental disorder (eg, psychoses and bipolar disorder) was 2.2, the odds ratio for moderate to severe mental disorder (eg, posttraumatic stress disorder and major depression) was 1.8, and the odds ratio for mild mental disorder (eg, anxiety disorders) was 1.9, compared with dopamine agonist-naïve patients.
“This is the first large-scale, real-world, claims-based study to examine the association between treatment of RLS with dopamine agonists and the development of psychiatric adverse events. Our findings are compelling, but need to be replicated in other patient populations,” said Dr. Hankin.
“Our retrospective analysis required careful consideration of matching,” said Daniel On-Fai Lee, MD, Clinical Professor of Neurology at the University of Kentucky College of Medicine in Lexington, who collaborated on the study. Although the investigators took care to match participants and to remove cases of secondary RLS from the analysis, they may have inadvertently overlooked one or more important matching variables that could affect the outcome, he added.
Arbor Pharmaceuticals provided funding for the study, but did not influence its methodology, analysis, results, or conclusion, said Dr. Lee.
—Erik Greb
Suggested Reading
Sierra M, Carnicella S, Strafella AP, et al. Apathy and impulse control disorders: yin & yang of dopamine dependent behaviors. J Parkinsons Dis. 2015;5(3):625-636.
Wilt TJ, MacDonald R, Ouellette J, et al. Pharmacologic therapy for primary restless legs syndrome: a systematic review and meta-analysis. JAMA Intern Med. 2013;173(7):496-505.
First Clinical Trial of a Genetic Therapy for Huntington’s Disease Nears Completion
VANCOUVER—Antisense oligonucleotides hold promise as treatments for Huntington’s disease, according to an overview delivered at the 21st International Congress of Parkinson’s Disease and Movement Disorders. Preclinical evidence suggests that these treatments are safe and will decrease levels of mutant huntingtin in the brain. The first clinical trial of an antisense oligonucleotide for Huntington’s disease is currently under way and fully enrolled. Results will be available in the near future, said Blair R. Leavitt, MDCM, Professor of Medical Genetics at the University of British Columbia in Vancouver. 
What Are Antisense Oligonucleotides?
Antisense oligonucleotides are small, artificial units of DNA that are modified chemically to have a long half-life. They can be targeted to bind to any RNA in the body, and when they bind with huntingtin messenger RNA, they prevent production of mutant huntingtin protein. In theory, this action should prevent all subsequent pathology and delay or prevent the onset of Huntington’s disease, said Dr. Leavitt.
Among the advantages of antisense oligonucleotides is that neurons and glia take them up freely. They reach the desired areas of the brain without requiring a vector to introduce them. Antisense oligonucleotides are stable, have a long term of activity, act in a dose-dependent manner, and have reversible effects. “They are much like our classic small-molecule drugs, so we are comfortable bringing these therapies into clinical development,” said Dr. Leavitt.
Preclinical Data Indicate Safety
Kordasiewicz and colleagues infused 75 mg of an antisense oligonucleotide directly into the brain of a mouse model of Huntington’s disease (ie, BACHD mice) over 14 days. They observed a decline in huntingtin RNA that endured for as long as three months. The treated mice had better motor coordination and performed better on the rotorod test. The treatment also slowed the loss of brain mass and improved hypoactivity and anxiety.
The investigators also showed that antisense oligonucleotide reached the brain after intrathecal administration to monkeys. The treatment reduced huntingtin levels by approximately 50% in the cortex, and by between 20% and 25% in deep brain structures.
A Potential Biomarker of Target Engagement
To gauge treatment efficacy in humans, neurologists need a noninvasive way to measure levels of huntingtin in the brain. It is not yet possible to measure brain huntingtin levels directly using imaging, but CSF levels of huntingtin could be a surrogate measure, Dr. Leavitt said.
Dr. Leavitt and colleagues developed an ultrasensitive single-molecule counting immunoassay that successfully quantified mutant huntingtin in the CSF of patients with Huntington’s disease. Mutant huntingtin was undetectable in healthy controls. Patients with manifest Huntington’s disease had three times more mutant huntingtin than asymptomatic mutation carriers did. Huntingtin levels increased as the disease progressed. In addition, huntingtin concentration predicted cognitive and motor dysfunction.
The investigators observed similar findings after they used microbead-based immunoprecipitation and flow cytometry to develop a second highly sensitive assay for detecting mutant huntingtin. They demonstrated that CSF levels of mutant huntingtin reflect brain levels of the protein in mouse models of Huntington’s disease, and in patients with Huntington’s disease, the levels increased with disease stage. They also demonstrated that CSF huntingtin levels decreased following suppression of huntingtin in the brain.
A Clinical Trial Nears Completion
Ionis Pharmaceuticals developed an antisense oligonucleotide that targets both the mutant and normal alleles of huntingtin. Investigators subsequently began a first-in-human phase I/IIa trial of the drug in patients with early Huntington’s disease. Participants were randomized 3:1 to drug or placebo at sites in the United Kingdom, Germany, and Canada. The drug is administered intrathecally, and maximal protein suppression occurs approximately four weeks later. Each study participant will undergo intrathecal injections every month for four months.
The trial’s primary objective is to evaluate the treatment’s safety and tolerability. Its secondary objective is to examine the drug’s CSF pharmacokinetics. Finally, an exploratory objective is to assess the treatment’s effect on pharmacodynamic biomarkers and on clinical end points of Huntington’s disease.
All of the participants have been enrolled in the study, and Dr. Leavitt administered an intrathecal infusion to the first subject at the Vancouver site in September 2015. Participants are generally in good health and have high levels of function. Thus far, the researchers have found no evidence of significant adverse events or safety concerns, and the drug appears tolerable, said Dr. Leavitt. Results of the trial should be available in the coming months, he added. “This is certainly exciting, and it is the first time we have been able to bring a genetic therapy into the clinic for this devastating disorder.”
Other Therapies in Development
Wave Life Sciences also has created an antisense oligonucleotide for Huntington’s disease that is in the late preclinical stages of development. The company uses a type of chemistry that allows it to control the stereoisomer composition of the nucleic acids. The therapy targets specific single-nucleotide polymorphisms on mutant huntingtin and therefore may not be appropriate for every patient with Huntington’s disease. “This [treatment] has at least the potential for allele-specific targeting … and will hopefully be entering the clinic fairly soon,” said Dr. Leavitt.
Other gene-therapy approaches require a vector, most often a nonpathogenic adeno-associated virus (AAV), to bring the treatment into the CNS. Several such therapeutic candidates in preclinical development are close to entering early human trials, said Dr. Leavitt.
UniQure is developing a form of AAV5 that expresses an artificial micro-RNA that targets huntingtin. The drug will require stereotaxic injection directly into the brain. In one study, direct intraparenchymal injection of the drug significantly reduced levels of mutant huntingtin in the putamen, caudate, and thalamus of a minipig model of Huntington’s disease. The drug had less effect in the cortex. Depending on where the virus is injected, viral approaches generally have good local targeting, but not necessarily widespread targeting, said Dr. Leavitt. Spark Therapeutics and Voyager Therapeutics are also developing therapies similar to that of UniQure.
—Erik Greb
Suggested Reading
Kordasiewicz HB, Stanek LM, Wancewicz EV, et al. Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis. Neuron. 2012; 74(6): 1031–1044.
Southwell AL, Smith SE, Davis TR, et al. Ultrasensitive measurement of huntingtin protein in cerebrospinal fluid demonstrates increase with Huntington disease stage and decrease following brain huntingtin suppression. Sci Rep. 2015;5:12166.
Wild EJ, Boggio R, Langbehn D, et al. Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington’s disease patients. J Clin Invest. 2015;125(5):1979-1986.
VANCOUVER—Antisense oligonucleotides hold promise as treatments for Huntington’s disease, according to an overview delivered at the 21st International Congress of Parkinson’s Disease and Movement Disorders. Preclinical evidence suggests that these treatments are safe and will decrease levels of mutant huntingtin in the brain. The first clinical trial of an antisense oligonucleotide for Huntington’s disease is currently under way and fully enrolled. Results will be available in the near future, said Blair R. Leavitt, MDCM, Professor of Medical Genetics at the University of British Columbia in Vancouver.
What Are Antisense Oligonucleotides?
Antisense oligonucleotides are small, artificial units of DNA that are modified chemically to have a long half-life. They can be targeted to bind to any RNA in the body, and when they bind with huntingtin messenger RNA, they prevent production of mutant huntingtin protein. In theory, this action should prevent all subsequent pathology and delay or prevent the onset of Huntington’s disease, said Dr. Leavitt.
Among the advantages of antisense oligonucleotides is that neurons and glia take them up freely. They reach the desired areas of the brain without requiring a vector to introduce them. Antisense oligonucleotides are stable, have a long term of activity, act in a dose-dependent manner, and have reversible effects. “They are much like our classic small-molecule drugs, so we are comfortable bringing these therapies into clinical development,” said Dr. Leavitt.
Preclinical Data Indicate Safety
Kordasiewicz and colleagues infused 75 mg of an antisense oligonucleotide directly into the brain of a mouse model of Huntington’s disease (ie, BACHD mice) over 14 days. They observed a decline in huntingtin RNA that endured for as long as three months. The treated mice had better motor coordination and performed better on the rotorod test. The treatment also slowed the loss of brain mass and improved hypoactivity and anxiety.
The investigators also showed that antisense oligonucleotide reached the brain after intrathecal administration to monkeys. The treatment reduced huntingtin levels by approximately 50% in the cortex, and by between 20% and 25% in deep brain structures.
A Potential Biomarker of Target Engagement
To gauge treatment efficacy in humans, neurologists need a noninvasive way to measure levels of huntingtin in the brain. It is not yet possible to measure brain huntingtin levels directly using imaging, but CSF levels of huntingtin could be a surrogate measure, Dr. Leavitt said.
Dr. Leavitt and colleagues developed an ultrasensitive single-molecule counting immunoassay that successfully quantified mutant huntingtin in the CSF of patients with Huntington’s disease. Mutant huntingtin was undetectable in healthy controls. Patients with manifest Huntington’s disease had three times more mutant huntingtin than asymptomatic mutation carriers did. Huntingtin levels increased as the disease progressed. In addition, huntingtin concentration predicted cognitive and motor dysfunction.
The investigators observed similar findings after they used microbead-based immunoprecipitation and flow cytometry to develop a second highly sensitive assay for detecting mutant huntingtin. They demonstrated that CSF levels of mutant huntingtin reflect brain levels of the protein in mouse models of Huntington’s disease, and in patients with Huntington’s disease, the levels increased with disease stage. They also demonstrated that CSF huntingtin levels decreased following suppression of huntingtin in the brain.
A Clinical Trial Nears Completion
Ionis Pharmaceuticals developed an antisense oligonucleotide that targets both the mutant and normal alleles of huntingtin. Investigators subsequently began a first-in-human phase I/IIa trial of the drug in patients with early Huntington’s disease. Participants were randomized 3:1 to drug or placebo at sites in the United Kingdom, Germany, and Canada. The drug is administered intrathecally, and maximal protein suppression occurs approximately four weeks later. Each study participant will undergo intrathecal injections every month for four months.
The trial’s primary objective is to evaluate the treatment’s safety and tolerability. Its secondary objective is to examine the drug’s CSF pharmacokinetics. Finally, an exploratory objective is to assess the treatment’s effect on pharmacodynamic biomarkers and on clinical end points of Huntington’s disease.
All of the participants have been enrolled in the study, and Dr. Leavitt administered an intrathecal infusion to the first subject at the Vancouver site in September 2015. Participants are generally in good health and have high levels of function. Thus far, the researchers have found no evidence of significant adverse events or safety concerns, and the drug appears tolerable, said Dr. Leavitt. Results of the trial should be available in the coming months, he added. “This is certainly exciting, and it is the first time we have been able to bring a genetic therapy into the clinic for this devastating disorder.”
Other Therapies in Development
Wave Life Sciences also has created an antisense oligonucleotide for Huntington’s disease that is in the late preclinical stages of development. The company uses a type of chemistry that allows it to control the stereoisomer composition of the nucleic acids. The therapy targets specific single-nucleotide polymorphisms on mutant huntingtin and therefore may not be appropriate for every patient with Huntington’s disease. “This [treatment] has at least the potential for allele-specific targeting … and will hopefully be entering the clinic fairly soon,” said Dr. Leavitt.
Other gene-therapy approaches require a vector, most often a nonpathogenic adeno-associated virus (AAV), to bring the treatment into the CNS. Several such therapeutic candidates in preclinical development are close to entering early human trials, said Dr. Leavitt.
UniQure is developing a form of AAV5 that expresses an artificial micro-RNA that targets huntingtin. The drug will require stereotaxic injection directly into the brain. In one study, direct intraparenchymal injection of the drug significantly reduced levels of mutant huntingtin in the putamen, caudate, and thalamus of a minipig model of Huntington’s disease. The drug had less effect in the cortex. Depending on where the virus is injected, viral approaches generally have good local targeting, but not necessarily widespread targeting, said Dr. Leavitt. Spark Therapeutics and Voyager Therapeutics are also developing therapies similar to that of UniQure.
—Erik Greb
Suggested Reading
Kordasiewicz HB, Stanek LM, Wancewicz EV, et al. Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis. Neuron. 2012; 74(6): 1031–1044.
Southwell AL, Smith SE, Davis TR, et al. Ultrasensitive measurement of huntingtin protein in cerebrospinal fluid demonstrates increase with Huntington disease stage and decrease following brain huntingtin suppression. Sci Rep. 2015;5:12166.
Wild EJ, Boggio R, Langbehn D, et al. Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington’s disease patients. J Clin Invest. 2015;125(5):1979-1986.
VANCOUVER—Antisense oligonucleotides hold promise as treatments for Huntington’s disease, according to an overview delivered at the 21st International Congress of Parkinson’s Disease and Movement Disorders. Preclinical evidence suggests that these treatments are safe and will decrease levels of mutant huntingtin in the brain. The first clinical trial of an antisense oligonucleotide for Huntington’s disease is currently under way and fully enrolled. Results will be available in the near future, said Blair R. Leavitt, MDCM, Professor of Medical Genetics at the University of British Columbia in Vancouver.
What Are Antisense Oligonucleotides?
Antisense oligonucleotides are small, artificial units of DNA that are modified chemically to have a long half-life. They can be targeted to bind to any RNA in the body, and when they bind with huntingtin messenger RNA, they prevent production of mutant huntingtin protein. In theory, this action should prevent all subsequent pathology and delay or prevent the onset of Huntington’s disease, said Dr. Leavitt.
Among the advantages of antisense oligonucleotides is that neurons and glia take them up freely. They reach the desired areas of the brain without requiring a vector to introduce them. Antisense oligonucleotides are stable, have a long term of activity, act in a dose-dependent manner, and have reversible effects. “They are much like our classic small-molecule drugs, so we are comfortable bringing these therapies into clinical development,” said Dr. Leavitt.
Preclinical Data Indicate Safety
Kordasiewicz and colleagues infused 75 mg of an antisense oligonucleotide directly into the brain of a mouse model of Huntington’s disease (ie, BACHD mice) over 14 days. They observed a decline in huntingtin RNA that endured for as long as three months. The treated mice had better motor coordination and performed better on the rotorod test. The treatment also slowed the loss of brain mass and improved hypoactivity and anxiety.
The investigators also showed that antisense oligonucleotide reached the brain after intrathecal administration to monkeys. The treatment reduced huntingtin levels by approximately 50% in the cortex, and by between 20% and 25% in deep brain structures.
A Potential Biomarker of Target Engagement
To gauge treatment efficacy in humans, neurologists need a noninvasive way to measure levels of huntingtin in the brain. It is not yet possible to measure brain huntingtin levels directly using imaging, but CSF levels of huntingtin could be a surrogate measure, Dr. Leavitt said.
Dr. Leavitt and colleagues developed an ultrasensitive single-molecule counting immunoassay that successfully quantified mutant huntingtin in the CSF of patients with Huntington’s disease. Mutant huntingtin was undetectable in healthy controls. Patients with manifest Huntington’s disease had three times more mutant huntingtin than asymptomatic mutation carriers did. Huntingtin levels increased as the disease progressed. In addition, huntingtin concentration predicted cognitive and motor dysfunction.
The investigators observed similar findings after they used microbead-based immunoprecipitation and flow cytometry to develop a second highly sensitive assay for detecting mutant huntingtin. They demonstrated that CSF levels of mutant huntingtin reflect brain levels of the protein in mouse models of Huntington’s disease, and in patients with Huntington’s disease, the levels increased with disease stage. They also demonstrated that CSF huntingtin levels decreased following suppression of huntingtin in the brain.
A Clinical Trial Nears Completion
Ionis Pharmaceuticals developed an antisense oligonucleotide that targets both the mutant and normal alleles of huntingtin. Investigators subsequently began a first-in-human phase I/IIa trial of the drug in patients with early Huntington’s disease. Participants were randomized 3:1 to drug or placebo at sites in the United Kingdom, Germany, and Canada. The drug is administered intrathecally, and maximal protein suppression occurs approximately four weeks later. Each study participant will undergo intrathecal injections every month for four months.
The trial’s primary objective is to evaluate the treatment’s safety and tolerability. Its secondary objective is to examine the drug’s CSF pharmacokinetics. Finally, an exploratory objective is to assess the treatment’s effect on pharmacodynamic biomarkers and on clinical end points of Huntington’s disease.
All of the participants have been enrolled in the study, and Dr. Leavitt administered an intrathecal infusion to the first subject at the Vancouver site in September 2015. Participants are generally in good health and have high levels of function. Thus far, the researchers have found no evidence of significant adverse events or safety concerns, and the drug appears tolerable, said Dr. Leavitt. Results of the trial should be available in the coming months, he added. “This is certainly exciting, and it is the first time we have been able to bring a genetic therapy into the clinic for this devastating disorder.”
Other Therapies in Development
Wave Life Sciences also has created an antisense oligonucleotide for Huntington’s disease that is in the late preclinical stages of development. The company uses a type of chemistry that allows it to control the stereoisomer composition of the nucleic acids. The therapy targets specific single-nucleotide polymorphisms on mutant huntingtin and therefore may not be appropriate for every patient with Huntington’s disease. “This [treatment] has at least the potential for allele-specific targeting … and will hopefully be entering the clinic fairly soon,” said Dr. Leavitt.
Other gene-therapy approaches require a vector, most often a nonpathogenic adeno-associated virus (AAV), to bring the treatment into the CNS. Several such therapeutic candidates in preclinical development are close to entering early human trials, said Dr. Leavitt.
UniQure is developing a form of AAV5 that expresses an artificial micro-RNA that targets huntingtin. The drug will require stereotaxic injection directly into the brain. In one study, direct intraparenchymal injection of the drug significantly reduced levels of mutant huntingtin in the putamen, caudate, and thalamus of a minipig model of Huntington’s disease. The drug had less effect in the cortex. Depending on where the virus is injected, viral approaches generally have good local targeting, but not necessarily widespread targeting, said Dr. Leavitt. Spark Therapeutics and Voyager Therapeutics are also developing therapies similar to that of UniQure.
—Erik Greb
Suggested Reading
Kordasiewicz HB, Stanek LM, Wancewicz EV, et al. Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis. Neuron. 2012; 74(6): 1031–1044.
Southwell AL, Smith SE, Davis TR, et al. Ultrasensitive measurement of huntingtin protein in cerebrospinal fluid demonstrates increase with Huntington disease stage and decrease following brain huntingtin suppression. Sci Rep. 2015;5:12166.
Wild EJ, Boggio R, Langbehn D, et al. Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington’s disease patients. J Clin Invest. 2015;125(5):1979-1986.
Fluid protocol takes aim at bariatric surgery readmissions
NEW YORK – With dehydration considered a contributor to hospital readmission after bariatric weight loss surgery, a multidisciplinary team of clinicians searched for a way to get patients to drink up. Specifically,
The project results were presented at a poster session at the American College of Surgeons Quality and Safety Conference.
“Our QI project was to streamline that process to ultimately eliminate or decrease those readmits,” Ms. Melei said.
They used 8-ounce water bottles. To track water consumption, they also numbered the bottles one through six for each patient. One-ounce cups were used during mealtimes. RNs, certified nursing assistants, and food service staff were educated about the fluid intake initiative. Only fluids provided by nursing were permitted and patients also received a clear message about fluid goals.
Another focus was standardizing communication with patients. They were not getting a consistent message from staff on what to expect before, during, and after surgery. “So we had to make sure [we] were all saying the same thing.”
The nurses and the other staff now ask the patients “Did you finish the bottle?” or “Where are you with the bottles?” Ms. Melei said. “At the end of a shift, the nurses document fluid consumption.”
During a 2-month baseline period, 12 patients drank an average 381.5 mL over 24 hours. Since the close of the project, the average daily fluid intake for patients undergoing bariatric surgery is 1,007 mL. In 12 months post implementation, average fluid intake for 39 patients jumped to 1,109.5 mL over 24 hours. “It was just such a hugely successful program. We had buy-in from every department, it worked really well, and we had great results,” said Cheryl Williams, the current bariatric program coordinator at Greenwich Hospital.
Sometimes dehydrated patients present to an emergency department complaining of vomiting, headache, and dizziness if they are not properly hydrated after surgery, Ms. Williams said. “Preventing dehydration helps to improve the patient’s recovery, as well as decrease emergency room visits and hospital admissions.”
Ashutosh Kaul, MD, FACS, medical director of the bariatric surgery program at Greenwich Hospital, said this study shows the importance of team building to improve patient care. “We built a core team that implemented a simple, low-cost, structured, and well-defined water distribution and documentation process, which resulted in better compliance of water intake. This reduced variability and improved postoperative intake progression, and we are presently studying its effect on reduction of readmissions and facilitating early discharge.”
Greenwich Hospital’s bariatric surgery center is accredited by the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP), a collaboration between the American College of Surgeons and the American Society for Metabolic and Bariatric Surgery. Ms. Williams and Ms. Melei had no relevant financial disclosures.
NEW YORK – With dehydration considered a contributor to hospital readmission after bariatric weight loss surgery, a multidisciplinary team of clinicians searched for a way to get patients to drink up. Specifically,
The project results were presented at a poster session at the American College of Surgeons Quality and Safety Conference.
“Our QI project was to streamline that process to ultimately eliminate or decrease those readmits,” Ms. Melei said.
They used 8-ounce water bottles. To track water consumption, they also numbered the bottles one through six for each patient. One-ounce cups were used during mealtimes. RNs, certified nursing assistants, and food service staff were educated about the fluid intake initiative. Only fluids provided by nursing were permitted and patients also received a clear message about fluid goals.
Another focus was standardizing communication with patients. They were not getting a consistent message from staff on what to expect before, during, and after surgery. “So we had to make sure [we] were all saying the same thing.”
The nurses and the other staff now ask the patients “Did you finish the bottle?” or “Where are you with the bottles?” Ms. Melei said. “At the end of a shift, the nurses document fluid consumption.”
During a 2-month baseline period, 12 patients drank an average 381.5 mL over 24 hours. Since the close of the project, the average daily fluid intake for patients undergoing bariatric surgery is 1,007 mL. In 12 months post implementation, average fluid intake for 39 patients jumped to 1,109.5 mL over 24 hours. “It was just such a hugely successful program. We had buy-in from every department, it worked really well, and we had great results,” said Cheryl Williams, the current bariatric program coordinator at Greenwich Hospital.
Sometimes dehydrated patients present to an emergency department complaining of vomiting, headache, and dizziness if they are not properly hydrated after surgery, Ms. Williams said. “Preventing dehydration helps to improve the patient’s recovery, as well as decrease emergency room visits and hospital admissions.”
Ashutosh Kaul, MD, FACS, medical director of the bariatric surgery program at Greenwich Hospital, said this study shows the importance of team building to improve patient care. “We built a core team that implemented a simple, low-cost, structured, and well-defined water distribution and documentation process, which resulted in better compliance of water intake. This reduced variability and improved postoperative intake progression, and we are presently studying its effect on reduction of readmissions and facilitating early discharge.”
Greenwich Hospital’s bariatric surgery center is accredited by the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP), a collaboration between the American College of Surgeons and the American Society for Metabolic and Bariatric Surgery. Ms. Williams and Ms. Melei had no relevant financial disclosures.
NEW YORK – With dehydration considered a contributor to hospital readmission after bariatric weight loss surgery, a multidisciplinary team of clinicians searched for a way to get patients to drink up. Specifically,
The project results were presented at a poster session at the American College of Surgeons Quality and Safety Conference.
“Our QI project was to streamline that process to ultimately eliminate or decrease those readmits,” Ms. Melei said.
They used 8-ounce water bottles. To track water consumption, they also numbered the bottles one through six for each patient. One-ounce cups were used during mealtimes. RNs, certified nursing assistants, and food service staff were educated about the fluid intake initiative. Only fluids provided by nursing were permitted and patients also received a clear message about fluid goals.
Another focus was standardizing communication with patients. They were not getting a consistent message from staff on what to expect before, during, and after surgery. “So we had to make sure [we] were all saying the same thing.”
The nurses and the other staff now ask the patients “Did you finish the bottle?” or “Where are you with the bottles?” Ms. Melei said. “At the end of a shift, the nurses document fluid consumption.”
During a 2-month baseline period, 12 patients drank an average 381.5 mL over 24 hours. Since the close of the project, the average daily fluid intake for patients undergoing bariatric surgery is 1,007 mL. In 12 months post implementation, average fluid intake for 39 patients jumped to 1,109.5 mL over 24 hours. “It was just such a hugely successful program. We had buy-in from every department, it worked really well, and we had great results,” said Cheryl Williams, the current bariatric program coordinator at Greenwich Hospital.
Sometimes dehydrated patients present to an emergency department complaining of vomiting, headache, and dizziness if they are not properly hydrated after surgery, Ms. Williams said. “Preventing dehydration helps to improve the patient’s recovery, as well as decrease emergency room visits and hospital admissions.”
Ashutosh Kaul, MD, FACS, medical director of the bariatric surgery program at Greenwich Hospital, said this study shows the importance of team building to improve patient care. “We built a core team that implemented a simple, low-cost, structured, and well-defined water distribution and documentation process, which resulted in better compliance of water intake. This reduced variability and improved postoperative intake progression, and we are presently studying its effect on reduction of readmissions and facilitating early discharge.”
Greenwich Hospital’s bariatric surgery center is accredited by the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP), a collaboration between the American College of Surgeons and the American Society for Metabolic and Bariatric Surgery. Ms. Williams and Ms. Melei had no relevant financial disclosures.
AT THE ACS QUALITY & SAFETY CONFERENCE
Key clinical point: QI project to increase water intake after bariatric surgery could decrease hospital readmission rates.
Major finding: Multidisciplinary protocol increases 24-hour fluid intake from 382 mL to 1,110 mL on average.
Data source: Comparison of water consumed by 12 patients before versus 39 patients after implementation.
Disclosures: Ms. Williams and Ms. Melei had no relevant financial disclosures.
Meningitis before age 3 months: Consider enterovirus and parechovirus
MADRID – Ninety-five percent of cases of enterovirus and parechovirus meningitis in infants younger than 90 days old in the United Kingdom and Ireland were diagnosed through lumbar puncture and identification of the virus in the CSF by PCR, Seilesh Kadambari, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.
“We recommend that routine testing of CSF for enterovirus and parechovirus in febrile infants should be promoted, even in the absence of pleocytosis,” said Dr. Kadambari of John Radcliffe Hospital in Oxford, England.
This active enhanced prospective surveillance study was undertaken because an earlier retrospective study concluded that the rate of viral meningitis across all pediatric and adult age groups had increased rapidly during a recent 10-year period in the United Kingdom and Ireland. Infants younger than 3 months of age were especially hard hit by enterovirus, which accounted in the earlier study for 92% of all viral meningitis cases in that age group. Dr. Kadambari and his coinvestigators decided to take a closer prospective look at the sub-3-month age group because it’s such an important time neurodevelopmentally.
During the 13-month period of June 2014 to June 2015, 710 patients younger than 90 days old were hospitalized for enterovirus or parechovirus meningitis across the United Kingdom and Republic of Ireland. Ninety-five percent were due to enterovirus. Only 6% of affected infants were born prematurely.
“One of the take-home messages for me from the study was that 12% of enterovirus cases and 23% of parechovirus meningitis cases required admission to an ICU setting,” the pediatrician observed.
Among the infants admitted to a pediatric ICU, half of those with enterovirus meningitis and all those with parechovirus meningitis required intubation and mechanical ventilation. One-fifth of the enterovirus meningitis patients in pediatric ICUs required inotropic support for cardiovascular stabilization, as did all young infants with parechovirus meningitis.
Among the 710 patients, the three most common clinical presenting features were fever, irritability, and reduced feeding, present in 85%, 66%, and 54%, respectively.
Upon physical examination, two noteworthy common findings were signs of shock, present in 27% of infants with enterovirus meningitis and 43% with parechovirus meningitis, and respiratory distress, seen in 12% and 26%, respectively.
None of the 710 infants had a secondary bacterial infection. “That has implications for antimicrobial stewardship programs,” according to Dr. Kadambari.
The majority of infants had a normal CSF WBC count and a normal-range C-reactive protein level.
“Raised inflammatory markers were not a common feature in our cohort,” he noted.
Two infants died: one of a massive pulmonary hemorrhage and the other as a result of septic shock. Of the remaining 708 patients, however, 699 (98.7%) were discharged without significant neurologic impairment. Seven infants with enterovirus meningitis and two with parechovirus meningitis were discharged with severe delay, including cases of fine motor and gross motor delay, visual abnormalities, and a single case of severe cardiac dysfunction requiring discharge on an ACE inhibitor.
This surveillance study was a collaboration between St. George’s University of London and Public Health England. Dr. Kadambari reported having no financial conflicts.
Future studies need to examine long-term neurodevelopmental outcomes in affected young infants out to age 24 months, he said.
MADRID – Ninety-five percent of cases of enterovirus and parechovirus meningitis in infants younger than 90 days old in the United Kingdom and Ireland were diagnosed through lumbar puncture and identification of the virus in the CSF by PCR, Seilesh Kadambari, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.
“We recommend that routine testing of CSF for enterovirus and parechovirus in febrile infants should be promoted, even in the absence of pleocytosis,” said Dr. Kadambari of John Radcliffe Hospital in Oxford, England.
This active enhanced prospective surveillance study was undertaken because an earlier retrospective study concluded that the rate of viral meningitis across all pediatric and adult age groups had increased rapidly during a recent 10-year period in the United Kingdom and Ireland. Infants younger than 3 months of age were especially hard hit by enterovirus, which accounted in the earlier study for 92% of all viral meningitis cases in that age group. Dr. Kadambari and his coinvestigators decided to take a closer prospective look at the sub-3-month age group because it’s such an important time neurodevelopmentally.
During the 13-month period of June 2014 to June 2015, 710 patients younger than 90 days old were hospitalized for enterovirus or parechovirus meningitis across the United Kingdom and Republic of Ireland. Ninety-five percent were due to enterovirus. Only 6% of affected infants were born prematurely.
“One of the take-home messages for me from the study was that 12% of enterovirus cases and 23% of parechovirus meningitis cases required admission to an ICU setting,” the pediatrician observed.
Among the infants admitted to a pediatric ICU, half of those with enterovirus meningitis and all those with parechovirus meningitis required intubation and mechanical ventilation. One-fifth of the enterovirus meningitis patients in pediatric ICUs required inotropic support for cardiovascular stabilization, as did all young infants with parechovirus meningitis.
Among the 710 patients, the three most common clinical presenting features were fever, irritability, and reduced feeding, present in 85%, 66%, and 54%, respectively.
Upon physical examination, two noteworthy common findings were signs of shock, present in 27% of infants with enterovirus meningitis and 43% with parechovirus meningitis, and respiratory distress, seen in 12% and 26%, respectively.
None of the 710 infants had a secondary bacterial infection. “That has implications for antimicrobial stewardship programs,” according to Dr. Kadambari.
The majority of infants had a normal CSF WBC count and a normal-range C-reactive protein level.
“Raised inflammatory markers were not a common feature in our cohort,” he noted.
Two infants died: one of a massive pulmonary hemorrhage and the other as a result of septic shock. Of the remaining 708 patients, however, 699 (98.7%) were discharged without significant neurologic impairment. Seven infants with enterovirus meningitis and two with parechovirus meningitis were discharged with severe delay, including cases of fine motor and gross motor delay, visual abnormalities, and a single case of severe cardiac dysfunction requiring discharge on an ACE inhibitor.
This surveillance study was a collaboration between St. George’s University of London and Public Health England. Dr. Kadambari reported having no financial conflicts.
Future studies need to examine long-term neurodevelopmental outcomes in affected young infants out to age 24 months, he said.
MADRID – Ninety-five percent of cases of enterovirus and parechovirus meningitis in infants younger than 90 days old in the United Kingdom and Ireland were diagnosed through lumbar puncture and identification of the virus in the CSF by PCR, Seilesh Kadambari, MD, reported at the annual meeting of the European Society for Paediatric Infectious Diseases.
“We recommend that routine testing of CSF for enterovirus and parechovirus in febrile infants should be promoted, even in the absence of pleocytosis,” said Dr. Kadambari of John Radcliffe Hospital in Oxford, England.
This active enhanced prospective surveillance study was undertaken because an earlier retrospective study concluded that the rate of viral meningitis across all pediatric and adult age groups had increased rapidly during a recent 10-year period in the United Kingdom and Ireland. Infants younger than 3 months of age were especially hard hit by enterovirus, which accounted in the earlier study for 92% of all viral meningitis cases in that age group. Dr. Kadambari and his coinvestigators decided to take a closer prospective look at the sub-3-month age group because it’s such an important time neurodevelopmentally.
During the 13-month period of June 2014 to June 2015, 710 patients younger than 90 days old were hospitalized for enterovirus or parechovirus meningitis across the United Kingdom and Republic of Ireland. Ninety-five percent were due to enterovirus. Only 6% of affected infants were born prematurely.
“One of the take-home messages for me from the study was that 12% of enterovirus cases and 23% of parechovirus meningitis cases required admission to an ICU setting,” the pediatrician observed.
Among the infants admitted to a pediatric ICU, half of those with enterovirus meningitis and all those with parechovirus meningitis required intubation and mechanical ventilation. One-fifth of the enterovirus meningitis patients in pediatric ICUs required inotropic support for cardiovascular stabilization, as did all young infants with parechovirus meningitis.
Among the 710 patients, the three most common clinical presenting features were fever, irritability, and reduced feeding, present in 85%, 66%, and 54%, respectively.
Upon physical examination, two noteworthy common findings were signs of shock, present in 27% of infants with enterovirus meningitis and 43% with parechovirus meningitis, and respiratory distress, seen in 12% and 26%, respectively.
None of the 710 infants had a secondary bacterial infection. “That has implications for antimicrobial stewardship programs,” according to Dr. Kadambari.
The majority of infants had a normal CSF WBC count and a normal-range C-reactive protein level.
“Raised inflammatory markers were not a common feature in our cohort,” he noted.
Two infants died: one of a massive pulmonary hemorrhage and the other as a result of septic shock. Of the remaining 708 patients, however, 699 (98.7%) were discharged without significant neurologic impairment. Seven infants with enterovirus meningitis and two with parechovirus meningitis were discharged with severe delay, including cases of fine motor and gross motor delay, visual abnormalities, and a single case of severe cardiac dysfunction requiring discharge on an ACE inhibitor.
This surveillance study was a collaboration between St. George’s University of London and Public Health England. Dr. Kadambari reported having no financial conflicts.
Future studies need to examine long-term neurodevelopmental outcomes in affected young infants out to age 24 months, he said.
AT ESPID 2017
Key clinical point:
Major finding: More than 98% of infants in the United Kingdom and Ireland younger than 90 days old with enterovirus or parechovirus meningitis were discharged without significant neurologic impairment.
Data source: A prospective active enhanced surveillance study including all 710 infants younger than 90 days old hospitalized for enterovirus or parechovirus meningitis in the United Kingdom and Ireland in a 13-month period.
Disclosures: The study was jointly sponsored by Public Health England and St. George’s University of London. The presenter reported having no financial conflicts.
New monotherapy approved for partial-onset seizures
The U.S. Food and Drug Administration has approved perampanel (Fycompa) for monotherapy treatment of partial-onset seizures (POS) in patients aged 12 years or older as of July 27. It was approved in 2012 for adjunctive use for POS and primary, generalized tonic-clonic seizures in patients aged 12 years or older.
Three clinical trials showed improvement in seizure control for the patients with POS taking perampanel, compared with placebo.
The drug is available in tablets from 2 mg to 12 mg and as an oral suspension formulation. It is taken once daily.
“Approximately one-third of people living with epilepsy have seizures that are not adequately controlled,” said Robert T. Wechsler, MD, PhD, medical director of the Idaho Comprehensive Epilepsy Center, in Eisai’s press release. “Having a new monotherapy option for partial-onset seizures that is once a day gives physicians and patients an effective treatment option that has the potential to make a difference in patients’ lives.”
The U.S. Food and Drug Administration has approved perampanel (Fycompa) for monotherapy treatment of partial-onset seizures (POS) in patients aged 12 years or older as of July 27. It was approved in 2012 for adjunctive use for POS and primary, generalized tonic-clonic seizures in patients aged 12 years or older.
Three clinical trials showed improvement in seizure control for the patients with POS taking perampanel, compared with placebo.
The drug is available in tablets from 2 mg to 12 mg and as an oral suspension formulation. It is taken once daily.
“Approximately one-third of people living with epilepsy have seizures that are not adequately controlled,” said Robert T. Wechsler, MD, PhD, medical director of the Idaho Comprehensive Epilepsy Center, in Eisai’s press release. “Having a new monotherapy option for partial-onset seizures that is once a day gives physicians and patients an effective treatment option that has the potential to make a difference in patients’ lives.”
The U.S. Food and Drug Administration has approved perampanel (Fycompa) for monotherapy treatment of partial-onset seizures (POS) in patients aged 12 years or older as of July 27. It was approved in 2012 for adjunctive use for POS and primary, generalized tonic-clonic seizures in patients aged 12 years or older.
Three clinical trials showed improvement in seizure control for the patients with POS taking perampanel, compared with placebo.
The drug is available in tablets from 2 mg to 12 mg and as an oral suspension formulation. It is taken once daily.
“Approximately one-third of people living with epilepsy have seizures that are not adequately controlled,” said Robert T. Wechsler, MD, PhD, medical director of the Idaho Comprehensive Epilepsy Center, in Eisai’s press release. “Having a new monotherapy option for partial-onset seizures that is once a day gives physicians and patients an effective treatment option that has the potential to make a difference in patients’ lives.”