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Taking Stroke Treatment to the Streets
A mobile stroke treatment unit using telemedicine is feasible, according to a study that reports on the initial experience with this type of unit in Ohio. In the February issue of JAMA Neurology, lead author Ahmed Itrat, MD, a neurologist at the Cerebrovascular Center at the Cleveland Clinic, and colleagues reported that their mobile stroke treatment unit had a low rate of technical failure and allowed a physician to cover multiple mobile stroke treatment units, thus broadening the geographic coverage and rendering the concept efficient and cost-effective.
Mobile stroke treatment units with on-site treatment teams that include a vascular neurologist can provide thrombolysis in the prehospital setting faster than treatment in the hospital. These units can be made more resource-efficient if the need for an on-site neurologist can be eliminated by relying solely on telemedicine for physician presence. With this idea in mind, Dr. Itrat and colleagues tested whether telemedicine is reliable and whether remote physician presence is adequate for acute stroke treatment using a mobile stoke treatment unit.
Real-World Data
Dr. Itrat and colleagues conducted a prospective observational study between July 18 and November 1, 2014. Their community-based study assessed telemedicine and the mobile stroke treatment unit in Cleveland. Participants were the first 100 Cleveland residents who had acute onset of stroke-like symptoms between 8 am and 8 pm and were evaluated by the mobile stroke treatment unit after implementation of the telemedicine stroke treatment program at the Cleveland Clinic. A vascular neurologist evaluated the first 100 patients via telemedicine, and a neuroradiologist remotely assessed images obtained by mobile CT. Data were entered into the medical records and a prospective registry.
The 3.5-month study compared the evaluation and treatment of patients on the mobile stroke treatment unit with the evaluation and treatment of a control group of patients brought to the emergency department by ambulance during the same year. Process times were measured from the time the patient entered the door of the mobile unit or emergency department. Any problems encountered during the stroke evaluation were recorded.
The researchers reported that 99 of 100 patients were evaluated successfully. The median duration of telemedicine evaluation was 20 minutes. One connection failure was due to crew error, and the patient was transported to the nearest emergency department. There were six telemedicine disconnections, none of which lasted longer than 60 seconds or affected clinical care. Sixteen patients received thrombolysis in the mobile stroke treatment unit. Times from the door to CT completion (13 minutes) and from door to IV thrombolysis (32 minutes) were significantly shorter in the mobile stroke treatment unit group, compared with the control group (18 minutes and 58 minutes, respectively). Times to CT interpretation did not differ significantly between the groups.
"While studies have modeled mobile stroke units to be cost-effective from the societal perspective, our investigation implies further reduction in operational costs of mobile stroke treatment units. Obviating the need for an on-site neurologist and neuroradiologist would allow multiple mobile units to be operated that are geographically distant from the physician," the researchers said.
A Wise Use of Limited Resources?
In an accompanying editorial, Martin Ebinger, MD, and Heinrich J. Audebert, MD, neurologists at Charité—Universitätsmedizin Berlin, state that "the occasionally emotional debate about prehospital thrombolysis usually revolves around the wise use of limited resources." Vascular neurologists, they point out, are a bottleneck for prehospital thrombolysis concepts. They are in short supply, and sending them out into the community seems counterintuitive, hence the appeal of telemedicine. The editorialists posit that "Stroke is a predestined disease for telemedicine because symptoms are audiovisually transmittable, and CT images can easily be accessed remotely. Obviously, replacing a personal encounter with a telemedicine consultation has its limitations. However, in a time-critical scenario such as stroke, the advantages of fast decisions about thrombolysis or thrombectomy may outweigh the shortcomings."
—Glenn S. Williams
Suggested Reading
Itrat A, Taqui A, Cerejo R, et al. Telemedicine in prehospital stroke evaluation and thrombolysis: taking stroke treatment to the doorstep. JAMA Neurol. 2016;73(2):162-168.
Ebinger M, Audebert HJ. Switched on—expert advice in prehospital thrombolysis via telemedicine. JAMA Neurol. 2016;73(2):153-154.
A mobile stroke treatment unit using telemedicine is feasible, according to a study that reports on the initial experience with this type of unit in Ohio. In the February issue of JAMA Neurology, lead author Ahmed Itrat, MD, a neurologist at the Cerebrovascular Center at the Cleveland Clinic, and colleagues reported that their mobile stroke treatment unit had a low rate of technical failure and allowed a physician to cover multiple mobile stroke treatment units, thus broadening the geographic coverage and rendering the concept efficient and cost-effective.
Mobile stroke treatment units with on-site treatment teams that include a vascular neurologist can provide thrombolysis in the prehospital setting faster than treatment in the hospital. These units can be made more resource-efficient if the need for an on-site neurologist can be eliminated by relying solely on telemedicine for physician presence. With this idea in mind, Dr. Itrat and colleagues tested whether telemedicine is reliable and whether remote physician presence is adequate for acute stroke treatment using a mobile stoke treatment unit.
Real-World Data
Dr. Itrat and colleagues conducted a prospective observational study between July 18 and November 1, 2014. Their community-based study assessed telemedicine and the mobile stroke treatment unit in Cleveland. Participants were the first 100 Cleveland residents who had acute onset of stroke-like symptoms between 8 am and 8 pm and were evaluated by the mobile stroke treatment unit after implementation of the telemedicine stroke treatment program at the Cleveland Clinic. A vascular neurologist evaluated the first 100 patients via telemedicine, and a neuroradiologist remotely assessed images obtained by mobile CT. Data were entered into the medical records and a prospective registry.
The 3.5-month study compared the evaluation and treatment of patients on the mobile stroke treatment unit with the evaluation and treatment of a control group of patients brought to the emergency department by ambulance during the same year. Process times were measured from the time the patient entered the door of the mobile unit or emergency department. Any problems encountered during the stroke evaluation were recorded.
The researchers reported that 99 of 100 patients were evaluated successfully. The median duration of telemedicine evaluation was 20 minutes. One connection failure was due to crew error, and the patient was transported to the nearest emergency department. There were six telemedicine disconnections, none of which lasted longer than 60 seconds or affected clinical care. Sixteen patients received thrombolysis in the mobile stroke treatment unit. Times from the door to CT completion (13 minutes) and from door to IV thrombolysis (32 minutes) were significantly shorter in the mobile stroke treatment unit group, compared with the control group (18 minutes and 58 minutes, respectively). Times to CT interpretation did not differ significantly between the groups.
"While studies have modeled mobile stroke units to be cost-effective from the societal perspective, our investigation implies further reduction in operational costs of mobile stroke treatment units. Obviating the need for an on-site neurologist and neuroradiologist would allow multiple mobile units to be operated that are geographically distant from the physician," the researchers said.
A Wise Use of Limited Resources?
In an accompanying editorial, Martin Ebinger, MD, and Heinrich J. Audebert, MD, neurologists at Charité—Universitätsmedizin Berlin, state that "the occasionally emotional debate about prehospital thrombolysis usually revolves around the wise use of limited resources." Vascular neurologists, they point out, are a bottleneck for prehospital thrombolysis concepts. They are in short supply, and sending them out into the community seems counterintuitive, hence the appeal of telemedicine. The editorialists posit that "Stroke is a predestined disease for telemedicine because symptoms are audiovisually transmittable, and CT images can easily be accessed remotely. Obviously, replacing a personal encounter with a telemedicine consultation has its limitations. However, in a time-critical scenario such as stroke, the advantages of fast decisions about thrombolysis or thrombectomy may outweigh the shortcomings."
—Glenn S. Williams
A mobile stroke treatment unit using telemedicine is feasible, according to a study that reports on the initial experience with this type of unit in Ohio. In the February issue of JAMA Neurology, lead author Ahmed Itrat, MD, a neurologist at the Cerebrovascular Center at the Cleveland Clinic, and colleagues reported that their mobile stroke treatment unit had a low rate of technical failure and allowed a physician to cover multiple mobile stroke treatment units, thus broadening the geographic coverage and rendering the concept efficient and cost-effective.
Mobile stroke treatment units with on-site treatment teams that include a vascular neurologist can provide thrombolysis in the prehospital setting faster than treatment in the hospital. These units can be made more resource-efficient if the need for an on-site neurologist can be eliminated by relying solely on telemedicine for physician presence. With this idea in mind, Dr. Itrat and colleagues tested whether telemedicine is reliable and whether remote physician presence is adequate for acute stroke treatment using a mobile stoke treatment unit.
Real-World Data
Dr. Itrat and colleagues conducted a prospective observational study between July 18 and November 1, 2014. Their community-based study assessed telemedicine and the mobile stroke treatment unit in Cleveland. Participants were the first 100 Cleveland residents who had acute onset of stroke-like symptoms between 8 am and 8 pm and were evaluated by the mobile stroke treatment unit after implementation of the telemedicine stroke treatment program at the Cleveland Clinic. A vascular neurologist evaluated the first 100 patients via telemedicine, and a neuroradiologist remotely assessed images obtained by mobile CT. Data were entered into the medical records and a prospective registry.
The 3.5-month study compared the evaluation and treatment of patients on the mobile stroke treatment unit with the evaluation and treatment of a control group of patients brought to the emergency department by ambulance during the same year. Process times were measured from the time the patient entered the door of the mobile unit or emergency department. Any problems encountered during the stroke evaluation were recorded.
The researchers reported that 99 of 100 patients were evaluated successfully. The median duration of telemedicine evaluation was 20 minutes. One connection failure was due to crew error, and the patient was transported to the nearest emergency department. There were six telemedicine disconnections, none of which lasted longer than 60 seconds or affected clinical care. Sixteen patients received thrombolysis in the mobile stroke treatment unit. Times from the door to CT completion (13 minutes) and from door to IV thrombolysis (32 minutes) were significantly shorter in the mobile stroke treatment unit group, compared with the control group (18 minutes and 58 minutes, respectively). Times to CT interpretation did not differ significantly between the groups.
"While studies have modeled mobile stroke units to be cost-effective from the societal perspective, our investigation implies further reduction in operational costs of mobile stroke treatment units. Obviating the need for an on-site neurologist and neuroradiologist would allow multiple mobile units to be operated that are geographically distant from the physician," the researchers said.
A Wise Use of Limited Resources?
In an accompanying editorial, Martin Ebinger, MD, and Heinrich J. Audebert, MD, neurologists at Charité—Universitätsmedizin Berlin, state that "the occasionally emotional debate about prehospital thrombolysis usually revolves around the wise use of limited resources." Vascular neurologists, they point out, are a bottleneck for prehospital thrombolysis concepts. They are in short supply, and sending them out into the community seems counterintuitive, hence the appeal of telemedicine. The editorialists posit that "Stroke is a predestined disease for telemedicine because symptoms are audiovisually transmittable, and CT images can easily be accessed remotely. Obviously, replacing a personal encounter with a telemedicine consultation has its limitations. However, in a time-critical scenario such as stroke, the advantages of fast decisions about thrombolysis or thrombectomy may outweigh the shortcomings."
—Glenn S. Williams
Suggested Reading
Itrat A, Taqui A, Cerejo R, et al. Telemedicine in prehospital stroke evaluation and thrombolysis: taking stroke treatment to the doorstep. JAMA Neurol. 2016;73(2):162-168.
Ebinger M, Audebert HJ. Switched on—expert advice in prehospital thrombolysis via telemedicine. JAMA Neurol. 2016;73(2):153-154.
Suggested Reading
Itrat A, Taqui A, Cerejo R, et al. Telemedicine in prehospital stroke evaluation and thrombolysis: taking stroke treatment to the doorstep. JAMA Neurol. 2016;73(2):162-168.
Ebinger M, Audebert HJ. Switched on—expert advice in prehospital thrombolysis via telemedicine. JAMA Neurol. 2016;73(2):153-154.
Looking for an Alternative to ABPN Maintenance of Certification?
The current American Board of Medical Specialties (ABMS)/American Board of Psychiatry and Neurology (ABPN) requirements for maintenance of certification (MOC) do not ensure that a practicing physician has maintained competency to practice neurology. The ABMS acknowledges this concept, and one ABMS member website included the following statement: “Many qualities are necessary to be a competent physician, and many of these qualities cannot be quantified or measured. Thus, certification is not a guarantee of the competence of the physician specialist.” In other words, board certification is meant to demonstrate competence, but the board does not guarantee competence. This concept nullifies the notion that the American College of Physicians (ACP) raised, that if you become involved in litigation, board certification will somehow protect you. The fact is that if you are negligent, no piece of paper hanging on your wall will protect you.
The costs to practicing neurologists, both in terms of time and money, to complete this process are considerable. In a recent study, the cost of physician compliance with MOC was found to range from $23,607 to $40,495 over a 10-year period, depending on specialty. Yet there is no published evidence that demonstrates that these requirements serve to improve quality of practice.
Action and Reaction
In an article published in the New England Journal of Medicine, Paul Teirstein, MD, Chief of Cardiology at the Scripps Clinic, criticized many aspects of MOC. Shortly after publication, the American Board of Internal Medicine issued a mea culpa and suspended some of the Practice Assessment, Patient Voice, and Patient Safety requirements.
On February 24, 2015, former American Academy of Neurology (AAN) President Timothy A. Pedley, MD, issued a statement on behalf of the AAN arguing that Part IV of MOC is an onerous requirement and that this ABPN requirement has imposed a hardship on neurologists.
In July 2015, the ABPN announced that as of January 1, 2016, the Feedback Module (patient or peer surveys) would become a highly recommended yet optional component of MOC. The Part IV Clinical Module component (chart review) will remain a requirement.
A New Pathway
Fortunately, there is a viable alternative to the ABMS/ABPN pathway to MOC. The National Board of Physicians and Surgeons (NBPAS) is offering recertification in ABMS medical specialties. The board of directors of the NBPAS comprises members representing many of the country’s top academic institutions and specialty organizations. All physician members of NBPAS are volunteers (there is a small paid administrative staff), in contradistinction to the ABMS boards. Members of the ABMS boards are paid six-figure salaries.
The NBPAS board recertification criteria can be found on its website (NBPAS.org). They are:
1. Previous certification by an ABMS member board.
2. Valid license to practice medicine.
3. At least 50 hours of Continuing Medical Education (CME) accredited by the Accreditation Council for CME within the past 24 months.
4. Active hospital privileges (for select specialties).
5. Clinical privileges in certified specialty have not been permanently revoked.
6. Cost: $169 for a two-year certification.
The MOC requirement itself is incorporated into Medicare law and under the Patient Protection and Affordable Care Act, although there is ambiguity regarding whether MOC must be obtained via the ABMS specialty boards. When these laws were written, the ABMS was essentially the only game in town for physicians. The ABMS has been challenged in terms of being a monopoly organization for specialty certification and recertification. Presumably because of this fact, or perhaps as a pre-emptive defense, the ABMS has recently acknowledged publicly that it does have competition in the form of the NBPAS. To punctuate this point, one ABMS member website has included the following statement, “Possession of a board certificate does not indicate total qualification for practice privileges, nor does it imply exclusion of other physicians not so certified.”
Due to pressure from NBPAS and others, the ABMS boards have had to reconsider their position on MOC. Beginning in 2016, the American Board of Anesthesiology decided to discontinue their 10-year recertification examination. Instead, their diplomates will be taking an online 30-question quiz per calendar quarter (120 questions per year). Although this is a positive change, making a 120-question, online, open-book exam for all diplomates recertifying must be significantly cheaper to produce and administer than a secured 10-year exam. That being said, the cost of this new MOC program is $210 per year instead of a lump sum of $2,100 to take the closed-book exam every 10 years. Clearly, the boards feel a reduction in cost of production for the boards should not translate to a reduction in cost to the diplomates, and that the boards should actually generate even greater revenues.
The ABPN has also responded positively by forming an MOC clinical advisory committee to evaluate how MOC impacts practice and “potentially” improves patient care. Their use of the word “potentially” is particularly encouraging, because it implicitly suggests that evidence needs to be found to support that claim.
The Future of Board Certification
The ABMS boards acknowledge that NBPAS exists as a legitimate alternative board, but they do not feel threatened at all. They are confident that physicians, like sheep to be herded, will continue to blindly pay to do unnecessary work in the name of board certification.
Unfortunately for the ABMS boards, more than 3,000 physicians have become diplomates of NBPAS, which has become accepted as a viable alternative to ABMS by an increasing number of hospital credentialing departments. It is only through an expanding number of diplomates that NBPAS can increase its acceptance and rival the inflexible, self-centered monopoly that ABMS has become.
With more institutions accepting NBPAS certification, the influence and leverage of NBPAS will grow, and physicians will be relieved of the burden of complying with costly and time-consuming requirements that do not improve practice. There is no harm in being dual-boarded, and becoming a diplomate of NBPAS prior to the expiration of an ABPN/ABMS board certification is a low-risk decision that supports a prophysician grassroots movement. During this time of unprecedented physician unity, organizations like NBPAS appear well positioned to help return the practice of medicine to physicians rather than detached administrators.
Suggested Reading
Mathew PG. An alternative pathway to the ABPN Maintenance of certification. Pract Neurol. 2016;14(1):17-21.
Teirstein PS. Boarded to death—why maintenance of certification is bad for doctors and patients. N Engl J Med. 2015;372(2):106-108.
The current American Board of Medical Specialties (ABMS)/American Board of Psychiatry and Neurology (ABPN) requirements for maintenance of certification (MOC) do not ensure that a practicing physician has maintained competency to practice neurology. The ABMS acknowledges this concept, and one ABMS member website included the following statement: “Many qualities are necessary to be a competent physician, and many of these qualities cannot be quantified or measured. Thus, certification is not a guarantee of the competence of the physician specialist.” In other words, board certification is meant to demonstrate competence, but the board does not guarantee competence. This concept nullifies the notion that the American College of Physicians (ACP) raised, that if you become involved in litigation, board certification will somehow protect you. The fact is that if you are negligent, no piece of paper hanging on your wall will protect you.
The costs to practicing neurologists, both in terms of time and money, to complete this process are considerable. In a recent study, the cost of physician compliance with MOC was found to range from $23,607 to $40,495 over a 10-year period, depending on specialty. Yet there is no published evidence that demonstrates that these requirements serve to improve quality of practice.
Action and Reaction
In an article published in the New England Journal of Medicine, Paul Teirstein, MD, Chief of Cardiology at the Scripps Clinic, criticized many aspects of MOC. Shortly after publication, the American Board of Internal Medicine issued a mea culpa and suspended some of the Practice Assessment, Patient Voice, and Patient Safety requirements.
On February 24, 2015, former American Academy of Neurology (AAN) President Timothy A. Pedley, MD, issued a statement on behalf of the AAN arguing that Part IV of MOC is an onerous requirement and that this ABPN requirement has imposed a hardship on neurologists.
In July 2015, the ABPN announced that as of January 1, 2016, the Feedback Module (patient or peer surveys) would become a highly recommended yet optional component of MOC. The Part IV Clinical Module component (chart review) will remain a requirement.
A New Pathway
Fortunately, there is a viable alternative to the ABMS/ABPN pathway to MOC. The National Board of Physicians and Surgeons (NBPAS) is offering recertification in ABMS medical specialties. The board of directors of the NBPAS comprises members representing many of the country’s top academic institutions and specialty organizations. All physician members of NBPAS are volunteers (there is a small paid administrative staff), in contradistinction to the ABMS boards. Members of the ABMS boards are paid six-figure salaries.
The NBPAS board recertification criteria can be found on its website (NBPAS.org). They are:
1. Previous certification by an ABMS member board.
2. Valid license to practice medicine.
3. At least 50 hours of Continuing Medical Education (CME) accredited by the Accreditation Council for CME within the past 24 months.
4. Active hospital privileges (for select specialties).
5. Clinical privileges in certified specialty have not been permanently revoked.
6. Cost: $169 for a two-year certification.
The MOC requirement itself is incorporated into Medicare law and under the Patient Protection and Affordable Care Act, although there is ambiguity regarding whether MOC must be obtained via the ABMS specialty boards. When these laws were written, the ABMS was essentially the only game in town for physicians. The ABMS has been challenged in terms of being a monopoly organization for specialty certification and recertification. Presumably because of this fact, or perhaps as a pre-emptive defense, the ABMS has recently acknowledged publicly that it does have competition in the form of the NBPAS. To punctuate this point, one ABMS member website has included the following statement, “Possession of a board certificate does not indicate total qualification for practice privileges, nor does it imply exclusion of other physicians not so certified.”
Due to pressure from NBPAS and others, the ABMS boards have had to reconsider their position on MOC. Beginning in 2016, the American Board of Anesthesiology decided to discontinue their 10-year recertification examination. Instead, their diplomates will be taking an online 30-question quiz per calendar quarter (120 questions per year). Although this is a positive change, making a 120-question, online, open-book exam for all diplomates recertifying must be significantly cheaper to produce and administer than a secured 10-year exam. That being said, the cost of this new MOC program is $210 per year instead of a lump sum of $2,100 to take the closed-book exam every 10 years. Clearly, the boards feel a reduction in cost of production for the boards should not translate to a reduction in cost to the diplomates, and that the boards should actually generate even greater revenues.
The ABPN has also responded positively by forming an MOC clinical advisory committee to evaluate how MOC impacts practice and “potentially” improves patient care. Their use of the word “potentially” is particularly encouraging, because it implicitly suggests that evidence needs to be found to support that claim.
The Future of Board Certification
The ABMS boards acknowledge that NBPAS exists as a legitimate alternative board, but they do not feel threatened at all. They are confident that physicians, like sheep to be herded, will continue to blindly pay to do unnecessary work in the name of board certification.
Unfortunately for the ABMS boards, more than 3,000 physicians have become diplomates of NBPAS, which has become accepted as a viable alternative to ABMS by an increasing number of hospital credentialing departments. It is only through an expanding number of diplomates that NBPAS can increase its acceptance and rival the inflexible, self-centered monopoly that ABMS has become.
With more institutions accepting NBPAS certification, the influence and leverage of NBPAS will grow, and physicians will be relieved of the burden of complying with costly and time-consuming requirements that do not improve practice. There is no harm in being dual-boarded, and becoming a diplomate of NBPAS prior to the expiration of an ABPN/ABMS board certification is a low-risk decision that supports a prophysician grassroots movement. During this time of unprecedented physician unity, organizations like NBPAS appear well positioned to help return the practice of medicine to physicians rather than detached administrators.
The current American Board of Medical Specialties (ABMS)/American Board of Psychiatry and Neurology (ABPN) requirements for maintenance of certification (MOC) do not ensure that a practicing physician has maintained competency to practice neurology. The ABMS acknowledges this concept, and one ABMS member website included the following statement: “Many qualities are necessary to be a competent physician, and many of these qualities cannot be quantified or measured. Thus, certification is not a guarantee of the competence of the physician specialist.” In other words, board certification is meant to demonstrate competence, but the board does not guarantee competence. This concept nullifies the notion that the American College of Physicians (ACP) raised, that if you become involved in litigation, board certification will somehow protect you. The fact is that if you are negligent, no piece of paper hanging on your wall will protect you.
The costs to practicing neurologists, both in terms of time and money, to complete this process are considerable. In a recent study, the cost of physician compliance with MOC was found to range from $23,607 to $40,495 over a 10-year period, depending on specialty. Yet there is no published evidence that demonstrates that these requirements serve to improve quality of practice.
Action and Reaction
In an article published in the New England Journal of Medicine, Paul Teirstein, MD, Chief of Cardiology at the Scripps Clinic, criticized many aspects of MOC. Shortly after publication, the American Board of Internal Medicine issued a mea culpa and suspended some of the Practice Assessment, Patient Voice, and Patient Safety requirements.
On February 24, 2015, former American Academy of Neurology (AAN) President Timothy A. Pedley, MD, issued a statement on behalf of the AAN arguing that Part IV of MOC is an onerous requirement and that this ABPN requirement has imposed a hardship on neurologists.
In July 2015, the ABPN announced that as of January 1, 2016, the Feedback Module (patient or peer surveys) would become a highly recommended yet optional component of MOC. The Part IV Clinical Module component (chart review) will remain a requirement.
A New Pathway
Fortunately, there is a viable alternative to the ABMS/ABPN pathway to MOC. The National Board of Physicians and Surgeons (NBPAS) is offering recertification in ABMS medical specialties. The board of directors of the NBPAS comprises members representing many of the country’s top academic institutions and specialty organizations. All physician members of NBPAS are volunteers (there is a small paid administrative staff), in contradistinction to the ABMS boards. Members of the ABMS boards are paid six-figure salaries.
The NBPAS board recertification criteria can be found on its website (NBPAS.org). They are:
1. Previous certification by an ABMS member board.
2. Valid license to practice medicine.
3. At least 50 hours of Continuing Medical Education (CME) accredited by the Accreditation Council for CME within the past 24 months.
4. Active hospital privileges (for select specialties).
5. Clinical privileges in certified specialty have not been permanently revoked.
6. Cost: $169 for a two-year certification.
The MOC requirement itself is incorporated into Medicare law and under the Patient Protection and Affordable Care Act, although there is ambiguity regarding whether MOC must be obtained via the ABMS specialty boards. When these laws were written, the ABMS was essentially the only game in town for physicians. The ABMS has been challenged in terms of being a monopoly organization for specialty certification and recertification. Presumably because of this fact, or perhaps as a pre-emptive defense, the ABMS has recently acknowledged publicly that it does have competition in the form of the NBPAS. To punctuate this point, one ABMS member website has included the following statement, “Possession of a board certificate does not indicate total qualification for practice privileges, nor does it imply exclusion of other physicians not so certified.”
Due to pressure from NBPAS and others, the ABMS boards have had to reconsider their position on MOC. Beginning in 2016, the American Board of Anesthesiology decided to discontinue their 10-year recertification examination. Instead, their diplomates will be taking an online 30-question quiz per calendar quarter (120 questions per year). Although this is a positive change, making a 120-question, online, open-book exam for all diplomates recertifying must be significantly cheaper to produce and administer than a secured 10-year exam. That being said, the cost of this new MOC program is $210 per year instead of a lump sum of $2,100 to take the closed-book exam every 10 years. Clearly, the boards feel a reduction in cost of production for the boards should not translate to a reduction in cost to the diplomates, and that the boards should actually generate even greater revenues.
The ABPN has also responded positively by forming an MOC clinical advisory committee to evaluate how MOC impacts practice and “potentially” improves patient care. Their use of the word “potentially” is particularly encouraging, because it implicitly suggests that evidence needs to be found to support that claim.
The Future of Board Certification
The ABMS boards acknowledge that NBPAS exists as a legitimate alternative board, but they do not feel threatened at all. They are confident that physicians, like sheep to be herded, will continue to blindly pay to do unnecessary work in the name of board certification.
Unfortunately for the ABMS boards, more than 3,000 physicians have become diplomates of NBPAS, which has become accepted as a viable alternative to ABMS by an increasing number of hospital credentialing departments. It is only through an expanding number of diplomates that NBPAS can increase its acceptance and rival the inflexible, self-centered monopoly that ABMS has become.
With more institutions accepting NBPAS certification, the influence and leverage of NBPAS will grow, and physicians will be relieved of the burden of complying with costly and time-consuming requirements that do not improve practice. There is no harm in being dual-boarded, and becoming a diplomate of NBPAS prior to the expiration of an ABPN/ABMS board certification is a low-risk decision that supports a prophysician grassroots movement. During this time of unprecedented physician unity, organizations like NBPAS appear well positioned to help return the practice of medicine to physicians rather than detached administrators.
Suggested Reading
Mathew PG. An alternative pathway to the ABPN Maintenance of certification. Pract Neurol. 2016;14(1):17-21.
Teirstein PS. Boarded to death—why maintenance of certification is bad for doctors and patients. N Engl J Med. 2015;372(2):106-108.
Suggested Reading
Mathew PG. An alternative pathway to the ABPN Maintenance of certification. Pract Neurol. 2016;14(1):17-21.
Teirstein PS. Boarded to death—why maintenance of certification is bad for doctors and patients. N Engl J Med. 2015;372(2):106-108.
Tool May Help Predict Persistent Postconcussion Symptoms
A clinical risk score may help identify which children and adolescents with recent head injury are at risk for persistent postconcussion symptoms, according to an investigation published March 8 in JAMA.
Approximately one-third of pediatric patients with concussion have ongoing somatic, cognitive, psychological, or behavioral symptoms at 28 days. At present, neurologists have no tools to help predict which patients will be affected in this way. The 5P (Preventing Postconcussive Problems in Pediatrics) study was performed to develop and validate a clinical risk score for this purpose, said Roger Zemek, MD, a scientist at Children’s Hospital of Eastern Ontario Research Institute in Ottawa, Canada, and his associates.
This prospective cohort study involved patients between ages 5 and 17 (median age, 12) who presented to one of nine Canadian pediatric emergency departments within 48 hours of sustaining a concussion.
In the derivation cohort, 510 of 1,701 participants (30%) met the criteria for persistent postconcussion symptoms. The investigators assessed 47 possible predictive variables for their usefulness in predicting persistent postconcussion symptoms in this cohort. The variables were collected from demographic data, patient history, injury characteristics, physical examination, results on the Acute Concussion Evaluation Inventory and the Postconcussion Symptom Inventory, and patient and parent responses to weekly follow-up surveys during the month after the injury.
The investigators devised a clinical risk score using the following nine predictors that they found to be most accurate: age, gender, presence or absence of prior concussion, migraine history, presence or absence of current headache, sensitivity to noise, fatigue, slow responses to questions, and an abnormal tandem stance. They then selected three cutoff points to stratify the risk of persistent postconcussion symptoms: 0–3 points indicated low risk, 4–8 points indicated intermediate risk, and 9 or more points indicated high risk. Treating physicians also were asked to predict the likelihood of persistent postconcussion symptoms.
In the validation cohort, 291 of 883 participants (33%) met the criteria for persistent postconcussion symptoms. For low-risk patients, the sensitivity of the clinical risk score was 94%, the specificity was 18%, the negative predictive value was 85%, and the positive predictive value was 36%. For high-risk patients, the sensitivity of the clinical risk score was 20%, the specificity was 94%, the negative predictive value was 70%, and the positive predictive value was 60%.
In both sets of patients, the clinical risk score was significantly better than physician judgment in predicting persistent postconcussion symptoms. The clinical risk score has modest accuracy, however, at distinguishing between who will and who will not have persistent symptoms. This tool could be refined further, perhaps, by adding information regarding biomarkers, genetic susceptibility, or advanced neuroimaging, said Dr. Zemek and his associates.
—Mary Ann Moon
Suggested Reading
Zemek R, Barrowman N, Freedman SB, et al. Clinical risk score for persistent postconcussion symptoms among children with acute concussion in the ED. JAMA. 2016;315(10):1014-1025.
A clinical risk score may help identify which children and adolescents with recent head injury are at risk for persistent postconcussion symptoms, according to an investigation published March 8 in JAMA.
Approximately one-third of pediatric patients with concussion have ongoing somatic, cognitive, psychological, or behavioral symptoms at 28 days. At present, neurologists have no tools to help predict which patients will be affected in this way. The 5P (Preventing Postconcussive Problems in Pediatrics) study was performed to develop and validate a clinical risk score for this purpose, said Roger Zemek, MD, a scientist at Children’s Hospital of Eastern Ontario Research Institute in Ottawa, Canada, and his associates.
This prospective cohort study involved patients between ages 5 and 17 (median age, 12) who presented to one of nine Canadian pediatric emergency departments within 48 hours of sustaining a concussion.
In the derivation cohort, 510 of 1,701 participants (30%) met the criteria for persistent postconcussion symptoms. The investigators assessed 47 possible predictive variables for their usefulness in predicting persistent postconcussion symptoms in this cohort. The variables were collected from demographic data, patient history, injury characteristics, physical examination, results on the Acute Concussion Evaluation Inventory and the Postconcussion Symptom Inventory, and patient and parent responses to weekly follow-up surveys during the month after the injury.
The investigators devised a clinical risk score using the following nine predictors that they found to be most accurate: age, gender, presence or absence of prior concussion, migraine history, presence or absence of current headache, sensitivity to noise, fatigue, slow responses to questions, and an abnormal tandem stance. They then selected three cutoff points to stratify the risk of persistent postconcussion symptoms: 0–3 points indicated low risk, 4–8 points indicated intermediate risk, and 9 or more points indicated high risk. Treating physicians also were asked to predict the likelihood of persistent postconcussion symptoms.
In the validation cohort, 291 of 883 participants (33%) met the criteria for persistent postconcussion symptoms. For low-risk patients, the sensitivity of the clinical risk score was 94%, the specificity was 18%, the negative predictive value was 85%, and the positive predictive value was 36%. For high-risk patients, the sensitivity of the clinical risk score was 20%, the specificity was 94%, the negative predictive value was 70%, and the positive predictive value was 60%.
In both sets of patients, the clinical risk score was significantly better than physician judgment in predicting persistent postconcussion symptoms. The clinical risk score has modest accuracy, however, at distinguishing between who will and who will not have persistent symptoms. This tool could be refined further, perhaps, by adding information regarding biomarkers, genetic susceptibility, or advanced neuroimaging, said Dr. Zemek and his associates.
—Mary Ann Moon
A clinical risk score may help identify which children and adolescents with recent head injury are at risk for persistent postconcussion symptoms, according to an investigation published March 8 in JAMA.
Approximately one-third of pediatric patients with concussion have ongoing somatic, cognitive, psychological, or behavioral symptoms at 28 days. At present, neurologists have no tools to help predict which patients will be affected in this way. The 5P (Preventing Postconcussive Problems in Pediatrics) study was performed to develop and validate a clinical risk score for this purpose, said Roger Zemek, MD, a scientist at Children’s Hospital of Eastern Ontario Research Institute in Ottawa, Canada, and his associates.
This prospective cohort study involved patients between ages 5 and 17 (median age, 12) who presented to one of nine Canadian pediatric emergency departments within 48 hours of sustaining a concussion.
In the derivation cohort, 510 of 1,701 participants (30%) met the criteria for persistent postconcussion symptoms. The investigators assessed 47 possible predictive variables for their usefulness in predicting persistent postconcussion symptoms in this cohort. The variables were collected from demographic data, patient history, injury characteristics, physical examination, results on the Acute Concussion Evaluation Inventory and the Postconcussion Symptom Inventory, and patient and parent responses to weekly follow-up surveys during the month after the injury.
The investigators devised a clinical risk score using the following nine predictors that they found to be most accurate: age, gender, presence or absence of prior concussion, migraine history, presence or absence of current headache, sensitivity to noise, fatigue, slow responses to questions, and an abnormal tandem stance. They then selected three cutoff points to stratify the risk of persistent postconcussion symptoms: 0–3 points indicated low risk, 4–8 points indicated intermediate risk, and 9 or more points indicated high risk. Treating physicians also were asked to predict the likelihood of persistent postconcussion symptoms.
In the validation cohort, 291 of 883 participants (33%) met the criteria for persistent postconcussion symptoms. For low-risk patients, the sensitivity of the clinical risk score was 94%, the specificity was 18%, the negative predictive value was 85%, and the positive predictive value was 36%. For high-risk patients, the sensitivity of the clinical risk score was 20%, the specificity was 94%, the negative predictive value was 70%, and the positive predictive value was 60%.
In both sets of patients, the clinical risk score was significantly better than physician judgment in predicting persistent postconcussion symptoms. The clinical risk score has modest accuracy, however, at distinguishing between who will and who will not have persistent symptoms. This tool could be refined further, perhaps, by adding information regarding biomarkers, genetic susceptibility, or advanced neuroimaging, said Dr. Zemek and his associates.
—Mary Ann Moon
Suggested Reading
Zemek R, Barrowman N, Freedman SB, et al. Clinical risk score for persistent postconcussion symptoms among children with acute concussion in the ED. JAMA. 2016;315(10):1014-1025.
Suggested Reading
Zemek R, Barrowman N, Freedman SB, et al. Clinical risk score for persistent postconcussion symptoms among children with acute concussion in the ED. JAMA. 2016;315(10):1014-1025.
High Coffee Consumption May Decrease Risk for MS
High coffee consumption decreases the odds of developing multiple sclerosis (MS), according to two case–control studies published online ahead of print March 3 in the Journal of Neurology, Neurosurgery & Psychiatry. Anna K. Hedström, MD, PhD, a postdoctoral researcher at the Karolinska Institute, Stockholm, and her associates conducted the studies.
The investigators analyzed coffee consumption among 1,620 adults with MS and 2,788 healthy controls in the Swedish Epidemiological Investigation of Multiple Sclerosis (EIMS). They also examined coffee consumption in 1,159 adults with MS and 1,172 healthy controls in the Kaiser Permanente Medical Care Plan, Northern California Region (KPNC).
In EIMS, the adjusted odds ratio (OR) for developing MS was 0.70 among participants who drank more than six cups of coffee (ie, greater than 900 mL) daily at the index year, which was defined as the year of the initial appearance of symptoms indicative of MS. The corresponding ORs for those who reported high coffee consumption at five or 10 years before the study were 0.72 and 0.71, respectively, but these results were not statistically significant.
In KPNC, those who consumed four or more cups of coffee (ie, more than 948 mL) daily were significantly less likely to develop MS than were those who never drank coffee (OR, 0.69). In addition, people who drank four or more cups of coffee daily at least five years prior to the index year had significantly reduced odds of MS (OR, 0.64).
A meta-analysis of the combined results of the two studies indicated a significant 29% reduction in the likelihood of developing MS among the people with the greatest coffee consumption (ie, greater than 900 mL daily in EIMS and greater than 948 mL in KPNC). The investigators adjusted all the analyses for many demographic and environmental risk factors for MS, including age, gender, residential area, ancestry, smoking habits, exposure to passive smoking, sun exposure habits, and BMI at age 20.
No evidence indicated any associations between increased amounts of tea or soda intake and MS.
“Further studies are required to establish if it is in fact caffeine, or if there is another molecule in coffee underlying the findings, to longitudinally assess the association between consumption of coffee and disease activity in MS, and to evaluate the mechanisms by which coffee may be acting, which could thus lead to new therapeutic targets,” the researchers concluded.
—Lori Laubach
Suggested Reading
Hedström AK, Mowry EM, Gianfrancesco MA, et al. High consumption of coffee is associated with decreased multiple sclerosis risk; results from two independent studies. J Neurol Neurosurg Psychiatry. 2016 March 3 [Epub ahead of print].
High coffee consumption decreases the odds of developing multiple sclerosis (MS), according to two case–control studies published online ahead of print March 3 in the Journal of Neurology, Neurosurgery & Psychiatry. Anna K. Hedström, MD, PhD, a postdoctoral researcher at the Karolinska Institute, Stockholm, and her associates conducted the studies.
The investigators analyzed coffee consumption among 1,620 adults with MS and 2,788 healthy controls in the Swedish Epidemiological Investigation of Multiple Sclerosis (EIMS). They also examined coffee consumption in 1,159 adults with MS and 1,172 healthy controls in the Kaiser Permanente Medical Care Plan, Northern California Region (KPNC).
In EIMS, the adjusted odds ratio (OR) for developing MS was 0.70 among participants who drank more than six cups of coffee (ie, greater than 900 mL) daily at the index year, which was defined as the year of the initial appearance of symptoms indicative of MS. The corresponding ORs for those who reported high coffee consumption at five or 10 years before the study were 0.72 and 0.71, respectively, but these results were not statistically significant.
In KPNC, those who consumed four or more cups of coffee (ie, more than 948 mL) daily were significantly less likely to develop MS than were those who never drank coffee (OR, 0.69). In addition, people who drank four or more cups of coffee daily at least five years prior to the index year had significantly reduced odds of MS (OR, 0.64).
A meta-analysis of the combined results of the two studies indicated a significant 29% reduction in the likelihood of developing MS among the people with the greatest coffee consumption (ie, greater than 900 mL daily in EIMS and greater than 948 mL in KPNC). The investigators adjusted all the analyses for many demographic and environmental risk factors for MS, including age, gender, residential area, ancestry, smoking habits, exposure to passive smoking, sun exposure habits, and BMI at age 20.
No evidence indicated any associations between increased amounts of tea or soda intake and MS.
“Further studies are required to establish if it is in fact caffeine, or if there is another molecule in coffee underlying the findings, to longitudinally assess the association between consumption of coffee and disease activity in MS, and to evaluate the mechanisms by which coffee may be acting, which could thus lead to new therapeutic targets,” the researchers concluded.
—Lori Laubach
High coffee consumption decreases the odds of developing multiple sclerosis (MS), according to two case–control studies published online ahead of print March 3 in the Journal of Neurology, Neurosurgery & Psychiatry. Anna K. Hedström, MD, PhD, a postdoctoral researcher at the Karolinska Institute, Stockholm, and her associates conducted the studies.
The investigators analyzed coffee consumption among 1,620 adults with MS and 2,788 healthy controls in the Swedish Epidemiological Investigation of Multiple Sclerosis (EIMS). They also examined coffee consumption in 1,159 adults with MS and 1,172 healthy controls in the Kaiser Permanente Medical Care Plan, Northern California Region (KPNC).
In EIMS, the adjusted odds ratio (OR) for developing MS was 0.70 among participants who drank more than six cups of coffee (ie, greater than 900 mL) daily at the index year, which was defined as the year of the initial appearance of symptoms indicative of MS. The corresponding ORs for those who reported high coffee consumption at five or 10 years before the study were 0.72 and 0.71, respectively, but these results were not statistically significant.
In KPNC, those who consumed four or more cups of coffee (ie, more than 948 mL) daily were significantly less likely to develop MS than were those who never drank coffee (OR, 0.69). In addition, people who drank four or more cups of coffee daily at least five years prior to the index year had significantly reduced odds of MS (OR, 0.64).
A meta-analysis of the combined results of the two studies indicated a significant 29% reduction in the likelihood of developing MS among the people with the greatest coffee consumption (ie, greater than 900 mL daily in EIMS and greater than 948 mL in KPNC). The investigators adjusted all the analyses for many demographic and environmental risk factors for MS, including age, gender, residential area, ancestry, smoking habits, exposure to passive smoking, sun exposure habits, and BMI at age 20.
No evidence indicated any associations between increased amounts of tea or soda intake and MS.
“Further studies are required to establish if it is in fact caffeine, or if there is another molecule in coffee underlying the findings, to longitudinally assess the association between consumption of coffee and disease activity in MS, and to evaluate the mechanisms by which coffee may be acting, which could thus lead to new therapeutic targets,” the researchers concluded.
—Lori Laubach
Suggested Reading
Hedström AK, Mowry EM, Gianfrancesco MA, et al. High consumption of coffee is associated with decreased multiple sclerosis risk; results from two independent studies. J Neurol Neurosurg Psychiatry. 2016 March 3 [Epub ahead of print].
Suggested Reading
Hedström AK, Mowry EM, Gianfrancesco MA, et al. High consumption of coffee is associated with decreased multiple sclerosis risk; results from two independent studies. J Neurol Neurosurg Psychiatry. 2016 March 3 [Epub ahead of print].
Intranasal Ketorolac Treats Migraine Effectively
Intranasal ketorolac is superior to placebo and noninferior to intranasal sumatriptan for the acute abortive treatment of moderate to severe migraine, according to data published in the February issue of Headache. Intranasal ketorolac may be appropriate for patients whose nausea makes the use of oral medications difficult, and the formulation also offers an effective alternative for patients who cannot or do not want to use a triptan nasal spray, according to the authors.
Research suggests that parenteral ketorolac may be as effective as or more effective than certain triptans and other acute abortive therapies. No previous study, however, had directly compared intranasal ketorolac with any migraine-specific therapy.
Aruna S. Rao, MD, Instructor of Neurology at Johns Hopkins University School of Medicine in Baltimore, and colleagues conducted a prospective, double-blind, double-dummy trial at an outpatient headache center in Baltimore from March 2013 to December 2014. Eligible patients were age 18 or older, had a history of episodic migraine for at least one year, and had two to 10 migraine attacks per month.
Participants were randomized in groups of equal size to one of six sequences of ketorolac nasal spray (31.5 mg), sumatriptan nasal spray (20 mg), and placebo. Each participant treated three moderate to severe migraine attacks and received a different treatment for each attack. During the 48 hours following the use of each treatment, patients used a four-point scale to assess headache severity, migraine-associated symptoms, and disability.
The study’s primary outcome was two-hour headache relief. Secondary outcomes included two-hour pain freedom, two-hour absence of migraine-associated symptoms, absence of allodynia, disability, and 24- and 48-hour sustained pain relief and sustained pain freedom.
In all, 72 participants were randomized, 54 used at least one dose of study medication, and 49 treated three attacks. A total of 152 attacks were analyzed. Patients’ mean age was 36. Approximately 80% of patients were Caucasian, and 98% were female.
About 73% of patients treated with ketorolac had two-hour pain relief, compared with 69% of patients treated with sumatriptan and 39% of controls. Ketorolac and sumatriptan thus were superior to placebo. In addition, 43% of patients treated with ketorolac had two-hour pain freedom, compared with 37% of patients treated with sumatriptan and 18% of controls. Ketorolac and sumatriptan were superior to placebo for time to pain relief, two-hour freedom from photophobia, and two-to-24-hour sustained pain relief. Only ketorolac was superior to placebo for two-hour freedom from nausea and phonophobia, two-to-24-hour sustained pain freedom, two-to-48-hour sustained pain relief, and two-to-48-hour sustained pain freedom.
The researchers found no statistically significant difference in two-hour freedom from allodynia in participants treated with ketorolac or sumatriptan, compared with placebo. In the first two hours after study treatment, participants who used ketorolac were 61% less likely, and participants who used sumatriptan were 53% less likely, to use rescue medication, compared with placebo. The most common adverse events reported for ketorolac and sumatriptan were nasal burning and an unusual taste. Both were mild to moderate for the majority of patients.
—Erik Greb
Suggested Reading
Rao AS, Gelaye B, Kurth T, et al. A randomized trial of ketorolac vs sumatripan vs placebo nasal spray (KSPN) for acute migraine. Headache. 2016;56(2):331-340.
Intranasal ketorolac is superior to placebo and noninferior to intranasal sumatriptan for the acute abortive treatment of moderate to severe migraine, according to data published in the February issue of Headache. Intranasal ketorolac may be appropriate for patients whose nausea makes the use of oral medications difficult, and the formulation also offers an effective alternative for patients who cannot or do not want to use a triptan nasal spray, according to the authors.
Research suggests that parenteral ketorolac may be as effective as or more effective than certain triptans and other acute abortive therapies. No previous study, however, had directly compared intranasal ketorolac with any migraine-specific therapy.
Aruna S. Rao, MD, Instructor of Neurology at Johns Hopkins University School of Medicine in Baltimore, and colleagues conducted a prospective, double-blind, double-dummy trial at an outpatient headache center in Baltimore from March 2013 to December 2014. Eligible patients were age 18 or older, had a history of episodic migraine for at least one year, and had two to 10 migraine attacks per month.
Participants were randomized in groups of equal size to one of six sequences of ketorolac nasal spray (31.5 mg), sumatriptan nasal spray (20 mg), and placebo. Each participant treated three moderate to severe migraine attacks and received a different treatment for each attack. During the 48 hours following the use of each treatment, patients used a four-point scale to assess headache severity, migraine-associated symptoms, and disability.
The study’s primary outcome was two-hour headache relief. Secondary outcomes included two-hour pain freedom, two-hour absence of migraine-associated symptoms, absence of allodynia, disability, and 24- and 48-hour sustained pain relief and sustained pain freedom.
In all, 72 participants were randomized, 54 used at least one dose of study medication, and 49 treated three attacks. A total of 152 attacks were analyzed. Patients’ mean age was 36. Approximately 80% of patients were Caucasian, and 98% were female.
About 73% of patients treated with ketorolac had two-hour pain relief, compared with 69% of patients treated with sumatriptan and 39% of controls. Ketorolac and sumatriptan thus were superior to placebo. In addition, 43% of patients treated with ketorolac had two-hour pain freedom, compared with 37% of patients treated with sumatriptan and 18% of controls. Ketorolac and sumatriptan were superior to placebo for time to pain relief, two-hour freedom from photophobia, and two-to-24-hour sustained pain relief. Only ketorolac was superior to placebo for two-hour freedom from nausea and phonophobia, two-to-24-hour sustained pain freedom, two-to-48-hour sustained pain relief, and two-to-48-hour sustained pain freedom.
The researchers found no statistically significant difference in two-hour freedom from allodynia in participants treated with ketorolac or sumatriptan, compared with placebo. In the first two hours after study treatment, participants who used ketorolac were 61% less likely, and participants who used sumatriptan were 53% less likely, to use rescue medication, compared with placebo. The most common adverse events reported for ketorolac and sumatriptan were nasal burning and an unusual taste. Both were mild to moderate for the majority of patients.
—Erik Greb
Intranasal ketorolac is superior to placebo and noninferior to intranasal sumatriptan for the acute abortive treatment of moderate to severe migraine, according to data published in the February issue of Headache. Intranasal ketorolac may be appropriate for patients whose nausea makes the use of oral medications difficult, and the formulation also offers an effective alternative for patients who cannot or do not want to use a triptan nasal spray, according to the authors.
Research suggests that parenteral ketorolac may be as effective as or more effective than certain triptans and other acute abortive therapies. No previous study, however, had directly compared intranasal ketorolac with any migraine-specific therapy.
Aruna S. Rao, MD, Instructor of Neurology at Johns Hopkins University School of Medicine in Baltimore, and colleagues conducted a prospective, double-blind, double-dummy trial at an outpatient headache center in Baltimore from March 2013 to December 2014. Eligible patients were age 18 or older, had a history of episodic migraine for at least one year, and had two to 10 migraine attacks per month.
Participants were randomized in groups of equal size to one of six sequences of ketorolac nasal spray (31.5 mg), sumatriptan nasal spray (20 mg), and placebo. Each participant treated three moderate to severe migraine attacks and received a different treatment for each attack. During the 48 hours following the use of each treatment, patients used a four-point scale to assess headache severity, migraine-associated symptoms, and disability.
The study’s primary outcome was two-hour headache relief. Secondary outcomes included two-hour pain freedom, two-hour absence of migraine-associated symptoms, absence of allodynia, disability, and 24- and 48-hour sustained pain relief and sustained pain freedom.
In all, 72 participants were randomized, 54 used at least one dose of study medication, and 49 treated three attacks. A total of 152 attacks were analyzed. Patients’ mean age was 36. Approximately 80% of patients were Caucasian, and 98% were female.
About 73% of patients treated with ketorolac had two-hour pain relief, compared with 69% of patients treated with sumatriptan and 39% of controls. Ketorolac and sumatriptan thus were superior to placebo. In addition, 43% of patients treated with ketorolac had two-hour pain freedom, compared with 37% of patients treated with sumatriptan and 18% of controls. Ketorolac and sumatriptan were superior to placebo for time to pain relief, two-hour freedom from photophobia, and two-to-24-hour sustained pain relief. Only ketorolac was superior to placebo for two-hour freedom from nausea and phonophobia, two-to-24-hour sustained pain freedom, two-to-48-hour sustained pain relief, and two-to-48-hour sustained pain freedom.
The researchers found no statistically significant difference in two-hour freedom from allodynia in participants treated with ketorolac or sumatriptan, compared with placebo. In the first two hours after study treatment, participants who used ketorolac were 61% less likely, and participants who used sumatriptan were 53% less likely, to use rescue medication, compared with placebo. The most common adverse events reported for ketorolac and sumatriptan were nasal burning and an unusual taste. Both were mild to moderate for the majority of patients.
—Erik Greb
Suggested Reading
Rao AS, Gelaye B, Kurth T, et al. A randomized trial of ketorolac vs sumatripan vs placebo nasal spray (KSPN) for acute migraine. Headache. 2016;56(2):331-340.
Suggested Reading
Rao AS, Gelaye B, Kurth T, et al. A randomized trial of ketorolac vs sumatripan vs placebo nasal spray (KSPN) for acute migraine. Headache. 2016;56(2):331-340.
How Often Do Antibiotics Cause Delirium?
Antibiotic-associated encephalopathy (AAE) may cause delirium more often than is recognized, according to research published March 8 in Neurology. AAE should be considered as a diagnosis for all patients who develop delirium after the initiation of antibiotics, the authors suggest. Improved recognition of AAE could reduce the period of delirium and improve patient outcomes through the early discontinuation of antibiotics.
Delirium occurs in as much as half of hospitalized patients and in as much as 80% of patients in intensive care. “People who have delirium are more likely to have other complications, go into a nursing home instead of going home after being in the hospital, and are more likely to die than people who do not develop delirium,” said Shamik Bhattacharyya, MD, Instructor in Neurology at Brigham and Women’s Hospital in Boston. “Any efforts we can make to help identify the cause of delirium have the potential to be greatly beneficial.”
Investigators Reviewed Case Reports
Although encephalopathy is reported as an adverse effect of antibiotics with a frequency of less than 1%, a 2013 retrospective study of 100 critically ill patients reported a 15% rate of encephalopathy associated with cefepime, a cephalosporin. The result suggests that AAE is underdiagnosed.
Dr. Bhattacharyya and colleagues conducted a comprehensive review of reported cases of AAE to define the specific clinical features, EEG changes, and neuroimaging findings associated with encephalopathy from particular antibiotic classes and individual antibiotics. The investigators excluded case series that did not describe individual patient data. For each described case, the researchers collected data on demographics, antibiotic used, comorbidities, clinical symptoms accompanying encephalopathy, time to toxicity onset and improvement, and laboratory investigations. They calculated a Naranjo score for each case to assess the likelihood that the given antibiotic caused encephalopathy.
Psychosis Was Common
The investigators identified 292 articles describing 391 individual cases from 1946 through 2013. Toxicity reports mentioned 54 antibiotics from 12 classes of antibiotic. Approximately 54% of the 391 cases were male, and the median age was 54.
About 47% of cases had psychosis, which was defined as the presence of delusions or hallucinations. Psychosis was most common in encephalopathy associated with sulfonamides (68%), quinolones (67%), macrolides (63%), and penicillin procaine (68%).
Overall, 14% of cases had seizures. This symptom was most common in AAE associated with penicillin (38%) and cephalosporins (35%). Seizures associated with cephalosporin-associated encephalopathy were nonconvulsive in 54% of patients, and nearly all other reported seizures were clinically apparent.
Approximately 15% of cases had myoclonus. Myoclonus was most common in cases of encephalopathy associated with penicillin (71%) and cephalosporins (41%), but infrequent (≤10%) with other antibiotic classes.
MRI of the brain was abnormal in AAE associated with metronidazole, but normal in all others, with the exception of one case of cefditoren pivoxil toxicity in the setting of acquired carnitine deficiency. Similarly, CT of the brain was normal in all cases except for one case of cerebellar hypodensity with metronidazole toxicity and one report of left thalamic hypodensity with imipenem toxicity associated with generalized seizures and epileptiform discharges on EEG.
EEG, however, was abnormal in 70% of cases of AAE in which EEG was performed, including 95% of cases of cephalosporin-associated encephalopathy. EEG was abnormal in 83% of cases of AAE associated with penicillin, 83% of cases associated with ciprofloxacin, and 69% of cases associated with isoniazid, but the test was performed much less frequently in patients with encephalopathy associated with these antibiotics, thus limiting interpretation of this finding.
AAE was apparent within a median of five days after antibiotic initiation for all individual antibiotics except isoniazid and metronidazole. For these antibiotics, the median length of time from initiation to emergence of encephalopathy was approximately three weeks. Time to resolution of encephalopathy after antibiotic discontinuation was within a median of five days for most antibiotic classes. Metronidazole, for which median time to resolution was 13 days, was an exception.
The median Naranjo scale score for all antibiotic classes was 4, indicating a possible association between the antibiotic and AAE. All reported cases had, by definition, an infection that could not be excluded as a potential cause of encephalopathy. When non-CNS infections were not considered a potential cause of encephalopathy, the median Naranjo scale score was 5, indicating a probable association.
Three Clinical Phenotypes of AAE
Based on these data, the investigators identified three clinical phenotypes of AAE. They characterized Type 1 AAE by onset within days of antibiotic initiation, common occurrence of myoclonus or seizures, abnormal EEG, normal MRI, and resolution within days. Type 1 AAE is associated with penicillin (as an individual antibiotic) and cephalosporins.
Type 2 AAE is marked by onset within days of antibiotic initiation, frequent occurrence of psychosis, rare occurrence of seizures, infrequently abnormal EEG, normal MRI, and resolution within days. This clinical phenotype is associated with procaine penicillin, sulfonamides, fluoroquinolones, and macrolides.
Type 3 AAE is seen only with metronidazole and is characterized by onset weeks after initiation, frequent occurrence of cerebellar dysfunction, rare seizures, rare and nonspecific EEG abnormalities, and omnipresence of abnormal MRI.
Reports’ Level of Detail Varied
Any review that relies exclusively on case reports and small series is subject to selection and publication bias, which may explain why the median age for AAE in reported cases was relatively young, said the authors. Also, AAE in the elderly may be underreported because delirium in this population may result from several factors.
The case reports that Dr. Bhattacharyya’s group collected had varying degrees of detail, and missing information prevented a precise estimation of the prevalence of reported symptoms and laboratory findings. The authors tried to reduce the effect of such variability on their analysis by reviewing a large number of cases. Many case reports, though, did not include enough clinical information to exclude other potential contributing factors to encephalopathy, and this lack of detail affected the strength of the association that the researchers found.
“More research is needed, but these antibiotics should be considered as a possible cause of delirium,” said Dr. Bhattacharyya. “Recognition of different patterns of toxicity could lead to a quicker diagnosis and hopefully prevent of some of the negative consequences for people with delirium and other brain problems.”
—Erik Greb
Suggested Reading
Bhattacharyya S, Darby RR, Raibagkar P, et al. Antibiotic-associated encephalopathy. Neurology. 2016;86(10):963-971.
Antibiotic-associated encephalopathy (AAE) may cause delirium more often than is recognized, according to research published March 8 in Neurology. AAE should be considered as a diagnosis for all patients who develop delirium after the initiation of antibiotics, the authors suggest. Improved recognition of AAE could reduce the period of delirium and improve patient outcomes through the early discontinuation of antibiotics.
Delirium occurs in as much as half of hospitalized patients and in as much as 80% of patients in intensive care. “People who have delirium are more likely to have other complications, go into a nursing home instead of going home after being in the hospital, and are more likely to die than people who do not develop delirium,” said Shamik Bhattacharyya, MD, Instructor in Neurology at Brigham and Women’s Hospital in Boston. “Any efforts we can make to help identify the cause of delirium have the potential to be greatly beneficial.”
Investigators Reviewed Case Reports
Although encephalopathy is reported as an adverse effect of antibiotics with a frequency of less than 1%, a 2013 retrospective study of 100 critically ill patients reported a 15% rate of encephalopathy associated with cefepime, a cephalosporin. The result suggests that AAE is underdiagnosed.
Dr. Bhattacharyya and colleagues conducted a comprehensive review of reported cases of AAE to define the specific clinical features, EEG changes, and neuroimaging findings associated with encephalopathy from particular antibiotic classes and individual antibiotics. The investigators excluded case series that did not describe individual patient data. For each described case, the researchers collected data on demographics, antibiotic used, comorbidities, clinical symptoms accompanying encephalopathy, time to toxicity onset and improvement, and laboratory investigations. They calculated a Naranjo score for each case to assess the likelihood that the given antibiotic caused encephalopathy.
Psychosis Was Common
The investigators identified 292 articles describing 391 individual cases from 1946 through 2013. Toxicity reports mentioned 54 antibiotics from 12 classes of antibiotic. Approximately 54% of the 391 cases were male, and the median age was 54.
About 47% of cases had psychosis, which was defined as the presence of delusions or hallucinations. Psychosis was most common in encephalopathy associated with sulfonamides (68%), quinolones (67%), macrolides (63%), and penicillin procaine (68%).
Overall, 14% of cases had seizures. This symptom was most common in AAE associated with penicillin (38%) and cephalosporins (35%). Seizures associated with cephalosporin-associated encephalopathy were nonconvulsive in 54% of patients, and nearly all other reported seizures were clinically apparent.
Approximately 15% of cases had myoclonus. Myoclonus was most common in cases of encephalopathy associated with penicillin (71%) and cephalosporins (41%), but infrequent (≤10%) with other antibiotic classes.
MRI of the brain was abnormal in AAE associated with metronidazole, but normal in all others, with the exception of one case of cefditoren pivoxil toxicity in the setting of acquired carnitine deficiency. Similarly, CT of the brain was normal in all cases except for one case of cerebellar hypodensity with metronidazole toxicity and one report of left thalamic hypodensity with imipenem toxicity associated with generalized seizures and epileptiform discharges on EEG.
EEG, however, was abnormal in 70% of cases of AAE in which EEG was performed, including 95% of cases of cephalosporin-associated encephalopathy. EEG was abnormal in 83% of cases of AAE associated with penicillin, 83% of cases associated with ciprofloxacin, and 69% of cases associated with isoniazid, but the test was performed much less frequently in patients with encephalopathy associated with these antibiotics, thus limiting interpretation of this finding.
AAE was apparent within a median of five days after antibiotic initiation for all individual antibiotics except isoniazid and metronidazole. For these antibiotics, the median length of time from initiation to emergence of encephalopathy was approximately three weeks. Time to resolution of encephalopathy after antibiotic discontinuation was within a median of five days for most antibiotic classes. Metronidazole, for which median time to resolution was 13 days, was an exception.
The median Naranjo scale score for all antibiotic classes was 4, indicating a possible association between the antibiotic and AAE. All reported cases had, by definition, an infection that could not be excluded as a potential cause of encephalopathy. When non-CNS infections were not considered a potential cause of encephalopathy, the median Naranjo scale score was 5, indicating a probable association.
Three Clinical Phenotypes of AAE
Based on these data, the investigators identified three clinical phenotypes of AAE. They characterized Type 1 AAE by onset within days of antibiotic initiation, common occurrence of myoclonus or seizures, abnormal EEG, normal MRI, and resolution within days. Type 1 AAE is associated with penicillin (as an individual antibiotic) and cephalosporins.
Type 2 AAE is marked by onset within days of antibiotic initiation, frequent occurrence of psychosis, rare occurrence of seizures, infrequently abnormal EEG, normal MRI, and resolution within days. This clinical phenotype is associated with procaine penicillin, sulfonamides, fluoroquinolones, and macrolides.
Type 3 AAE is seen only with metronidazole and is characterized by onset weeks after initiation, frequent occurrence of cerebellar dysfunction, rare seizures, rare and nonspecific EEG abnormalities, and omnipresence of abnormal MRI.
Reports’ Level of Detail Varied
Any review that relies exclusively on case reports and small series is subject to selection and publication bias, which may explain why the median age for AAE in reported cases was relatively young, said the authors. Also, AAE in the elderly may be underreported because delirium in this population may result from several factors.
The case reports that Dr. Bhattacharyya’s group collected had varying degrees of detail, and missing information prevented a precise estimation of the prevalence of reported symptoms and laboratory findings. The authors tried to reduce the effect of such variability on their analysis by reviewing a large number of cases. Many case reports, though, did not include enough clinical information to exclude other potential contributing factors to encephalopathy, and this lack of detail affected the strength of the association that the researchers found.
“More research is needed, but these antibiotics should be considered as a possible cause of delirium,” said Dr. Bhattacharyya. “Recognition of different patterns of toxicity could lead to a quicker diagnosis and hopefully prevent of some of the negative consequences for people with delirium and other brain problems.”
—Erik Greb
Antibiotic-associated encephalopathy (AAE) may cause delirium more often than is recognized, according to research published March 8 in Neurology. AAE should be considered as a diagnosis for all patients who develop delirium after the initiation of antibiotics, the authors suggest. Improved recognition of AAE could reduce the period of delirium and improve patient outcomes through the early discontinuation of antibiotics.
Delirium occurs in as much as half of hospitalized patients and in as much as 80% of patients in intensive care. “People who have delirium are more likely to have other complications, go into a nursing home instead of going home after being in the hospital, and are more likely to die than people who do not develop delirium,” said Shamik Bhattacharyya, MD, Instructor in Neurology at Brigham and Women’s Hospital in Boston. “Any efforts we can make to help identify the cause of delirium have the potential to be greatly beneficial.”
Investigators Reviewed Case Reports
Although encephalopathy is reported as an adverse effect of antibiotics with a frequency of less than 1%, a 2013 retrospective study of 100 critically ill patients reported a 15% rate of encephalopathy associated with cefepime, a cephalosporin. The result suggests that AAE is underdiagnosed.
Dr. Bhattacharyya and colleagues conducted a comprehensive review of reported cases of AAE to define the specific clinical features, EEG changes, and neuroimaging findings associated with encephalopathy from particular antibiotic classes and individual antibiotics. The investigators excluded case series that did not describe individual patient data. For each described case, the researchers collected data on demographics, antibiotic used, comorbidities, clinical symptoms accompanying encephalopathy, time to toxicity onset and improvement, and laboratory investigations. They calculated a Naranjo score for each case to assess the likelihood that the given antibiotic caused encephalopathy.
Psychosis Was Common
The investigators identified 292 articles describing 391 individual cases from 1946 through 2013. Toxicity reports mentioned 54 antibiotics from 12 classes of antibiotic. Approximately 54% of the 391 cases were male, and the median age was 54.
About 47% of cases had psychosis, which was defined as the presence of delusions or hallucinations. Psychosis was most common in encephalopathy associated with sulfonamides (68%), quinolones (67%), macrolides (63%), and penicillin procaine (68%).
Overall, 14% of cases had seizures. This symptom was most common in AAE associated with penicillin (38%) and cephalosporins (35%). Seizures associated with cephalosporin-associated encephalopathy were nonconvulsive in 54% of patients, and nearly all other reported seizures were clinically apparent.
Approximately 15% of cases had myoclonus. Myoclonus was most common in cases of encephalopathy associated with penicillin (71%) and cephalosporins (41%), but infrequent (≤10%) with other antibiotic classes.
MRI of the brain was abnormal in AAE associated with metronidazole, but normal in all others, with the exception of one case of cefditoren pivoxil toxicity in the setting of acquired carnitine deficiency. Similarly, CT of the brain was normal in all cases except for one case of cerebellar hypodensity with metronidazole toxicity and one report of left thalamic hypodensity with imipenem toxicity associated with generalized seizures and epileptiform discharges on EEG.
EEG, however, was abnormal in 70% of cases of AAE in which EEG was performed, including 95% of cases of cephalosporin-associated encephalopathy. EEG was abnormal in 83% of cases of AAE associated with penicillin, 83% of cases associated with ciprofloxacin, and 69% of cases associated with isoniazid, but the test was performed much less frequently in patients with encephalopathy associated with these antibiotics, thus limiting interpretation of this finding.
AAE was apparent within a median of five days after antibiotic initiation for all individual antibiotics except isoniazid and metronidazole. For these antibiotics, the median length of time from initiation to emergence of encephalopathy was approximately three weeks. Time to resolution of encephalopathy after antibiotic discontinuation was within a median of five days for most antibiotic classes. Metronidazole, for which median time to resolution was 13 days, was an exception.
The median Naranjo scale score for all antibiotic classes was 4, indicating a possible association between the antibiotic and AAE. All reported cases had, by definition, an infection that could not be excluded as a potential cause of encephalopathy. When non-CNS infections were not considered a potential cause of encephalopathy, the median Naranjo scale score was 5, indicating a probable association.
Three Clinical Phenotypes of AAE
Based on these data, the investigators identified three clinical phenotypes of AAE. They characterized Type 1 AAE by onset within days of antibiotic initiation, common occurrence of myoclonus or seizures, abnormal EEG, normal MRI, and resolution within days. Type 1 AAE is associated with penicillin (as an individual antibiotic) and cephalosporins.
Type 2 AAE is marked by onset within days of antibiotic initiation, frequent occurrence of psychosis, rare occurrence of seizures, infrequently abnormal EEG, normal MRI, and resolution within days. This clinical phenotype is associated with procaine penicillin, sulfonamides, fluoroquinolones, and macrolides.
Type 3 AAE is seen only with metronidazole and is characterized by onset weeks after initiation, frequent occurrence of cerebellar dysfunction, rare seizures, rare and nonspecific EEG abnormalities, and omnipresence of abnormal MRI.
Reports’ Level of Detail Varied
Any review that relies exclusively on case reports and small series is subject to selection and publication bias, which may explain why the median age for AAE in reported cases was relatively young, said the authors. Also, AAE in the elderly may be underreported because delirium in this population may result from several factors.
The case reports that Dr. Bhattacharyya’s group collected had varying degrees of detail, and missing information prevented a precise estimation of the prevalence of reported symptoms and laboratory findings. The authors tried to reduce the effect of such variability on their analysis by reviewing a large number of cases. Many case reports, though, did not include enough clinical information to exclude other potential contributing factors to encephalopathy, and this lack of detail affected the strength of the association that the researchers found.
“More research is needed, but these antibiotics should be considered as a possible cause of delirium,” said Dr. Bhattacharyya. “Recognition of different patterns of toxicity could lead to a quicker diagnosis and hopefully prevent of some of the negative consequences for people with delirium and other brain problems.”
—Erik Greb
Suggested Reading
Bhattacharyya S, Darby RR, Raibagkar P, et al. Antibiotic-associated encephalopathy. Neurology. 2016;86(10):963-971.
Suggested Reading
Bhattacharyya S, Darby RR, Raibagkar P, et al. Antibiotic-associated encephalopathy. Neurology. 2016;86(10):963-971.
Headache Worsening After IV DHE May Not Predict Outcome of Chronic Migraine
Headache worsening after treatment with IV dihydroergotamine (DHE) does not predict poor headache outcome in the medium term among patients with chronic migraine, according to research published March 1 in Neurology. Headache exacerbation thus is not a sufficient reason to stop treatment. Instead, neurologists should focus on controlling nausea, which is the most important modifiable factor in achieving a good headache outcome, according to the researchers.
Neurologists have used IV DHE to treat patients with migraine for decades. After receiving this therapy, some patients have transient headache worsening, and this development may be interpreted as a reason to stop the infusions. Michael Eller, MD, Assistant Clinical Professor of Neurology at the University of California, San Francisco (UCSF), and colleagues performed a retrospective chart review to determine whether transient headache worsening after IV DHE infusion predicts medium-term headache outcome in patients with chronic migraine.
The investigators included all patients with chronic migraine admitted by the UCSF Headache Service between January 1, 2008, and December 31, 2012, in their analysis. All patients received IV DHE according to a standard protocol, which included 1-mg doses administered over five days to a typical target dose of 11.25 mg. In addition, patients were premedicated with ondansetron, domperidone, or both. Participants with medication overuse (approximately 30% of the population) also received IV aspirin before receiving IV DHE.
Dr. Eller and colleagues retrospectively analyzed the prospectively collected inpatient headache diaries, progress notes, and discharge summaries. Physicians did not routinely ask patients whether they had headache exacerbation. The researchers defined DHE worsening as headache (typically, exacerbation of the underlying phenotype) or nausea increase within 30 minutes of the infusion. The treating clinician assessed and recorded medium-term headache outcome at follow-up approximately six weeks after discharge.
During the study period, 274 patients with chronic migraine had inpatient treatment with DHE. Mean age was 44, and 77% of the population was female. In all, 153 patients had been receiving migraine preventives. Headache outcome information was available for 214 patients, and patients with missing outcome data did not differ from the others in terms of age, sex, or likelihood of having nausea or medication overuse. Approximately 78% of patients with follow-up data had medium-term headache benefit following IV DHE.
Forty-one participants (19%) had headache worsening with DHE infusions. Of these patients, 66% had medium-term headache benefit, compared with 82% of patients who did not have headache exacerbation. A univariate analysis indicated that headache exacerbation with DHE infusion was associated with reduced odds of medium-term headache benefit. Multivariate logistic regression analysis adjusted for nausea, leg cramping, medication overuse, sex, and age, however, indicated that headache exacerbation with DHE was not an independent predictor of medium-term headache benefit.
Nausea was the modifiable risk factor with the greatest effect on headache outcome. In an adjusted model, nausea was significantly associated with headache exacerbation with DHE infusion. Nausea also was an independent predictor of decreased likelihood of medium-term headache benefit in the fully adjusted model, as was medication overuse. Older age was strongly associated with increased odds of headache benefit.
The results suggest that adequate nausea control might help prevent headache exacerbation, said the authors. “Clinicians in all settings should focus their efforts on aggressive nausea control during a course of IV DHE for chronic migraine,” they added. Younger patients with chronic migraine were less likely to benefit from an inpatient course of IV DHE, and this finding “highlights an even greater need for nausea control in that population.”
The study’s retrospective design was a limitation, said Dr. Eller. Some exacerbations of headache may have gone unreported, and future studies should systematically query patients for this symptom, he added.
Data Improve the Understanding of DHE
The investigation by Dr. Eller and colleagues improves our current understanding of the effects of DHE, said Andrew Charles, MD, Director of the Headache Research and Treatment Program at the University of California, Los Angeles, in an accompanying editorial. The careful documentation and systematic reporting of patient experience, although retrospective, can be valuable in characterizing common patient-management issues, he added.
In population studies, persistent frequent nausea has been associated with increased risk of progression from episodic migraine to chronic migraine. “Whether or not treatment of nausea as a ‘modifiable risk factor’ actually changes the clinical course of migraine remains unclear,” said Dr. Charles. “What is clear, however, is that nausea is a frequently disabling component of migraine that warrants aggressive therapy.” Various therapeutic options exist, but no evidence clearly supports one option over the others. “This study underscores the importance of optimizing therapy of migraine-related nausea, and of coming to a better understanding of the role of nausea and its treatment in the short- and long-term outcomes of patients with migraine,” Dr. Charles concluded.
—Erik Greb
Suggested Reading
Charles A. Comment: Outcomes of migraine therapy with IV dihydroergotamine. Neurology. 2016;86(9):859.
Eller M, Gelfand AA, Riggins NY, et al. Exacerbation of headache during dihydroergotamine for chronic migraine does not alter outcome. Neurology. 2016;86(9):856-859.
Headache worsening after treatment with IV dihydroergotamine (DHE) does not predict poor headache outcome in the medium term among patients with chronic migraine, according to research published March 1 in Neurology. Headache exacerbation thus is not a sufficient reason to stop treatment. Instead, neurologists should focus on controlling nausea, which is the most important modifiable factor in achieving a good headache outcome, according to the researchers.
Neurologists have used IV DHE to treat patients with migraine for decades. After receiving this therapy, some patients have transient headache worsening, and this development may be interpreted as a reason to stop the infusions. Michael Eller, MD, Assistant Clinical Professor of Neurology at the University of California, San Francisco (UCSF), and colleagues performed a retrospective chart review to determine whether transient headache worsening after IV DHE infusion predicts medium-term headache outcome in patients with chronic migraine.
The investigators included all patients with chronic migraine admitted by the UCSF Headache Service between January 1, 2008, and December 31, 2012, in their analysis. All patients received IV DHE according to a standard protocol, which included 1-mg doses administered over five days to a typical target dose of 11.25 mg. In addition, patients were premedicated with ondansetron, domperidone, or both. Participants with medication overuse (approximately 30% of the population) also received IV aspirin before receiving IV DHE.
Dr. Eller and colleagues retrospectively analyzed the prospectively collected inpatient headache diaries, progress notes, and discharge summaries. Physicians did not routinely ask patients whether they had headache exacerbation. The researchers defined DHE worsening as headache (typically, exacerbation of the underlying phenotype) or nausea increase within 30 minutes of the infusion. The treating clinician assessed and recorded medium-term headache outcome at follow-up approximately six weeks after discharge.
During the study period, 274 patients with chronic migraine had inpatient treatment with DHE. Mean age was 44, and 77% of the population was female. In all, 153 patients had been receiving migraine preventives. Headache outcome information was available for 214 patients, and patients with missing outcome data did not differ from the others in terms of age, sex, or likelihood of having nausea or medication overuse. Approximately 78% of patients with follow-up data had medium-term headache benefit following IV DHE.
Forty-one participants (19%) had headache worsening with DHE infusions. Of these patients, 66% had medium-term headache benefit, compared with 82% of patients who did not have headache exacerbation. A univariate analysis indicated that headache exacerbation with DHE infusion was associated with reduced odds of medium-term headache benefit. Multivariate logistic regression analysis adjusted for nausea, leg cramping, medication overuse, sex, and age, however, indicated that headache exacerbation with DHE was not an independent predictor of medium-term headache benefit.
Nausea was the modifiable risk factor with the greatest effect on headache outcome. In an adjusted model, nausea was significantly associated with headache exacerbation with DHE infusion. Nausea also was an independent predictor of decreased likelihood of medium-term headache benefit in the fully adjusted model, as was medication overuse. Older age was strongly associated with increased odds of headache benefit.
The results suggest that adequate nausea control might help prevent headache exacerbation, said the authors. “Clinicians in all settings should focus their efforts on aggressive nausea control during a course of IV DHE for chronic migraine,” they added. Younger patients with chronic migraine were less likely to benefit from an inpatient course of IV DHE, and this finding “highlights an even greater need for nausea control in that population.”
The study’s retrospective design was a limitation, said Dr. Eller. Some exacerbations of headache may have gone unreported, and future studies should systematically query patients for this symptom, he added.
Data Improve the Understanding of DHE
The investigation by Dr. Eller and colleagues improves our current understanding of the effects of DHE, said Andrew Charles, MD, Director of the Headache Research and Treatment Program at the University of California, Los Angeles, in an accompanying editorial. The careful documentation and systematic reporting of patient experience, although retrospective, can be valuable in characterizing common patient-management issues, he added.
In population studies, persistent frequent nausea has been associated with increased risk of progression from episodic migraine to chronic migraine. “Whether or not treatment of nausea as a ‘modifiable risk factor’ actually changes the clinical course of migraine remains unclear,” said Dr. Charles. “What is clear, however, is that nausea is a frequently disabling component of migraine that warrants aggressive therapy.” Various therapeutic options exist, but no evidence clearly supports one option over the others. “This study underscores the importance of optimizing therapy of migraine-related nausea, and of coming to a better understanding of the role of nausea and its treatment in the short- and long-term outcomes of patients with migraine,” Dr. Charles concluded.
—Erik Greb
Headache worsening after treatment with IV dihydroergotamine (DHE) does not predict poor headache outcome in the medium term among patients with chronic migraine, according to research published March 1 in Neurology. Headache exacerbation thus is not a sufficient reason to stop treatment. Instead, neurologists should focus on controlling nausea, which is the most important modifiable factor in achieving a good headache outcome, according to the researchers.
Neurologists have used IV DHE to treat patients with migraine for decades. After receiving this therapy, some patients have transient headache worsening, and this development may be interpreted as a reason to stop the infusions. Michael Eller, MD, Assistant Clinical Professor of Neurology at the University of California, San Francisco (UCSF), and colleagues performed a retrospective chart review to determine whether transient headache worsening after IV DHE infusion predicts medium-term headache outcome in patients with chronic migraine.
The investigators included all patients with chronic migraine admitted by the UCSF Headache Service between January 1, 2008, and December 31, 2012, in their analysis. All patients received IV DHE according to a standard protocol, which included 1-mg doses administered over five days to a typical target dose of 11.25 mg. In addition, patients were premedicated with ondansetron, domperidone, or both. Participants with medication overuse (approximately 30% of the population) also received IV aspirin before receiving IV DHE.
Dr. Eller and colleagues retrospectively analyzed the prospectively collected inpatient headache diaries, progress notes, and discharge summaries. Physicians did not routinely ask patients whether they had headache exacerbation. The researchers defined DHE worsening as headache (typically, exacerbation of the underlying phenotype) or nausea increase within 30 minutes of the infusion. The treating clinician assessed and recorded medium-term headache outcome at follow-up approximately six weeks after discharge.
During the study period, 274 patients with chronic migraine had inpatient treatment with DHE. Mean age was 44, and 77% of the population was female. In all, 153 patients had been receiving migraine preventives. Headache outcome information was available for 214 patients, and patients with missing outcome data did not differ from the others in terms of age, sex, or likelihood of having nausea or medication overuse. Approximately 78% of patients with follow-up data had medium-term headache benefit following IV DHE.
Forty-one participants (19%) had headache worsening with DHE infusions. Of these patients, 66% had medium-term headache benefit, compared with 82% of patients who did not have headache exacerbation. A univariate analysis indicated that headache exacerbation with DHE infusion was associated with reduced odds of medium-term headache benefit. Multivariate logistic regression analysis adjusted for nausea, leg cramping, medication overuse, sex, and age, however, indicated that headache exacerbation with DHE was not an independent predictor of medium-term headache benefit.
Nausea was the modifiable risk factor with the greatest effect on headache outcome. In an adjusted model, nausea was significantly associated with headache exacerbation with DHE infusion. Nausea also was an independent predictor of decreased likelihood of medium-term headache benefit in the fully adjusted model, as was medication overuse. Older age was strongly associated with increased odds of headache benefit.
The results suggest that adequate nausea control might help prevent headache exacerbation, said the authors. “Clinicians in all settings should focus their efforts on aggressive nausea control during a course of IV DHE for chronic migraine,” they added. Younger patients with chronic migraine were less likely to benefit from an inpatient course of IV DHE, and this finding “highlights an even greater need for nausea control in that population.”
The study’s retrospective design was a limitation, said Dr. Eller. Some exacerbations of headache may have gone unreported, and future studies should systematically query patients for this symptom, he added.
Data Improve the Understanding of DHE
The investigation by Dr. Eller and colleagues improves our current understanding of the effects of DHE, said Andrew Charles, MD, Director of the Headache Research and Treatment Program at the University of California, Los Angeles, in an accompanying editorial. The careful documentation and systematic reporting of patient experience, although retrospective, can be valuable in characterizing common patient-management issues, he added.
In population studies, persistent frequent nausea has been associated with increased risk of progression from episodic migraine to chronic migraine. “Whether or not treatment of nausea as a ‘modifiable risk factor’ actually changes the clinical course of migraine remains unclear,” said Dr. Charles. “What is clear, however, is that nausea is a frequently disabling component of migraine that warrants aggressive therapy.” Various therapeutic options exist, but no evidence clearly supports one option over the others. “This study underscores the importance of optimizing therapy of migraine-related nausea, and of coming to a better understanding of the role of nausea and its treatment in the short- and long-term outcomes of patients with migraine,” Dr. Charles concluded.
—Erik Greb
Suggested Reading
Charles A. Comment: Outcomes of migraine therapy with IV dihydroergotamine. Neurology. 2016;86(9):859.
Eller M, Gelfand AA, Riggins NY, et al. Exacerbation of headache during dihydroergotamine for chronic migraine does not alter outcome. Neurology. 2016;86(9):856-859.
Suggested Reading
Charles A. Comment: Outcomes of migraine therapy with IV dihydroergotamine. Neurology. 2016;86(9):859.
Eller M, Gelfand AA, Riggins NY, et al. Exacerbation of headache during dihydroergotamine for chronic migraine does not alter outcome. Neurology. 2016;86(9):856-859.
VTEP Guidelines Can Be Systematically Implemented in Pediatric Inpatients
Clinical question: Can venous thromboembolism prophylaxis (VTEP) guidelines be systematically implemented in a pediatric inpatient population?
Background: VTEP for hospitalized adult medical patients has been characterized in the literature as being safe and efficacious, although mortality benefits are unclear.1 Systematic risk stratification based on electronic medical records (EMRs) with resultant implementation of pharmacologic and mechanical thromboprophylaxis has been shown to improve appropriate VTEP ordering in the adult inpatient population.2
Although the incidence of VTE is known to be increasing in the pediatric population, systematic VTEP implementation in hospitalized children is not well-described. Prior studies have shown the safety of systematic VTEP implementation through a protocol identifying high-risk pediatric inpatients with resultant initiation of appropriate VTEP. 3,4
Risk stratification in prior studies has taken into consideration risk factors such as altered mobility, presence of a central venous catheter (CVC), spinal cord injury (SCI), major lower-extremity orthopedic surgery, major trauma, active malignancy, acute infection, obesity, estrogen use, inflammatory bowel disease (IBD), prior VTE, and family history of VTE.4
Study design: Prospective cohort study using QI methodology.
Setting: A 455-bed, tertiary, freestanding children’s hospital.
Synopsis: After reviewing current literature for VTEP in adults and children and existing institutional pathways for VTEP in adults, traumatic brain injury, and SCI, a multidisciplinary committee formulated VTEP guidelines for 12- to 17-year-old patients. Pharmacologic prophylaxis was considered appropriate in the absence of contraindications and only if CVC and altered mobility were present as risk factors. Using a previously published logistic regression model evaluating VTE risk factors, patients were further categorized as high, moderate, or low risk.
Initial risk-factor categorization was via EMR-based order set, where risk factors were displayed, but subsequently was performed by an integrated tool based on an initial screening form completed by providers upon admission. Logic rules applied by the EMR led to specific VTEP recommendations, which were then selectable by the provider.
Over the first 17 months of EMR tool use, 148 patients on average were admitted each month. VTEP screening rates via the EMR tool increased from 48% in the first month to 81% in the final month. Despite EMR tool usage, VTEP orders did not always correlate with recommendations. Although not a stated objective of the study, none of the screened patients developed a VTE (compared to three cases of VTE in patients between 12 and 17 years of age the year prior).
Bottom line: VTEP guidelines can be systematically implemented via an EMR-based tool in a pediatric inpatient population.
Citation: Mahajerin A, Webber E, Morris J, Taylor K, Saysana M. Development and implementation results of a venous thromboembolism prophylaxis guideline in a tertiary care pediatric hospital. Hosp Pediatr. 2015;5(12):630-636.
References
- Spyropoulos AC, Mahan C. Venous thromboembolism prophylaxis in the medical patient: controversies and perspectives. Am J Med. 2009;122(12):1077-1084.
- Kahn SR, Morrison DR, Cohen JM, et al. Interventions for implementation of thromboprophylaxis in hospitalized medical and surgical patients at risk for venous thromboembolism. Cochrane Database Syst Rev. 2013;7:CD008201.
- Takemoto CM, Sohi S, Desai K, et al. Hospital-associated venous thromboembolism in children: incidence and clinical characteristics. J Pediatr. 2014;164(2):332-338.
- Raffini L, Trimarchi T, Beliveau J, Davis D. Thromboprophylaxis in a pediatric hospital: a patient-safety and quality-improvement initiative. Pediatrics. 2011;127(5):e1326-1332.
Clinical question: Can venous thromboembolism prophylaxis (VTEP) guidelines be systematically implemented in a pediatric inpatient population?
Background: VTEP for hospitalized adult medical patients has been characterized in the literature as being safe and efficacious, although mortality benefits are unclear.1 Systematic risk stratification based on electronic medical records (EMRs) with resultant implementation of pharmacologic and mechanical thromboprophylaxis has been shown to improve appropriate VTEP ordering in the adult inpatient population.2
Although the incidence of VTE is known to be increasing in the pediatric population, systematic VTEP implementation in hospitalized children is not well-described. Prior studies have shown the safety of systematic VTEP implementation through a protocol identifying high-risk pediatric inpatients with resultant initiation of appropriate VTEP. 3,4
Risk stratification in prior studies has taken into consideration risk factors such as altered mobility, presence of a central venous catheter (CVC), spinal cord injury (SCI), major lower-extremity orthopedic surgery, major trauma, active malignancy, acute infection, obesity, estrogen use, inflammatory bowel disease (IBD), prior VTE, and family history of VTE.4
Study design: Prospective cohort study using QI methodology.
Setting: A 455-bed, tertiary, freestanding children’s hospital.
Synopsis: After reviewing current literature for VTEP in adults and children and existing institutional pathways for VTEP in adults, traumatic brain injury, and SCI, a multidisciplinary committee formulated VTEP guidelines for 12- to 17-year-old patients. Pharmacologic prophylaxis was considered appropriate in the absence of contraindications and only if CVC and altered mobility were present as risk factors. Using a previously published logistic regression model evaluating VTE risk factors, patients were further categorized as high, moderate, or low risk.
Initial risk-factor categorization was via EMR-based order set, where risk factors were displayed, but subsequently was performed by an integrated tool based on an initial screening form completed by providers upon admission. Logic rules applied by the EMR led to specific VTEP recommendations, which were then selectable by the provider.
Over the first 17 months of EMR tool use, 148 patients on average were admitted each month. VTEP screening rates via the EMR tool increased from 48% in the first month to 81% in the final month. Despite EMR tool usage, VTEP orders did not always correlate with recommendations. Although not a stated objective of the study, none of the screened patients developed a VTE (compared to three cases of VTE in patients between 12 and 17 years of age the year prior).
Bottom line: VTEP guidelines can be systematically implemented via an EMR-based tool in a pediatric inpatient population.
Citation: Mahajerin A, Webber E, Morris J, Taylor K, Saysana M. Development and implementation results of a venous thromboembolism prophylaxis guideline in a tertiary care pediatric hospital. Hosp Pediatr. 2015;5(12):630-636.
References
- Spyropoulos AC, Mahan C. Venous thromboembolism prophylaxis in the medical patient: controversies and perspectives. Am J Med. 2009;122(12):1077-1084.
- Kahn SR, Morrison DR, Cohen JM, et al. Interventions for implementation of thromboprophylaxis in hospitalized medical and surgical patients at risk for venous thromboembolism. Cochrane Database Syst Rev. 2013;7:CD008201.
- Takemoto CM, Sohi S, Desai K, et al. Hospital-associated venous thromboembolism in children: incidence and clinical characteristics. J Pediatr. 2014;164(2):332-338.
- Raffini L, Trimarchi T, Beliveau J, Davis D. Thromboprophylaxis in a pediatric hospital: a patient-safety and quality-improvement initiative. Pediatrics. 2011;127(5):e1326-1332.
Clinical question: Can venous thromboembolism prophylaxis (VTEP) guidelines be systematically implemented in a pediatric inpatient population?
Background: VTEP for hospitalized adult medical patients has been characterized in the literature as being safe and efficacious, although mortality benefits are unclear.1 Systematic risk stratification based on electronic medical records (EMRs) with resultant implementation of pharmacologic and mechanical thromboprophylaxis has been shown to improve appropriate VTEP ordering in the adult inpatient population.2
Although the incidence of VTE is known to be increasing in the pediatric population, systematic VTEP implementation in hospitalized children is not well-described. Prior studies have shown the safety of systematic VTEP implementation through a protocol identifying high-risk pediatric inpatients with resultant initiation of appropriate VTEP. 3,4
Risk stratification in prior studies has taken into consideration risk factors such as altered mobility, presence of a central venous catheter (CVC), spinal cord injury (SCI), major lower-extremity orthopedic surgery, major trauma, active malignancy, acute infection, obesity, estrogen use, inflammatory bowel disease (IBD), prior VTE, and family history of VTE.4
Study design: Prospective cohort study using QI methodology.
Setting: A 455-bed, tertiary, freestanding children’s hospital.
Synopsis: After reviewing current literature for VTEP in adults and children and existing institutional pathways for VTEP in adults, traumatic brain injury, and SCI, a multidisciplinary committee formulated VTEP guidelines for 12- to 17-year-old patients. Pharmacologic prophylaxis was considered appropriate in the absence of contraindications and only if CVC and altered mobility were present as risk factors. Using a previously published logistic regression model evaluating VTE risk factors, patients were further categorized as high, moderate, or low risk.
Initial risk-factor categorization was via EMR-based order set, where risk factors were displayed, but subsequently was performed by an integrated tool based on an initial screening form completed by providers upon admission. Logic rules applied by the EMR led to specific VTEP recommendations, which were then selectable by the provider.
Over the first 17 months of EMR tool use, 148 patients on average were admitted each month. VTEP screening rates via the EMR tool increased from 48% in the first month to 81% in the final month. Despite EMR tool usage, VTEP orders did not always correlate with recommendations. Although not a stated objective of the study, none of the screened patients developed a VTE (compared to three cases of VTE in patients between 12 and 17 years of age the year prior).
Bottom line: VTEP guidelines can be systematically implemented via an EMR-based tool in a pediatric inpatient population.
Citation: Mahajerin A, Webber E, Morris J, Taylor K, Saysana M. Development and implementation results of a venous thromboembolism prophylaxis guideline in a tertiary care pediatric hospital. Hosp Pediatr. 2015;5(12):630-636.
References
- Spyropoulos AC, Mahan C. Venous thromboembolism prophylaxis in the medical patient: controversies and perspectives. Am J Med. 2009;122(12):1077-1084.
- Kahn SR, Morrison DR, Cohen JM, et al. Interventions for implementation of thromboprophylaxis in hospitalized medical and surgical patients at risk for venous thromboembolism. Cochrane Database Syst Rev. 2013;7:CD008201.
- Takemoto CM, Sohi S, Desai K, et al. Hospital-associated venous thromboembolism in children: incidence and clinical characteristics. J Pediatr. 2014;164(2):332-338.
- Raffini L, Trimarchi T, Beliveau J, Davis D. Thromboprophylaxis in a pediatric hospital: a patient-safety and quality-improvement initiative. Pediatrics. 2011;127(5):e1326-1332.
Continuous Chest Compressions Do Not Improve Outcome Compared to Chest Compressions Interrupted for Ventilation
Clinical question: In cardiopulmonary resuscitation, do continuous chest compressions improve survival or neurologic outcome compared to chest compressions interrupted for ventilation?
Background: Animal models have demonstrated that interruptions in chest compressions are associated with decreased survival and worse neurologic outcome in cardiac arrests. Observational studies in humans have suggested that for out-of-hospital cardiac arrests, continuous compressions result in improved survival.
Study Design: Unblinded, randomized, cluster design with crossover.
Setting: One hundred fourteen emergency medical service (EMS) agencies across eight clinical sites in North America.
Synopsis: Patients with out-of-hospital cardiac arrest received either continuous chest compressions with asynchronous positive-pressure ventilations or interrupted compressions at a rate of 30 compressions to two ventilations. EMS agencies were divided into clusters and randomly assigned to deliver either resuscitation strategy. Twice per year, each cluster switched treatment strategies.
During the active enrollment phase, 12,653 patients were enrolled in the intervention arm and 11,058 were enrolled in the control arm. The primary outcome of survival to hospital discharge was comparable between the two groups, with 9.0% survival rate in the intervention group as compared to 9.7% in the control group (P=0.07). The secondary outcome of survivorship with favorable neurologic status was similar at 7.0% in the intervention group and 7.7% in the control group.
There was only a small difference in the proportion of minutes devoted to compressions between the two groups, so the similarity in outcomes may be reflective of high-quality chest compressions. Additional limitations include a lack of standardization of post-resuscitation care and a lack of measurement of oxygen or ventilation delivered.
Bottom line: For out-of-hospital cardiac arrests, continuous chest compressions with positive-pressure ventilation did not increase survival or improve neurologic outcome compared to interrupted chest compressions.
Citation: Nichol G, Lerou B, Wang H, et al. Trial of continuous or interrupted chest compressions during CPR. N Engl J Med. 2015;373(23):2203-2214.
Clinical question: In cardiopulmonary resuscitation, do continuous chest compressions improve survival or neurologic outcome compared to chest compressions interrupted for ventilation?
Background: Animal models have demonstrated that interruptions in chest compressions are associated with decreased survival and worse neurologic outcome in cardiac arrests. Observational studies in humans have suggested that for out-of-hospital cardiac arrests, continuous compressions result in improved survival.
Study Design: Unblinded, randomized, cluster design with crossover.
Setting: One hundred fourteen emergency medical service (EMS) agencies across eight clinical sites in North America.
Synopsis: Patients with out-of-hospital cardiac arrest received either continuous chest compressions with asynchronous positive-pressure ventilations or interrupted compressions at a rate of 30 compressions to two ventilations. EMS agencies were divided into clusters and randomly assigned to deliver either resuscitation strategy. Twice per year, each cluster switched treatment strategies.
During the active enrollment phase, 12,653 patients were enrolled in the intervention arm and 11,058 were enrolled in the control arm. The primary outcome of survival to hospital discharge was comparable between the two groups, with 9.0% survival rate in the intervention group as compared to 9.7% in the control group (P=0.07). The secondary outcome of survivorship with favorable neurologic status was similar at 7.0% in the intervention group and 7.7% in the control group.
There was only a small difference in the proportion of minutes devoted to compressions between the two groups, so the similarity in outcomes may be reflective of high-quality chest compressions. Additional limitations include a lack of standardization of post-resuscitation care and a lack of measurement of oxygen or ventilation delivered.
Bottom line: For out-of-hospital cardiac arrests, continuous chest compressions with positive-pressure ventilation did not increase survival or improve neurologic outcome compared to interrupted chest compressions.
Citation: Nichol G, Lerou B, Wang H, et al. Trial of continuous or interrupted chest compressions during CPR. N Engl J Med. 2015;373(23):2203-2214.
Clinical question: In cardiopulmonary resuscitation, do continuous chest compressions improve survival or neurologic outcome compared to chest compressions interrupted for ventilation?
Background: Animal models have demonstrated that interruptions in chest compressions are associated with decreased survival and worse neurologic outcome in cardiac arrests. Observational studies in humans have suggested that for out-of-hospital cardiac arrests, continuous compressions result in improved survival.
Study Design: Unblinded, randomized, cluster design with crossover.
Setting: One hundred fourteen emergency medical service (EMS) agencies across eight clinical sites in North America.
Synopsis: Patients with out-of-hospital cardiac arrest received either continuous chest compressions with asynchronous positive-pressure ventilations or interrupted compressions at a rate of 30 compressions to two ventilations. EMS agencies were divided into clusters and randomly assigned to deliver either resuscitation strategy. Twice per year, each cluster switched treatment strategies.
During the active enrollment phase, 12,653 patients were enrolled in the intervention arm and 11,058 were enrolled in the control arm. The primary outcome of survival to hospital discharge was comparable between the two groups, with 9.0% survival rate in the intervention group as compared to 9.7% in the control group (P=0.07). The secondary outcome of survivorship with favorable neurologic status was similar at 7.0% in the intervention group and 7.7% in the control group.
There was only a small difference in the proportion of minutes devoted to compressions between the two groups, so the similarity in outcomes may be reflective of high-quality chest compressions. Additional limitations include a lack of standardization of post-resuscitation care and a lack of measurement of oxygen or ventilation delivered.
Bottom line: For out-of-hospital cardiac arrests, continuous chest compressions with positive-pressure ventilation did not increase survival or improve neurologic outcome compared to interrupted chest compressions.
Citation: Nichol G, Lerou B, Wang H, et al. Trial of continuous or interrupted chest compressions during CPR. N Engl J Med. 2015;373(23):2203-2214.
ATRIA Better at Predicting Stroke Risk in Patients with Atrial Fibrillation Than CHADS2, CHA2DS2-VAS
Clinical question: Does the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) risk score more accurately identify patients with atrial fibrillation (Afib) who are at low risk for ischemic stroke than the CHADS2 or CHA2DS2-VASc score?
Background: More accurate and reliable stroke risk prediction tools are needed to optimize anticoagulation decision making in patients with Afib. Recently, a new clinically based risk score, the ATRIA, has been developed and validated. This risk score assigns points based on four age categories (as well as an interaction of age and prior stroke); female gender; renal function; and history of diabetes, congestive heart failure, and hypertension. This study compared the predictive ability of the ATRIA risk score with the CHADS2 and CHA2DS2-VASc risk scores and their implications for anticoagulant treatment in Afib patients.
Study Design: Retrospective cohort study.
Setting: Afib patients not using warfarin from the United Kingdom’s Clinical Practice Research Datalink (CPRD) database, January 1998 to January 2012.
Synopsis: A total of 60,594 patients with Afib were followed until occurrence of ischemic stroke, prescription of warfarin, death, or the study’s end. The annualized stroke rate was 2.99%. Patients with moderate and high-risk CHA2DS2-VASc scores had lower event rates than those with corresponding ATRIA and CHADS2 scores. C-statistics for full point scores were 0.70 (95% CI, 0.69–0.71) for ATRIA and 0.68 (95% CI, 0.67–0.69) for both CHADS2 and CHA2DS2-VASc scores. The net reclassification index of ATRIA compared with CHADS2 and CHA2DS2-VASc risk scores were 0.137 and 0.233, respectively, reflecting that the ATRIA risk score better categorizes patients developing an event.
ATRIA risk score more accurately identified low-risk patients than the CHA2DS2-VASc score assigned to higher-risk categories. The results persisted even after restricting analysis to more recent follow-up, excluding unspecified strokes and excluding renal dysfunction as a predictor. Most improvements with ATRIA were the result of “down classification,” suggesting that using the CHA2DS2-VASc risk score could lead to overtreatment of patients at very low risk of stroke.
Bottom line: The ATRIA risk score better identifies Afib patients who are at low risk for stroke compared to CHADS2 and CHA2DS2-VASc scores.
Citation: van den Ham HA, Klungel OH, Singer DE, Leufkens HG, van Staa TP. Comparative performance of ATRIA, CHADS2, and CHA2DS2-VASc risk scores predicting stroke in patients with atrial fibrillation: results from a national primary care database. J Am Coll Cardiol. 2015;66(17):1851-1959.
Clinical question: Does the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) risk score more accurately identify patients with atrial fibrillation (Afib) who are at low risk for ischemic stroke than the CHADS2 or CHA2DS2-VASc score?
Background: More accurate and reliable stroke risk prediction tools are needed to optimize anticoagulation decision making in patients with Afib. Recently, a new clinically based risk score, the ATRIA, has been developed and validated. This risk score assigns points based on four age categories (as well as an interaction of age and prior stroke); female gender; renal function; and history of diabetes, congestive heart failure, and hypertension. This study compared the predictive ability of the ATRIA risk score with the CHADS2 and CHA2DS2-VASc risk scores and their implications for anticoagulant treatment in Afib patients.
Study Design: Retrospective cohort study.
Setting: Afib patients not using warfarin from the United Kingdom’s Clinical Practice Research Datalink (CPRD) database, January 1998 to January 2012.
Synopsis: A total of 60,594 patients with Afib were followed until occurrence of ischemic stroke, prescription of warfarin, death, or the study’s end. The annualized stroke rate was 2.99%. Patients with moderate and high-risk CHA2DS2-VASc scores had lower event rates than those with corresponding ATRIA and CHADS2 scores. C-statistics for full point scores were 0.70 (95% CI, 0.69–0.71) for ATRIA and 0.68 (95% CI, 0.67–0.69) for both CHADS2 and CHA2DS2-VASc scores. The net reclassification index of ATRIA compared with CHADS2 and CHA2DS2-VASc risk scores were 0.137 and 0.233, respectively, reflecting that the ATRIA risk score better categorizes patients developing an event.
ATRIA risk score more accurately identified low-risk patients than the CHA2DS2-VASc score assigned to higher-risk categories. The results persisted even after restricting analysis to more recent follow-up, excluding unspecified strokes and excluding renal dysfunction as a predictor. Most improvements with ATRIA were the result of “down classification,” suggesting that using the CHA2DS2-VASc risk score could lead to overtreatment of patients at very low risk of stroke.
Bottom line: The ATRIA risk score better identifies Afib patients who are at low risk for stroke compared to CHADS2 and CHA2DS2-VASc scores.
Citation: van den Ham HA, Klungel OH, Singer DE, Leufkens HG, van Staa TP. Comparative performance of ATRIA, CHADS2, and CHA2DS2-VASc risk scores predicting stroke in patients with atrial fibrillation: results from a national primary care database. J Am Coll Cardiol. 2015;66(17):1851-1959.
Clinical question: Does the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) risk score more accurately identify patients with atrial fibrillation (Afib) who are at low risk for ischemic stroke than the CHADS2 or CHA2DS2-VASc score?
Background: More accurate and reliable stroke risk prediction tools are needed to optimize anticoagulation decision making in patients with Afib. Recently, a new clinically based risk score, the ATRIA, has been developed and validated. This risk score assigns points based on four age categories (as well as an interaction of age and prior stroke); female gender; renal function; and history of diabetes, congestive heart failure, and hypertension. This study compared the predictive ability of the ATRIA risk score with the CHADS2 and CHA2DS2-VASc risk scores and their implications for anticoagulant treatment in Afib patients.
Study Design: Retrospective cohort study.
Setting: Afib patients not using warfarin from the United Kingdom’s Clinical Practice Research Datalink (CPRD) database, January 1998 to January 2012.
Synopsis: A total of 60,594 patients with Afib were followed until occurrence of ischemic stroke, prescription of warfarin, death, or the study’s end. The annualized stroke rate was 2.99%. Patients with moderate and high-risk CHA2DS2-VASc scores had lower event rates than those with corresponding ATRIA and CHADS2 scores. C-statistics for full point scores were 0.70 (95% CI, 0.69–0.71) for ATRIA and 0.68 (95% CI, 0.67–0.69) for both CHADS2 and CHA2DS2-VASc scores. The net reclassification index of ATRIA compared with CHADS2 and CHA2DS2-VASc risk scores were 0.137 and 0.233, respectively, reflecting that the ATRIA risk score better categorizes patients developing an event.
ATRIA risk score more accurately identified low-risk patients than the CHA2DS2-VASc score assigned to higher-risk categories. The results persisted even after restricting analysis to more recent follow-up, excluding unspecified strokes and excluding renal dysfunction as a predictor. Most improvements with ATRIA were the result of “down classification,” suggesting that using the CHA2DS2-VASc risk score could lead to overtreatment of patients at very low risk of stroke.
Bottom line: The ATRIA risk score better identifies Afib patients who are at low risk for stroke compared to CHADS2 and CHA2DS2-VASc scores.
Citation: van den Ham HA, Klungel OH, Singer DE, Leufkens HG, van Staa TP. Comparative performance of ATRIA, CHADS2, and CHA2DS2-VASc risk scores predicting stroke in patients with atrial fibrillation: results from a national primary care database. J Am Coll Cardiol. 2015;66(17):1851-1959.