The enthusiasm surrounding point-of-care ultrasound (POCUS) is clear and well founded. POCUS is a powerful tool that produces valuable diagnostic information for common and important clinical problems faced by hospitalists, such as pneumonia, soft-tissue infections,¹ and myriad other applications. It can inform the evaluation and management of complex clinical problems such as dyspnea.² Beyond its diagnostic potential, POCUS is well known to improve common procedures performed by adult and pediatric hospitalists by improving success rates and decreasing complications.

Excitement surrounding this technology continues to grow among hospitalists, leading to a proliferation of high-quality educational programs over the last 5 years. Most notable among these offerings has been the more comprehensive training available through the Society of Hospital Medicine (SHM) certificate-based pathway, though many other strong options exist, including institution-based curricula, such as the HealthPartners CHAMP program,³ and pediatric-focused programs. Growth in training is also occurring among medical students and residents. As of a 2012 survey, the majority (51%) of US medical schools had begun to weave ultrasound into their curricula,⁴ and this growth is also occurring in internal medicine and pediatric residency programs.⁵

Given the high potential for this technology and the growth in interest, it is an excellent time to pause and review some of the challenges faced by practitioners, hospitalist groups, and educators seeking to optimize POCUS implementation. A deliberate approach to POCUS education, the development of shared standards for high-quality use, and an ongoing dedication to develop specialty-specific practices will largely determine how much of this potential is fulfilled.

The largest challenge is likely to be educational. Educating clinicians to be able to integrate POCUS into practice is a complex, multistep process requiring not only an adequate core of didactic training and access to machines, but also the structured opportunity to develop rudimentary hands-on skills. Such initial training should be followed by continued practice and feedback as developing POCUS users progress toward independent practice. The study by Kumar et al.⁶ reaffirms that brief didactic lectures and access to machines are necessary, but they are clearly insufficient for learners to be able to use POCUS independently for a wide variety of applications. Their intervention also contrasts markedly with the 20 hours of didactics and 150 supervised scans recommended by the American College of Emergency Physicians prior to independent use for a core of six applications.⁷

Shared standards for education, use, and oversight will be crucial to fulfilling the potential of POCUS within hospital medicine. Our belief is that much can be learned from the thoughtful approach taken during the development of POCUS as a mainstream tool in emergency medicine in the early 2000s. In this approach, emergency physicians determined a sufficient and achievable standard of training for core POCUS applications, which was widely adopted. Based on completion of this training, physicians who were required to complete credentialing from their hospitals were widely able to achieve it, without any need for external certification. Emergency medicine guidelines further mandated the documentation of examinations and the creation of an exam report, features that improve clinical communication and facilitate quality improvement. Quality assurance processes that reviewed images and clinician interpretations were established as mandatory, which they should be in hospital medicine. Evidence was produced as to which exams physicians could do reliably with this focused training and which they could not. In the context of these thoughtful constructs, lawsuits have been noted to be exceedingly rare; and when they do occur, they have typically been for the failure to use POCUS rather than the converse.⁸

While many of these precepts deserve replication, others should also be modified to reflect changes in technology, medical education, and medical practice over the last 20 years and to improve upon this base of success. For example, with POCUS training now appearing in many medical school and residency curricula, training paradigms for both residents and attendings will need to accommodate a wider range of incoming skills. Emphasis should continue to be shifted toward competency-based assessments and entrustment and away from a fixed training time or exam number threshold. Important financial aspects have also changed. The cost of practical machines has dropped considerably, and medicine is shifting away from a fee-for-service model. While it remains appropriate that physicians may bill for POCUS examinations, it is likely that improved diagnosis, improved throughput, and a reduction in complications will yield greater value and should be the emphasis of cost/value discussions.⁹ Finally, while hospitals may impose credentialing, this process can also create a burden not present for most other noninvasive skills and may deter appropriate use. If this approach is chosen by a hospital, requirements should ideally remain modest, and as these skills become more widespread, POCUS should ultimately be built into board examinations and core credentialing.⁹

Thoughtful and concerted effort will be required by hospitalist leaders, educational innovators, and professional societies in developing POCUS to best serve hospitalists and their patients. This work has already begun. For example, in 2019 SHM offered a position statement outlining important aspects such as current evidence-based applications, training pathways, quality assurance, and program management.¹⁰ These recommendations should guide both adult and pediatric hospitalists. The Alliance for Academic Internal Medicine offered a similar position statement for resident training.¹¹ Interest groups are growing in numerous professional societies, which will facilitate collaboration and promote propagation of best practices. High-quality educational tools are continuing to be developed by numerous organizations.

While further development is needed to add the detail, granularity, and practical tools that educational and practice leaders need to assure that POCUS achieves its potential in hospital medicine, the foundation for POCUS use within the specialty is being thoughtfully constructed. As this process proceeds, it will be vital to continue to learn from our emergency medicine colleagues, who have already met similar challenges, while at the same time be able to develop a modern POCUS model optimized for hospital medicine workflow, training, and patient care.

The enthusiasm surrounding point-of-care ultrasound (POCUS) is clear and well founded. POCUS is a powerful tool that produces valuable diagnostic information for common and important clinical problems faced by hospitalists, such as pneumonia, soft-tissue infections,¹ and myriad other applications. It can inform the evaluation and management of complex clinical problems such as dyspnea.² Beyond its diagnostic potential, POCUS is well known to improve common procedures performed by adult and pediatric hospitalists by improving success rates and decreasing complications.

Excitement surrounding this technology continues to grow among hospitalists, leading to a proliferation of high-quality educational programs over the last 5 years. Most notable among these offerings has been the more comprehensive training available through the Society of Hospital Medicine (SHM) certificate-based pathway, though many other strong options exist, including institution-based curricula, such as the HealthPartners CHAMP program,³ and pediatric-focused programs. Growth in training is also occurring among medical students and residents. As of a 2012 survey, the majority (51%) of US medical schools had begun to weave ultrasound into their curricula,⁴ and this growth is also occurring in internal medicine and pediatric residency programs.⁵

Given the high potential for this technology and the growth in interest, it is an excellent time to pause and review some of the challenges faced by practitioners, hospitalist groups, and educators seeking to optimize POCUS implementation. A deliberate approach to POCUS education, the development of shared standards for high-quality use, and an ongoing dedication to develop specialty-specific practices will largely determine how much of this potential is fulfilled.

The largest challenge is likely to be educational. Educating clinicians to be able to integrate POCUS into practice is a complex, multistep process requiring not only an adequate core of didactic training and access to machines, but also the structured opportunity to develop rudimentary hands-on skills. Such initial training should be followed by continued practice and feedback as developing POCUS users progress toward independent practice. The study by Kumar et al.⁶ reaffirms that brief didactic lectures and access to machines are necessary, but they are clearly insufficient for learners to be able to use POCUS independently for a wide variety of applications. Their intervention also contrasts markedly with the 20 hours of didactics and 150 supervised scans recommended by the American College of Emergency Physicians prior to independent use for a core of six applications.⁷

Shared standards for education, use, and oversight will be crucial to fulfilling the potential of POCUS within hospital medicine. Our belief is that much can be learned from the thoughtful approach taken during the development of POCUS as a mainstream tool in emergency medicine in the early 2000s. In this approach, emergency physicians determined a sufficient and achievable standard of training for core POCUS applications, which was widely adopted. Based on completion of this training, physicians who were required to complete credentialing from their hospitals were widely able to achieve it, without any need for external certification. Emergency medicine guidelines further mandated the documentation of examinations and the creation of an exam report, features that improve clinical communication and facilitate quality improvement. Quality assurance processes that reviewed images and clinician interpretations were established as mandatory, which they should be in hospital medicine. Evidence was produced as to which exams physicians could do reliably with this focused training and which they could not. In the context of these thoughtful constructs, lawsuits have been noted to be exceedingly rare; and when they do occur, they have typically been for the failure to use POCUS rather than the converse.⁸

While many of these precepts deserve replication, others should also be modified to reflect changes in technology, medical education, and medical practice over the last 20 years and to improve upon this base of success. For example, with POCUS training now appearing in many medical school and residency curricula, training paradigms for both residents and attendings will need to accommodate a wider range of incoming skills. Emphasis should continue to be shifted toward competency-based assessments and entrustment and away from a fixed training time or exam number threshold. Important financial aspects have also changed. The cost of practical machines has dropped considerably, and medicine is shifting away from a fee-for-service model. While it remains appropriate that physicians may bill for POCUS examinations, it is likely that improved diagnosis, improved throughput, and a reduction in complications will yield greater value and should be the emphasis of cost/value discussions.⁹ Finally, while hospitals may impose credentialing, this process can also create a burden not present for most other noninvasive skills and may deter appropriate use. If this approach is chosen by a hospital, requirements should ideally remain modest, and as these skills become more widespread, POCUS should ultimately be built into board examinations and core credentialing.⁹

Thoughtful and concerted effort will be required by hospitalist leaders, educational innovators, and professional societies in developing POCUS to best serve hospitalists and their patients. This work has already begun. For example, in 2019 SHM offered a position statement outlining important aspects such as current evidence-based applications, training pathways, quality assurance, and program management.¹⁰ These recommendations should guide both adult and pediatric hospitalists. The Alliance for Academic Internal Medicine offered a similar position statement for resident training.¹¹ Interest groups are growing in numerous professional societies, which will facilitate collaboration and promote propagation of best practices. High-quality educational tools are continuing to be developed by numerous organizations.

While further development is needed to add the detail, granularity, and practical tools that educational and practice leaders need to assure that POCUS achieves its potential in hospital medicine, the foundation for POCUS use within the specialty is being thoughtfully constructed. As this process proceeds, it will be vital to continue to learn from our emergency medicine colleagues, who have already met similar challenges, while at the same time be able to develop a modern POCUS model optimized for hospital medicine workflow, training, and patient care.

The enthusiasm surrounding point-of-care ultrasound (POCUS) is clear and well founded. POCUS is a powerful tool that produces valuable diagnostic information for common and important clinical problems faced by hospitalists, such as pneumonia, soft-tissue infections,¹ and myriad other applications. It can inform the evaluation and management of complex clinical problems such as dyspnea.² Beyond its diagnostic potential, POCUS is well known to improve common procedures performed by adult and pediatric hospitalists by improving success rates and decreasing complications.

Excitement surrounding this technology continues to grow among hospitalists, leading to a proliferation of high-quality educational programs over the last 5 years. Most notable among these offerings has been the more comprehensive training available through the Society of Hospital Medicine (SHM) certificate-based pathway, though many other strong options exist, including institution-based curricula, such as the HealthPartners CHAMP program,³ and pediatric-focused programs. Growth in training is also occurring among medical students and residents. As of a 2012 survey, the majority (51%) of US medical schools had begun to weave ultrasound into their curricula,⁴ and this growth is also occurring in internal medicine and pediatric residency programs.⁵

Given the high potential for this technology and the growth in interest, it is an excellent time to pause and review some of the challenges faced by practitioners, hospitalist groups, and educators seeking to optimize POCUS implementation. A deliberate approach to POCUS education, the development of shared standards for high-quality use, and an ongoing dedication to develop specialty-specific practices will largely determine how much of this potential is fulfilled.

The largest challenge is likely to be educational. Educating clinicians to be able to integrate POCUS into practice is a complex, multistep process requiring not only an adequate core of didactic training and access to machines, but also the structured opportunity to develop rudimentary hands-on skills. Such initial training should be followed by continued practice and feedback as developing POCUS users progress toward independent practice. The study by Kumar et al.⁶ reaffirms that brief didactic lectures and access to machines are necessary, but they are clearly insufficient for learners to be able to use POCUS independently for a wide variety of applications. Their intervention also contrasts markedly with the 20 hours of didactics and 150 supervised scans recommended by the American College of Emergency Physicians prior to independent use for a core of six applications.⁷

Shared standards for education, use, and oversight will be crucial to fulfilling the potential of POCUS within hospital medicine. Our belief is that much can be learned from the thoughtful approach taken during the development of POCUS as a mainstream tool in emergency medicine in the early 2000s. In this approach, emergency physicians determined a sufficient and achievable standard of training for core POCUS applications, which was widely adopted. Based on completion of this training, physicians who were required to complete credentialing from their hospitals were widely able to achieve it, without any need for external certification. Emergency medicine guidelines further mandated the documentation of examinations and the creation of an exam report, features that improve clinical communication and facilitate quality improvement. Quality assurance processes that reviewed images and clinician interpretations were established as mandatory, which they should be in hospital medicine. Evidence was produced as to which exams physicians could do reliably with this focused training and which they could not. In the context of these thoughtful constructs, lawsuits have been noted to be exceedingly rare; and when they do occur, they have typically been for the failure to use POCUS rather than the converse.⁸

While many of these precepts deserve replication, others should also be modified to reflect changes in technology, medical education, and medical practice over the last 20 years and to improve upon this base of success. For example, with POCUS training now appearing in many medical school and residency curricula, training paradigms for both residents and attendings will need to accommodate a wider range of incoming skills. Emphasis should continue to be shifted toward competency-based assessments and entrustment and away from a fixed training time or exam number threshold. Important financial aspects have also changed. The cost of practical machines has dropped considerably, and medicine is shifting away from a fee-for-service model. While it remains appropriate that physicians may bill for POCUS examinations, it is likely that improved diagnosis, improved throughput, and a reduction in complications will yield greater value and should be the emphasis of cost/value discussions.⁹ Finally, while hospitals may impose credentialing, this process can also create a burden not present for most other noninvasive skills and may deter appropriate use. If this approach is chosen by a hospital, requirements should ideally remain modest, and as these skills become more widespread, POCUS should ultimately be built into board examinations and core credentialing.⁹

Thoughtful and concerted effort will be required by hospitalist leaders, educational innovators, and professional societies in developing POCUS to best serve hospitalists and their patients. This work has already begun. For example, in 2019 SHM offered a position statement outlining important aspects such as current evidence-based applications, training pathways, quality assurance, and program management.¹⁰ These recommendations should guide both adult and pediatric hospitalists. The Alliance for Academic Internal Medicine offered a similar position statement for resident training.¹¹ Interest groups are growing in numerous professional societies, which will facilitate collaboration and promote propagation of best practices. High-quality educational tools are continuing to be developed by numerous organizations.

While further development is needed to add the detail, granularity, and practical tools that educational and practice leaders need to assure that POCUS achieves its potential in hospital medicine, the foundation for POCUS use within the specialty is being thoughtfully constructed. As this process proceeds, it will be vital to continue to learn from our emergency medicine colleagues, who have already met similar challenges, while at the same time be able to develop a modern POCUS model optimized for hospital medicine workflow, training, and patient care.

What childhood game better captures communication exchange than “telephone”: as whispers pass from ear to ear, the original message degrades or transforms entirely. In complex healthcare systems, a more perilous version of “telephone” emerges, distinct from the well-worn metaphor: the signal never arrives at all. The primary care provider never even knew the patient was in the hospital; the discharge summary was never received; the patient cannot remember important details; and key medications are missing. In this edition of the Journal, Roman Ayele et al.¹ used qualitative methods to explore this transitional black box between community hospitals and Veterans’ Affairs (VA) primary care clinics, illuminating how signal fragmentation may render the increasing use of care services outside the VA system as inversely proportionate to quality.

To understand why, a small amount of historical context is necessary. The VA has increasingly focused on expanding healthcare options to its nine million veterans. On June 6, 2019, the VA Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act was passed to consolidate existing programs and lower barriers for Veterans to seek care in non-VA urgent care and subspecialty settings.² Though this act is not specifically focused on access to community hospitals, patients seeking urgent and subspecialty care are likely to be increasingly hospitalized outside of the VA due to geographic factors affecting point-of-care decisions. Concurrent with this expansion of options is the planned replacement of the VA’s legacy electronic health record, VistA.³ Both transformations indicate the need for the VA to be watchful and to intensify its focus on safe, effective exchanges of information.

Against this backdrop, Ayele et al.³ use stakeholder interviews with veterans and both non-VA and VA clinicians to identify the current lack of standardized practices for transitions of veteran care from community hospitals to VA primary care in Eastern Colorado. The themes most linked to care fragmentation included difficulty in identifying veterans and notifying VA primary care of hospital discharges, transferring medical records, making follow-up appointments, and coordinating prescribing with VA pharmacies. Participants identified incomplete or delayed information exchanges that were further complicated by the inability to confirm transmission across systems. A patchwork of postacute care solutions failed to prevent wasteful, low-value transitional care, including unscheduled primary care walk-ins and ED visits for medication refills. Participants arrived at a simple common solution: develop a clinically trained “VA liaison” to work at the interface between VA primary care and non-VA community hospitals so as to provide a single point of contact to coordinate these transitions. In short, to have someone to pick up the phone.

The strengths of this qualitative study lie in its insights into the current gaps in care transitions through the eyes of key stakeholders. By engaging patients and providers in imagining system changes that are actionable in the near- (clinical VA liaisons) and longer-term (pharmacy and EHR integration), Ayele et al. have provided a helpful starting place in studying and improving the interface between VA and non-VA care. Stakeholders emphasized the importance of a clear access point so that outside providers can easily notify VA clinics, arrange follow-ups, and streamline physician prescribing to avoid dangerous and costly delays in care.⁴ Though similar issues have been illuminated in prior work on care fragmentation,⁴ perspective in context is a fundamental strength of qualitative research, and further highlights the urgency of this period in veteran care.

There is the old adage: “if you have seen one VA, you have seen one VA”. This is arguably reflected in how each VA medical center is situated in a different regional and local healthcare delivery context, despite a common national infrastructure. The authors acknowledge limited generalizability but provide a framework for reproducing such work in regional VA systems. A national model for transitioning patients from regional community partners to VA primary care would require further testing, and to be a credible system-wide investment, would necessitate meaningful measurement across multiple sites. Given recent evidence of strong internal VA performance compared to the private sector,⁵ it is time for the VA to intensify focus on external care transitions. Given its history and continued commitment to funding innovation,⁶ the VA ought to be up to the task. Yet, as VA hospitalists, we know only too well that the system is increasingly under pressure to apply constrained resources inside and outside its own walls. Sending business elsewhere might not only fail at improving care but also weaken the fragile care delivery infrastructure.⁷

The idea that access and continuity may be in conflict raises an ethical question in modern practice and shared decision-making: how do we advise patients navigating complicated and imperfect health systems to understand the choices they are making and the risks they are taking when they spread care across systems? How are access and convenience weighed against the troubled movement of information across systems? How great is the risk if their care teams do not hear the same message? Knowing that increased fragmentation disproportionately affects the marginalized and vulnerable, especially those with complex chronic care needs,⁸ should we advise certain patients to stay in place within a single system?

As hospitalists, we are implied players in this dangerous version of the telephone game at a fascinating time in healthcare. Unlike when we advise patients on the risks and benefits of treatment, we have little evidence to guide our patients on when to stay put and when to leave to get care outside the system, inviting the risk of lost signals, garbled messages, and worst of all, frustrating, duplicative, unsafe care. As we strive for incremental improvements toward sweeping transformations in healthcare, we may for a few more years have to remind each other—and our students—of the incredible value of one more phone call: to make sure the intended message was received.

Disclaimer

The contents of this publication do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.

What childhood game better captures communication exchange than “telephone”: as whispers pass from ear to ear, the original message degrades or transforms entirely. In complex healthcare systems, a more perilous version of “telephone” emerges, distinct from the well-worn metaphor: the signal never arrives at all. The primary care provider never even knew the patient was in the hospital; the discharge summary was never received; the patient cannot remember important details; and key medications are missing. In this edition of the Journal, Roman Ayele et al.¹ used qualitative methods to explore this transitional black box between community hospitals and Veterans’ Affairs (VA) primary care clinics, illuminating how signal fragmentation may render the increasing use of care services outside the VA system as inversely proportionate to quality.

To understand why, a small amount of historical context is necessary. The VA has increasingly focused on expanding healthcare options to its nine million veterans. On June 6, 2019, the VA Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act was passed to consolidate existing programs and lower barriers for Veterans to seek care in non-VA urgent care and subspecialty settings.² Though this act is not specifically focused on access to community hospitals, patients seeking urgent and subspecialty care are likely to be increasingly hospitalized outside of the VA due to geographic factors affecting point-of-care decisions. Concurrent with this expansion of options is the planned replacement of the VA’s legacy electronic health record, VistA.³ Both transformations indicate the need for the VA to be watchful and to intensify its focus on safe, effective exchanges of information.

Against this backdrop, Ayele et al.³ use stakeholder interviews with veterans and both non-VA and VA clinicians to identify the current lack of standardized practices for transitions of veteran care from community hospitals to VA primary care in Eastern Colorado. The themes most linked to care fragmentation included difficulty in identifying veterans and notifying VA primary care of hospital discharges, transferring medical records, making follow-up appointments, and coordinating prescribing with VA pharmacies. Participants identified incomplete or delayed information exchanges that were further complicated by the inability to confirm transmission across systems. A patchwork of postacute care solutions failed to prevent wasteful, low-value transitional care, including unscheduled primary care walk-ins and ED visits for medication refills. Participants arrived at a simple common solution: develop a clinically trained “VA liaison” to work at the interface between VA primary care and non-VA community hospitals so as to provide a single point of contact to coordinate these transitions. In short, to have someone to pick up the phone.

The strengths of this qualitative study lie in its insights into the current gaps in care transitions through the eyes of key stakeholders. By engaging patients and providers in imagining system changes that are actionable in the near- (clinical VA liaisons) and longer-term (pharmacy and EHR integration), Ayele et al. have provided a helpful starting place in studying and improving the interface between VA and non-VA care. Stakeholders emphasized the importance of a clear access point so that outside providers can easily notify VA clinics, arrange follow-ups, and streamline physician prescribing to avoid dangerous and costly delays in care.⁴ Though similar issues have been illuminated in prior work on care fragmentation,⁴ perspective in context is a fundamental strength of qualitative research, and further highlights the urgency of this period in veteran care.

There is the old adage: “if you have seen one VA, you have seen one VA”. This is arguably reflected in how each VA medical center is situated in a different regional and local healthcare delivery context, despite a common national infrastructure. The authors acknowledge limited generalizability but provide a framework for reproducing such work in regional VA systems. A national model for transitioning patients from regional community partners to VA primary care would require further testing, and to be a credible system-wide investment, would necessitate meaningful measurement across multiple sites. Given recent evidence of strong internal VA performance compared to the private sector,⁵ it is time for the VA to intensify focus on external care transitions. Given its history and continued commitment to funding innovation,⁶ the VA ought to be up to the task. Yet, as VA hospitalists, we know only too well that the system is increasingly under pressure to apply constrained resources inside and outside its own walls. Sending business elsewhere might not only fail at improving care but also weaken the fragile care delivery infrastructure.⁷

The idea that access and continuity may be in conflict raises an ethical question in modern practice and shared decision-making: how do we advise patients navigating complicated and imperfect health systems to understand the choices they are making and the risks they are taking when they spread care across systems? How are access and convenience weighed against the troubled movement of information across systems? How great is the risk if their care teams do not hear the same message? Knowing that increased fragmentation disproportionately affects the marginalized and vulnerable, especially those with complex chronic care needs,⁸ should we advise certain patients to stay in place within a single system?

As hospitalists, we are implied players in this dangerous version of the telephone game at a fascinating time in healthcare. Unlike when we advise patients on the risks and benefits of treatment, we have little evidence to guide our patients on when to stay put and when to leave to get care outside the system, inviting the risk of lost signals, garbled messages, and worst of all, frustrating, duplicative, unsafe care. As we strive for incremental improvements toward sweeping transformations in healthcare, we may for a few more years have to remind each other—and our students—of the incredible value of one more phone call: to make sure the intended message was received.

Disclaimer

The contents of this publication do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.

What childhood game better captures communication exchange than “telephone”: as whispers pass from ear to ear, the original message degrades or transforms entirely. In complex healthcare systems, a more perilous version of “telephone” emerges, distinct from the well-worn metaphor: the signal never arrives at all. The primary care provider never even knew the patient was in the hospital; the discharge summary was never received; the patient cannot remember important details; and key medications are missing. In this edition of the Journal, Roman Ayele et al.¹ used qualitative methods to explore this transitional black box between community hospitals and Veterans’ Affairs (VA) primary care clinics, illuminating how signal fragmentation may render the increasing use of care services outside the VA system as inversely proportionate to quality.

To understand why, a small amount of historical context is necessary. The VA has increasingly focused on expanding healthcare options to its nine million veterans. On June 6, 2019, the VA Maintaining Internal Systems and Strengthening Integrated Outside Networks (MISSION) Act was passed to consolidate existing programs and lower barriers for Veterans to seek care in non-VA urgent care and subspecialty settings.² Though this act is not specifically focused on access to community hospitals, patients seeking urgent and subspecialty care are likely to be increasingly hospitalized outside of the VA due to geographic factors affecting point-of-care decisions. Concurrent with this expansion of options is the planned replacement of the VA’s legacy electronic health record, VistA.³ Both transformations indicate the need for the VA to be watchful and to intensify its focus on safe, effective exchanges of information.

Against this backdrop, Ayele et al.³ use stakeholder interviews with veterans and both non-VA and VA clinicians to identify the current lack of standardized practices for transitions of veteran care from community hospitals to VA primary care in Eastern Colorado. The themes most linked to care fragmentation included difficulty in identifying veterans and notifying VA primary care of hospital discharges, transferring medical records, making follow-up appointments, and coordinating prescribing with VA pharmacies. Participants identified incomplete or delayed information exchanges that were further complicated by the inability to confirm transmission across systems. A patchwork of postacute care solutions failed to prevent wasteful, low-value transitional care, including unscheduled primary care walk-ins and ED visits for medication refills. Participants arrived at a simple common solution: develop a clinically trained “VA liaison” to work at the interface between VA primary care and non-VA community hospitals so as to provide a single point of contact to coordinate these transitions. In short, to have someone to pick up the phone.

The strengths of this qualitative study lie in its insights into the current gaps in care transitions through the eyes of key stakeholders. By engaging patients and providers in imagining system changes that are actionable in the near- (clinical VA liaisons) and longer-term (pharmacy and EHR integration), Ayele et al. have provided a helpful starting place in studying and improving the interface between VA and non-VA care. Stakeholders emphasized the importance of a clear access point so that outside providers can easily notify VA clinics, arrange follow-ups, and streamline physician prescribing to avoid dangerous and costly delays in care.⁴ Though similar issues have been illuminated in prior work on care fragmentation,⁴ perspective in context is a fundamental strength of qualitative research, and further highlights the urgency of this period in veteran care.

There is the old adage: “if you have seen one VA, you have seen one VA”. This is arguably reflected in how each VA medical center is situated in a different regional and local healthcare delivery context, despite a common national infrastructure. The authors acknowledge limited generalizability but provide a framework for reproducing such work in regional VA systems. A national model for transitioning patients from regional community partners to VA primary care would require further testing, and to be a credible system-wide investment, would necessitate meaningful measurement across multiple sites. Given recent evidence of strong internal VA performance compared to the private sector,⁵ it is time for the VA to intensify focus on external care transitions. Given its history and continued commitment to funding innovation,⁶ the VA ought to be up to the task. Yet, as VA hospitalists, we know only too well that the system is increasingly under pressure to apply constrained resources inside and outside its own walls. Sending business elsewhere might not only fail at improving care but also weaken the fragile care delivery infrastructure.⁷

The idea that access and continuity may be in conflict raises an ethical question in modern practice and shared decision-making: how do we advise patients navigating complicated and imperfect health systems to understand the choices they are making and the risks they are taking when they spread care across systems? How are access and convenience weighed against the troubled movement of information across systems? How great is the risk if their care teams do not hear the same message? Knowing that increased fragmentation disproportionately affects the marginalized and vulnerable, especially those with complex chronic care needs,⁸ should we advise certain patients to stay in place within a single system?

As hospitalists, we are implied players in this dangerous version of the telephone game at a fascinating time in healthcare. Unlike when we advise patients on the risks and benefits of treatment, we have little evidence to guide our patients on when to stay put and when to leave to get care outside the system, inviting the risk of lost signals, garbled messages, and worst of all, frustrating, duplicative, unsafe care. As we strive for incremental improvements toward sweeping transformations in healthcare, we may for a few more years have to remind each other—and our students—of the incredible value of one more phone call: to make sure the intended message was received.

Disclaimer

The contents of this publication do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.

Porphyria cutanea tarda (PCT) is the most common type of porphyria. The accumulation of porphyrin in various organ systems results from a deficiency of uroporphyrinogen decarboxylase (UROD).^1-3 Chronic hepatitis C virus (HCV) causes a hepatic decrease in hepcidin production, resulting in increased iron absorption. Iron loading and increased oxidative stress in the liver leads to nonporphyrin inhibition of UROD production and to oxidation of porphyrinogens to porphyrins.⁴ This in turn leads to accumulation of uroporphyrins and carboxylated metabolites that can be detected in urine.⁴

Signs of PCT include blisters, vesicles, and possibly milia developing on sun-exposed areas of the skin, such as the face, forearms, and dorsal hands.⁴ Case reports have demonstrated a resolution of PCT in patients with chronic HCV with treatment with direct-acting antivirals (DAAs), such as ledipasvir/sofosbuvir.^1,3 However, here we present 2 cases of patients who developed blistering diseases during treatment of chronic HCV with ledipasvir/sofosbuvir. Neither demonstrated complete resolution of symptoms during the treatment regimen.

Cases

Patient 1

A 63-year-old white male with a history of chronic HCV (genotype 1a), bipolar disorder, hyperlipidemia, tobacco dependence, and cirrhosis (F4 by elastography) presented with minimally to moderately painful blisters on his bilateral dorsal hands that had developed around weeks 8 to 9 of treatment with ledipasvir/sofosbuvir. The patient reported that no new blisters had appeared following completion of 12 weeks of treatment and that his current blisters were in various stages of healing. He reported alcohol use of 1 to 2 twelve-ounce beers daily and no history of dioxin exposure. His medications included doxepin, hydralazine, hydrochlorothiazide, quetiapine, folic acid, and thiamine. His hepatitis C viral load was 440,000 IU/mL prior to treatment. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron level was 135 µg/dL, total iron-binding capacity (TIBC) was 323 µg/dL, and ferritin was 299.0 ng/mL. His HFEgene was negative for mutations. Following 4 weeks of treatment with ledipasvir/sofosbuvir, a hepatitis C viral load was not detected.

A physical examination on presentation revealed erosions with overlying hemorrhagic crusts on the bilateral dorsal hands (Figure). 

At the 4-month follow-up, the patient reported no new blister formations. A physical examination revealed well-healed scars and several clustered milia on bilateral dorsal hands with no active vesicles or bullae noted.

Patient 2

An African American male aged 63 years presented with a 1-month history of moderately painful blisters on his bilateral dorsal hands during treatment of chronic HCV (genotype 1a) with ledipasvir/sofosbuvir. His medical history included gout, tobacco and alcohol addiction, osteoarthritis, and hepatic fibrosis (F3 by elastography). The patient’s medications included allopurinol, lisinopril, and hydrochlorothiazide. He reported no history of dioxin exposure. On the day of presentation, he was on week 9 of the 12-week treatment ledipasvir/sofosbuvir regimen. Laboratory results included an initial HCV viral load of 1,618,605 IU/mL. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron was 191 µg/dL, TIBC 388 µg/dL, and ferritin 459.0 ng/mL. After 4 weeks of treatment, the patient’s hepatitis C viral load was undetectable.

A physical examination revealed several resolving erosions to his bilateral dorsal hands, some of which had overlying crusting along with one small hemorrhagic vesicle on the right dorsal hand. A punch biopsy of the hemorrhagic vesicle was performed and demonstrated a cell-poor subepidermal blister with festooning of the dermal papilla. A direct immunofluorescence study showed immunoglobulin (Ig) G fluorescence along the dermal-epidermal junction and within vessel walls in the superficial dermis. Weak IgM and C3 fluorescence also was noted within vessel walls in the superficial dermis. All of the patient findings and history were consistent with PCT, although pseudo-PCT also was a consideration. A 24-hour urine sample yielded negative results for porphobilinogen. Urine porphyrin test results were not available, leading to a presumptive histological diagnosis of PCT.

The patient completed 11 of the prescribed 12 weeks of ledipasvir/sofosbuvir. The blisters resolved shortly thereafter.

Discussion

PCT has a well-established association with chronic HCV infection.⁴ We present 2 cases of a blistering disease clinically and histologically compatible with PCT that developed in patients only after initiation of treatment for chronic HCV with ledipasvir/sofosbuvir. One case was confirmed as PCT on the basis of compatible histopathologic findings and a urine porphyrin assay that showed elevated levels of uroporphyrins and carboxylated metabolites. The second case was clinically and histologically suggestive of PCT but not confirmed by urine porphyrin testing. In both patients, after 8 to 9 weeks of a 12-week course of antiviral therapy, the blistering lesions were noted but appeared to be resolving, and no new lesions were noted after discontinuation of therapy. It appeared that the antiviral treatment temporally triggered the initiation of the blistering skin disease, and as the chronic HCV infection cleared after treatment, the blistering lesions also began to resolve.

Mechanistically, it is known that the virally-induced hepatic damage leads to inhibition of uroporphyrinogen decarboxylase, and the subsequent oxidation of porphyrinogens to porphyrins. Cofactors such as HIV infection also may contribute to development of PCT.⁵

De novo PCT has been documented during therapy using interferon and ribavirin.⁶ The hemolytic anemia and increased hepatic iron were implicated as potential etiologies.⁶ Patients with HCV and PCT treated with the newer direct-acting antiviral therapies have been described to have experienced improvement in PCT symptoms.³

Although there were rare reports of deterioration in renal and liver function,⁷ reactivation of HBV infection,⁸ and Stevens-Johnson syndrome⁹ with antiviral therapy, these complications were not observed in these patients. Both patients also had successful resolution of HCV infection, and by completion of the antiviral therapy, the blistering also resolved.

Conclusion

PCT is an extrahepatic manifestation of HCV infection. Health care providers should be aware of the association of chronic HCV infection with PCT. The findings of PCT should not result in the delay or discontinuation of antiviral therapy.

Porphyria cutanea tarda (PCT) is the most common type of porphyria. The accumulation of porphyrin in various organ systems results from a deficiency of uroporphyrinogen decarboxylase (UROD).^1-3 Chronic hepatitis C virus (HCV) causes a hepatic decrease in hepcidin production, resulting in increased iron absorption. Iron loading and increased oxidative stress in the liver leads to nonporphyrin inhibition of UROD production and to oxidation of porphyrinogens to porphyrins.⁴ This in turn leads to accumulation of uroporphyrins and carboxylated metabolites that can be detected in urine.⁴

Signs of PCT include blisters, vesicles, and possibly milia developing on sun-exposed areas of the skin, such as the face, forearms, and dorsal hands.⁴ Case reports have demonstrated a resolution of PCT in patients with chronic HCV with treatment with direct-acting antivirals (DAAs), such as ledipasvir/sofosbuvir.^1,3 However, here we present 2 cases of patients who developed blistering diseases during treatment of chronic HCV with ledipasvir/sofosbuvir. Neither demonstrated complete resolution of symptoms during the treatment regimen.

Cases

Patient 1

A 63-year-old white male with a history of chronic HCV (genotype 1a), bipolar disorder, hyperlipidemia, tobacco dependence, and cirrhosis (F4 by elastography) presented with minimally to moderately painful blisters on his bilateral dorsal hands that had developed around weeks 8 to 9 of treatment with ledipasvir/sofosbuvir. The patient reported that no new blisters had appeared following completion of 12 weeks of treatment and that his current blisters were in various stages of healing. He reported alcohol use of 1 to 2 twelve-ounce beers daily and no history of dioxin exposure. His medications included doxepin, hydralazine, hydrochlorothiazide, quetiapine, folic acid, and thiamine. His hepatitis C viral load was 440,000 IU/mL prior to treatment. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron level was 135 µg/dL, total iron-binding capacity (TIBC) was 323 µg/dL, and ferritin was 299.0 ng/mL. His HFEgene was negative for mutations. Following 4 weeks of treatment with ledipasvir/sofosbuvir, a hepatitis C viral load was not detected.

A physical examination on presentation revealed erosions with overlying hemorrhagic crusts on the bilateral dorsal hands (Figure). 

At the 4-month follow-up, the patient reported no new blister formations. A physical examination revealed well-healed scars and several clustered milia on bilateral dorsal hands with no active vesicles or bullae noted.

Patient 2

An African American male aged 63 years presented with a 1-month history of moderately painful blisters on his bilateral dorsal hands during treatment of chronic HCV (genotype 1a) with ledipasvir/sofosbuvir. His medical history included gout, tobacco and alcohol addiction, osteoarthritis, and hepatic fibrosis (F3 by elastography). The patient’s medications included allopurinol, lisinopril, and hydrochlorothiazide. He reported no history of dioxin exposure. On the day of presentation, he was on week 9 of the 12-week treatment ledipasvir/sofosbuvir regimen. Laboratory results included an initial HCV viral load of 1,618,605 IU/mL. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron was 191 µg/dL, TIBC 388 µg/dL, and ferritin 459.0 ng/mL. After 4 weeks of treatment, the patient’s hepatitis C viral load was undetectable.

A physical examination revealed several resolving erosions to his bilateral dorsal hands, some of which had overlying crusting along with one small hemorrhagic vesicle on the right dorsal hand. A punch biopsy of the hemorrhagic vesicle was performed and demonstrated a cell-poor subepidermal blister with festooning of the dermal papilla. A direct immunofluorescence study showed immunoglobulin (Ig) G fluorescence along the dermal-epidermal junction and within vessel walls in the superficial dermis. Weak IgM and C3 fluorescence also was noted within vessel walls in the superficial dermis. All of the patient findings and history were consistent with PCT, although pseudo-PCT also was a consideration. A 24-hour urine sample yielded negative results for porphobilinogen. Urine porphyrin test results were not available, leading to a presumptive histological diagnosis of PCT.

The patient completed 11 of the prescribed 12 weeks of ledipasvir/sofosbuvir. The blisters resolved shortly thereafter.

Discussion

PCT has a well-established association with chronic HCV infection.⁴ We present 2 cases of a blistering disease clinically and histologically compatible with PCT that developed in patients only after initiation of treatment for chronic HCV with ledipasvir/sofosbuvir. One case was confirmed as PCT on the basis of compatible histopathologic findings and a urine porphyrin assay that showed elevated levels of uroporphyrins and carboxylated metabolites. The second case was clinically and histologically suggestive of PCT but not confirmed by urine porphyrin testing. In both patients, after 8 to 9 weeks of a 12-week course of antiviral therapy, the blistering lesions were noted but appeared to be resolving, and no new lesions were noted after discontinuation of therapy. It appeared that the antiviral treatment temporally triggered the initiation of the blistering skin disease, and as the chronic HCV infection cleared after treatment, the blistering lesions also began to resolve.

Mechanistically, it is known that the virally-induced hepatic damage leads to inhibition of uroporphyrinogen decarboxylase, and the subsequent oxidation of porphyrinogens to porphyrins. Cofactors such as HIV infection also may contribute to development of PCT.⁵

De novo PCT has been documented during therapy using interferon and ribavirin.⁶ The hemolytic anemia and increased hepatic iron were implicated as potential etiologies.⁶ Patients with HCV and PCT treated with the newer direct-acting antiviral therapies have been described to have experienced improvement in PCT symptoms.³

Although there were rare reports of deterioration in renal and liver function,⁷ reactivation of HBV infection,⁸ and Stevens-Johnson syndrome⁹ with antiviral therapy, these complications were not observed in these patients. Both patients also had successful resolution of HCV infection, and by completion of the antiviral therapy, the blistering also resolved.

Conclusion

PCT is an extrahepatic manifestation of HCV infection. Health care providers should be aware of the association of chronic HCV infection with PCT. The findings of PCT should not result in the delay or discontinuation of antiviral therapy.

Porphyria cutanea tarda (PCT) is the most common type of porphyria. The accumulation of porphyrin in various organ systems results from a deficiency of uroporphyrinogen decarboxylase (UROD).^1-3 Chronic hepatitis C virus (HCV) causes a hepatic decrease in hepcidin production, resulting in increased iron absorption. Iron loading and increased oxidative stress in the liver leads to nonporphyrin inhibition of UROD production and to oxidation of porphyrinogens to porphyrins.⁴ This in turn leads to accumulation of uroporphyrins and carboxylated metabolites that can be detected in urine.⁴

Signs of PCT include blisters, vesicles, and possibly milia developing on sun-exposed areas of the skin, such as the face, forearms, and dorsal hands.⁴ Case reports have demonstrated a resolution of PCT in patients with chronic HCV with treatment with direct-acting antivirals (DAAs), such as ledipasvir/sofosbuvir.^1,3 However, here we present 2 cases of patients who developed blistering diseases during treatment of chronic HCV with ledipasvir/sofosbuvir. Neither demonstrated complete resolution of symptoms during the treatment regimen.

Cases

Patient 1

A 63-year-old white male with a history of chronic HCV (genotype 1a), bipolar disorder, hyperlipidemia, tobacco dependence, and cirrhosis (F4 by elastography) presented with minimally to moderately painful blisters on his bilateral dorsal hands that had developed around weeks 8 to 9 of treatment with ledipasvir/sofosbuvir. The patient reported that no new blisters had appeared following completion of 12 weeks of treatment and that his current blisters were in various stages of healing. He reported alcohol use of 1 to 2 twelve-ounce beers daily and no history of dioxin exposure. His medications included doxepin, hydralazine, hydrochlorothiazide, quetiapine, folic acid, and thiamine. His hepatitis C viral load was 440,000 IU/mL prior to treatment. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron level was 135 µg/dL, total iron-binding capacity (TIBC) was 323 µg/dL, and ferritin was 299.0 ng/mL. His HFEgene was negative for mutations. Following 4 weeks of treatment with ledipasvir/sofosbuvir, a hepatitis C viral load was not detected.

A physical examination on presentation revealed erosions with overlying hemorrhagic crusts on the bilateral dorsal hands (Figure). 

At the 4-month follow-up, the patient reported no new blister formations. A physical examination revealed well-healed scars and several clustered milia on bilateral dorsal hands with no active vesicles or bullae noted.

Patient 2

An African American male aged 63 years presented with a 1-month history of moderately painful blisters on his bilateral dorsal hands during treatment of chronic HCV (genotype 1a) with ledipasvir/sofosbuvir. His medical history included gout, tobacco and alcohol addiction, osteoarthritis, and hepatic fibrosis (F3 by elastography). The patient’s medications included allopurinol, lisinopril, and hydrochlorothiazide. He reported no history of dioxin exposure. On the day of presentation, he was on week 9 of the 12-week treatment ledipasvir/sofosbuvir regimen. Laboratory results included an initial HCV viral load of 1,618,605 IU/mL. Tests for hepatitis B surface antigen and HIV antibodies were negative. His iron was 191 µg/dL, TIBC 388 µg/dL, and ferritin 459.0 ng/mL. After 4 weeks of treatment, the patient’s hepatitis C viral load was undetectable.

A physical examination revealed several resolving erosions to his bilateral dorsal hands, some of which had overlying crusting along with one small hemorrhagic vesicle on the right dorsal hand. A punch biopsy of the hemorrhagic vesicle was performed and demonstrated a cell-poor subepidermal blister with festooning of the dermal papilla. A direct immunofluorescence study showed immunoglobulin (Ig) G fluorescence along the dermal-epidermal junction and within vessel walls in the superficial dermis. Weak IgM and C3 fluorescence also was noted within vessel walls in the superficial dermis. All of the patient findings and history were consistent with PCT, although pseudo-PCT also was a consideration. A 24-hour urine sample yielded negative results for porphobilinogen. Urine porphyrin test results were not available, leading to a presumptive histological diagnosis of PCT.

The patient completed 11 of the prescribed 12 weeks of ledipasvir/sofosbuvir. The blisters resolved shortly thereafter.

Discussion

PCT has a well-established association with chronic HCV infection.⁴ We present 2 cases of a blistering disease clinically and histologically compatible with PCT that developed in patients only after initiation of treatment for chronic HCV with ledipasvir/sofosbuvir. One case was confirmed as PCT on the basis of compatible histopathologic findings and a urine porphyrin assay that showed elevated levels of uroporphyrins and carboxylated metabolites. The second case was clinically and histologically suggestive of PCT but not confirmed by urine porphyrin testing. In both patients, after 8 to 9 weeks of a 12-week course of antiviral therapy, the blistering lesions were noted but appeared to be resolving, and no new lesions were noted after discontinuation of therapy. It appeared that the antiviral treatment temporally triggered the initiation of the blistering skin disease, and as the chronic HCV infection cleared after treatment, the blistering lesions also began to resolve.

Mechanistically, it is known that the virally-induced hepatic damage leads to inhibition of uroporphyrinogen decarboxylase, and the subsequent oxidation of porphyrinogens to porphyrins. Cofactors such as HIV infection also may contribute to development of PCT.⁵

De novo PCT has been documented during therapy using interferon and ribavirin.⁶ The hemolytic anemia and increased hepatic iron were implicated as potential etiologies.⁶ Patients with HCV and PCT treated with the newer direct-acting antiviral therapies have been described to have experienced improvement in PCT symptoms.³

Although there were rare reports of deterioration in renal and liver function,⁷ reactivation of HBV infection,⁸ and Stevens-Johnson syndrome⁹ with antiviral therapy, these complications were not observed in these patients. Both patients also had successful resolution of HCV infection, and by completion of the antiviral therapy, the blistering also resolved.

Conclusion

PCT is an extrahepatic manifestation of HCV infection. Health care providers should be aware of the association of chronic HCV infection with PCT. The findings of PCT should not result in the delay or discontinuation of antiviral therapy.

Sepsis is a major public health concern: 10% of patients with sepsis die, and mortality quadruples with progression to septic shock.¹ Systemic inflammatory response syndrome (SIRS) criteria, originally published in 1992, are commonly used to detect sepsis, but as early as 2001, these criteria were recognized as lacking specificity.² Nonetheless, the use of SIRS criteria has persisted in practice. Sepsis was redefined in Sepsis-3 (2016) to guide earlier and more appropriate identification and treatment, which has been shown to greatly improve patient outcomes.^1,3 Key recommendations in Sepsis 3 included eliminating SIRS criteria, defining organ dysfunction by the Sequential Organ Failure Assessment (SOFA) score, and introducing the quick SOFA (qSOFA) score.¹

The qSOFA combines 3 clinical variables to provide a rapid, simple bedside score that measures the likelihood of poor outcomes, such as admission to an intensive care unit (ICU) or mortality in adults with suspected infection.^1,3 The qSOFA score is intended to aid healthcare professionals in more timely stratification of those patients who need escalated care to prevent deterioration.¹ The assessment also has been explored as a screening tool for sepsis in clinical practice; however, limited data exists concerning the comparative utility of qSOFA and SIRS in this capacity, and study results are inconsistent.^4-6

The most important attribute of a screening tool is high sensitivity, but high specificity also is desired. The qSOFA could supplant SIRS as a screening tool for sepsis if it maintained similarly high sensitivity but achieved superior specificity. Therefore, our primary objective for this study was to determine the effectiveness of qSOFA as a screening assessment for sepsis in the setting of a general inpatient medicine service by contrasting the sensitivity and specificity of qSOFA with SIRS in predicting sepsis, using a retrospective chart review design.

Methods

Administrative data from the Department of Veterans Affairs (VA) Corporate Data Warehouse were accessed via the VA Informatics and Computing Infrastructure (VINCI) and used to identify VA inpatient admissions and obtain the laboratory and vital sign data necessary to calculate SIRS, qSOFA, and SOFA scores. The data were supplemented by manual review of VA health records to obtain information that was not readily available in administrative records, including septic shock outcomes and laboratory and vital sign data obtained in the ICU. This study was approved by the institutional review board at the University of Iowa and the research and development committee at the Iowa City VA Medical Center (ICVAMC).

Patients

The study population included veterans admitted to the nonsurgical medicine unit at ICVAMC between August 1, 2014 and August 1, 2016 who were transferred to an ICU after admission; direct ICU admissions were not included as the qSOFA has been shown in studies to be more beneficial and offer better predictive validity outside the ICU. Excluding these direct admissions prevented any potential skewing of the data. To control for possible selection bias, veterans also were excluded if they transferred from another facility, were admitted under observation status, or if they had been admitted within the prior 30 days. These patients may have been more critically ill than those who presented directly to our facility and any prior treatment could affect the clinical status of the patient and assessment for sepsis at the time of presentation to the VA. Veterans were further required to have evidence of suspected infection based on manual review of the health record, which was determined by receipt of an antibiotic relevant to the empiric treatment of sepsis within 48 hours of admission.

Sepsis and Septic Shock Assessment Tools

As outlined in the Sepsis-3 guidelines, sepsis was defined as suspected or confirmed infection with an acute change in the SOFA score of ≥ 2 points, which is assumed to be 0 in those not known to have preexisting dysfunction.¹ The SOFA score includes variables from the respiratory, coagulation, hepatic, cardiovascular, renal, and central nervous systems.¹ Septic shock was defined as vasopressor administration and a serum lactic acid level > 2 mmol/L occurring up to 24 hours apart and within 3 days of the first antibiotic dose administered.

The SIRS assessment includes 4 clinical variables (temperature, heart rate, respiratory rate, and white blood cell count) while qSOFA is comprised of 3 variables (respiratory rate, systolic blood pressure, and altered mental status).¹ With both assessments, a score ≥ 2 is considered positive, which indicates increased risk for sepsis in patients with suspected infection.¹ In keeping with existing studies, qSOFA and SIRS assessments were scored using maximum values found within 48 hours before and 24 hours after the first administered antibiotic dose.³

Outcomes

The primary outcome variable was the presence of sepsis in adults with evidence of infection within 48 hours of admission. Secondary outcome measures included 30-day mortality and septic shock.

Performance between the SIRS and qSOFA assessments was contrasted using sensitivity, specificity, and positive and negative predictive value measurements. Associations of qSOFA and SIRS with septic shock and 30-day mortality were evaluated using a 2-tailed Fisher’s exact test with a threshold of α = 0.05 to determine statistical significance.

Results

The study sample of 481 veterans had a mean age of 67.4 years, 94% were male, and 91.1% were white (Table 1). 

Scores for qSOFA, but not SIRS, were significantly associated with septic shock (Fisher’s exact test; qSOFA: P = .009; SIRS: P = .58) (Table 3). 

Discussion

High sensitivity is critical for a sepsis screening tool. To be clinically useful, it has been suggested that biomarkers predicting poor outcomes for sepsis should have a sensitivity of > 80%.⁴ Although qSOFA demonstrated greater specificity than SIRS in our study (83.6% vs 25.7%), qSOFA showed lower sensitivity (44.7% vs 80.0%), which resulted in a greater potential for false negatives; 55.3% of those with sepsis would go undetected. Therefore, our study does not support qSOFA as a better screening assessment than SIRS for sepsis in the veteran population.

Most studies concur with our findings of low sensitivity and high specificity of qSOFA. In a systematic review and meta-analysis, Serafim and colleagues identified 10 studies published after Sepsis-3 that reported sensitivity or specificity of qSOFA and SIRS for sepsis diagnosis.⁵ Seven of the 10 studies reported sensitivities and favored SIRS in the diagnosis of sepsis (Relative risk: 1.32; 95% CI: 0.40-2.24; P < .0001; I² = 100%). The authors noted that substantial heterogeneity among studies, including differences in study design, sample size, and criteria for determination of infection, was an important limitation. In addition, most studies that contrast qSOFA and SIRS center on prognostic value in predicting mortality, rather than as a screening test for a diagnosis of sepsis.

We concluded SIRS was more sensitive and thus superior to qSOFA when used as a screening tool for sepsis but conceded that more prospective and homogenous investigations were necessary. To our knowledge, only 1 published study has deviated from this conclusion and reported comparable sensitivity between SIRS (92%) and qSOFA (90%).⁶ Our study adds to existing literature as it is the first conducted in a veteran population. Additionally, we performed our investigation in a general medicine population with methods similar to existing literature, including the key study validating clinical criteria for sepsis by Seymour and colleagues.³

Limitations

This study is not without limitations, including potential misclassification of cases if essential data points were not available during data collection via health record review or the data points were not representative of a true change from baseline (eg, the Glasgow Coma Scale score for altered mental status in the qSOFA or the SOFA score for organ dysfunction). Generalizability of the results also may be limited due to our retrospective, single-center design and characteristics typical of a veteran population (eg, older, white males). Additionally, many veterans were excluded from the study if they transferred from another facility. These veterans may have been more critically ill than those who presented directly to our facility, which possibly introduced selection bias.

Conclusion

Our findings do not support use of the qSOFA as a suitable replacement for SIRS as a sepsis screening tool among patients with suspected infection in the general medicine inpatient setting. The clinical concern with SIRS is that unfavorable specificity leads to unnecessary antibiotic exposure among patients who are falsely positive. While qSOFA has demonstrated higher specificity, its use would cause many sepsis cases to go undetected due to the technique’s low sensitivity. Frequent false negative qSOFA results could thus serve to impede, rather than enhance, early recognition and intervention for sepsis.

The ideal sepsis screening tool is rapid and possesses high sensitivity and specificity to promptly identify and manage sepsis and avert unfavorable outcomes such as septic shock and death. While the SIRS criteria do not satisfy these ideal features, its measurement characteristics are more suitable for the application of sepsis screening than the qSOFA and should thus remain the standard tool in this setting. Future prospectively designed studies with more uniform methodologies are necessary to ascertain the most effective approach to identify sepsis for which novel screening approaches with more clinically suitable measurement properties are greatly needed.

Acknowledgements
This research was supported by the Iowa City VA Health Care System, Department of Pharmacy Services. Additional support was provided by the Health Services Research and Development Service, Department of Veterans Affairs.

Sepsis is a major public health concern: 10% of patients with sepsis die, and mortality quadruples with progression to septic shock.¹ Systemic inflammatory response syndrome (SIRS) criteria, originally published in 1992, are commonly used to detect sepsis, but as early as 2001, these criteria were recognized as lacking specificity.² Nonetheless, the use of SIRS criteria has persisted in practice. Sepsis was redefined in Sepsis-3 (2016) to guide earlier and more appropriate identification and treatment, which has been shown to greatly improve patient outcomes.^1,3 Key recommendations in Sepsis 3 included eliminating SIRS criteria, defining organ dysfunction by the Sequential Organ Failure Assessment (SOFA) score, and introducing the quick SOFA (qSOFA) score.¹

The qSOFA combines 3 clinical variables to provide a rapid, simple bedside score that measures the likelihood of poor outcomes, such as admission to an intensive care unit (ICU) or mortality in adults with suspected infection.^1,3 The qSOFA score is intended to aid healthcare professionals in more timely stratification of those patients who need escalated care to prevent deterioration.¹ The assessment also has been explored as a screening tool for sepsis in clinical practice; however, limited data exists concerning the comparative utility of qSOFA and SIRS in this capacity, and study results are inconsistent.^4-6

The most important attribute of a screening tool is high sensitivity, but high specificity also is desired. The qSOFA could supplant SIRS as a screening tool for sepsis if it maintained similarly high sensitivity but achieved superior specificity. Therefore, our primary objective for this study was to determine the effectiveness of qSOFA as a screening assessment for sepsis in the setting of a general inpatient medicine service by contrasting the sensitivity and specificity of qSOFA with SIRS in predicting sepsis, using a retrospective chart review design.

Methods

Administrative data from the Department of Veterans Affairs (VA) Corporate Data Warehouse were accessed via the VA Informatics and Computing Infrastructure (VINCI) and used to identify VA inpatient admissions and obtain the laboratory and vital sign data necessary to calculate SIRS, qSOFA, and SOFA scores. The data were supplemented by manual review of VA health records to obtain information that was not readily available in administrative records, including septic shock outcomes and laboratory and vital sign data obtained in the ICU. This study was approved by the institutional review board at the University of Iowa and the research and development committee at the Iowa City VA Medical Center (ICVAMC).

Patients

The study population included veterans admitted to the nonsurgical medicine unit at ICVAMC between August 1, 2014 and August 1, 2016 who were transferred to an ICU after admission; direct ICU admissions were not included as the qSOFA has been shown in studies to be more beneficial and offer better predictive validity outside the ICU. Excluding these direct admissions prevented any potential skewing of the data. To control for possible selection bias, veterans also were excluded if they transferred from another facility, were admitted under observation status, or if they had been admitted within the prior 30 days. These patients may have been more critically ill than those who presented directly to our facility and any prior treatment could affect the clinical status of the patient and assessment for sepsis at the time of presentation to the VA. Veterans were further required to have evidence of suspected infection based on manual review of the health record, which was determined by receipt of an antibiotic relevant to the empiric treatment of sepsis within 48 hours of admission.

Sepsis and Septic Shock Assessment Tools

As outlined in the Sepsis-3 guidelines, sepsis was defined as suspected or confirmed infection with an acute change in the SOFA score of ≥ 2 points, which is assumed to be 0 in those not known to have preexisting dysfunction.¹ The SOFA score includes variables from the respiratory, coagulation, hepatic, cardiovascular, renal, and central nervous systems.¹ Septic shock was defined as vasopressor administration and a serum lactic acid level > 2 mmol/L occurring up to 24 hours apart and within 3 days of the first antibiotic dose administered.

The SIRS assessment includes 4 clinical variables (temperature, heart rate, respiratory rate, and white blood cell count) while qSOFA is comprised of 3 variables (respiratory rate, systolic blood pressure, and altered mental status).¹ With both assessments, a score ≥ 2 is considered positive, which indicates increased risk for sepsis in patients with suspected infection.¹ In keeping with existing studies, qSOFA and SIRS assessments were scored using maximum values found within 48 hours before and 24 hours after the first administered antibiotic dose.³

Outcomes

The primary outcome variable was the presence of sepsis in adults with evidence of infection within 48 hours of admission. Secondary outcome measures included 30-day mortality and septic shock.

Performance between the SIRS and qSOFA assessments was contrasted using sensitivity, specificity, and positive and negative predictive value measurements. Associations of qSOFA and SIRS with septic shock and 30-day mortality were evaluated using a 2-tailed Fisher’s exact test with a threshold of α = 0.05 to determine statistical significance.

Results

The study sample of 481 veterans had a mean age of 67.4 years, 94% were male, and 91.1% were white (Table 1). 

Scores for qSOFA, but not SIRS, were significantly associated with septic shock (Fisher’s exact test; qSOFA: P = .009; SIRS: P = .58) (Table 3). 

Discussion

High sensitivity is critical for a sepsis screening tool. To be clinically useful, it has been suggested that biomarkers predicting poor outcomes for sepsis should have a sensitivity of > 80%.⁴ Although qSOFA demonstrated greater specificity than SIRS in our study (83.6% vs 25.7%), qSOFA showed lower sensitivity (44.7% vs 80.0%), which resulted in a greater potential for false negatives; 55.3% of those with sepsis would go undetected. Therefore, our study does not support qSOFA as a better screening assessment than SIRS for sepsis in the veteran population.

Most studies concur with our findings of low sensitivity and high specificity of qSOFA. In a systematic review and meta-analysis, Serafim and colleagues identified 10 studies published after Sepsis-3 that reported sensitivity or specificity of qSOFA and SIRS for sepsis diagnosis.⁵ Seven of the 10 studies reported sensitivities and favored SIRS in the diagnosis of sepsis (Relative risk: 1.32; 95% CI: 0.40-2.24; P < .0001; I² = 100%). The authors noted that substantial heterogeneity among studies, including differences in study design, sample size, and criteria for determination of infection, was an important limitation. In addition, most studies that contrast qSOFA and SIRS center on prognostic value in predicting mortality, rather than as a screening test for a diagnosis of sepsis.

We concluded SIRS was more sensitive and thus superior to qSOFA when used as a screening tool for sepsis but conceded that more prospective and homogenous investigations were necessary. To our knowledge, only 1 published study has deviated from this conclusion and reported comparable sensitivity between SIRS (92%) and qSOFA (90%).⁶ Our study adds to existing literature as it is the first conducted in a veteran population. Additionally, we performed our investigation in a general medicine population with methods similar to existing literature, including the key study validating clinical criteria for sepsis by Seymour and colleagues.³

Limitations

This study is not without limitations, including potential misclassification of cases if essential data points were not available during data collection via health record review or the data points were not representative of a true change from baseline (eg, the Glasgow Coma Scale score for altered mental status in the qSOFA or the SOFA score for organ dysfunction). Generalizability of the results also may be limited due to our retrospective, single-center design and characteristics typical of a veteran population (eg, older, white males). Additionally, many veterans were excluded from the study if they transferred from another facility. These veterans may have been more critically ill than those who presented directly to our facility, which possibly introduced selection bias.

Conclusion

Our findings do not support use of the qSOFA as a suitable replacement for SIRS as a sepsis screening tool among patients with suspected infection in the general medicine inpatient setting. The clinical concern with SIRS is that unfavorable specificity leads to unnecessary antibiotic exposure among patients who are falsely positive. While qSOFA has demonstrated higher specificity, its use would cause many sepsis cases to go undetected due to the technique’s low sensitivity. Frequent false negative qSOFA results could thus serve to impede, rather than enhance, early recognition and intervention for sepsis.

The ideal sepsis screening tool is rapid and possesses high sensitivity and specificity to promptly identify and manage sepsis and avert unfavorable outcomes such as septic shock and death. While the SIRS criteria do not satisfy these ideal features, its measurement characteristics are more suitable for the application of sepsis screening than the qSOFA and should thus remain the standard tool in this setting. Future prospectively designed studies with more uniform methodologies are necessary to ascertain the most effective approach to identify sepsis for which novel screening approaches with more clinically suitable measurement properties are greatly needed.

Acknowledgements
This research was supported by the Iowa City VA Health Care System, Department of Pharmacy Services. Additional support was provided by the Health Services Research and Development Service, Department of Veterans Affairs.

Sepsis is a major public health concern: 10% of patients with sepsis die, and mortality quadruples with progression to septic shock.¹ Systemic inflammatory response syndrome (SIRS) criteria, originally published in 1992, are commonly used to detect sepsis, but as early as 2001, these criteria were recognized as lacking specificity.² Nonetheless, the use of SIRS criteria has persisted in practice. Sepsis was redefined in Sepsis-3 (2016) to guide earlier and more appropriate identification and treatment, which has been shown to greatly improve patient outcomes.^1,3 Key recommendations in Sepsis 3 included eliminating SIRS criteria, defining organ dysfunction by the Sequential Organ Failure Assessment (SOFA) score, and introducing the quick SOFA (qSOFA) score.¹

The qSOFA combines 3 clinical variables to provide a rapid, simple bedside score that measures the likelihood of poor outcomes, such as admission to an intensive care unit (ICU) or mortality in adults with suspected infection.^1,3 The qSOFA score is intended to aid healthcare professionals in more timely stratification of those patients who need escalated care to prevent deterioration.¹ The assessment also has been explored as a screening tool for sepsis in clinical practice; however, limited data exists concerning the comparative utility of qSOFA and SIRS in this capacity, and study results are inconsistent.^4-6

The most important attribute of a screening tool is high sensitivity, but high specificity also is desired. The qSOFA could supplant SIRS as a screening tool for sepsis if it maintained similarly high sensitivity but achieved superior specificity. Therefore, our primary objective for this study was to determine the effectiveness of qSOFA as a screening assessment for sepsis in the setting of a general inpatient medicine service by contrasting the sensitivity and specificity of qSOFA with SIRS in predicting sepsis, using a retrospective chart review design.

Methods

Administrative data from the Department of Veterans Affairs (VA) Corporate Data Warehouse were accessed via the VA Informatics and Computing Infrastructure (VINCI) and used to identify VA inpatient admissions and obtain the laboratory and vital sign data necessary to calculate SIRS, qSOFA, and SOFA scores. The data were supplemented by manual review of VA health records to obtain information that was not readily available in administrative records, including septic shock outcomes and laboratory and vital sign data obtained in the ICU. This study was approved by the institutional review board at the University of Iowa and the research and development committee at the Iowa City VA Medical Center (ICVAMC).

Patients

The study population included veterans admitted to the nonsurgical medicine unit at ICVAMC between August 1, 2014 and August 1, 2016 who were transferred to an ICU after admission; direct ICU admissions were not included as the qSOFA has been shown in studies to be more beneficial and offer better predictive validity outside the ICU. Excluding these direct admissions prevented any potential skewing of the data. To control for possible selection bias, veterans also were excluded if they transferred from another facility, were admitted under observation status, or if they had been admitted within the prior 30 days. These patients may have been more critically ill than those who presented directly to our facility and any prior treatment could affect the clinical status of the patient and assessment for sepsis at the time of presentation to the VA. Veterans were further required to have evidence of suspected infection based on manual review of the health record, which was determined by receipt of an antibiotic relevant to the empiric treatment of sepsis within 48 hours of admission.

Sepsis and Septic Shock Assessment Tools

As outlined in the Sepsis-3 guidelines, sepsis was defined as suspected or confirmed infection with an acute change in the SOFA score of ≥ 2 points, which is assumed to be 0 in those not known to have preexisting dysfunction.¹ The SOFA score includes variables from the respiratory, coagulation, hepatic, cardiovascular, renal, and central nervous systems.¹ Septic shock was defined as vasopressor administration and a serum lactic acid level > 2 mmol/L occurring up to 24 hours apart and within 3 days of the first antibiotic dose administered.

The SIRS assessment includes 4 clinical variables (temperature, heart rate, respiratory rate, and white blood cell count) while qSOFA is comprised of 3 variables (respiratory rate, systolic blood pressure, and altered mental status).¹ With both assessments, a score ≥ 2 is considered positive, which indicates increased risk for sepsis in patients with suspected infection.¹ In keeping with existing studies, qSOFA and SIRS assessments were scored using maximum values found within 48 hours before and 24 hours after the first administered antibiotic dose.³

Outcomes

The primary outcome variable was the presence of sepsis in adults with evidence of infection within 48 hours of admission. Secondary outcome measures included 30-day mortality and septic shock.

Performance between the SIRS and qSOFA assessments was contrasted using sensitivity, specificity, and positive and negative predictive value measurements. Associations of qSOFA and SIRS with septic shock and 30-day mortality were evaluated using a 2-tailed Fisher’s exact test with a threshold of α = 0.05 to determine statistical significance.

Results

The study sample of 481 veterans had a mean age of 67.4 years, 94% were male, and 91.1% were white (Table 1). 

Scores for qSOFA, but not SIRS, were significantly associated with septic shock (Fisher’s exact test; qSOFA: P = .009; SIRS: P = .58) (Table 3). 

Discussion

High sensitivity is critical for a sepsis screening tool. To be clinically useful, it has been suggested that biomarkers predicting poor outcomes for sepsis should have a sensitivity of > 80%.⁴ Although qSOFA demonstrated greater specificity than SIRS in our study (83.6% vs 25.7%), qSOFA showed lower sensitivity (44.7% vs 80.0%), which resulted in a greater potential for false negatives; 55.3% of those with sepsis would go undetected. Therefore, our study does not support qSOFA as a better screening assessment than SIRS for sepsis in the veteran population.

Most studies concur with our findings of low sensitivity and high specificity of qSOFA. In a systematic review and meta-analysis, Serafim and colleagues identified 10 studies published after Sepsis-3 that reported sensitivity or specificity of qSOFA and SIRS for sepsis diagnosis.⁵ Seven of the 10 studies reported sensitivities and favored SIRS in the diagnosis of sepsis (Relative risk: 1.32; 95% CI: 0.40-2.24; P < .0001; I² = 100%). The authors noted that substantial heterogeneity among studies, including differences in study design, sample size, and criteria for determination of infection, was an important limitation. In addition, most studies that contrast qSOFA and SIRS center on prognostic value in predicting mortality, rather than as a screening test for a diagnosis of sepsis.

We concluded SIRS was more sensitive and thus superior to qSOFA when used as a screening tool for sepsis but conceded that more prospective and homogenous investigations were necessary. To our knowledge, only 1 published study has deviated from this conclusion and reported comparable sensitivity between SIRS (92%) and qSOFA (90%).⁶ Our study adds to existing literature as it is the first conducted in a veteran population. Additionally, we performed our investigation in a general medicine population with methods similar to existing literature, including the key study validating clinical criteria for sepsis by Seymour and colleagues.³

Limitations

This study is not without limitations, including potential misclassification of cases if essential data points were not available during data collection via health record review or the data points were not representative of a true change from baseline (eg, the Glasgow Coma Scale score for altered mental status in the qSOFA or the SOFA score for organ dysfunction). Generalizability of the results also may be limited due to our retrospective, single-center design and characteristics typical of a veteran population (eg, older, white males). Additionally, many veterans were excluded from the study if they transferred from another facility. These veterans may have been more critically ill than those who presented directly to our facility, which possibly introduced selection bias.

Conclusion

Our findings do not support use of the qSOFA as a suitable replacement for SIRS as a sepsis screening tool among patients with suspected infection in the general medicine inpatient setting. The clinical concern with SIRS is that unfavorable specificity leads to unnecessary antibiotic exposure among patients who are falsely positive. While qSOFA has demonstrated higher specificity, its use would cause many sepsis cases to go undetected due to the technique’s low sensitivity. Frequent false negative qSOFA results could thus serve to impede, rather than enhance, early recognition and intervention for sepsis.

The ideal sepsis screening tool is rapid and possesses high sensitivity and specificity to promptly identify and manage sepsis and avert unfavorable outcomes such as septic shock and death. While the SIRS criteria do not satisfy these ideal features, its measurement characteristics are more suitable for the application of sepsis screening than the qSOFA and should thus remain the standard tool in this setting. Future prospectively designed studies with more uniform methodologies are necessary to ascertain the most effective approach to identify sepsis for which novel screening approaches with more clinically suitable measurement properties are greatly needed.

Acknowledgements
This research was supported by the Iowa City VA Health Care System, Department of Pharmacy Services. Additional support was provided by the Health Services Research and Development Service, Department of Veterans Affairs.

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

The first death in the United States from the novel coronavirus (COVID-19) was a Washington state man in his 50s who had underlying health conditions, state health officials announced on Feb 29. At the same time, officials there are investigating a possible COVID-19 outbreak at a long-term care facility.

Washington state officials reported two other presumptive positive cases of COVID-19, both of whom are associated with LifeCare of Kirkland, Washington. One is a woman in her 70s who is a resident at the facility and the other is a woman in her 40s who is a health care worker at the facility.

Additionally, many residents and staff members at the facility have reported respiratory symptoms, according to Jeff Duchin, MD, health officer for public health in Seattle and King County. Among the more than 100 residents at the facility, 27 have respiratory symptoms; while among the 180 staff members, 25 have reported symptoms.

Overall, these reports bring the total number of U.S. COVID-19 cases detected by the public health system to 22, though that number is expected to climb as these investigations continue.

The general risk to the American public is still low, including residents in long-term care facilities, Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the Centers for Disease Control and Prevention, said during the Feb. 29 press briefing. Older people are are higher risk, however, and long-term care facilities should emphasize handwashing and the early identification of individuals with symptoms.

Dr. Duchin added that health care workers who are sick should stay home and that visitors should be screened for symptoms, the same advice offered to limit the spread of influenza at long-term care facilities.

Whitehouse.gov

The CDC briefing comes after President Trump held his own press conference at the White House where he identified the person who had died as being a woman in her 50s who was medically at risk.

During that press conference, Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said that the current pattern of disease with COVID-19 suggests that 75%-80% of patients will have mild illness and recover, while 15%-20% will require advanced medical care.

For the most part, the more serious cases will occur in those who are elderly or have underlying medical conditions. There is “no indication” that individuals who recover from the virus are becoming re-infected, Dr. Fauci said.

The administration also announced a series of actions aimed at slowing the spread of the virus and responding to it. On March 2, President Trump will meet with leaders in the pharmaceutical industry at the White House to discuss vaccine development. The administration is also working to ensure an adequate supply of face masks. Vice President Mike Pence said there are currently more than 40 million masks available, but that the administration has received promises of 35 million more masks per month from manufacturers. Access to masks will be prioritized for high-risk health care workers, Vice President Pence said. “The average American does not need to go out and buy a mask,” he added.

Additionally, Vice President Pence announced new travel restrictions with Iran that would bar entry to the United States for any foreign national who visited Iran in the last 14 days. The federal government is also advising Americans not to travel to the regions in Italy and South Korea that have been most affected by COVID-19. The government is also working with officials in Italy and South Korea to conduct medical screening of anyone coming into the United States from those countries.

mschneider@mdedge.com

The first death in the United States from the novel coronavirus (COVID-19) was a Washington state man in his 50s who had underlying health conditions, state health officials announced on Feb 29. At the same time, officials there are investigating a possible COVID-19 outbreak at a long-term care facility.

Washington state officials reported two other presumptive positive cases of COVID-19, both of whom are associated with LifeCare of Kirkland, Washington. One is a woman in her 70s who is a resident at the facility and the other is a woman in her 40s who is a health care worker at the facility.

Additionally, many residents and staff members at the facility have reported respiratory symptoms, according to Jeff Duchin, MD, health officer for public health in Seattle and King County. Among the more than 100 residents at the facility, 27 have respiratory symptoms; while among the 180 staff members, 25 have reported symptoms.

Overall, these reports bring the total number of U.S. COVID-19 cases detected by the public health system to 22, though that number is expected to climb as these investigations continue.

The general risk to the American public is still low, including residents in long-term care facilities, Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the Centers for Disease Control and Prevention, said during the Feb. 29 press briefing. Older people are are higher risk, however, and long-term care facilities should emphasize handwashing and the early identification of individuals with symptoms.

Dr. Duchin added that health care workers who are sick should stay home and that visitors should be screened for symptoms, the same advice offered to limit the spread of influenza at long-term care facilities.

Whitehouse.gov

The CDC briefing comes after President Trump held his own press conference at the White House where he identified the person who had died as being a woman in her 50s who was medically at risk.

During that press conference, Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said that the current pattern of disease with COVID-19 suggests that 75%-80% of patients will have mild illness and recover, while 15%-20% will require advanced medical care.

For the most part, the more serious cases will occur in those who are elderly or have underlying medical conditions. There is “no indication” that individuals who recover from the virus are becoming re-infected, Dr. Fauci said.

The administration also announced a series of actions aimed at slowing the spread of the virus and responding to it. On March 2, President Trump will meet with leaders in the pharmaceutical industry at the White House to discuss vaccine development. The administration is also working to ensure an adequate supply of face masks. Vice President Mike Pence said there are currently more than 40 million masks available, but that the administration has received promises of 35 million more masks per month from manufacturers. Access to masks will be prioritized for high-risk health care workers, Vice President Pence said. “The average American does not need to go out and buy a mask,” he added.

Additionally, Vice President Pence announced new travel restrictions with Iran that would bar entry to the United States for any foreign national who visited Iran in the last 14 days. The federal government is also advising Americans not to travel to the regions in Italy and South Korea that have been most affected by COVID-19. The government is also working with officials in Italy and South Korea to conduct medical screening of anyone coming into the United States from those countries.

mschneider@mdedge.com

The first death in the United States from the novel coronavirus (COVID-19) was a Washington state man in his 50s who had underlying health conditions, state health officials announced on Feb 29. At the same time, officials there are investigating a possible COVID-19 outbreak at a long-term care facility.

Washington state officials reported two other presumptive positive cases of COVID-19, both of whom are associated with LifeCare of Kirkland, Washington. One is a woman in her 70s who is a resident at the facility and the other is a woman in her 40s who is a health care worker at the facility.

Additionally, many residents and staff members at the facility have reported respiratory symptoms, according to Jeff Duchin, MD, health officer for public health in Seattle and King County. Among the more than 100 residents at the facility, 27 have respiratory symptoms; while among the 180 staff members, 25 have reported symptoms.

Overall, these reports bring the total number of U.S. COVID-19 cases detected by the public health system to 22, though that number is expected to climb as these investigations continue.

The general risk to the American public is still low, including residents in long-term care facilities, Nancy Messonnier, MD, director of the National Center for Immunization and Respiratory Diseases at the Centers for Disease Control and Prevention, said during the Feb. 29 press briefing. Older people are are higher risk, however, and long-term care facilities should emphasize handwashing and the early identification of individuals with symptoms.

Dr. Duchin added that health care workers who are sick should stay home and that visitors should be screened for symptoms, the same advice offered to limit the spread of influenza at long-term care facilities.

Whitehouse.gov

The CDC briefing comes after President Trump held his own press conference at the White House where he identified the person who had died as being a woman in her 50s who was medically at risk.

During that press conference, Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said that the current pattern of disease with COVID-19 suggests that 75%-80% of patients will have mild illness and recover, while 15%-20% will require advanced medical care.

For the most part, the more serious cases will occur in those who are elderly or have underlying medical conditions. There is “no indication” that individuals who recover from the virus are becoming re-infected, Dr. Fauci said.

The administration also announced a series of actions aimed at slowing the spread of the virus and responding to it. On March 2, President Trump will meet with leaders in the pharmaceutical industry at the White House to discuss vaccine development. The administration is also working to ensure an adequate supply of face masks. Vice President Mike Pence said there are currently more than 40 million masks available, but that the administration has received promises of 35 million more masks per month from manufacturers. Access to masks will be prioritized for high-risk health care workers, Vice President Pence said. “The average American does not need to go out and buy a mask,” he added.

Additionally, Vice President Pence announced new travel restrictions with Iran that would bar entry to the United States for any foreign national who visited Iran in the last 14 days. The federal government is also advising Americans not to travel to the regions in Italy and South Korea that have been most affected by COVID-19. The government is also working with officials in Italy and South Korea to conduct medical screening of anyone coming into the United States from those countries.

mschneider@mdedge.com

WEST PALM BEACH, FLA. – Among patients with relapsing-remitting multiple sclerosis (MS), depression increases the likelihood of having worse neurologic function one year later, according to a study presented at ACTRIMS Forum 2020. Patients’ subjective descriptions of disease activity did not significantly change during that time, which “suggests that depression is not merely a reactive phenomenon, but rather an independent contributor to clinical worsening in the long term,” said Jenny Feng, MD, a neuroimmunology fellow at the Mellen Center for MS Treatment and Research at the Cleveland Clinic.

The researchers hypothesize that depression’s influence on psychomotor function may contribute to clinical worsening in MS.

More than half of patients with MS have depression, and there is a higher prevalence of depression in relapsing-remitting MS than in progressive disease. “Depression is associated with systemic inflammation,” Dr. Feng said at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “We know that depressed individuals tend to have slower walking speeds, slower processing speeds, and worse quality of life measures.” But neurologists do not know whether patients feel depressed because the disease is getting worse, or whether depression is an independent contributing factor to MS, Dr. Feng said.

To examine whether depression affects neurologic performance and disease activity in patients with MS, Dr. Feng and colleagues analyzed real-world data from about 2,400 patients in MS PATHS (Multiple Sclerosis Partners Advancing Technology and Health Solutions), a network of centers in the United States and Europe. The researchers assessed the longitudinal relationship between depression, measures of neurologic function, and MRI metrics.

The researchers included patients with relapsing-remitting MS who had clinical and imaging data available at baseline and about 1 year later. Patients completed tests of manual dexterity, walking speed, and processing speed that are based on the Multiple Sclerosis Functional Composite. A worsening of 20% on any measure is considered clinically significant.

Patients had a mean age of about 45 years and mean disease duration of about 14 years. Patients with a T score greater than 45 on the Neuro-QoL depression questionnaire were classified as having depression, and approximately half of the population had depression. Patients with depression were more likely to have an employment status of disabled and to receive infusion medications.

The investigators used propensity score analysis to adjust for baseline differences between patients with and without depression and evaluated the effect of depression on year 1 outcome measures using logistic regression for categorical variables and linear regression for continuous variables.

“After propensity weighting for baseline covariates including neuroperformance scores, individuals with depression continued to worsen,” Dr. Feng said. Patients with depression were more likely to have a 20% worsening in at least one measure of neurologic performance at year 1 (odds ratio, 1.31). “There was a trend for increased odds of interval relapses, increased T2 lesion burden, and contrast-enhancing lesions at year 1” in patients with depression, but the results were not statistically significant. “Despite worsening neuroperformance at year 1 in individuals with baseline depression, their [patient-reported outcomes] at year 1 were not significantly worse.”

The researcher lacked information about the date of depression onset and medication compliance, Dr. Feng said. In addition, propensity weighting does not account for potential bias due to missing data.

The findings support the existing practice of actively screening for and treating depression in patients with MS, Dr. Feng said.

Dr. Feng had no disclosures. Coauthors have consulted for and received research support from pharmaceutical companies. MS PATHS is supported by Biogen.

jremaly@mdedge.com

SOURCE: Feng JJ et al. ACTRIMS Forum 2020. Abstract P226.

WEST PALM BEACH, FLA. – Among patients with relapsing-remitting multiple sclerosis (MS), depression increases the likelihood of having worse neurologic function one year later, according to a study presented at ACTRIMS Forum 2020. Patients’ subjective descriptions of disease activity did not significantly change during that time, which “suggests that depression is not merely a reactive phenomenon, but rather an independent contributor to clinical worsening in the long term,” said Jenny Feng, MD, a neuroimmunology fellow at the Mellen Center for MS Treatment and Research at the Cleveland Clinic.

The researchers hypothesize that depression’s influence on psychomotor function may contribute to clinical worsening in MS.

More than half of patients with MS have depression, and there is a higher prevalence of depression in relapsing-remitting MS than in progressive disease. “Depression is associated with systemic inflammation,” Dr. Feng said at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “We know that depressed individuals tend to have slower walking speeds, slower processing speeds, and worse quality of life measures.” But neurologists do not know whether patients feel depressed because the disease is getting worse, or whether depression is an independent contributing factor to MS, Dr. Feng said.

To examine whether depression affects neurologic performance and disease activity in patients with MS, Dr. Feng and colleagues analyzed real-world data from about 2,400 patients in MS PATHS (Multiple Sclerosis Partners Advancing Technology and Health Solutions), a network of centers in the United States and Europe. The researchers assessed the longitudinal relationship between depression, measures of neurologic function, and MRI metrics.

The researchers included patients with relapsing-remitting MS who had clinical and imaging data available at baseline and about 1 year later. Patients completed tests of manual dexterity, walking speed, and processing speed that are based on the Multiple Sclerosis Functional Composite. A worsening of 20% on any measure is considered clinically significant.

Patients had a mean age of about 45 years and mean disease duration of about 14 years. Patients with a T score greater than 45 on the Neuro-QoL depression questionnaire were classified as having depression, and approximately half of the population had depression. Patients with depression were more likely to have an employment status of disabled and to receive infusion medications.

The investigators used propensity score analysis to adjust for baseline differences between patients with and without depression and evaluated the effect of depression on year 1 outcome measures using logistic regression for categorical variables and linear regression for continuous variables.

“After propensity weighting for baseline covariates including neuroperformance scores, individuals with depression continued to worsen,” Dr. Feng said. Patients with depression were more likely to have a 20% worsening in at least one measure of neurologic performance at year 1 (odds ratio, 1.31). “There was a trend for increased odds of interval relapses, increased T2 lesion burden, and contrast-enhancing lesions at year 1” in patients with depression, but the results were not statistically significant. “Despite worsening neuroperformance at year 1 in individuals with baseline depression, their [patient-reported outcomes] at year 1 were not significantly worse.”

The researcher lacked information about the date of depression onset and medication compliance, Dr. Feng said. In addition, propensity weighting does not account for potential bias due to missing data.

The findings support the existing practice of actively screening for and treating depression in patients with MS, Dr. Feng said.

Dr. Feng had no disclosures. Coauthors have consulted for and received research support from pharmaceutical companies. MS PATHS is supported by Biogen.

jremaly@mdedge.com

SOURCE: Feng JJ et al. ACTRIMS Forum 2020. Abstract P226.

WEST PALM BEACH, FLA. – Among patients with relapsing-remitting multiple sclerosis (MS), depression increases the likelihood of having worse neurologic function one year later, according to a study presented at ACTRIMS Forum 2020. Patients’ subjective descriptions of disease activity did not significantly change during that time, which “suggests that depression is not merely a reactive phenomenon, but rather an independent contributor to clinical worsening in the long term,” said Jenny Feng, MD, a neuroimmunology fellow at the Mellen Center for MS Treatment and Research at the Cleveland Clinic.

The researchers hypothesize that depression’s influence on psychomotor function may contribute to clinical worsening in MS.

More than half of patients with MS have depression, and there is a higher prevalence of depression in relapsing-remitting MS than in progressive disease. “Depression is associated with systemic inflammation,” Dr. Feng said at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. “We know that depressed individuals tend to have slower walking speeds, slower processing speeds, and worse quality of life measures.” But neurologists do not know whether patients feel depressed because the disease is getting worse, or whether depression is an independent contributing factor to MS, Dr. Feng said.

To examine whether depression affects neurologic performance and disease activity in patients with MS, Dr. Feng and colleagues analyzed real-world data from about 2,400 patients in MS PATHS (Multiple Sclerosis Partners Advancing Technology and Health Solutions), a network of centers in the United States and Europe. The researchers assessed the longitudinal relationship between depression, measures of neurologic function, and MRI metrics.

The researchers included patients with relapsing-remitting MS who had clinical and imaging data available at baseline and about 1 year later. Patients completed tests of manual dexterity, walking speed, and processing speed that are based on the Multiple Sclerosis Functional Composite. A worsening of 20% on any measure is considered clinically significant.

Patients had a mean age of about 45 years and mean disease duration of about 14 years. Patients with a T score greater than 45 on the Neuro-QoL depression questionnaire were classified as having depression, and approximately half of the population had depression. Patients with depression were more likely to have an employment status of disabled and to receive infusion medications.

The investigators used propensity score analysis to adjust for baseline differences between patients with and without depression and evaluated the effect of depression on year 1 outcome measures using logistic regression for categorical variables and linear regression for continuous variables.

“After propensity weighting for baseline covariates including neuroperformance scores, individuals with depression continued to worsen,” Dr. Feng said. Patients with depression were more likely to have a 20% worsening in at least one measure of neurologic performance at year 1 (odds ratio, 1.31). “There was a trend for increased odds of interval relapses, increased T2 lesion burden, and contrast-enhancing lesions at year 1” in patients with depression, but the results were not statistically significant. “Despite worsening neuroperformance at year 1 in individuals with baseline depression, their [patient-reported outcomes] at year 1 were not significantly worse.”

The researcher lacked information about the date of depression onset and medication compliance, Dr. Feng said. In addition, propensity weighting does not account for potential bias due to missing data.

The findings support the existing practice of actively screening for and treating depression in patients with MS, Dr. Feng said.

Dr. Feng had no disclosures. Coauthors have consulted for and received research support from pharmaceutical companies. MS PATHS is supported by Biogen.

jremaly@mdedge.com

SOURCE: Feng JJ et al. ACTRIMS Forum 2020. Abstract P226.

WEST PALM BEACH, FLA. – About a third of patients with multiple sclerosis (MS) switch to a more potent disease-modifying therapy (DMT) within 1 year of disease activity being detected on MRI, according to a study of prescribing practices. The number of T2 lesions on MRI may be associated with the likelihood of switching DMTs, said Ryan Canissario, MD, a neurology resident at University of Rochester (New York) Medical Center, and colleagues.

The researchers had hypothesized that “the majority of patients would undergo a change in DMT in response to MRI activity,” they said. Delays in follow-up or therapy start times may partly explain the relatively low rates of switching during the first few months. “We speculate that other reasons ... include clinician or patient risk tolerance, patient age, prior longstanding stability on existing therapy, recent therapy change prior to MRI, or high baseline DMT potency,” the researchers said. Future studies will try to clarify the findings and assess outcomes related to prescribing practices.

Preventing new lesions on MRI is a primary treatment target in MS. “Following this principle, change in [DMT] should be considered in the setting of MRI evidence of disease activity,” but prescribing practices have not been well characterized, Dr. Canissario and colleagues said.

To identify and characterize patients who underwent a DMT change after the detection of brain MRI disease activity, Dr. Canissario and colleagues analyzed data from more than 1,300 patients in MS PATHS (MS Partners Advancing Technology and Health Solutions), a research network of 10 health care institutions. The investigators presented their results at ACTRIMS Forum 2020, the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

By consensus, the investigators classified DMTs as low potency (for example, interferons, immunoglobulin G, glatiramer acetate, and teriflunomide), medium potency (azathioprine, cladribine, daclizumab, dimethyl fumarate, fingolimod, methotrexate, and mycophenolate mofetil), or high potency (alemtuzumab, cyclophosphamide, mitoxantrone, natalizumab, ocrelizumab, ofatumumab, and rituximab).

The researchers reviewed available imaging data from Apr. 2015 to Aug. 2019 to identify patients with new T2 or gadolinium-enhancing lesions. They determined whether these patients had an escalation in DMT potency or a lateral switch at 3, 6, 9, and 12 months after a radiologist reviewed the MRI.

The number of patients with MRI evidence of disease activity and complete DMT data ranged from 1,364 at 3 months to 952 at 12 months. The proportion of patients who had an escalation in therapy was 17.4% at 3 months, 25.5% at 6 months, 30.4% at 9 months, and 34.3% at 12 months. The proportion with a lateral change was 2% at 3 months, 3.4% at 6 months, 4.3% at 9 months, and 6% at 12 months.

The percentage of patients with DMT escalation or lateral change at 9 months increased with an increasing number of new T2 lesions. About 27% of patients with one new lesion switched therapy, compared with 43.5% of those with more than three new lesions.

Dr. Canissario had no disclosures. Coauthors disclosed research support from and consulting for pharmaceutical companies. MS PATHS is funded by Biogen.

jremaly@mdedge.com

SOURCE: Canissario R et al. ACTRIMS Forum 2020. Abstract P112.

WEST PALM BEACH, FLA. – About a third of patients with multiple sclerosis (MS) switch to a more potent disease-modifying therapy (DMT) within 1 year of disease activity being detected on MRI, according to a study of prescribing practices. The number of T2 lesions on MRI may be associated with the likelihood of switching DMTs, said Ryan Canissario, MD, a neurology resident at University of Rochester (New York) Medical Center, and colleagues.

The researchers had hypothesized that “the majority of patients would undergo a change in DMT in response to MRI activity,” they said. Delays in follow-up or therapy start times may partly explain the relatively low rates of switching during the first few months. “We speculate that other reasons ... include clinician or patient risk tolerance, patient age, prior longstanding stability on existing therapy, recent therapy change prior to MRI, or high baseline DMT potency,” the researchers said. Future studies will try to clarify the findings and assess outcomes related to prescribing practices.

Preventing new lesions on MRI is a primary treatment target in MS. “Following this principle, change in [DMT] should be considered in the setting of MRI evidence of disease activity,” but prescribing practices have not been well characterized, Dr. Canissario and colleagues said.

To identify and characterize patients who underwent a DMT change after the detection of brain MRI disease activity, Dr. Canissario and colleagues analyzed data from more than 1,300 patients in MS PATHS (MS Partners Advancing Technology and Health Solutions), a research network of 10 health care institutions. The investigators presented their results at ACTRIMS Forum 2020, the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

By consensus, the investigators classified DMTs as low potency (for example, interferons, immunoglobulin G, glatiramer acetate, and teriflunomide), medium potency (azathioprine, cladribine, daclizumab, dimethyl fumarate, fingolimod, methotrexate, and mycophenolate mofetil), or high potency (alemtuzumab, cyclophosphamide, mitoxantrone, natalizumab, ocrelizumab, ofatumumab, and rituximab).

The researchers reviewed available imaging data from Apr. 2015 to Aug. 2019 to identify patients with new T2 or gadolinium-enhancing lesions. They determined whether these patients had an escalation in DMT potency or a lateral switch at 3, 6, 9, and 12 months after a radiologist reviewed the MRI.

The number of patients with MRI evidence of disease activity and complete DMT data ranged from 1,364 at 3 months to 952 at 12 months. The proportion of patients who had an escalation in therapy was 17.4% at 3 months, 25.5% at 6 months, 30.4% at 9 months, and 34.3% at 12 months. The proportion with a lateral change was 2% at 3 months, 3.4% at 6 months, 4.3% at 9 months, and 6% at 12 months.

The percentage of patients with DMT escalation or lateral change at 9 months increased with an increasing number of new T2 lesions. About 27% of patients with one new lesion switched therapy, compared with 43.5% of those with more than three new lesions.

Dr. Canissario had no disclosures. Coauthors disclosed research support from and consulting for pharmaceutical companies. MS PATHS is funded by Biogen.

jremaly@mdedge.com

SOURCE: Canissario R et al. ACTRIMS Forum 2020. Abstract P112.

WEST PALM BEACH, FLA. – About a third of patients with multiple sclerosis (MS) switch to a more potent disease-modifying therapy (DMT) within 1 year of disease activity being detected on MRI, according to a study of prescribing practices. The number of T2 lesions on MRI may be associated with the likelihood of switching DMTs, said Ryan Canissario, MD, a neurology resident at University of Rochester (New York) Medical Center, and colleagues.

The researchers had hypothesized that “the majority of patients would undergo a change in DMT in response to MRI activity,” they said. Delays in follow-up or therapy start times may partly explain the relatively low rates of switching during the first few months. “We speculate that other reasons ... include clinician or patient risk tolerance, patient age, prior longstanding stability on existing therapy, recent therapy change prior to MRI, or high baseline DMT potency,” the researchers said. Future studies will try to clarify the findings and assess outcomes related to prescribing practices.

Preventing new lesions on MRI is a primary treatment target in MS. “Following this principle, change in [DMT] should be considered in the setting of MRI evidence of disease activity,” but prescribing practices have not been well characterized, Dr. Canissario and colleagues said.

To identify and characterize patients who underwent a DMT change after the detection of brain MRI disease activity, Dr. Canissario and colleagues analyzed data from more than 1,300 patients in MS PATHS (MS Partners Advancing Technology and Health Solutions), a research network of 10 health care institutions. The investigators presented their results at ACTRIMS Forum 2020, the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

By consensus, the investigators classified DMTs as low potency (for example, interferons, immunoglobulin G, glatiramer acetate, and teriflunomide), medium potency (azathioprine, cladribine, daclizumab, dimethyl fumarate, fingolimod, methotrexate, and mycophenolate mofetil), or high potency (alemtuzumab, cyclophosphamide, mitoxantrone, natalizumab, ocrelizumab, ofatumumab, and rituximab).

The researchers reviewed available imaging data from Apr. 2015 to Aug. 2019 to identify patients with new T2 or gadolinium-enhancing lesions. They determined whether these patients had an escalation in DMT potency or a lateral switch at 3, 6, 9, and 12 months after a radiologist reviewed the MRI.

The number of patients with MRI evidence of disease activity and complete DMT data ranged from 1,364 at 3 months to 952 at 12 months. The proportion of patients who had an escalation in therapy was 17.4% at 3 months, 25.5% at 6 months, 30.4% at 9 months, and 34.3% at 12 months. The proportion with a lateral change was 2% at 3 months, 3.4% at 6 months, 4.3% at 9 months, and 6% at 12 months.

The percentage of patients with DMT escalation or lateral change at 9 months increased with an increasing number of new T2 lesions. About 27% of patients with one new lesion switched therapy, compared with 43.5% of those with more than three new lesions.

Dr. Canissario had no disclosures. Coauthors disclosed research support from and consulting for pharmaceutical companies. MS PATHS is funded by Biogen.

jremaly@mdedge.com

SOURCE: Canissario R et al. ACTRIMS Forum 2020. Abstract P112.

WEST PALM BEACH, FLA. – The incidence rate of many cardiovascular events is more than doubled in patients with multiple sclerosis (MS), compared with matched controls without MS, according to a study presented at ACTRIMS Forum 2020. The risk of a major adverse cardiac event (MACE) – that is, a first myocardial infarction, stroke, or cardiac arrest – is approximately twofold higher. Venous thromboembolism and peripheral vascular disease also occur at notably increased rates, reported Rebecca Persson, MPH, and colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. Ms. Persson is an epidemiologist at the Boston Collaborative Drug Surveillance Program in Lexington, Mass.

Vascular comorbidities are more prevalent in patients with MS than in the general population, but few studies have reported on the incidence of cardiovascular disease after MS diagnosis. To describe rates of incident cardiovascular disease after MS diagnosis and compare them with rates in a matched population without MS, the researchers analyzed data from a U.S. Department of Defense database.

The study included a cohort of 6,406 patients with MS diagnosed and treated during Jan. 2004–Aug. 2017 who had at least one prescription for an MS disease-modifying treatment.

A cohort of 66,281 patients without MS were matched to the patients with MS 10:1 based on age, sex, geographic region, and cohort entry date. The researchers excluded patients with a history of cardiovascular disease or select comorbidities such as dyslipidemia, atrial fibrillation, or a disorder related to peripheral vascular disease. They also excluded patients with a history of treated hypertension or treated type 2 diabetes, defined as diagnosis and treatment within 90 days of each other.

Researchers considered a patient to have a cardiovascular disease outcome – including MI, stroke, cardiac arrest, heart failure, angina or unspecified ischemic heart disease, transient ischemic attack or unspecified cerebrovascular disease, venous thromboembolism, peripheral vascular disease, pericardial disease, bradycardia or heart block, or arrhythmia other than atrial fibrillation or atrial flutter – if the disease was recorded five or more times.

The researchers followed patients from cohort entry until study outcome (separate for each outcome), loss of eligibility, death, or end of data collection. Ms. Persson and colleagues calculated incidence rates (IRs) using the Byar method and incidence rate ratios (IRRs) using Poisson regression for each outcome.

The median age at MS diagnosis or at the matched date was 38 years, and 71% were female. The median duration of record after patients entered the cohort was 7.2 years for patients with MS and 5.3 years for patients without MS.

The IRs of all cardiovascular disease types, with the exception of bradycardia or heart block, were higher for patients with MS, compared with non-MS patients, the researchers reported. Many cardiovascular disease outcomes had IRRs greater than 2. “The incidence of MI was higher among MS patients than among non-MS patients,” the researchers said (IR, 12.4 vs. 5.9 per 10,000 person-years; IRR, 2.11).

“Risk of MACE and risk of stroke were higher among MS patients than among non-MS patients,” the researchers said. Relative risks also were higher among women than among men (2.47 vs. 1.55 for MACE, and 2.19 vs. 1.71 for stroke). When the investigators performed a sensitivity analysis to address the possibility that physicians might misdiagnosis MS symptoms as stroke, the rate of stroke was attenuated among patients with MS, but remained elevated relative to the rate among patients without MS (IRR, 1.63).

The IR of venous thromboembolism was more than 2 times higher among patients with MS than among non-MS patients (38.4 vs. 15.1 per 10,000 person-years; IRR, 2.54), as was the risk of peripheral vascular disease (14.9 vs. 6.0 per 10,000 person-years; IRR, 2.49). The relative risk of peripheral vascular disease was higher in women than men, and the risk in patients with MS increased after age 40 years.

The study was funded by a grant from Celgene, a subsidiary of Bristol-Myers Squibb. Four of Ms. Persson’s coauthors are employees of BMS, and one works for a company that has a business relationship with Celgene.

jremaly@mdedge.com

SOURCE: Persson R et al. ACTRIMS Forum 2020. Abstract P082.

WEST PALM BEACH, FLA. – The incidence rate of many cardiovascular events is more than doubled in patients with multiple sclerosis (MS), compared with matched controls without MS, according to a study presented at ACTRIMS Forum 2020. The risk of a major adverse cardiac event (MACE) – that is, a first myocardial infarction, stroke, or cardiac arrest – is approximately twofold higher. Venous thromboembolism and peripheral vascular disease also occur at notably increased rates, reported Rebecca Persson, MPH, and colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. Ms. Persson is an epidemiologist at the Boston Collaborative Drug Surveillance Program in Lexington, Mass.

Vascular comorbidities are more prevalent in patients with MS than in the general population, but few studies have reported on the incidence of cardiovascular disease after MS diagnosis. To describe rates of incident cardiovascular disease after MS diagnosis and compare them with rates in a matched population without MS, the researchers analyzed data from a U.S. Department of Defense database.

The study included a cohort of 6,406 patients with MS diagnosed and treated during Jan. 2004–Aug. 2017 who had at least one prescription for an MS disease-modifying treatment.

A cohort of 66,281 patients without MS were matched to the patients with MS 10:1 based on age, sex, geographic region, and cohort entry date. The researchers excluded patients with a history of cardiovascular disease or select comorbidities such as dyslipidemia, atrial fibrillation, or a disorder related to peripheral vascular disease. They also excluded patients with a history of treated hypertension or treated type 2 diabetes, defined as diagnosis and treatment within 90 days of each other.

Researchers considered a patient to have a cardiovascular disease outcome – including MI, stroke, cardiac arrest, heart failure, angina or unspecified ischemic heart disease, transient ischemic attack or unspecified cerebrovascular disease, venous thromboembolism, peripheral vascular disease, pericardial disease, bradycardia or heart block, or arrhythmia other than atrial fibrillation or atrial flutter – if the disease was recorded five or more times.

The researchers followed patients from cohort entry until study outcome (separate for each outcome), loss of eligibility, death, or end of data collection. Ms. Persson and colleagues calculated incidence rates (IRs) using the Byar method and incidence rate ratios (IRRs) using Poisson regression for each outcome.

The median age at MS diagnosis or at the matched date was 38 years, and 71% were female. The median duration of record after patients entered the cohort was 7.2 years for patients with MS and 5.3 years for patients without MS.

The IRs of all cardiovascular disease types, with the exception of bradycardia or heart block, were higher for patients with MS, compared with non-MS patients, the researchers reported. Many cardiovascular disease outcomes had IRRs greater than 2. “The incidence of MI was higher among MS patients than among non-MS patients,” the researchers said (IR, 12.4 vs. 5.9 per 10,000 person-years; IRR, 2.11).

“Risk of MACE and risk of stroke were higher among MS patients than among non-MS patients,” the researchers said. Relative risks also were higher among women than among men (2.47 vs. 1.55 for MACE, and 2.19 vs. 1.71 for stroke). When the investigators performed a sensitivity analysis to address the possibility that physicians might misdiagnosis MS symptoms as stroke, the rate of stroke was attenuated among patients with MS, but remained elevated relative to the rate among patients without MS (IRR, 1.63).

The IR of venous thromboembolism was more than 2 times higher among patients with MS than among non-MS patients (38.4 vs. 15.1 per 10,000 person-years; IRR, 2.54), as was the risk of peripheral vascular disease (14.9 vs. 6.0 per 10,000 person-years; IRR, 2.49). The relative risk of peripheral vascular disease was higher in women than men, and the risk in patients with MS increased after age 40 years.

The study was funded by a grant from Celgene, a subsidiary of Bristol-Myers Squibb. Four of Ms. Persson’s coauthors are employees of BMS, and one works for a company that has a business relationship with Celgene.

jremaly@mdedge.com

SOURCE: Persson R et al. ACTRIMS Forum 2020. Abstract P082.

WEST PALM BEACH, FLA. – The incidence rate of many cardiovascular events is more than doubled in patients with multiple sclerosis (MS), compared with matched controls without MS, according to a study presented at ACTRIMS Forum 2020. The risk of a major adverse cardiac event (MACE) – that is, a first myocardial infarction, stroke, or cardiac arrest – is approximately twofold higher. Venous thromboembolism and peripheral vascular disease also occur at notably increased rates, reported Rebecca Persson, MPH, and colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. Ms. Persson is an epidemiologist at the Boston Collaborative Drug Surveillance Program in Lexington, Mass.

Vascular comorbidities are more prevalent in patients with MS than in the general population, but few studies have reported on the incidence of cardiovascular disease after MS diagnosis. To describe rates of incident cardiovascular disease after MS diagnosis and compare them with rates in a matched population without MS, the researchers analyzed data from a U.S. Department of Defense database.

The study included a cohort of 6,406 patients with MS diagnosed and treated during Jan. 2004–Aug. 2017 who had at least one prescription for an MS disease-modifying treatment.

A cohort of 66,281 patients without MS were matched to the patients with MS 10:1 based on age, sex, geographic region, and cohort entry date. The researchers excluded patients with a history of cardiovascular disease or select comorbidities such as dyslipidemia, atrial fibrillation, or a disorder related to peripheral vascular disease. They also excluded patients with a history of treated hypertension or treated type 2 diabetes, defined as diagnosis and treatment within 90 days of each other.

Researchers considered a patient to have a cardiovascular disease outcome – including MI, stroke, cardiac arrest, heart failure, angina or unspecified ischemic heart disease, transient ischemic attack or unspecified cerebrovascular disease, venous thromboembolism, peripheral vascular disease, pericardial disease, bradycardia or heart block, or arrhythmia other than atrial fibrillation or atrial flutter – if the disease was recorded five or more times.

The researchers followed patients from cohort entry until study outcome (separate for each outcome), loss of eligibility, death, or end of data collection. Ms. Persson and colleagues calculated incidence rates (IRs) using the Byar method and incidence rate ratios (IRRs) using Poisson regression for each outcome.

The median age at MS diagnosis or at the matched date was 38 years, and 71% were female. The median duration of record after patients entered the cohort was 7.2 years for patients with MS and 5.3 years for patients without MS.

The IRs of all cardiovascular disease types, with the exception of bradycardia or heart block, were higher for patients with MS, compared with non-MS patients, the researchers reported. Many cardiovascular disease outcomes had IRRs greater than 2. “The incidence of MI was higher among MS patients than among non-MS patients,” the researchers said (IR, 12.4 vs. 5.9 per 10,000 person-years; IRR, 2.11).

“Risk of MACE and risk of stroke were higher among MS patients than among non-MS patients,” the researchers said. Relative risks also were higher among women than among men (2.47 vs. 1.55 for MACE, and 2.19 vs. 1.71 for stroke). When the investigators performed a sensitivity analysis to address the possibility that physicians might misdiagnosis MS symptoms as stroke, the rate of stroke was attenuated among patients with MS, but remained elevated relative to the rate among patients without MS (IRR, 1.63).

The IR of venous thromboembolism was more than 2 times higher among patients with MS than among non-MS patients (38.4 vs. 15.1 per 10,000 person-years; IRR, 2.54), as was the risk of peripheral vascular disease (14.9 vs. 6.0 per 10,000 person-years; IRR, 2.49). The relative risk of peripheral vascular disease was higher in women than men, and the risk in patients with MS increased after age 40 years.

The study was funded by a grant from Celgene, a subsidiary of Bristol-Myers Squibb. Four of Ms. Persson’s coauthors are employees of BMS, and one works for a company that has a business relationship with Celgene.

jremaly@mdedge.com

SOURCE: Persson R et al. ACTRIMS Forum 2020. Abstract P082.

WEST PALM BEACH, FLA. – A machine learning model that combines data on the brain’s functional connectivity with clinical information such as age, sex and disease duration shows the potential to provide an accurate assessment of clinical impairment in patients with multiple sclerosis (MS).

“This is the first study to show that dynamic functional connectivity is useful to identify the impairment level in MS, and can be used for personalized treatment by clinicians,” first author Ceren Tozlu, PhD, of Weill Cornell Medicine, New York, said in an interview.

“We found out that structural connectivity is the most important feature that distinguishes MS patients from healthy controls, while dynamic functional connectivity was more discriminative compared to the static functional connectivity in MS patient classification regarding their impairment level.”

The findings were presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Statistical assessment of the clinical impairment of MS using MRI is hindered by a relatively weak correlation between the impairment and disease burden, such as lesion load.

However, the brain’s functional connectivity network, which is indicative of the disruption of the transmission of signals of gray matter regions, could provide a deeper understanding of connectome-level mechanisms that underlie variability in MS-related impairments, Dr. Tozlu and colleagues say.

With no previous study pulling together multimodal imaging data including static and dynamic functional connectivity to classify MS patients with a clinically significant impairment versus non–clinically significant impairment, Dr. Tozlu and the team sought to build a machine-learning–based model to do so.

For the study, they enrolled 79 patients with MS, including 42 with Expanded Disability Status scores of 2 or higher, representing clinically significant impairment at baseline.

The patients, who had a mean age of 45 years, were 66% female and had a mean disease duration of 12.48 years. The ensemble model that was used incorporated functional connectivity and a clinical dataset of age, sex, and disease duration. Functional connectivity was measured by evaluating blood oxygen level dependent (BOLD) signal activity between 86 FreeSurfer-based gray matter regions.

“Functional connectivity is a statistical correlation (Pearson’s correlation coefficient) between two time series of BOLD signals measured on two distinct region of interest of the brain during MRI scan,” Dr. Tozlu explained. “In our study, BOLD time series were measured using resting-state functional MRI technique that last 7 minutes.”

The ensemble model was able to classify low-adapting MS patients with an area under ROC curve (AUC) of 0.638 and a balanced accuracy of 0.659. The model performed well in accurately classifying the MS patients with clinically significant impairment with a sensitivity of 0.719.

“The models in which we applied functional and structural connectivity showed a high performance in classifying MS patients regarding their impairment level,” Dr. Tozlu said.

She noted that “these models may be extended to predict change in impairment level in a longitudinal study, for instance, identifying MS patients who may have a clinically significant impairment.”

In further evaluating which particular functional connections were most related to MS disease activity, Dr. Tozlu and colleagues found the most discriminative areas were between the right superior parietal and right inferior temporal, between right lateral occipital and left pericalcarine, and between right pericalcarine and right side of frontal pole.

If further validated, the approach could have important, broader clinical implications, Dr. Tozlu said.

“If the validation of these models on a larger dataset is successful, this model may be used to decide for personalized treatment,” Dr. Tozlu added. “The model could offer guidance in providing more powerful treatment for MS patients who may have a clinically significant impairment and less powerful treatment for MS patients who may not have a clinically significant impairment in order to avoid the side effects of treatments.

“Therefore, we believe that dynamics in functional connectivity should be taken into account in the next studies in MS.”

In commenting on the research, Eric Klawiter, MD, associate professor of neurology, Harvard Medical School and associate neurologist at Massachusetts General Hospital, both in Boston, said the findings offer valuable insights in the use of machine learning and MS imaging.

“This research shows very nicely the power of machine learning and connectivity techniques to differentiate MS phenotypes based on disability level,” he said in an interview.

“The future direction of this work is to develop predictive markers for disability progression and this would have significant impact in how we evaluate newly diagnosed patients and counsel their treatment decisions.”

Dr. Tozlu and Dr. Klawiter had no disclosures to report.

SOURCE: Tozlu C et al. ACTRIMS Forum 2020. Abstract P025.

WEST PALM BEACH, FLA. – A machine learning model that combines data on the brain’s functional connectivity with clinical information such as age, sex and disease duration shows the potential to provide an accurate assessment of clinical impairment in patients with multiple sclerosis (MS).

“This is the first study to show that dynamic functional connectivity is useful to identify the impairment level in MS, and can be used for personalized treatment by clinicians,” first author Ceren Tozlu, PhD, of Weill Cornell Medicine, New York, said in an interview.

“We found out that structural connectivity is the most important feature that distinguishes MS patients from healthy controls, while dynamic functional connectivity was more discriminative compared to the static functional connectivity in MS patient classification regarding their impairment level.”

The findings were presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Statistical assessment of the clinical impairment of MS using MRI is hindered by a relatively weak correlation between the impairment and disease burden, such as lesion load.

However, the brain’s functional connectivity network, which is indicative of the disruption of the transmission of signals of gray matter regions, could provide a deeper understanding of connectome-level mechanisms that underlie variability in MS-related impairments, Dr. Tozlu and colleagues say.

With no previous study pulling together multimodal imaging data including static and dynamic functional connectivity to classify MS patients with a clinically significant impairment versus non–clinically significant impairment, Dr. Tozlu and the team sought to build a machine-learning–based model to do so.

For the study, they enrolled 79 patients with MS, including 42 with Expanded Disability Status scores of 2 or higher, representing clinically significant impairment at baseline.

The patients, who had a mean age of 45 years, were 66% female and had a mean disease duration of 12.48 years. The ensemble model that was used incorporated functional connectivity and a clinical dataset of age, sex, and disease duration. Functional connectivity was measured by evaluating blood oxygen level dependent (BOLD) signal activity between 86 FreeSurfer-based gray matter regions.

“Functional connectivity is a statistical correlation (Pearson’s correlation coefficient) between two time series of BOLD signals measured on two distinct region of interest of the brain during MRI scan,” Dr. Tozlu explained. “In our study, BOLD time series were measured using resting-state functional MRI technique that last 7 minutes.”

The ensemble model was able to classify low-adapting MS patients with an area under ROC curve (AUC) of 0.638 and a balanced accuracy of 0.659. The model performed well in accurately classifying the MS patients with clinically significant impairment with a sensitivity of 0.719.

“The models in which we applied functional and structural connectivity showed a high performance in classifying MS patients regarding their impairment level,” Dr. Tozlu said.

She noted that “these models may be extended to predict change in impairment level in a longitudinal study, for instance, identifying MS patients who may have a clinically significant impairment.”

In further evaluating which particular functional connections were most related to MS disease activity, Dr. Tozlu and colleagues found the most discriminative areas were between the right superior parietal and right inferior temporal, between right lateral occipital and left pericalcarine, and between right pericalcarine and right side of frontal pole.

If further validated, the approach could have important, broader clinical implications, Dr. Tozlu said.

“If the validation of these models on a larger dataset is successful, this model may be used to decide for personalized treatment,” Dr. Tozlu added. “The model could offer guidance in providing more powerful treatment for MS patients who may have a clinically significant impairment and less powerful treatment for MS patients who may not have a clinically significant impairment in order to avoid the side effects of treatments.

“Therefore, we believe that dynamics in functional connectivity should be taken into account in the next studies in MS.”

In commenting on the research, Eric Klawiter, MD, associate professor of neurology, Harvard Medical School and associate neurologist at Massachusetts General Hospital, both in Boston, said the findings offer valuable insights in the use of machine learning and MS imaging.

“This research shows very nicely the power of machine learning and connectivity techniques to differentiate MS phenotypes based on disability level,” he said in an interview.

“The future direction of this work is to develop predictive markers for disability progression and this would have significant impact in how we evaluate newly diagnosed patients and counsel their treatment decisions.”

Dr. Tozlu and Dr. Klawiter had no disclosures to report.

SOURCE: Tozlu C et al. ACTRIMS Forum 2020. Abstract P025.

WEST PALM BEACH, FLA. – A machine learning model that combines data on the brain’s functional connectivity with clinical information such as age, sex and disease duration shows the potential to provide an accurate assessment of clinical impairment in patients with multiple sclerosis (MS).

“This is the first study to show that dynamic functional connectivity is useful to identify the impairment level in MS, and can be used for personalized treatment by clinicians,” first author Ceren Tozlu, PhD, of Weill Cornell Medicine, New York, said in an interview.

“We found out that structural connectivity is the most important feature that distinguishes MS patients from healthy controls, while dynamic functional connectivity was more discriminative compared to the static functional connectivity in MS patient classification regarding their impairment level.”

The findings were presented at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Statistical assessment of the clinical impairment of MS using MRI is hindered by a relatively weak correlation between the impairment and disease burden, such as lesion load.

However, the brain’s functional connectivity network, which is indicative of the disruption of the transmission of signals of gray matter regions, could provide a deeper understanding of connectome-level mechanisms that underlie variability in MS-related impairments, Dr. Tozlu and colleagues say.

With no previous study pulling together multimodal imaging data including static and dynamic functional connectivity to classify MS patients with a clinically significant impairment versus non–clinically significant impairment, Dr. Tozlu and the team sought to build a machine-learning–based model to do so.

For the study, they enrolled 79 patients with MS, including 42 with Expanded Disability Status scores of 2 or higher, representing clinically significant impairment at baseline.

The patients, who had a mean age of 45 years, were 66% female and had a mean disease duration of 12.48 years. The ensemble model that was used incorporated functional connectivity and a clinical dataset of age, sex, and disease duration. Functional connectivity was measured by evaluating blood oxygen level dependent (BOLD) signal activity between 86 FreeSurfer-based gray matter regions.

“Functional connectivity is a statistical correlation (Pearson’s correlation coefficient) between two time series of BOLD signals measured on two distinct region of interest of the brain during MRI scan,” Dr. Tozlu explained. “In our study, BOLD time series were measured using resting-state functional MRI technique that last 7 minutes.”

The ensemble model was able to classify low-adapting MS patients with an area under ROC curve (AUC) of 0.638 and a balanced accuracy of 0.659. The model performed well in accurately classifying the MS patients with clinically significant impairment with a sensitivity of 0.719.

“The models in which we applied functional and structural connectivity showed a high performance in classifying MS patients regarding their impairment level,” Dr. Tozlu said.

She noted that “these models may be extended to predict change in impairment level in a longitudinal study, for instance, identifying MS patients who may have a clinically significant impairment.”

In further evaluating which particular functional connections were most related to MS disease activity, Dr. Tozlu and colleagues found the most discriminative areas were between the right superior parietal and right inferior temporal, between right lateral occipital and left pericalcarine, and between right pericalcarine and right side of frontal pole.

If further validated, the approach could have important, broader clinical implications, Dr. Tozlu said.

“If the validation of these models on a larger dataset is successful, this model may be used to decide for personalized treatment,” Dr. Tozlu added. “The model could offer guidance in providing more powerful treatment for MS patients who may have a clinically significant impairment and less powerful treatment for MS patients who may not have a clinically significant impairment in order to avoid the side effects of treatments.

“Therefore, we believe that dynamics in functional connectivity should be taken into account in the next studies in MS.”

In commenting on the research, Eric Klawiter, MD, associate professor of neurology, Harvard Medical School and associate neurologist at Massachusetts General Hospital, both in Boston, said the findings offer valuable insights in the use of machine learning and MS imaging.

“This research shows very nicely the power of machine learning and connectivity techniques to differentiate MS phenotypes based on disability level,” he said in an interview.

“The future direction of this work is to develop predictive markers for disability progression and this would have significant impact in how we evaluate newly diagnosed patients and counsel their treatment decisions.”

Dr. Tozlu and Dr. Klawiter had no disclosures to report.

SOURCE: Tozlu C et al. ACTRIMS Forum 2020. Abstract P025.