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The Road Less Traveled: Why Rural Dermatology Could Be Your Path After Residency
The Road Less Traveled: Why Rural Dermatology Could Be Your Path After Residency
The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.
What Does Rural Really Mean?
Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term nonmetropolitan is preferred. The US Department of Agriculture’s Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.
A Day in Rural Practice
Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.
Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.
Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.
Hybrid Partnerships and Hospital-Based Practice
Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.
Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.
Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.
The Hub-and-Spoke Model
Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).
The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.
Finding the Right Fit
The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.
Getting Started: A 90-Day Outline
Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2
Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.
Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.
Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.
Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.
Compensation and Career Sustainability
Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.
Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.
Broader Efforts and Community
No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.
Teledermatology and Academic Tracks
Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.
Final Thoughts
So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.
- Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
- Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.
What Does Rural Really Mean?
Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term nonmetropolitan is preferred. The US Department of Agriculture’s Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.
A Day in Rural Practice
Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.
Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.
Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.
Hybrid Partnerships and Hospital-Based Practice
Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.
Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.
Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.
The Hub-and-Spoke Model
Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).
The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.
Finding the Right Fit
The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.
Getting Started: A 90-Day Outline
Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2
Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.
Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.
Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.
Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.
Compensation and Career Sustainability
Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.
Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.
Broader Efforts and Community
No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.
Teledermatology and Academic Tracks
Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.
Final Thoughts
So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.
The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.
What Does Rural Really Mean?
Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term nonmetropolitan is preferred. The US Department of Agriculture’s Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.
A Day in Rural Practice
Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.
Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.
Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.
Hybrid Partnerships and Hospital-Based Practice
Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.
Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.
Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.
The Hub-and-Spoke Model
Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).
The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.
Finding the Right Fit
The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.
Getting Started: A 90-Day Outline
Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2
Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.
Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.
Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.
Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.
Compensation and Career Sustainability
Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.
Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.
Broader Efforts and Community
No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.
Teledermatology and Academic Tracks
Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.
Final Thoughts
So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.
- Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
- Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
- Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
- Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
The Road Less Traveled: Why Rural Dermatology Could Be Your Path After Residency
The Road Less Traveled: Why Rural Dermatology Could Be Your Path After Residency
Cobblestonelike Papules on the Neck
The Diagnosis: Fibroelastolytic Papulosis
Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief.
Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1
Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype.
Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis.
Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1
Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1
Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5
Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6
In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9
- Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
- Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
- Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
- Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
- Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
- Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
- Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
- Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
The Diagnosis: Fibroelastolytic Papulosis
Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief.
Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1
Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype.
Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis.
Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1
Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1
Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5
Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6
In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9
The Diagnosis: Fibroelastolytic Papulosis
Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief.
Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1
Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype.
Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis.
Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1
Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1
Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5
Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6
In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9
- Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
- Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
- Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
- Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
- Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
- Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
- Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
- Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
- Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
- Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
- Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
- Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
- Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
- Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
- Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
- Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
A 76-year-old woman presented to the dermatology clinic for evaluation of a pruritic rash on the posterior lateral neck of several years’ duration. The rash had been slowly worsening and was intermittently symptomatic. Physical examination revealed monomorphous flesh-colored papules coalescing on the neck, yielding a cobblestonelike texture. The patient had been treated previously by dermatology with topical steroids, but symptoms persisted. A punch biopsy of the left lateral neck was performed.
Thoracic Intramedullary Mass Causing Neurologic Weakness
Thoracic Intramedullary Mass Causing Neurologic Weakness
Discussion
A diagnosis of dural arteriovenous fistula (dAVF) was made. Lesions involving the spinal cord are traditionally classified by location as extradural, intradural/extramedullary, or intramedullary. Intramedullary spinal cord abnormalities pose considerable diagnostic and management challenges because of the risks of biopsy in this location and the added potential for morbidity and mortality from improperly treated lesions. Although MRI is the preferred imaging modality, PET/CT and magnetic resonance angiography (MRA) may also help narrow the differential diagnosis and potentially avoid complications from an invasive biopsy.1 This patient’s intramedullary lesion, which represented a dAVF, posed a diagnostic challenge; after diagnosis, it was successfully managed conservatively with dexamethasone and physical therapy.
Intradural tumors account for 2% to 4% of all primary central nervous system (CNS) tumors.2 Ependymomas account for 50% to 60% of intramedullary tumors in adults, while astrocytomas account for about 60% of all lesions in children and adolescents.3,4 The differential diagnosis for intramedullary tumors also includes hemangioblastoma, metastases, primary CNS lymphoma, germ cell tumors, and gangliogliomas.5,6
Intramedullary metastases remain rare, although the incidence is rising with improvements in oncologic and supportive treatments. Autopsy studies conducted decades ago demonstrated that about 0.9% to 2.1% of patients with systemic cancer have intramedullary metastases at death.7,8 In patients with an established history of malignancy, a metastatic intramedullary tumor should be placed higher on the differential diagnosis. Intramedullary metastases most often occur in the setting of widespread metastatic disease. A systematic review of the literature on patients with lung cancer (small cell and non-small cell lung carcinomas) and ≥ 1 intramedullary spinal cord metastasis demonstrated that 55.8% of patients had concurrent brain metastases, 20.0% had leptomeningeal carcinomatosis, and 19.5% had vertebral metastases.9 While about half of all intramedullary metastases are associated with lung cancer, other common malignancies that metastasize to this area include colorectal, breast, and renal cell carcinoma, as well as lymphoma and melanoma primaries.10,11
On imaging, intramedullary metastases often appear as several short, studded segments with surrounding edema, typically out of proportion to the size of the lesion.1 By contrast, astrocytomas and ependymomas often span multiple segments, and enhancement patterns can vary depending on the subtype and grade. Glioblastoma multiforme, or grade 4 IDH wild-type astrocytomas, demonstrate an irregular, heterogeneous pattern of enhancement. Hemangioblastomas vary in size and are classically hypointense to isointense on T1-weighted sequences, isointense to hyperintense on T2-weighted sequences, and demonstrate avid enhancement on T1- postcontrast images. In large hemangioblastomas, flow voids due to prominent vasculature may be visualized.
Numerous nonneoplastic tumor mimics can obscure the differential diagnosis. Vascular malformations, including cavernomas and dAVFs, can also present with enhancement and edema. dAVFs are the most common type of spinal vascular malformation, accounting for about 70% of cases.12 They are supplied by the radiculomeningeal arteries, whereas pial arteriovenous malformations (AVMs) are supplied by the radiculomedullary and radiculopial arteries. On MRI, dAVFs usually have venous congestion with intramedullary edema, which appears as an ill-defined centromedullary hyperintensity on T2-weighted imaging over multiple segments. The spinal cord may appear swollen with atrophic changes in chronic cases. Spinal cord AVMs are rarer and have an intramedullary nidus. They usually demonstrate mixed heterogeneous signal on T1- and T2-weighted imaging due to blood products, while the nidus demonstrates a variable degree of enhancement. Serpiginous flow voids are seen both within the nidus and at the cord surface.
Demyelinating lesions of the spine may be seen in neuroinflammatory conditions such as multiple sclerosis, neuromyelitis optica spectrum disorder, acute transverse myelitis, and acute disseminated encephalomyelitis. In multiple sclerosis, lesions typically extend ≤ 2 vertebral segments in length, cover less than half of the vertebral cross-sectional area, and have a dorsolateral predilection.13 Active lesions may demonstrate enhancement along the rim or in a patchy pattern. In the presence of demyelinating lesions, there may occasionally appear to be an expansile mass with a syrinx.14
Infections such as tuberculosis and neurosarcoidosis should also remain on the differential diagnosis. On MRI, tuberculosis usually involves the thoracic cord and is typically rim-enhancing.15 If there are caseating granulomas, T2-weighted images may also demonstrate rim enhancement.16 Spinal sarcoidosis is unusual without intracranial involvement, and its appearance may include leptomeningeal enhancement, cord expansion, and hyperintense signal on T2- weighted imaging.17
Finally, iatrogenic causes are also possible, including radiation myelopathy and mechanical spinal cord injury. For radiation myelopathy, it is important to ascertain whether a patient has undergone prior radiotherapy in the region and to obtain the pertinent dosimetry. Spinal cord injury may cause a focal signal abnormality within the cord, with T2 hyperintensity; these foci may or may not present with enhancement, edema, or hematoma and therefore may resemble tumors.13
This patient presented with progressive right-sided lower extremity weakness and hypoesthesia and a history of a low-grade right renal/pelvic ureteral tumor. The immediate impression was that the thoracic intramedullary lesion represented a metastatic lesion. However, in the absence of any systemic or intracranial metastases, this progression was much less likely. An extensive interdisciplinary workup was conducted that included medical oncology, neurology, neuroradiology, neuro-oncology, neurosurgery, nuclear medicine, and radiation oncology. Neuroradiology and nuclear medicine identified a slightly hypermetabolic focus on the PET/CT from 1.5 years prior that correlated exactly with the same location as the lesion on the recent spinal MRI. This finding, along with the MRA, confirmed the diagnosis of a dAVF, which was successfully managed conservatively with dexamethasone and physical therapy, rather than through oncologic treatments such as radiotherapy
There remains debate regarding the utility of steroids in treating patients with dAVF. Although there are some case reports documenting that the edema associated with the dAVF responds to steroids, other case series have found that steroids may worsen outcomes in patients with dAVF, possibly due to increased venous hydrostatic pressure.
This case demonstrates the importance of an interdisciplinary workup when evaluating an intramedullary lesion, as well as maintaining a wide differential diagnosis, particularly in the absence of a history of polymetastatic cancer. All the clues (such as the slightly hypermetabolic focus on a PET/CT from 1.5 years prior) need to be obtained to comfortably reach a diagnosis in the absence of pathologic confirmation. These cases can be especially challenging due to the lack of pathologic confirmation, but by understanding the main differentiating features among the various etiologies and obtaining all available information, a correct diagnosis can be made without unnecessary interventions.
- Moghaddam SM, Bhatt AA. Location, length, and enhancement: systematic approach to differentiating intramedullary spinal cord lesions. Insights Imaging. 2018;9:511-526. doi:10.1007/s13244-018-0608-3
- Grimm S, Chamberlain MC. Adult primary spinal cord tumors. Expert Rev Neurother. 2009;9:1487-1495. doi:10.1586/ern.09.101
- Miller DJ, McCutcheon IE. Hemangioblastomas and other uncommon intramedullary tumors. J Neurooncol. 2000;47:253- 270. doi:10.1023/a:1006403500801
- Mottl H, Koutecky J. Treatment of spinal cord tumors in children. Med Pediatr Oncol. 1997;29:293-295.
- Kandemirli SG, Reddy A, Hitchon P, et al. Intramedullary tumours and tumour mimics. Clin Radiol. 2020;75:876.e17-876. e32. doi:10.1016/j.crad.2020.05.010
- Tobin MK, Geraghty JR, Engelhard HH, et al. Intramedullary spinal cord tumors: a review of current and future treatment strategies. Neurosurg Focus. 2015;39:E14. doi:10.3171/2015.5.FOCUS15158
- Chason JL, Walker FB, Landers JW. Metastatic carcinoma in the central nervous system and dorsal root ganglia. A prospective autopsy study. Cancer. 1963;16:781-787.
- Costigan DA, Winkelman MD. Intramedullary spinal cord metastasis. A clinicopathological study of 13 cases. J Neurosurg. 1985;62:227-233.
- Wu L, Wang L, Yang J, et al. Clinical features, treatments, and prognosis of intramedullary spinal cord metastases from lung cancer: a case series and systematic review. Neurospine. 2022;19:65-76. doi:10.14245/ns.2142910.455
- Lv J, Liu B, Quan X, et al. Intramedullary spinal cord metastasis in malignancies: an institutional analysis and review. Onco Targets Ther. 2019;12:4741-4753. doi:10.2147/OTT.S193235
- Goyal A, Yolcu Y, Kerezoudis P, et al. Intramedullary spinal cord metastases: an institutional review of survival and outcomes. J Neurooncol. 2019;142:347-354. doi:10.1007/s11060-019-03105-2
- Krings T. Vascular malformations of the spine and spinal cord: anatomy, classification, treatment. Clin Neuroradiol. 2010;20:5-24. doi:10.1007/s00062-010-9036-6
- Maj E, Wojtowicz K, Aleksandra PP, et al. Intramedullary spinal tumor-like lesions. Acta Radiol. 2019;60:994-1010. doi:10.1177/0284185118809540
- Waziri A, Vonsattel JP, Kaiser MG, et al. Expansile, enhancing cervical cord lesion with an associated syrinx secondary to demyelination. Case report and review of the literature. J Neurosurg Spine. 2007;6:52-56. doi:10.3171/spi.2007.6.1.52
- Nussbaum ES, Rockswold GL, Bergman TA, et al. Spinal tuberculosis: a diagnostic and management challenge. J Neurosurg. 1995;83:243-247. doi:10.3171/jns.1995.83.2.0243
- Lu M. Imaging diagnosis of spinal intramedullary tuberculoma: case reports and literature review. J Spinal Cord Med. 2010;33:159-162. doi:10.1080/10790268.2010.11689691
- Do-Dai DD, Brooks MK, Goldkamp A, et al. Magnetic resonance imaging of intramedullary spinal cord lesions: a pictorial review. Curr Probl Diagn Radiol. 2010;39:160-185. doi:10.1067/j.cpradiol.2009.05.004
Discussion
A diagnosis of dural arteriovenous fistula (dAVF) was made. Lesions involving the spinal cord are traditionally classified by location as extradural, intradural/extramedullary, or intramedullary. Intramedullary spinal cord abnormalities pose considerable diagnostic and management challenges because of the risks of biopsy in this location and the added potential for morbidity and mortality from improperly treated lesions. Although MRI is the preferred imaging modality, PET/CT and magnetic resonance angiography (MRA) may also help narrow the differential diagnosis and potentially avoid complications from an invasive biopsy.1 This patient’s intramedullary lesion, which represented a dAVF, posed a diagnostic challenge; after diagnosis, it was successfully managed conservatively with dexamethasone and physical therapy.
Intradural tumors account for 2% to 4% of all primary central nervous system (CNS) tumors.2 Ependymomas account for 50% to 60% of intramedullary tumors in adults, while astrocytomas account for about 60% of all lesions in children and adolescents.3,4 The differential diagnosis for intramedullary tumors also includes hemangioblastoma, metastases, primary CNS lymphoma, germ cell tumors, and gangliogliomas.5,6
Intramedullary metastases remain rare, although the incidence is rising with improvements in oncologic and supportive treatments. Autopsy studies conducted decades ago demonstrated that about 0.9% to 2.1% of patients with systemic cancer have intramedullary metastases at death.7,8 In patients with an established history of malignancy, a metastatic intramedullary tumor should be placed higher on the differential diagnosis. Intramedullary metastases most often occur in the setting of widespread metastatic disease. A systematic review of the literature on patients with lung cancer (small cell and non-small cell lung carcinomas) and ≥ 1 intramedullary spinal cord metastasis demonstrated that 55.8% of patients had concurrent brain metastases, 20.0% had leptomeningeal carcinomatosis, and 19.5% had vertebral metastases.9 While about half of all intramedullary metastases are associated with lung cancer, other common malignancies that metastasize to this area include colorectal, breast, and renal cell carcinoma, as well as lymphoma and melanoma primaries.10,11
On imaging, intramedullary metastases often appear as several short, studded segments with surrounding edema, typically out of proportion to the size of the lesion.1 By contrast, astrocytomas and ependymomas often span multiple segments, and enhancement patterns can vary depending on the subtype and grade. Glioblastoma multiforme, or grade 4 IDH wild-type astrocytomas, demonstrate an irregular, heterogeneous pattern of enhancement. Hemangioblastomas vary in size and are classically hypointense to isointense on T1-weighted sequences, isointense to hyperintense on T2-weighted sequences, and demonstrate avid enhancement on T1- postcontrast images. In large hemangioblastomas, flow voids due to prominent vasculature may be visualized.
Numerous nonneoplastic tumor mimics can obscure the differential diagnosis. Vascular malformations, including cavernomas and dAVFs, can also present with enhancement and edema. dAVFs are the most common type of spinal vascular malformation, accounting for about 70% of cases.12 They are supplied by the radiculomeningeal arteries, whereas pial arteriovenous malformations (AVMs) are supplied by the radiculomedullary and radiculopial arteries. On MRI, dAVFs usually have venous congestion with intramedullary edema, which appears as an ill-defined centromedullary hyperintensity on T2-weighted imaging over multiple segments. The spinal cord may appear swollen with atrophic changes in chronic cases. Spinal cord AVMs are rarer and have an intramedullary nidus. They usually demonstrate mixed heterogeneous signal on T1- and T2-weighted imaging due to blood products, while the nidus demonstrates a variable degree of enhancement. Serpiginous flow voids are seen both within the nidus and at the cord surface.
Demyelinating lesions of the spine may be seen in neuroinflammatory conditions such as multiple sclerosis, neuromyelitis optica spectrum disorder, acute transverse myelitis, and acute disseminated encephalomyelitis. In multiple sclerosis, lesions typically extend ≤ 2 vertebral segments in length, cover less than half of the vertebral cross-sectional area, and have a dorsolateral predilection.13 Active lesions may demonstrate enhancement along the rim or in a patchy pattern. In the presence of demyelinating lesions, there may occasionally appear to be an expansile mass with a syrinx.14
Infections such as tuberculosis and neurosarcoidosis should also remain on the differential diagnosis. On MRI, tuberculosis usually involves the thoracic cord and is typically rim-enhancing.15 If there are caseating granulomas, T2-weighted images may also demonstrate rim enhancement.16 Spinal sarcoidosis is unusual without intracranial involvement, and its appearance may include leptomeningeal enhancement, cord expansion, and hyperintense signal on T2- weighted imaging.17
Finally, iatrogenic causes are also possible, including radiation myelopathy and mechanical spinal cord injury. For radiation myelopathy, it is important to ascertain whether a patient has undergone prior radiotherapy in the region and to obtain the pertinent dosimetry. Spinal cord injury may cause a focal signal abnormality within the cord, with T2 hyperintensity; these foci may or may not present with enhancement, edema, or hematoma and therefore may resemble tumors.13
This patient presented with progressive right-sided lower extremity weakness and hypoesthesia and a history of a low-grade right renal/pelvic ureteral tumor. The immediate impression was that the thoracic intramedullary lesion represented a metastatic lesion. However, in the absence of any systemic or intracranial metastases, this progression was much less likely. An extensive interdisciplinary workup was conducted that included medical oncology, neurology, neuroradiology, neuro-oncology, neurosurgery, nuclear medicine, and radiation oncology. Neuroradiology and nuclear medicine identified a slightly hypermetabolic focus on the PET/CT from 1.5 years prior that correlated exactly with the same location as the lesion on the recent spinal MRI. This finding, along with the MRA, confirmed the diagnosis of a dAVF, which was successfully managed conservatively with dexamethasone and physical therapy, rather than through oncologic treatments such as radiotherapy
There remains debate regarding the utility of steroids in treating patients with dAVF. Although there are some case reports documenting that the edema associated with the dAVF responds to steroids, other case series have found that steroids may worsen outcomes in patients with dAVF, possibly due to increased venous hydrostatic pressure.
This case demonstrates the importance of an interdisciplinary workup when evaluating an intramedullary lesion, as well as maintaining a wide differential diagnosis, particularly in the absence of a history of polymetastatic cancer. All the clues (such as the slightly hypermetabolic focus on a PET/CT from 1.5 years prior) need to be obtained to comfortably reach a diagnosis in the absence of pathologic confirmation. These cases can be especially challenging due to the lack of pathologic confirmation, but by understanding the main differentiating features among the various etiologies and obtaining all available information, a correct diagnosis can be made without unnecessary interventions.
Discussion
A diagnosis of dural arteriovenous fistula (dAVF) was made. Lesions involving the spinal cord are traditionally classified by location as extradural, intradural/extramedullary, or intramedullary. Intramedullary spinal cord abnormalities pose considerable diagnostic and management challenges because of the risks of biopsy in this location and the added potential for morbidity and mortality from improperly treated lesions. Although MRI is the preferred imaging modality, PET/CT and magnetic resonance angiography (MRA) may also help narrow the differential diagnosis and potentially avoid complications from an invasive biopsy.1 This patient’s intramedullary lesion, which represented a dAVF, posed a diagnostic challenge; after diagnosis, it was successfully managed conservatively with dexamethasone and physical therapy.
Intradural tumors account for 2% to 4% of all primary central nervous system (CNS) tumors.2 Ependymomas account for 50% to 60% of intramedullary tumors in adults, while astrocytomas account for about 60% of all lesions in children and adolescents.3,4 The differential diagnosis for intramedullary tumors also includes hemangioblastoma, metastases, primary CNS lymphoma, germ cell tumors, and gangliogliomas.5,6
Intramedullary metastases remain rare, although the incidence is rising with improvements in oncologic and supportive treatments. Autopsy studies conducted decades ago demonstrated that about 0.9% to 2.1% of patients with systemic cancer have intramedullary metastases at death.7,8 In patients with an established history of malignancy, a metastatic intramedullary tumor should be placed higher on the differential diagnosis. Intramedullary metastases most often occur in the setting of widespread metastatic disease. A systematic review of the literature on patients with lung cancer (small cell and non-small cell lung carcinomas) and ≥ 1 intramedullary spinal cord metastasis demonstrated that 55.8% of patients had concurrent brain metastases, 20.0% had leptomeningeal carcinomatosis, and 19.5% had vertebral metastases.9 While about half of all intramedullary metastases are associated with lung cancer, other common malignancies that metastasize to this area include colorectal, breast, and renal cell carcinoma, as well as lymphoma and melanoma primaries.10,11
On imaging, intramedullary metastases often appear as several short, studded segments with surrounding edema, typically out of proportion to the size of the lesion.1 By contrast, astrocytomas and ependymomas often span multiple segments, and enhancement patterns can vary depending on the subtype and grade. Glioblastoma multiforme, or grade 4 IDH wild-type astrocytomas, demonstrate an irregular, heterogeneous pattern of enhancement. Hemangioblastomas vary in size and are classically hypointense to isointense on T1-weighted sequences, isointense to hyperintense on T2-weighted sequences, and demonstrate avid enhancement on T1- postcontrast images. In large hemangioblastomas, flow voids due to prominent vasculature may be visualized.
Numerous nonneoplastic tumor mimics can obscure the differential diagnosis. Vascular malformations, including cavernomas and dAVFs, can also present with enhancement and edema. dAVFs are the most common type of spinal vascular malformation, accounting for about 70% of cases.12 They are supplied by the radiculomeningeal arteries, whereas pial arteriovenous malformations (AVMs) are supplied by the radiculomedullary and radiculopial arteries. On MRI, dAVFs usually have venous congestion with intramedullary edema, which appears as an ill-defined centromedullary hyperintensity on T2-weighted imaging over multiple segments. The spinal cord may appear swollen with atrophic changes in chronic cases. Spinal cord AVMs are rarer and have an intramedullary nidus. They usually demonstrate mixed heterogeneous signal on T1- and T2-weighted imaging due to blood products, while the nidus demonstrates a variable degree of enhancement. Serpiginous flow voids are seen both within the nidus and at the cord surface.
Demyelinating lesions of the spine may be seen in neuroinflammatory conditions such as multiple sclerosis, neuromyelitis optica spectrum disorder, acute transverse myelitis, and acute disseminated encephalomyelitis. In multiple sclerosis, lesions typically extend ≤ 2 vertebral segments in length, cover less than half of the vertebral cross-sectional area, and have a dorsolateral predilection.13 Active lesions may demonstrate enhancement along the rim or in a patchy pattern. In the presence of demyelinating lesions, there may occasionally appear to be an expansile mass with a syrinx.14
Infections such as tuberculosis and neurosarcoidosis should also remain on the differential diagnosis. On MRI, tuberculosis usually involves the thoracic cord and is typically rim-enhancing.15 If there are caseating granulomas, T2-weighted images may also demonstrate rim enhancement.16 Spinal sarcoidosis is unusual without intracranial involvement, and its appearance may include leptomeningeal enhancement, cord expansion, and hyperintense signal on T2- weighted imaging.17
Finally, iatrogenic causes are also possible, including radiation myelopathy and mechanical spinal cord injury. For radiation myelopathy, it is important to ascertain whether a patient has undergone prior radiotherapy in the region and to obtain the pertinent dosimetry. Spinal cord injury may cause a focal signal abnormality within the cord, with T2 hyperintensity; these foci may or may not present with enhancement, edema, or hematoma and therefore may resemble tumors.13
This patient presented with progressive right-sided lower extremity weakness and hypoesthesia and a history of a low-grade right renal/pelvic ureteral tumor. The immediate impression was that the thoracic intramedullary lesion represented a metastatic lesion. However, in the absence of any systemic or intracranial metastases, this progression was much less likely. An extensive interdisciplinary workup was conducted that included medical oncology, neurology, neuroradiology, neuro-oncology, neurosurgery, nuclear medicine, and radiation oncology. Neuroradiology and nuclear medicine identified a slightly hypermetabolic focus on the PET/CT from 1.5 years prior that correlated exactly with the same location as the lesion on the recent spinal MRI. This finding, along with the MRA, confirmed the diagnosis of a dAVF, which was successfully managed conservatively with dexamethasone and physical therapy, rather than through oncologic treatments such as radiotherapy
There remains debate regarding the utility of steroids in treating patients with dAVF. Although there are some case reports documenting that the edema associated with the dAVF responds to steroids, other case series have found that steroids may worsen outcomes in patients with dAVF, possibly due to increased venous hydrostatic pressure.
This case demonstrates the importance of an interdisciplinary workup when evaluating an intramedullary lesion, as well as maintaining a wide differential diagnosis, particularly in the absence of a history of polymetastatic cancer. All the clues (such as the slightly hypermetabolic focus on a PET/CT from 1.5 years prior) need to be obtained to comfortably reach a diagnosis in the absence of pathologic confirmation. These cases can be especially challenging due to the lack of pathologic confirmation, but by understanding the main differentiating features among the various etiologies and obtaining all available information, a correct diagnosis can be made without unnecessary interventions.
- Moghaddam SM, Bhatt AA. Location, length, and enhancement: systematic approach to differentiating intramedullary spinal cord lesions. Insights Imaging. 2018;9:511-526. doi:10.1007/s13244-018-0608-3
- Grimm S, Chamberlain MC. Adult primary spinal cord tumors. Expert Rev Neurother. 2009;9:1487-1495. doi:10.1586/ern.09.101
- Miller DJ, McCutcheon IE. Hemangioblastomas and other uncommon intramedullary tumors. J Neurooncol. 2000;47:253- 270. doi:10.1023/a:1006403500801
- Mottl H, Koutecky J. Treatment of spinal cord tumors in children. Med Pediatr Oncol. 1997;29:293-295.
- Kandemirli SG, Reddy A, Hitchon P, et al. Intramedullary tumours and tumour mimics. Clin Radiol. 2020;75:876.e17-876. e32. doi:10.1016/j.crad.2020.05.010
- Tobin MK, Geraghty JR, Engelhard HH, et al. Intramedullary spinal cord tumors: a review of current and future treatment strategies. Neurosurg Focus. 2015;39:E14. doi:10.3171/2015.5.FOCUS15158
- Chason JL, Walker FB, Landers JW. Metastatic carcinoma in the central nervous system and dorsal root ganglia. A prospective autopsy study. Cancer. 1963;16:781-787.
- Costigan DA, Winkelman MD. Intramedullary spinal cord metastasis. A clinicopathological study of 13 cases. J Neurosurg. 1985;62:227-233.
- Wu L, Wang L, Yang J, et al. Clinical features, treatments, and prognosis of intramedullary spinal cord metastases from lung cancer: a case series and systematic review. Neurospine. 2022;19:65-76. doi:10.14245/ns.2142910.455
- Lv J, Liu B, Quan X, et al. Intramedullary spinal cord metastasis in malignancies: an institutional analysis and review. Onco Targets Ther. 2019;12:4741-4753. doi:10.2147/OTT.S193235
- Goyal A, Yolcu Y, Kerezoudis P, et al. Intramedullary spinal cord metastases: an institutional review of survival and outcomes. J Neurooncol. 2019;142:347-354. doi:10.1007/s11060-019-03105-2
- Krings T. Vascular malformations of the spine and spinal cord: anatomy, classification, treatment. Clin Neuroradiol. 2010;20:5-24. doi:10.1007/s00062-010-9036-6
- Maj E, Wojtowicz K, Aleksandra PP, et al. Intramedullary spinal tumor-like lesions. Acta Radiol. 2019;60:994-1010. doi:10.1177/0284185118809540
- Waziri A, Vonsattel JP, Kaiser MG, et al. Expansile, enhancing cervical cord lesion with an associated syrinx secondary to demyelination. Case report and review of the literature. J Neurosurg Spine. 2007;6:52-56. doi:10.3171/spi.2007.6.1.52
- Nussbaum ES, Rockswold GL, Bergman TA, et al. Spinal tuberculosis: a diagnostic and management challenge. J Neurosurg. 1995;83:243-247. doi:10.3171/jns.1995.83.2.0243
- Lu M. Imaging diagnosis of spinal intramedullary tuberculoma: case reports and literature review. J Spinal Cord Med. 2010;33:159-162. doi:10.1080/10790268.2010.11689691
- Do-Dai DD, Brooks MK, Goldkamp A, et al. Magnetic resonance imaging of intramedullary spinal cord lesions: a pictorial review. Curr Probl Diagn Radiol. 2010;39:160-185. doi:10.1067/j.cpradiol.2009.05.004
- Moghaddam SM, Bhatt AA. Location, length, and enhancement: systematic approach to differentiating intramedullary spinal cord lesions. Insights Imaging. 2018;9:511-526. doi:10.1007/s13244-018-0608-3
- Grimm S, Chamberlain MC. Adult primary spinal cord tumors. Expert Rev Neurother. 2009;9:1487-1495. doi:10.1586/ern.09.101
- Miller DJ, McCutcheon IE. Hemangioblastomas and other uncommon intramedullary tumors. J Neurooncol. 2000;47:253- 270. doi:10.1023/a:1006403500801
- Mottl H, Koutecky J. Treatment of spinal cord tumors in children. Med Pediatr Oncol. 1997;29:293-295.
- Kandemirli SG, Reddy A, Hitchon P, et al. Intramedullary tumours and tumour mimics. Clin Radiol. 2020;75:876.e17-876. e32. doi:10.1016/j.crad.2020.05.010
- Tobin MK, Geraghty JR, Engelhard HH, et al. Intramedullary spinal cord tumors: a review of current and future treatment strategies. Neurosurg Focus. 2015;39:E14. doi:10.3171/2015.5.FOCUS15158
- Chason JL, Walker FB, Landers JW. Metastatic carcinoma in the central nervous system and dorsal root ganglia. A prospective autopsy study. Cancer. 1963;16:781-787.
- Costigan DA, Winkelman MD. Intramedullary spinal cord metastasis. A clinicopathological study of 13 cases. J Neurosurg. 1985;62:227-233.
- Wu L, Wang L, Yang J, et al. Clinical features, treatments, and prognosis of intramedullary spinal cord metastases from lung cancer: a case series and systematic review. Neurospine. 2022;19:65-76. doi:10.14245/ns.2142910.455
- Lv J, Liu B, Quan X, et al. Intramedullary spinal cord metastasis in malignancies: an institutional analysis and review. Onco Targets Ther. 2019;12:4741-4753. doi:10.2147/OTT.S193235
- Goyal A, Yolcu Y, Kerezoudis P, et al. Intramedullary spinal cord metastases: an institutional review of survival and outcomes. J Neurooncol. 2019;142:347-354. doi:10.1007/s11060-019-03105-2
- Krings T. Vascular malformations of the spine and spinal cord: anatomy, classification, treatment. Clin Neuroradiol. 2010;20:5-24. doi:10.1007/s00062-010-9036-6
- Maj E, Wojtowicz K, Aleksandra PP, et al. Intramedullary spinal tumor-like lesions. Acta Radiol. 2019;60:994-1010. doi:10.1177/0284185118809540
- Waziri A, Vonsattel JP, Kaiser MG, et al. Expansile, enhancing cervical cord lesion with an associated syrinx secondary to demyelination. Case report and review of the literature. J Neurosurg Spine. 2007;6:52-56. doi:10.3171/spi.2007.6.1.52
- Nussbaum ES, Rockswold GL, Bergman TA, et al. Spinal tuberculosis: a diagnostic and management challenge. J Neurosurg. 1995;83:243-247. doi:10.3171/jns.1995.83.2.0243
- Lu M. Imaging diagnosis of spinal intramedullary tuberculoma: case reports and literature review. J Spinal Cord Med. 2010;33:159-162. doi:10.1080/10790268.2010.11689691
- Do-Dai DD, Brooks MK, Goldkamp A, et al. Magnetic resonance imaging of intramedullary spinal cord lesions: a pictorial review. Curr Probl Diagn Radiol. 2010;39:160-185. doi:10.1067/j.cpradiol.2009.05.004
Thoracic Intramedullary Mass Causing Neurologic Weakness
Thoracic Intramedullary Mass Causing Neurologic Weakness
An 87-year-old man presented to the emergency department reporting a 1-month history of right lower extremity weakness, progressing to an inability to ambulate. The patient had a history of hyperlipidemia, hypertension, benign prostatic hyperplasia, chronic obstructive pulmonary disease, low-grade right urothelial carcinoma status postbiopsy 2 years earlier, and atrial fibrillation following cardioversion 6 years earlier without anticoagulation therapy. He also reported severe right groin pain and increasing urinary obstruction.
On admission, neurology evaluated the patient’s lower extremity strength as 5/5 on his left, 1/5 on his right hip, and 2/5 on his right knee, with hypoesthesia of his right lower extremity. Computed tomography (CT) with contrast of the chest, abdomen, and pelvis demonstrated moderate to severe right-sided hydronephrosis, possibly due to a proximal right ureteric mass; no evidence of systemic metastases was found. He underwent a gadolinium-enhanced magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine, which showed a mass at T7-T8, a mass effect in the central cord, and abnormal spinal cord enhancement from T7 through the conus medullaris. A review of fluorodeoxyglucose- 18 (FDG-18) positron emission tomography (PET)-CT imaging from 1.5 years prior showed a low-grade focus (Figures 1-3). A gadolinium-enhanced brain MRI did not demonstrate any intracranial metastatic disease, acute infarct, hemorrhage, mass effect, or extra-axial fluid collections.



Early Infantile Hemangioma Diagnosis Is Key in Skin of Color
Early Infantile Hemangioma Diagnosis Is Key in Skin of Color
Richard P. Usatine, MD
Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.1 It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.2 It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.1-3
Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).4 In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.4 Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.3 Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.5-7
Epidemiology
Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.1 The most common type is superficial IH, typically found on the head or neck.5 Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.1,3
Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.
Key Clinical Features
Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.5 Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.5
Worth Noting
Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.2,3
The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent life-threatening complications.1-3
Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.10 It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.11 As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.1,4,10
For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.4,10
Health Disparity Highlight
Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.12
A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.6 Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.6 Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.6
An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).7
These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.
- Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
- Mitra R, Fitzsimons HL, Hale T, et al. Recent advances in understanding the molecular basis of infantile haemangioma development. Br J Dermatol. 2024;191:661-669.
- Rodríguez Bandera AI, Sebaratnam DF, Wargon O, et al. Infantile hemangioma. Part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392.
- Sebaratnam DF, Rodríguez Bandera AL, Wong LCF, et al. Infantile hemangioma. Part 2: management. J Am Acad Dermatol. 2021;85:1395-1404.
- Taye ME, Shah J, Seiverling EV, et al. Diagnosis of vascular anomalies in patients with skin of color. J Clin Aesthet Dermatol. 2024;17:54-62.
- Lie E, Psoter KJ, Püttgen KB. Lower socioeconomic status is associated with delayed access to care for infantile hemangioma: a cohort study. J Am Acad Dermatol. 2023;88:E221-E230.
- Kumar KD, Desai AD, Shah VP, et al. Racial discrepancies in presentation of hospitalized infantile hemangioma cases using the Kids’ Inpatient Database. Health Sci Rep. 2023;6:E1092.
- Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567.
- Léauté-Labrèze C, Baselga Torres E, Weibel L, et al. The infantile hemangioma referral score: a validated tool for physicians. Pediatrics. 2020;145:E20191628.
- Macca L, Altavilla D, Di Bartolomeo L, et al. Update on treatment of infantile hemangiomas: what’s new in the last five years? Front Pharmacol. 2022;13:879602.
- Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475.
- Frieden IJ, Püttgen KB, Drolet BA, et al. Management of infantile hemangiomas during the COVID pandemic. Pediatr Dermatol. 2020;37:412-418.
Richard P. Usatine, MD
Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.1 It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.2 It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.1-3
Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).4 In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.4 Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.3 Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.5-7
Epidemiology
Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.1 The most common type is superficial IH, typically found on the head or neck.5 Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.1,3
Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.
Key Clinical Features
Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.5 Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.5
Worth Noting
Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.2,3
The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent life-threatening complications.1-3
Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.10 It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.11 As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.1,4,10
For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.4,10
Health Disparity Highlight
Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.12
A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.6 Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.6 Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.6
An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).7
These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.
Richard P. Usatine, MD
Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.1 It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.2 It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.1-3
Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).4 In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.4 Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.3 Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.5-7
Epidemiology
Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.1 The most common type is superficial IH, typically found on the head or neck.5 Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.1,3
Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.
Key Clinical Features
Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.5 Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.5
Worth Noting
Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.2,3
The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent life-threatening complications.1-3
Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.10 It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.11 As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.1,4,10
For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.4,10
Health Disparity Highlight
Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.12
A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.6 Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.6 Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.6
An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).7
These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.
- Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
- Mitra R, Fitzsimons HL, Hale T, et al. Recent advances in understanding the molecular basis of infantile haemangioma development. Br J Dermatol. 2024;191:661-669.
- Rodríguez Bandera AI, Sebaratnam DF, Wargon O, et al. Infantile hemangioma. Part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392.
- Sebaratnam DF, Rodríguez Bandera AL, Wong LCF, et al. Infantile hemangioma. Part 2: management. J Am Acad Dermatol. 2021;85:1395-1404.
- Taye ME, Shah J, Seiverling EV, et al. Diagnosis of vascular anomalies in patients with skin of color. J Clin Aesthet Dermatol. 2024;17:54-62.
- Lie E, Psoter KJ, Püttgen KB. Lower socioeconomic status is associated with delayed access to care for infantile hemangioma: a cohort study. J Am Acad Dermatol. 2023;88:E221-E230.
- Kumar KD, Desai AD, Shah VP, et al. Racial discrepancies in presentation of hospitalized infantile hemangioma cases using the Kids’ Inpatient Database. Health Sci Rep. 2023;6:E1092.
- Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567.
- Léauté-Labrèze C, Baselga Torres E, Weibel L, et al. The infantile hemangioma referral score: a validated tool for physicians. Pediatrics. 2020;145:E20191628.
- Macca L, Altavilla D, Di Bartolomeo L, et al. Update on treatment of infantile hemangiomas: what’s new in the last five years? Front Pharmacol. 2022;13:879602.
- Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475.
- Frieden IJ, Püttgen KB, Drolet BA, et al. Management of infantile hemangiomas during the COVID pandemic. Pediatr Dermatol. 2020;37:412-418.
- Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
- Mitra R, Fitzsimons HL, Hale T, et al. Recent advances in understanding the molecular basis of infantile haemangioma development. Br J Dermatol. 2024;191:661-669.
- Rodríguez Bandera AI, Sebaratnam DF, Wargon O, et al. Infantile hemangioma. Part 1: epidemiology, pathogenesis, clinical presentation and assessment. J Am Acad Dermatol. 2021;85:1379-1392.
- Sebaratnam DF, Rodríguez Bandera AL, Wong LCF, et al. Infantile hemangioma. Part 2: management. J Am Acad Dermatol. 2021;85:1395-1404.
- Taye ME, Shah J, Seiverling EV, et al. Diagnosis of vascular anomalies in patients with skin of color. J Clin Aesthet Dermatol. 2024;17:54-62.
- Lie E, Psoter KJ, Püttgen KB. Lower socioeconomic status is associated with delayed access to care for infantile hemangioma: a cohort study. J Am Acad Dermatol. 2023;88:E221-E230.
- Kumar KD, Desai AD, Shah VP, et al. Racial discrepancies in presentation of hospitalized infantile hemangioma cases using the Kids’ Inpatient Database. Health Sci Rep. 2023;6:E1092.
- Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567.
- Léauté-Labrèze C, Baselga Torres E, Weibel L, et al. The infantile hemangioma referral score: a validated tool for physicians. Pediatrics. 2020;145:E20191628.
- Macca L, Altavilla D, Di Bartolomeo L, et al. Update on treatment of infantile hemangiomas: what’s new in the last five years? Front Pharmacol. 2022;13:879602.
- Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143:E20183475.
- Frieden IJ, Püttgen KB, Drolet BA, et al. Management of infantile hemangiomas during the COVID pandemic. Pediatr Dermatol. 2020;37:412-418.
Early Infantile Hemangioma Diagnosis Is Key in Skin of Color
Early Infantile Hemangioma Diagnosis Is Key in Skin of Color
Following the Hyperkalemia Trail: A Case Report of ECG Changes and Treatment Responses
Following the Hyperkalemia Trail: A Case Report of ECG Changes and Treatment Responses
Hyperkalemia involves elevated serum potassium levels (> 5.0 mEq/L) and represents an important electrolyte disturbance due to its potentially severe consequences, including cardiac effects that can lead to dysrhythmia and even asystole and death.1,2 In a US Medicare population, the prevalence of hyperkalemia has been estimated at 2.7% and is associated with substantial health care costs.3 The prevalence is even more marked in patients with preexisting conditions such as chronic kidney disease (CKD) and heart failure.4,5
Hyperkalemia can result from multiple factors, including impaired renal function, adrenal disease, adverse drug reactions of angiotensin-converting enzyme inhibitors (ACEIs) and other medications, and heritable mutations.6 Hyperkalemia poses a considerable clinical risk, associated with adverse outcomes such as myocardial infarction and increased mortality in patients with CKD.5,7,8 Electrocardiographic (ECG) changes associated with hyperkalemia play a vital role in guiding clinical decisions and treatment strategies.9 Understanding the pathophysiology, risk factors, and consequences of hyperkalemia, as well as the significance of ECG changes in its management, is essential for health care practitioners.
Case Presentation
An 81-year-old Hispanic man with a history of hypertension, hypothyroidism, gout, and CKD stage 3B presented to the emergency department with progressive weakness resulting in falls and culminating in an inability to ambulate independently. Additional symptoms included nausea, diarrhea, and myalgia. His vital signs were notable for a pulse of 41 beats/min. The physical examination was remarkable for significant weakness of the bilateral upper extremities, inability to bear his own weight, and bilateral lower extremity edema. His initial ECG upon arrival showed bradycardia with wide QRS, absent P waves, and peaked T waves (Figure 1a). These findings differed from his baseline ECG taken 1 year earlier, which showed sinus rhythm with premature atrial complexes and an old right bundle branch block (Figure 1b).

Medication review revealed that the patient was currently prescribed 100 mg allopurinol daily, 2.5 mg amlodipine daily, 10 mg atorvastatin at bedtime, 4 mg doxazosin daily, 112 mcg levothyroxine daily, 100 mg losartan daily, 25 mg metoprolol daily, and 0.4 mg tamsulosin daily. The patient had also been taking over-the-counter indomethacin for knee pain.
Based on the ECG results, he was treated with 0.083%/6 mL nebulized albuterol, 4.65 Mq/250 mL saline solution intravenous (IV) calcium gluconate, 10 units IV insulin with concomitant 50%/25 mL IV dextrose and 8.4 g of oral patiromer suspension. IV furosemide was held due to concern for renal function. The decision to proceed with hemodialysis was made. Repeat laboratory tests were performed, and an ECG obtained after treatment initiation but prior to hemodialysis demonstrated improvement of rate and T wave shortening (Figure 1c). The serum potassium level dropped from 9.8 mEq/L to 7.9 mEq/L (reference range, 3.5-5.0 mEq/L) (Table 1).

In addition to hemodialysis, sodium zirconium 10 g orally 3 times daily was added. Laboratory test results and an ECG was performed after dialysis continued to demonstrate improvement (Figure 1d). The patient’s potassium level decreased to 5.8 mEq/L, with the ECG demonstrating stability of heart rate and further improvement of the PR interval, QRS complex, and T waves.
Despite the established treatment regimen, potassium levels again rose to 6.7 mEq/L, but there were no significant changes in the ECG, and thus no medication changes were made (Figure 1e). Subsequent monitoring demonstrated a further increase in potassium to 7.4 mEq/L, with an ECG demonstrating a return to the baseline of 1 year prior. The patient underwent hemodialysis again and was given oral furosemide 60 mg every 12 hours. The potassium concentration after dialysis decreased to 4.7 mEq/L and remained stable, not going above 5.0 mEq/L on subsequent monitoring. The patient had resolution of all symptoms and was discharged.
Discussion
We have described in detail the presentation of each pathology and mechanisms of each treatment, starting with the patient’s initial condition that brought him to the emergency room—muscle weakness. Skeletal muscle weakness is a common manifestation of hyperkalemia, occurring in 20% to 40% of cases, and is more prevalent in severe elevations of potassium. Rarely, the weakness can progress to flaccid paralysis of the patient’s extremities and, in extreme cases, the diaphragm.
Muscle weakness progression occurs in a manner that resembles Guillain-Barré syndrome, starting in the lower extremities and ascending toward the upper extremities.10 This is known as secondary hyperkalemic periodic paralysis. Hyperkalemia lowers the transmembrane gradient in neurons, leading to neuronal depolarization independent of the degree of hyperkalemia. If the degree of hyperkalemia is large enough, this depolarization inactivates voltage-gated sodium channels, making neurons refractory to excitation. Electromyographical studies have shown reduction in the compounded muscle action potential.11 The transient nature of this paralysis is reflected by rapid correction of weakness and paralysis when the electrolyte disorder is corrected.
The patient in this case also presented with bradycardia. The ECG manifestations of hyperkalemia can include atrial asystole, intraventricular conduction disturbances, peaked T waves, and widened QRS complexes. However, some patients with renal insufficiency may not exhibit ECG changes despite significantly elevated serum potassium levels.12
The severity of hyperkalemia is crucial in determining the associated ECG changes, with levels > 6.0 mEq/L presenting with abnormalities.13 ECG findings alone may not always accurately reflect the severity of hyperkalemia, as up to 60% of patients with potassium levels > 6.0 mEq/L may not show ECG changes.14 Additionally, extreme hyperkalemia can lead to inconsistent ECG findings, making it challenging to rely solely on ECG for diagnosis and monitoring.8 The level of potassium that causes these effects varies widely through patient populations.
The main mechanism by which hyperkalemia affects the heart’s conduction system is through voltage differences across the conduction fibers and eventual steady-state inactivation of sodium channels. This combination of mechanisms shortens the action potential duration, allowing more cardiomyocytes to undergo synchronized depolarization. This amalgamation of cardiomyocytes repolarizing can be reflected on ECGs as peaked T waves. As the action potential decreases, there is a period during which cardiomyocytes are prone to tachyarrhythmias and ventricular fibrillation.
A reduced action potential may lead to increased rates of depolarization and thus conduction, which in some scenarios may increase heart rate. As the levels of potassium rise, intracellular accumulation impedes the entry of sodium by decreasing the cation gradient across the cell membrane. This effectively slows the sinus nodes and prolongs the QRS by slowing the overall propagation of action potentials. By this mechanism, conduction delays, blocks, or asystole are manifested. The patient in this case showed conduction delays, peaked T waves, and disappearance of P waves when he first arrived.
Hyperkalemia Treatment
Hyperkalemia develops most commonly due to acute or chronic kidney diseases, as was the case with this patient. The patient’s hyperkalemia was also augmented by the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which can directly affect renal function. A properly functioning kidney is responsible for excretion of up to 90% of ingested potassium, while the remainder is excreted through the gastrointestinal (GI) tract. Definitive treatment of hyperkalemia is mitigated primarily through these 2 organ systems. The treatment also includes transitory mechanisms of potassium reduction. The goal of each method is to preserve the action potential of cardiomyocytes and myocytes. This patient presented with acute symptomatic hyperkalemia and received various medications to acutely, transitorily, and definitively treat it.
Initial therapy included calcium gluconate, which functions to stabilize the myocardial cell membrane. Hyperkalemia decreases the resting membrane action potential of excitable cells and predisposes them to early depolarization and thus dysrhythmias. Calcium decreases the threshold potential across cells and offsets the overall gradient back to near normal levels.15 Calcium can be delivered through calcium gluconate or calcium chloride. Calcium chloride is not preferred because extravasation can cause pain, blistering and tissue ischemia. Central venous access is required, potentially delaying prompt treatment. Calcium acts rapidly after administration—within 1 to 3 minutes—but only lasts 30 to 60 minutes.16 Administration of calcium gluconate can be repeated as often as necessary, but patients must be monitored for adverse effects of calcium such as nausea, abdominal pain, polydipsia, polyuria, muscle weakness, and paresthesia. Care must be taken when patients are taking digoxin, because calcium may potentiate toxicity.17 Although calcium provides immediate benefits it does little to correct the underlying cause; other medications are required to remove potassium from the body.
Two medication classes have been proven to shift potassium intracellularly. The first are β-2 agonists, such as albuterol/levalbuterol, and the second is insulin. Both work through sodium-potassium-ATPase in a direct manner. β-2 agonists stimulate sodium-potassium-ATPase to move more potassium intracellularly, but these effects have been seen only with high doses of albuterol, typically 4× the standard dose of 0.5 mg in nebulized solutions to achieve decreases in potassium of 0.3 to 0.6 mEq/L, although some trials have reported decreases of 0.62 to 0.98 mEq/L.15,18 These potassium-lowering effects of β-2 agonist are modest, but can be seen 20 to 30 minutes after administration and persist up to 1 to 2 hours. β-2 agonists are also readily affected by β blockers, which may reduce or negate the desired effect in hyperkalemia. For these reasons, a β-2 agonist should not be given as monotherapy and should be provided as an adjuvant to more independent therapies such as insulin. Insulin binds to receptors on muscle cells and increases the quantity of sodium-potassium-ATPase and glucose transporters. With this increase in influx pumps, surrounding tissues with higher resting membrane potentials can absorb the potassium load, thereby protecting cardiomyocytes.
Potassium Removal
Three methods are currently available to remove potassium from the body: GI excretion, renal excretion, and direct removal from the bloodstream. Under normal physiologic conditions, the kidneys account for about 90% of the body’s ability to remove potassium. Loop diuretics facilitate the removal of potassium by increasing urine production and have an additional potassium-wasting effect. Although the onset of action of loop diuretics is typically 30 to 60 minutes after oral administration, their effect can last for several hours. In this patient, furosemide was introduced later in the treatment plan to manage recurring hyperkalemia by enhancing renal potassium excretion.
Potassium binders such as patiromer act in the GI tract, effectively reducing serum potassium levels although with a slower onset of action than furosemide, generally taking hours to days to exert its effect. Both medications illustrate a tailored approach to managing potassium levels, adapted to the evolving needs and renal function of the patient. The last method is using hemodialysis—by far the most rapid method to remove potassium, but also the most invasive. The different methods of treating hyperkalemia are summarized in Table 2. This patient required multiple days of hemodialysis to completely correct the electrolyte disorder. Upon discharge, the patient continued oral furosemide 40 mg daily and eventually discontinued hemodialysis due to stable renal function.

Often, after correcting an inciting event, potassium stores in the body eventually stabilize and do not require additional follow-up. Patients prone to hyperkalemia should be thoroughly educated on medications to avoid (NSAIDs, ACEIs/ARBs, trimethoprim), an adequate low potassium diet, and symptoms that may warrant medical attention.19
Conclusions
This case illustrates the importance of recognizing the spectrum of manifestations of hyperkalemia, which ranged from muscle weakness to cardiac dysrhythmias. Management strategies for the patient included stabilization of cardiac membranes, potassium shifting, and potassium removal, each tailored to the patient’s individual clinical findings.
The case further illustrates the critical role of continuous monitoring and dynamic adjustment of therapeutic strategies in response to evolving clinical and laboratory findings. The initial and subsequent ECGs, alongside laboratory tests, were instrumental in guiding the adjustments needed in the treatment regimen, ensuring both the efficacy and safety of the interventions. This proactive approach can mitigate the risk of recurrent hyperkalemia and its complications.
- Youn JH, McDonough AA. Recent advances in understanding integrative control of potassium homeostasis. Annu Rev Physiol. 2009;71:381-401. doi:10.1146/annurev.physiol.010908.163241 2.
- Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. In: StatPearls. StatPearls Publishing; September 4, 2023. Accessed October 22, 2025.
- Mu F, Betts KA, Woolley JM, et al. Prevalence and economic burden of hyperkalemia in the United States Medicare population. Curr Med Res Opin. 2020;36:1333-1341. doi:10.1080/03007995.2020.1775072
- Loutradis C, Tolika P, Skodra A, et al. Prevalence of hyperkalemia in diabetic and non-diabetic patients with chronic kidney disease: a nested case-control study. Am J Nephrol. 2015;42:351-360. doi:10.1159/000442393
- Grodzinsky A, Goyal A, Gosch K, et al. Prevalence and prognosis of hyperkalemia in patients with acute myocardial infarction. Am J Med. 2016;129:858-865. doi:10.1016/j.amjmed.2016.03.008
- Hunter RW, Bailey MA. Hyperkalemia: pathophysiology, risk factors and consequences. Nephrol Dial Transplant. 2019;34(suppl 3):iii2-iii11. doi:10.1093/ndt/gfz206
- Luo J, Brunelli SM, Jensen DE, Yang A. Association between serum potassium and outcomes in patients with reduced kidney function. Clin J Am Soc Nephrol. 2016;11:90-100. doi:10.2215/CJN.01730215
- Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28:3155-3165. doi:10.1681/ASN.2016121344
- Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000;18:721-729. doi:10.1053/ajem.2000.7344
- Kimmons LA, Usery JB. Acute ascending muscle weakness secondary to medication-induced hyperkalemia. Case Rep Med. 2014;2014:789529. doi:10.1155/2014/789529
- Naik KR, Saroja AO, Khanpet MS. Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis. Ann Indian Acad Neurol. 2012;15:339-343. doi:10.4103/0972-2327.104354
- Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3:324-330. doi:10.2215/CJN.04611007
- Larivée NL, Michaud JB, More KM, Wilson JA, Tennankore KK. Hyperkalemia: prevalence, predictors and emerging treatments. Cardiol Ther. 2023;12:35-63. doi:10.1007/s40119-022-00289-z
- Shingarev R, Allon M. A physiologic-based approach to the treatment of acute hyperkalemia. Am J Kidney Dis. 2010;56:578-584. doi:10.1053/j.ajkd.2010.03.014
- Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33:40-47.
- Ng KE, Lee CS. Updated treatment options in the management of hyperkalemia. U.S. Pharmacist. February 16, 2017. Accessed October 1, 2025. www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia
- Quick G, Bastani B. Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae. Ann Emerg Med. 1994;24:305-311. doi:10.1016/s0196-0644(94)70144-x 18.
- Allon M, Dunlay R, Copkney C. Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Ann Intern Med. 1989;110:426-429. doi:10.7326/0003-4819-110-6-42619.
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4 suppl):S117-S314. doi:10.1016/j.kint.2023.10.018
Hyperkalemia involves elevated serum potassium levels (> 5.0 mEq/L) and represents an important electrolyte disturbance due to its potentially severe consequences, including cardiac effects that can lead to dysrhythmia and even asystole and death.1,2 In a US Medicare population, the prevalence of hyperkalemia has been estimated at 2.7% and is associated with substantial health care costs.3 The prevalence is even more marked in patients with preexisting conditions such as chronic kidney disease (CKD) and heart failure.4,5
Hyperkalemia can result from multiple factors, including impaired renal function, adrenal disease, adverse drug reactions of angiotensin-converting enzyme inhibitors (ACEIs) and other medications, and heritable mutations.6 Hyperkalemia poses a considerable clinical risk, associated with adverse outcomes such as myocardial infarction and increased mortality in patients with CKD.5,7,8 Electrocardiographic (ECG) changes associated with hyperkalemia play a vital role in guiding clinical decisions and treatment strategies.9 Understanding the pathophysiology, risk factors, and consequences of hyperkalemia, as well as the significance of ECG changes in its management, is essential for health care practitioners.
Case Presentation
An 81-year-old Hispanic man with a history of hypertension, hypothyroidism, gout, and CKD stage 3B presented to the emergency department with progressive weakness resulting in falls and culminating in an inability to ambulate independently. Additional symptoms included nausea, diarrhea, and myalgia. His vital signs were notable for a pulse of 41 beats/min. The physical examination was remarkable for significant weakness of the bilateral upper extremities, inability to bear his own weight, and bilateral lower extremity edema. His initial ECG upon arrival showed bradycardia with wide QRS, absent P waves, and peaked T waves (Figure 1a). These findings differed from his baseline ECG taken 1 year earlier, which showed sinus rhythm with premature atrial complexes and an old right bundle branch block (Figure 1b).

Medication review revealed that the patient was currently prescribed 100 mg allopurinol daily, 2.5 mg amlodipine daily, 10 mg atorvastatin at bedtime, 4 mg doxazosin daily, 112 mcg levothyroxine daily, 100 mg losartan daily, 25 mg metoprolol daily, and 0.4 mg tamsulosin daily. The patient had also been taking over-the-counter indomethacin for knee pain.
Based on the ECG results, he was treated with 0.083%/6 mL nebulized albuterol, 4.65 Mq/250 mL saline solution intravenous (IV) calcium gluconate, 10 units IV insulin with concomitant 50%/25 mL IV dextrose and 8.4 g of oral patiromer suspension. IV furosemide was held due to concern for renal function. The decision to proceed with hemodialysis was made. Repeat laboratory tests were performed, and an ECG obtained after treatment initiation but prior to hemodialysis demonstrated improvement of rate and T wave shortening (Figure 1c). The serum potassium level dropped from 9.8 mEq/L to 7.9 mEq/L (reference range, 3.5-5.0 mEq/L) (Table 1).

In addition to hemodialysis, sodium zirconium 10 g orally 3 times daily was added. Laboratory test results and an ECG was performed after dialysis continued to demonstrate improvement (Figure 1d). The patient’s potassium level decreased to 5.8 mEq/L, with the ECG demonstrating stability of heart rate and further improvement of the PR interval, QRS complex, and T waves.
Despite the established treatment regimen, potassium levels again rose to 6.7 mEq/L, but there were no significant changes in the ECG, and thus no medication changes were made (Figure 1e). Subsequent monitoring demonstrated a further increase in potassium to 7.4 mEq/L, with an ECG demonstrating a return to the baseline of 1 year prior. The patient underwent hemodialysis again and was given oral furosemide 60 mg every 12 hours. The potassium concentration after dialysis decreased to 4.7 mEq/L and remained stable, not going above 5.0 mEq/L on subsequent monitoring. The patient had resolution of all symptoms and was discharged.
Discussion
We have described in detail the presentation of each pathology and mechanisms of each treatment, starting with the patient’s initial condition that brought him to the emergency room—muscle weakness. Skeletal muscle weakness is a common manifestation of hyperkalemia, occurring in 20% to 40% of cases, and is more prevalent in severe elevations of potassium. Rarely, the weakness can progress to flaccid paralysis of the patient’s extremities and, in extreme cases, the diaphragm.
Muscle weakness progression occurs in a manner that resembles Guillain-Barré syndrome, starting in the lower extremities and ascending toward the upper extremities.10 This is known as secondary hyperkalemic periodic paralysis. Hyperkalemia lowers the transmembrane gradient in neurons, leading to neuronal depolarization independent of the degree of hyperkalemia. If the degree of hyperkalemia is large enough, this depolarization inactivates voltage-gated sodium channels, making neurons refractory to excitation. Electromyographical studies have shown reduction in the compounded muscle action potential.11 The transient nature of this paralysis is reflected by rapid correction of weakness and paralysis when the electrolyte disorder is corrected.
The patient in this case also presented with bradycardia. The ECG manifestations of hyperkalemia can include atrial asystole, intraventricular conduction disturbances, peaked T waves, and widened QRS complexes. However, some patients with renal insufficiency may not exhibit ECG changes despite significantly elevated serum potassium levels.12
The severity of hyperkalemia is crucial in determining the associated ECG changes, with levels > 6.0 mEq/L presenting with abnormalities.13 ECG findings alone may not always accurately reflect the severity of hyperkalemia, as up to 60% of patients with potassium levels > 6.0 mEq/L may not show ECG changes.14 Additionally, extreme hyperkalemia can lead to inconsistent ECG findings, making it challenging to rely solely on ECG for diagnosis and monitoring.8 The level of potassium that causes these effects varies widely through patient populations.
The main mechanism by which hyperkalemia affects the heart’s conduction system is through voltage differences across the conduction fibers and eventual steady-state inactivation of sodium channels. This combination of mechanisms shortens the action potential duration, allowing more cardiomyocytes to undergo synchronized depolarization. This amalgamation of cardiomyocytes repolarizing can be reflected on ECGs as peaked T waves. As the action potential decreases, there is a period during which cardiomyocytes are prone to tachyarrhythmias and ventricular fibrillation.
A reduced action potential may lead to increased rates of depolarization and thus conduction, which in some scenarios may increase heart rate. As the levels of potassium rise, intracellular accumulation impedes the entry of sodium by decreasing the cation gradient across the cell membrane. This effectively slows the sinus nodes and prolongs the QRS by slowing the overall propagation of action potentials. By this mechanism, conduction delays, blocks, or asystole are manifested. The patient in this case showed conduction delays, peaked T waves, and disappearance of P waves when he first arrived.
Hyperkalemia Treatment
Hyperkalemia develops most commonly due to acute or chronic kidney diseases, as was the case with this patient. The patient’s hyperkalemia was also augmented by the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which can directly affect renal function. A properly functioning kidney is responsible for excretion of up to 90% of ingested potassium, while the remainder is excreted through the gastrointestinal (GI) tract. Definitive treatment of hyperkalemia is mitigated primarily through these 2 organ systems. The treatment also includes transitory mechanisms of potassium reduction. The goal of each method is to preserve the action potential of cardiomyocytes and myocytes. This patient presented with acute symptomatic hyperkalemia and received various medications to acutely, transitorily, and definitively treat it.
Initial therapy included calcium gluconate, which functions to stabilize the myocardial cell membrane. Hyperkalemia decreases the resting membrane action potential of excitable cells and predisposes them to early depolarization and thus dysrhythmias. Calcium decreases the threshold potential across cells and offsets the overall gradient back to near normal levels.15 Calcium can be delivered through calcium gluconate or calcium chloride. Calcium chloride is not preferred because extravasation can cause pain, blistering and tissue ischemia. Central venous access is required, potentially delaying prompt treatment. Calcium acts rapidly after administration—within 1 to 3 minutes—but only lasts 30 to 60 minutes.16 Administration of calcium gluconate can be repeated as often as necessary, but patients must be monitored for adverse effects of calcium such as nausea, abdominal pain, polydipsia, polyuria, muscle weakness, and paresthesia. Care must be taken when patients are taking digoxin, because calcium may potentiate toxicity.17 Although calcium provides immediate benefits it does little to correct the underlying cause; other medications are required to remove potassium from the body.
Two medication classes have been proven to shift potassium intracellularly. The first are β-2 agonists, such as albuterol/levalbuterol, and the second is insulin. Both work through sodium-potassium-ATPase in a direct manner. β-2 agonists stimulate sodium-potassium-ATPase to move more potassium intracellularly, but these effects have been seen only with high doses of albuterol, typically 4× the standard dose of 0.5 mg in nebulized solutions to achieve decreases in potassium of 0.3 to 0.6 mEq/L, although some trials have reported decreases of 0.62 to 0.98 mEq/L.15,18 These potassium-lowering effects of β-2 agonist are modest, but can be seen 20 to 30 minutes after administration and persist up to 1 to 2 hours. β-2 agonists are also readily affected by β blockers, which may reduce or negate the desired effect in hyperkalemia. For these reasons, a β-2 agonist should not be given as monotherapy and should be provided as an adjuvant to more independent therapies such as insulin. Insulin binds to receptors on muscle cells and increases the quantity of sodium-potassium-ATPase and glucose transporters. With this increase in influx pumps, surrounding tissues with higher resting membrane potentials can absorb the potassium load, thereby protecting cardiomyocytes.
Potassium Removal
Three methods are currently available to remove potassium from the body: GI excretion, renal excretion, and direct removal from the bloodstream. Under normal physiologic conditions, the kidneys account for about 90% of the body’s ability to remove potassium. Loop diuretics facilitate the removal of potassium by increasing urine production and have an additional potassium-wasting effect. Although the onset of action of loop diuretics is typically 30 to 60 minutes after oral administration, their effect can last for several hours. In this patient, furosemide was introduced later in the treatment plan to manage recurring hyperkalemia by enhancing renal potassium excretion.
Potassium binders such as patiromer act in the GI tract, effectively reducing serum potassium levels although with a slower onset of action than furosemide, generally taking hours to days to exert its effect. Both medications illustrate a tailored approach to managing potassium levels, adapted to the evolving needs and renal function of the patient. The last method is using hemodialysis—by far the most rapid method to remove potassium, but also the most invasive. The different methods of treating hyperkalemia are summarized in Table 2. This patient required multiple days of hemodialysis to completely correct the electrolyte disorder. Upon discharge, the patient continued oral furosemide 40 mg daily and eventually discontinued hemodialysis due to stable renal function.

Often, after correcting an inciting event, potassium stores in the body eventually stabilize and do not require additional follow-up. Patients prone to hyperkalemia should be thoroughly educated on medications to avoid (NSAIDs, ACEIs/ARBs, trimethoprim), an adequate low potassium diet, and symptoms that may warrant medical attention.19
Conclusions
This case illustrates the importance of recognizing the spectrum of manifestations of hyperkalemia, which ranged from muscle weakness to cardiac dysrhythmias. Management strategies for the patient included stabilization of cardiac membranes, potassium shifting, and potassium removal, each tailored to the patient’s individual clinical findings.
The case further illustrates the critical role of continuous monitoring and dynamic adjustment of therapeutic strategies in response to evolving clinical and laboratory findings. The initial and subsequent ECGs, alongside laboratory tests, were instrumental in guiding the adjustments needed in the treatment regimen, ensuring both the efficacy and safety of the interventions. This proactive approach can mitigate the risk of recurrent hyperkalemia and its complications.
Hyperkalemia involves elevated serum potassium levels (> 5.0 mEq/L) and represents an important electrolyte disturbance due to its potentially severe consequences, including cardiac effects that can lead to dysrhythmia and even asystole and death.1,2 In a US Medicare population, the prevalence of hyperkalemia has been estimated at 2.7% and is associated with substantial health care costs.3 The prevalence is even more marked in patients with preexisting conditions such as chronic kidney disease (CKD) and heart failure.4,5
Hyperkalemia can result from multiple factors, including impaired renal function, adrenal disease, adverse drug reactions of angiotensin-converting enzyme inhibitors (ACEIs) and other medications, and heritable mutations.6 Hyperkalemia poses a considerable clinical risk, associated with adverse outcomes such as myocardial infarction and increased mortality in patients with CKD.5,7,8 Electrocardiographic (ECG) changes associated with hyperkalemia play a vital role in guiding clinical decisions and treatment strategies.9 Understanding the pathophysiology, risk factors, and consequences of hyperkalemia, as well as the significance of ECG changes in its management, is essential for health care practitioners.
Case Presentation
An 81-year-old Hispanic man with a history of hypertension, hypothyroidism, gout, and CKD stage 3B presented to the emergency department with progressive weakness resulting in falls and culminating in an inability to ambulate independently. Additional symptoms included nausea, diarrhea, and myalgia. His vital signs were notable for a pulse of 41 beats/min. The physical examination was remarkable for significant weakness of the bilateral upper extremities, inability to bear his own weight, and bilateral lower extremity edema. His initial ECG upon arrival showed bradycardia with wide QRS, absent P waves, and peaked T waves (Figure 1a). These findings differed from his baseline ECG taken 1 year earlier, which showed sinus rhythm with premature atrial complexes and an old right bundle branch block (Figure 1b).

Medication review revealed that the patient was currently prescribed 100 mg allopurinol daily, 2.5 mg amlodipine daily, 10 mg atorvastatin at bedtime, 4 mg doxazosin daily, 112 mcg levothyroxine daily, 100 mg losartan daily, 25 mg metoprolol daily, and 0.4 mg tamsulosin daily. The patient had also been taking over-the-counter indomethacin for knee pain.
Based on the ECG results, he was treated with 0.083%/6 mL nebulized albuterol, 4.65 Mq/250 mL saline solution intravenous (IV) calcium gluconate, 10 units IV insulin with concomitant 50%/25 mL IV dextrose and 8.4 g of oral patiromer suspension. IV furosemide was held due to concern for renal function. The decision to proceed with hemodialysis was made. Repeat laboratory tests were performed, and an ECG obtained after treatment initiation but prior to hemodialysis demonstrated improvement of rate and T wave shortening (Figure 1c). The serum potassium level dropped from 9.8 mEq/L to 7.9 mEq/L (reference range, 3.5-5.0 mEq/L) (Table 1).

In addition to hemodialysis, sodium zirconium 10 g orally 3 times daily was added. Laboratory test results and an ECG was performed after dialysis continued to demonstrate improvement (Figure 1d). The patient’s potassium level decreased to 5.8 mEq/L, with the ECG demonstrating stability of heart rate and further improvement of the PR interval, QRS complex, and T waves.
Despite the established treatment regimen, potassium levels again rose to 6.7 mEq/L, but there were no significant changes in the ECG, and thus no medication changes were made (Figure 1e). Subsequent monitoring demonstrated a further increase in potassium to 7.4 mEq/L, with an ECG demonstrating a return to the baseline of 1 year prior. The patient underwent hemodialysis again and was given oral furosemide 60 mg every 12 hours. The potassium concentration after dialysis decreased to 4.7 mEq/L and remained stable, not going above 5.0 mEq/L on subsequent monitoring. The patient had resolution of all symptoms and was discharged.
Discussion
We have described in detail the presentation of each pathology and mechanisms of each treatment, starting with the patient’s initial condition that brought him to the emergency room—muscle weakness. Skeletal muscle weakness is a common manifestation of hyperkalemia, occurring in 20% to 40% of cases, and is more prevalent in severe elevations of potassium. Rarely, the weakness can progress to flaccid paralysis of the patient’s extremities and, in extreme cases, the diaphragm.
Muscle weakness progression occurs in a manner that resembles Guillain-Barré syndrome, starting in the lower extremities and ascending toward the upper extremities.10 This is known as secondary hyperkalemic periodic paralysis. Hyperkalemia lowers the transmembrane gradient in neurons, leading to neuronal depolarization independent of the degree of hyperkalemia. If the degree of hyperkalemia is large enough, this depolarization inactivates voltage-gated sodium channels, making neurons refractory to excitation. Electromyographical studies have shown reduction in the compounded muscle action potential.11 The transient nature of this paralysis is reflected by rapid correction of weakness and paralysis when the electrolyte disorder is corrected.
The patient in this case also presented with bradycardia. The ECG manifestations of hyperkalemia can include atrial asystole, intraventricular conduction disturbances, peaked T waves, and widened QRS complexes. However, some patients with renal insufficiency may not exhibit ECG changes despite significantly elevated serum potassium levels.12
The severity of hyperkalemia is crucial in determining the associated ECG changes, with levels > 6.0 mEq/L presenting with abnormalities.13 ECG findings alone may not always accurately reflect the severity of hyperkalemia, as up to 60% of patients with potassium levels > 6.0 mEq/L may not show ECG changes.14 Additionally, extreme hyperkalemia can lead to inconsistent ECG findings, making it challenging to rely solely on ECG for diagnosis and monitoring.8 The level of potassium that causes these effects varies widely through patient populations.
The main mechanism by which hyperkalemia affects the heart’s conduction system is through voltage differences across the conduction fibers and eventual steady-state inactivation of sodium channels. This combination of mechanisms shortens the action potential duration, allowing more cardiomyocytes to undergo synchronized depolarization. This amalgamation of cardiomyocytes repolarizing can be reflected on ECGs as peaked T waves. As the action potential decreases, there is a period during which cardiomyocytes are prone to tachyarrhythmias and ventricular fibrillation.
A reduced action potential may lead to increased rates of depolarization and thus conduction, which in some scenarios may increase heart rate. As the levels of potassium rise, intracellular accumulation impedes the entry of sodium by decreasing the cation gradient across the cell membrane. This effectively slows the sinus nodes and prolongs the QRS by slowing the overall propagation of action potentials. By this mechanism, conduction delays, blocks, or asystole are manifested. The patient in this case showed conduction delays, peaked T waves, and disappearance of P waves when he first arrived.
Hyperkalemia Treatment
Hyperkalemia develops most commonly due to acute or chronic kidney diseases, as was the case with this patient. The patient’s hyperkalemia was also augmented by the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which can directly affect renal function. A properly functioning kidney is responsible for excretion of up to 90% of ingested potassium, while the remainder is excreted through the gastrointestinal (GI) tract. Definitive treatment of hyperkalemia is mitigated primarily through these 2 organ systems. The treatment also includes transitory mechanisms of potassium reduction. The goal of each method is to preserve the action potential of cardiomyocytes and myocytes. This patient presented with acute symptomatic hyperkalemia and received various medications to acutely, transitorily, and definitively treat it.
Initial therapy included calcium gluconate, which functions to stabilize the myocardial cell membrane. Hyperkalemia decreases the resting membrane action potential of excitable cells and predisposes them to early depolarization and thus dysrhythmias. Calcium decreases the threshold potential across cells and offsets the overall gradient back to near normal levels.15 Calcium can be delivered through calcium gluconate or calcium chloride. Calcium chloride is not preferred because extravasation can cause pain, blistering and tissue ischemia. Central venous access is required, potentially delaying prompt treatment. Calcium acts rapidly after administration—within 1 to 3 minutes—but only lasts 30 to 60 minutes.16 Administration of calcium gluconate can be repeated as often as necessary, but patients must be monitored for adverse effects of calcium such as nausea, abdominal pain, polydipsia, polyuria, muscle weakness, and paresthesia. Care must be taken when patients are taking digoxin, because calcium may potentiate toxicity.17 Although calcium provides immediate benefits it does little to correct the underlying cause; other medications are required to remove potassium from the body.
Two medication classes have been proven to shift potassium intracellularly. The first are β-2 agonists, such as albuterol/levalbuterol, and the second is insulin. Both work through sodium-potassium-ATPase in a direct manner. β-2 agonists stimulate sodium-potassium-ATPase to move more potassium intracellularly, but these effects have been seen only with high doses of albuterol, typically 4× the standard dose of 0.5 mg in nebulized solutions to achieve decreases in potassium of 0.3 to 0.6 mEq/L, although some trials have reported decreases of 0.62 to 0.98 mEq/L.15,18 These potassium-lowering effects of β-2 agonist are modest, but can be seen 20 to 30 minutes after administration and persist up to 1 to 2 hours. β-2 agonists are also readily affected by β blockers, which may reduce or negate the desired effect in hyperkalemia. For these reasons, a β-2 agonist should not be given as monotherapy and should be provided as an adjuvant to more independent therapies such as insulin. Insulin binds to receptors on muscle cells and increases the quantity of sodium-potassium-ATPase and glucose transporters. With this increase in influx pumps, surrounding tissues with higher resting membrane potentials can absorb the potassium load, thereby protecting cardiomyocytes.
Potassium Removal
Three methods are currently available to remove potassium from the body: GI excretion, renal excretion, and direct removal from the bloodstream. Under normal physiologic conditions, the kidneys account for about 90% of the body’s ability to remove potassium. Loop diuretics facilitate the removal of potassium by increasing urine production and have an additional potassium-wasting effect. Although the onset of action of loop diuretics is typically 30 to 60 minutes after oral administration, their effect can last for several hours. In this patient, furosemide was introduced later in the treatment plan to manage recurring hyperkalemia by enhancing renal potassium excretion.
Potassium binders such as patiromer act in the GI tract, effectively reducing serum potassium levels although with a slower onset of action than furosemide, generally taking hours to days to exert its effect. Both medications illustrate a tailored approach to managing potassium levels, adapted to the evolving needs and renal function of the patient. The last method is using hemodialysis—by far the most rapid method to remove potassium, but also the most invasive. The different methods of treating hyperkalemia are summarized in Table 2. This patient required multiple days of hemodialysis to completely correct the electrolyte disorder. Upon discharge, the patient continued oral furosemide 40 mg daily and eventually discontinued hemodialysis due to stable renal function.

Often, after correcting an inciting event, potassium stores in the body eventually stabilize and do not require additional follow-up. Patients prone to hyperkalemia should be thoroughly educated on medications to avoid (NSAIDs, ACEIs/ARBs, trimethoprim), an adequate low potassium diet, and symptoms that may warrant medical attention.19
Conclusions
This case illustrates the importance of recognizing the spectrum of manifestations of hyperkalemia, which ranged from muscle weakness to cardiac dysrhythmias. Management strategies for the patient included stabilization of cardiac membranes, potassium shifting, and potassium removal, each tailored to the patient’s individual clinical findings.
The case further illustrates the critical role of continuous monitoring and dynamic adjustment of therapeutic strategies in response to evolving clinical and laboratory findings. The initial and subsequent ECGs, alongside laboratory tests, were instrumental in guiding the adjustments needed in the treatment regimen, ensuring both the efficacy and safety of the interventions. This proactive approach can mitigate the risk of recurrent hyperkalemia and its complications.
- Youn JH, McDonough AA. Recent advances in understanding integrative control of potassium homeostasis. Annu Rev Physiol. 2009;71:381-401. doi:10.1146/annurev.physiol.010908.163241 2.
- Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. In: StatPearls. StatPearls Publishing; September 4, 2023. Accessed October 22, 2025.
- Mu F, Betts KA, Woolley JM, et al. Prevalence and economic burden of hyperkalemia in the United States Medicare population. Curr Med Res Opin. 2020;36:1333-1341. doi:10.1080/03007995.2020.1775072
- Loutradis C, Tolika P, Skodra A, et al. Prevalence of hyperkalemia in diabetic and non-diabetic patients with chronic kidney disease: a nested case-control study. Am J Nephrol. 2015;42:351-360. doi:10.1159/000442393
- Grodzinsky A, Goyal A, Gosch K, et al. Prevalence and prognosis of hyperkalemia in patients with acute myocardial infarction. Am J Med. 2016;129:858-865. doi:10.1016/j.amjmed.2016.03.008
- Hunter RW, Bailey MA. Hyperkalemia: pathophysiology, risk factors and consequences. Nephrol Dial Transplant. 2019;34(suppl 3):iii2-iii11. doi:10.1093/ndt/gfz206
- Luo J, Brunelli SM, Jensen DE, Yang A. Association between serum potassium and outcomes in patients with reduced kidney function. Clin J Am Soc Nephrol. 2016;11:90-100. doi:10.2215/CJN.01730215
- Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28:3155-3165. doi:10.1681/ASN.2016121344
- Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000;18:721-729. doi:10.1053/ajem.2000.7344
- Kimmons LA, Usery JB. Acute ascending muscle weakness secondary to medication-induced hyperkalemia. Case Rep Med. 2014;2014:789529. doi:10.1155/2014/789529
- Naik KR, Saroja AO, Khanpet MS. Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis. Ann Indian Acad Neurol. 2012;15:339-343. doi:10.4103/0972-2327.104354
- Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3:324-330. doi:10.2215/CJN.04611007
- Larivée NL, Michaud JB, More KM, Wilson JA, Tennankore KK. Hyperkalemia: prevalence, predictors and emerging treatments. Cardiol Ther. 2023;12:35-63. doi:10.1007/s40119-022-00289-z
- Shingarev R, Allon M. A physiologic-based approach to the treatment of acute hyperkalemia. Am J Kidney Dis. 2010;56:578-584. doi:10.1053/j.ajkd.2010.03.014
- Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33:40-47.
- Ng KE, Lee CS. Updated treatment options in the management of hyperkalemia. U.S. Pharmacist. February 16, 2017. Accessed October 1, 2025. www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia
- Quick G, Bastani B. Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae. Ann Emerg Med. 1994;24:305-311. doi:10.1016/s0196-0644(94)70144-x 18.
- Allon M, Dunlay R, Copkney C. Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Ann Intern Med. 1989;110:426-429. doi:10.7326/0003-4819-110-6-42619.
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4 suppl):S117-S314. doi:10.1016/j.kint.2023.10.018
- Youn JH, McDonough AA. Recent advances in understanding integrative control of potassium homeostasis. Annu Rev Physiol. 2009;71:381-401. doi:10.1146/annurev.physiol.010908.163241 2.
- Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. In: StatPearls. StatPearls Publishing; September 4, 2023. Accessed October 22, 2025.
- Mu F, Betts KA, Woolley JM, et al. Prevalence and economic burden of hyperkalemia in the United States Medicare population. Curr Med Res Opin. 2020;36:1333-1341. doi:10.1080/03007995.2020.1775072
- Loutradis C, Tolika P, Skodra A, et al. Prevalence of hyperkalemia in diabetic and non-diabetic patients with chronic kidney disease: a nested case-control study. Am J Nephrol. 2015;42:351-360. doi:10.1159/000442393
- Grodzinsky A, Goyal A, Gosch K, et al. Prevalence and prognosis of hyperkalemia in patients with acute myocardial infarction. Am J Med. 2016;129:858-865. doi:10.1016/j.amjmed.2016.03.008
- Hunter RW, Bailey MA. Hyperkalemia: pathophysiology, risk factors and consequences. Nephrol Dial Transplant. 2019;34(suppl 3):iii2-iii11. doi:10.1093/ndt/gfz206
- Luo J, Brunelli SM, Jensen DE, Yang A. Association between serum potassium and outcomes in patients with reduced kidney function. Clin J Am Soc Nephrol. 2016;11:90-100. doi:10.2215/CJN.01730215
- Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28:3155-3165. doi:10.1681/ASN.2016121344
- Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000;18:721-729. doi:10.1053/ajem.2000.7344
- Kimmons LA, Usery JB. Acute ascending muscle weakness secondary to medication-induced hyperkalemia. Case Rep Med. 2014;2014:789529. doi:10.1155/2014/789529
- Naik KR, Saroja AO, Khanpet MS. Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis. Ann Indian Acad Neurol. 2012;15:339-343. doi:10.4103/0972-2327.104354
- Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3:324-330. doi:10.2215/CJN.04611007
- Larivée NL, Michaud JB, More KM, Wilson JA, Tennankore KK. Hyperkalemia: prevalence, predictors and emerging treatments. Cardiol Ther. 2023;12:35-63. doi:10.1007/s40119-022-00289-z
- Shingarev R, Allon M. A physiologic-based approach to the treatment of acute hyperkalemia. Am J Kidney Dis. 2010;56:578-584. doi:10.1053/j.ajkd.2010.03.014
- Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33:40-47.
- Ng KE, Lee CS. Updated treatment options in the management of hyperkalemia. U.S. Pharmacist. February 16, 2017. Accessed October 1, 2025. www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia
- Quick G, Bastani B. Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae. Ann Emerg Med. 1994;24:305-311. doi:10.1016/s0196-0644(94)70144-x 18.
- Allon M, Dunlay R, Copkney C. Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Ann Intern Med. 1989;110:426-429. doi:10.7326/0003-4819-110-6-42619.
- Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4 suppl):S117-S314. doi:10.1016/j.kint.2023.10.018
Following the Hyperkalemia Trail: A Case Report of ECG Changes and Treatment Responses
Following the Hyperkalemia Trail: A Case Report of ECG Changes and Treatment Responses
Evaluation of Pharmacist-Driven Inhaled Corticosteroid De-escalation in Veterans
Evaluation of Pharmacist-Driven Inhaled Corticosteroid De-escalation in Veterans
Systemic glucocorticoids play an important role in the treatment of chronic obstructive pulmonary disease (COPD) exacerbations. They are recommended to shorten recovery time and increase forced expiratory volume in 1 second (FEV1) during exacerbations.1 However, the role of the chronic use of inhaled corticosteroids (ICSs) in the treatment of COPD is less clear.
When added to inhaled β-2 agonists and muscarinic antagonists, ICSs can decrease the risk of exacerbations.1 However, not all patients with COPD benefit from ICS therapy. The degree of benefit an ICS can provide has been shown to correlate with eosinophil count—a marker of inflammation. The expected benefit of using an ICS increases as the eosinophil count increases.1 Maximum benefit can be observed with eosinophil counts ≥ 300 cells/µL, and minimal benefit is observed with eosinophil counts < 100 cells/µL. Adverse effects (AEs) of ICSs include a hoarse voice, oral candidiasis, and an increased risk of pneumonia.1 Given the risk of AEs, it is important to limit ICS use in patients who are unlikely to reap any benefits.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest the use of ICSs in patients who experience exacerbations while using long-acting β agonist (LABA) plus long-acting muscarinic antagonist (LAMA) therapy and have an eosinophil count ≥ 100 cells/µL. Switching from LABA or LAMA monotherapy to triple therapy with LAMA/LABA/ICS may be considered if patients have continued exacerbations and an eosinophil count ≥ 300 cells/µL. De-escalation of ICS therapy should be considered if patients do not meet these criteria or if patients experience ICS AEs, such as pneumonia. The patients most likely to have increased exacerbations or decreased FEV1 with ICS withdrawal are those with eosinophil counts ≥ 300 cells/µL.1,2
Several studies have explored the effects of ICS de-escalation in real-world clinical settings. A systematic review of 11 studies indicated that de-escalation of ICS in COPD does not result in increased exacerbations.3 A prospective study by Rossi et al found that in a 6-month period, 141 of 482 patients on ICS therapy (29%) had an exacerbation. In the opposing arm of the study, 88 of 334 patients (26%) with deprescribed ICS experienced an exacerbation. The difference between these 2 groups was not statistically significant.4 The researchers concluded that in real-world practice, ICS withdrawal can be safe in patients at low risk of exacerbation.
About 25% of veterans (1.25 million) have been diagnosed with COPD.5 To address this, the US Department of Veterans Affairs (VA) and US Department of Defense published updated COPD guidelines in 2021 that specify criteria for de-escalation of ICS.6 Guidelines, however, may not be reflected in common clinical practice for several years following publication. The VA Academic Detailing Service (ADS) provides tools to help clinicians identify patients who may benefit from changes in treatment plans. A recent ADS focus was the implementation of a COPD dashboard, which identifies patients with COPD who are candidates for ICS de-escalation based on comorbid diagnoses, exacerbation history, and eosinophil count. VA pharmacists have an expanded role in the management of primary care disease states and are therefore well-positioned to increase adherence to guideline-directed therapy. The objective of this quality improvement project was to determine the impact of pharmacist-driven de-escalation on ICS usage in veterans with COPD.
Methods
This project was conducted in an outpatient clinic at the Robley Rex VA Medical Center beginning September 21, 2023, with a progress note in the Computerized Patient Record System (CPRS). Eligible patients were selected using the COPD Dashboard provided by ADS. The COPD Dashboard defined patients with COPD as those with ≥ 2 outpatient COPD diagnoses in the past 2 years, 1 inpatient discharge COPD diagnosis in the past year, or COPD listed as an active problem. COPD diagnoses were identified using International Statistical Classification of Disease, Tenth Revision (ICD-10) codes
Candidates identified for ICS de-escalation by the dashboard were excluded if they had a history of COPD exacerbation in the previous 2 years. The dashboard identified COPD exacerbations via ICD-10 codes for COPD or acute respiratory failure for inpatient discharges, emergency department (ED) visits, urgent care visits, and community care consults with 1 of the following terms: emergency, inpatient, hospital, urgent, ED (self). The COPD dashboard excluded patients with a diagnosis of asthma.
After patients were selected, they were screened for additional exclusion criteria. Patients were excluded if a pulmonary care practitioner managed their COPD; if identified via an active pulmonary consult in CPRS; if a non-VA clinician prescribed their ICS; or if they were being treated with roflumilast, theophylline, or chronic azithromycin. Individuals taking these 3 drugs were excluded due to potential severe and/or refractory COPD. Patients also were excluded if they: (1) had prior ICS de-escalation failure (defined as a COPD exacerbation following ICS de-escalation that resulted in ICS resumption); (2) had a COPD exacerbation requiring systemic corticosteroids or antibiotics in the previous year; (3) had active lung cancer; (4) did not have any eosinophil levels in CPRS within the previous 2 years; or (5) had any eosinophil levels ≥ 300 cells/µL in the previous year.
Each patient who met the inclusion criteria and was not excluded received a focused medication review by a pharmacist who created a templated progress note, with patient-specific recommendations, that was entered in the CPRS (eAppendix). The recommendations were also attached as an addendum to the patient’s last primary care visit note, and the primary care practitioner (PCP) was alerted via CPRS to consider ICS de-escalation and non-ICS alternatives. Tapering of ICS therapy was offered as an option to de-escalate if abrupt discontinuation was deemed inappropriate. PCPs were also prompted to consider referral to a primary care clinical pharmacy specialist for management and follow-up of ICS de-escalation.
The primary outcome was the number of patients with de-escalated ICS at 3 and 6 months following the recommendation. Secondary outcomes included the number of: patients who were no longer prescribed an ICS or who had a non-ICS alternative initiated at a pharmacist’s recommendation; patients who were referred to a primary care clinical pharmacy specialist for ICS de-escalation; COPD exacerbations requiring systemic steroids or antibiotics, or requiring an ED visit, inpatient admission, or urgent-care clinic visit; and cases of pneumonia or oral candidiasis. Primary and secondary outcomes were evaluated via chart review in CPRS. For secondary outcomes of pneumonia and COPD exacerbation, identification was made by documented diagnosis in CPRS. For continuous data such as age, the mean was calculated.
Results
Pharmacist ICS de-escalation recommendations were made between September 21, 2023, and November 19, 2023, for 106 patients. The mean age was 72 years and 99 (93%) patients were male (Table 1). Forty-one (39%) of the patients used tobacco at the time of the study. FEV1 was available for 69 patients with a mean of 63% (GOLD grade 2).1 Based on FEV1 values, 16 patients had mild COPD (GOLD grade 1), 37 patients had moderate COPD (GOLD grade 2), 14 patients had severe COPD (GOLD grade 3), and 2 patients had very severe COPD (GOLD grade 4).1 Thirty-four patients received LABA + LAMA + ICS, 65 received LABA + ICS, 2 received LAMA + ICS, and 5 received ICS monotherapy. The most common dose of ICS was a moderate dose (Table 2). Only 2 patients had an ICS AE in the previous year.


ICS de-escalation recommendations resulted in ICS de-escalation in 50 (47.2%) and 62 (58.5%) patients at 3 and 6 months, respectively. The 6-month ICS de-escalation rate by ICS dose at baseline was 72.2% (high dose), 60.0% (moderate), and 30.8% (low). De-escalation at 6 months by GOLD grade at baseline was 56.3% (9 of 16 patients, GOLD 1), 64.9% (24 of 37 patients, GOLD 2), 50% (7 of 14 patients, GOLD 3), and 50% (1 of 2 patients, GOLD 4). Six months after the ICS de-escalation recommendation appeared in the CPRS, the percentage of patients on LABA + ICS therapy dropped from 65 patients (61.3%) at baseline to 25 patients (23.6%).
Secondary outcomes were assessed at 3 and 6 months following the recommendation. Most patients with de-escalated ICS had their ICS discontinued and a non-ICS alternative initiated per pharmacist recommendations. At 6 months, 39 patients (36.8%) patients were referred to a patient aligned care team (PACT) pharmacist for de-escalation. Of the 39 patients referred to pharmacists, 69.2% (27 patients) were de-escalated; this compared to 52.2% (35 patients) who were not referred to pharmacists (Table 3).

ICS use increases the risk of pneumonia.1 At 6 months, 11 patients were diagnosed with pneumonia; 3 patients were diagnosed with pneumonia twice, resulting in a total of 14 cases. Ten cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation. One patient had a documented case of oral candidiasis that occurred while on ICS therapy; no patients with discontinued ICS were diagnosed with oral candidiasis. In addition, 10 patients had COPD exacerbations; however no patients had exacerbations both before and after de-escalation. Six patients were on ICS therapy when they experienced an exacerbation, and 4 patients had an exacerbation after ICS de-escalation.
Discussion
More than half of patients receiving the pharmacist intervention achieved the primary outcome of ICS de-escalation at 6 months. Furthermore, a larger percentage of patients referred to pharmacists for the management of ICS de-escalation successfully achieved de-escalation compared to those who were not referred. These outcomes reflect the important role pharmacists can play in identifying appropriate candidates for ICS de-escalation and assisting in the management of ICS de-escalation. Patients referred to pharmacists also received other services such as smoking cessation pharmacotherapy and counseling on inhaler technique and adherence. These interventions can support improved COPD clinical outcomes.
The purpose of de-escalating ICS therapy is to reduce the risk of AEs such as pneumonia and oral candidiasis.1 The secondary outcomes of this study support previous evidence that patients who have de-escalated ICS therapy may have reduced risk of AEs compared to those who remain on ICS therapy.3 Specifically, of the 14 cases of pneumonia that occurred during the study, 10 cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation.
ICS de-escalation may increase risk of increased COPD exacerbations.1 However, the secondary outcomes of this study do not indicate that those with de-escalated ICS had more COPD exacerbations compared to those who continued on ICS. Pharmacists’ recommendations were more effective for patients with less severe COPD based on baseline FEV1.
The previous GOLD Guidelines for COPD suggested LABA + ICS therapy as an option for patients with a high symptom and exacerbation burden (previously known as GOLD Group D). Guidelines no longer recommend LABA + ICS therapy due to the superiority of triple inhaled therapy for exacerbations and the superiority of LAMA + LABA therapy for dyspnea.7 A majority of identified patients in this project were on LABA + ICS therapy alone at baseline. The ICS de-escalation recommendation resulted in a 61.5% reduction in patients on LABA + ICS therapy at 6 months. By decreasing the number of patients on LABA + ICS without LAMA, recommendations increased the number of patients on guideline-directed therapy.
Limitations
This study lacked a control group, and the rate of ICS de-escalation in patients who did not receive a pharmacist recommendation was not assessed. Therefore, it could not be determined whether the pharmacist recommendation is more effective than no recommendation. Another limitation was our inability to access records from non-VA health care facilities. This may have resulted in missed COPD exacerbations, pneumonia, and oral candidiasis prior to or following the pharmacist recommendation.
In addition, the method used to notify PCPs of the pharmacist recommendation was a CPRS alert. Clinicians often receive multiple daily alerts and may not always pay close attention to them due to alert fatigue. Early in the study, some PCPs were unknowingly omitted from the alert of the pharmacist recommendation for 10 patients due to human error. For 8 of these 10 patients, the PCP was notified of the recommendations during the 3-month follow-up period. However, 2 patients had COPD exacerbations during the 3-month follow-up period. In these cases, the PCP was not alerted to de-escalate ICS. The data for these patients were collected at 3 and 6 months in the same manner as all other patients. Also, 7 of 35 patients who were referred to a pharmacist for ICS de-escalation did not have a scheduled appointment. These patients were considered to be lost to follow-up and this may have resulted in an underestimation of the ability of pharmacists to successfully de-escalate ICS in patients with COPD.
Other studies have evaluated the efficacy of a pharmacy-driven ICS de-escalation.8,9 Hegland et al reported ICS de-escalation for 22% of 141 eligible ambulatory patients with COPD on triple inhaled therapy following pharmacist appointments.8 A study by Hahn et al resulted in 63.8% of 58 patients with COPD being maintained off ICS following a pharmacist de-escalation initiative.9 However, these studies relied upon more time-consuming de-escalation interventions, including at least 1 phone, video, or in-person patient visit.8,9
This project used a single chart review and templated progress note to recommend ICS de-escalation and achieved similar or improved de-escalation rates compared to previous studies.8,9 Previous studies were conducted prior to the updated 2023 GOLD guidelines for COPD which no longer recommend LABA + ICS therapy. This project addressed ICS de-escalation in patients on LABA + ICS therapy in addition to those on triple inhaled therapy. Additionally, previous studies did not address rates of moderate to severe COPD exacerbation and adverse events to ICS following the pharmacist intervention.8,9
This study included COPD exacerbations and cases of pneumonia or oral candidiasis as secondary outcomes to assess the safety and efficacy of the ICS de-escalation. It appeared there were similar or lower rates of COPD exacerbations, pneumonia, and oral candidiasis in those with de-escalated ICS therapy in this study. However, these secondary outcomes are exploratory and would need to be confirmed by larger studies powered to address these outcomes.
CONCLUSIONS
Pharmacist-driven ICS de-escalation may be an effective method for reducing ICS usage in veterans as seen in this study. Additional controlled studies are required to evaluate the efficacy and safety of pharmacist-driven ICS de-escalation.

- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2024 Report). Accessed October 14, 2025. https://goldcopd.org/2024-gold-report/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2025 Report). Accessed November 14, 2025. https://goldcopd.org/2025-gold-report/
- Rogliani P, Ritondo BL, Gabriele M, et al. Optimizing de-escalation of inhaled corticosteroids in COPD: a systematic review of real-world findings. Expert Rev Clin Pharmacol. 2020;13(9):977-990. doi:10.1080/17512433.2020.1817739
- Rossi A, Guerriero M, Corrado A; OPTIMO/AIPO Study Group. Withdrawal of inhaled corticosteroids can be safe in COPD patients at low risk of exacerbation: a real-life study on the appropriateness of treatment in moderate COPD patients (OPTIMO). Respir Res. 2014;15(1):77. doi:10.1186/1465-9921-15-77
- Anderson E, Wiener RS, Resnick K, et al. Care coordination for veterans with COPD: a positive deviance study. Am J Manag Care. 2020;26(2):63-68. doi:10.37765/ajmc.2020.42394
- US Department of Veterans Affairs, US Department of Defense. VA/DoD Clinical Practice Guideline for the Management of Chronic Obstructive Pulmonary Disease. 2021. Accessed October 14, 2025. https://www.healthquality.va.gov/guidelines/CD/copd/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2023 Report). Accessed October 14, 2025. https://goldcopd.org/wp-content/uploads/2023/03/GOLD-2023-ver-1.3-17Feb2023_WMV.pdf
- Hegland AJ, Bolduc J, Jones L, Kunisaki KM, Melzer AC. Pharmacist-driven deprescribing of inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2021;18(4):730-733. doi:10.1513/AnnalsATS.202007-871RL
- Hahn NM, Nagy MW. Implementation of a targeted inhaled corticosteroid de-escalation process in patients with chronic obstructive pulmonary disease in the primary care setting. Innov Pharm. 2022;13(1):10.24926/iip.v13i1.4349. doi:10.24926/iip.v13i1.4349
Systemic glucocorticoids play an important role in the treatment of chronic obstructive pulmonary disease (COPD) exacerbations. They are recommended to shorten recovery time and increase forced expiratory volume in 1 second (FEV1) during exacerbations.1 However, the role of the chronic use of inhaled corticosteroids (ICSs) in the treatment of COPD is less clear.
When added to inhaled β-2 agonists and muscarinic antagonists, ICSs can decrease the risk of exacerbations.1 However, not all patients with COPD benefit from ICS therapy. The degree of benefit an ICS can provide has been shown to correlate with eosinophil count—a marker of inflammation. The expected benefit of using an ICS increases as the eosinophil count increases.1 Maximum benefit can be observed with eosinophil counts ≥ 300 cells/µL, and minimal benefit is observed with eosinophil counts < 100 cells/µL. Adverse effects (AEs) of ICSs include a hoarse voice, oral candidiasis, and an increased risk of pneumonia.1 Given the risk of AEs, it is important to limit ICS use in patients who are unlikely to reap any benefits.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest the use of ICSs in patients who experience exacerbations while using long-acting β agonist (LABA) plus long-acting muscarinic antagonist (LAMA) therapy and have an eosinophil count ≥ 100 cells/µL. Switching from LABA or LAMA monotherapy to triple therapy with LAMA/LABA/ICS may be considered if patients have continued exacerbations and an eosinophil count ≥ 300 cells/µL. De-escalation of ICS therapy should be considered if patients do not meet these criteria or if patients experience ICS AEs, such as pneumonia. The patients most likely to have increased exacerbations or decreased FEV1 with ICS withdrawal are those with eosinophil counts ≥ 300 cells/µL.1,2
Several studies have explored the effects of ICS de-escalation in real-world clinical settings. A systematic review of 11 studies indicated that de-escalation of ICS in COPD does not result in increased exacerbations.3 A prospective study by Rossi et al found that in a 6-month period, 141 of 482 patients on ICS therapy (29%) had an exacerbation. In the opposing arm of the study, 88 of 334 patients (26%) with deprescribed ICS experienced an exacerbation. The difference between these 2 groups was not statistically significant.4 The researchers concluded that in real-world practice, ICS withdrawal can be safe in patients at low risk of exacerbation.
About 25% of veterans (1.25 million) have been diagnosed with COPD.5 To address this, the US Department of Veterans Affairs (VA) and US Department of Defense published updated COPD guidelines in 2021 that specify criteria for de-escalation of ICS.6 Guidelines, however, may not be reflected in common clinical practice for several years following publication. The VA Academic Detailing Service (ADS) provides tools to help clinicians identify patients who may benefit from changes in treatment plans. A recent ADS focus was the implementation of a COPD dashboard, which identifies patients with COPD who are candidates for ICS de-escalation based on comorbid diagnoses, exacerbation history, and eosinophil count. VA pharmacists have an expanded role in the management of primary care disease states and are therefore well-positioned to increase adherence to guideline-directed therapy. The objective of this quality improvement project was to determine the impact of pharmacist-driven de-escalation on ICS usage in veterans with COPD.
Methods
This project was conducted in an outpatient clinic at the Robley Rex VA Medical Center beginning September 21, 2023, with a progress note in the Computerized Patient Record System (CPRS). Eligible patients were selected using the COPD Dashboard provided by ADS. The COPD Dashboard defined patients with COPD as those with ≥ 2 outpatient COPD diagnoses in the past 2 years, 1 inpatient discharge COPD diagnosis in the past year, or COPD listed as an active problem. COPD diagnoses were identified using International Statistical Classification of Disease, Tenth Revision (ICD-10) codes
Candidates identified for ICS de-escalation by the dashboard were excluded if they had a history of COPD exacerbation in the previous 2 years. The dashboard identified COPD exacerbations via ICD-10 codes for COPD or acute respiratory failure for inpatient discharges, emergency department (ED) visits, urgent care visits, and community care consults with 1 of the following terms: emergency, inpatient, hospital, urgent, ED (self). The COPD dashboard excluded patients with a diagnosis of asthma.
After patients were selected, they were screened for additional exclusion criteria. Patients were excluded if a pulmonary care practitioner managed their COPD; if identified via an active pulmonary consult in CPRS; if a non-VA clinician prescribed their ICS; or if they were being treated with roflumilast, theophylline, or chronic azithromycin. Individuals taking these 3 drugs were excluded due to potential severe and/or refractory COPD. Patients also were excluded if they: (1) had prior ICS de-escalation failure (defined as a COPD exacerbation following ICS de-escalation that resulted in ICS resumption); (2) had a COPD exacerbation requiring systemic corticosteroids or antibiotics in the previous year; (3) had active lung cancer; (4) did not have any eosinophil levels in CPRS within the previous 2 years; or (5) had any eosinophil levels ≥ 300 cells/µL in the previous year.
Each patient who met the inclusion criteria and was not excluded received a focused medication review by a pharmacist who created a templated progress note, with patient-specific recommendations, that was entered in the CPRS (eAppendix). The recommendations were also attached as an addendum to the patient’s last primary care visit note, and the primary care practitioner (PCP) was alerted via CPRS to consider ICS de-escalation and non-ICS alternatives. Tapering of ICS therapy was offered as an option to de-escalate if abrupt discontinuation was deemed inappropriate. PCPs were also prompted to consider referral to a primary care clinical pharmacy specialist for management and follow-up of ICS de-escalation.
The primary outcome was the number of patients with de-escalated ICS at 3 and 6 months following the recommendation. Secondary outcomes included the number of: patients who were no longer prescribed an ICS or who had a non-ICS alternative initiated at a pharmacist’s recommendation; patients who were referred to a primary care clinical pharmacy specialist for ICS de-escalation; COPD exacerbations requiring systemic steroids or antibiotics, or requiring an ED visit, inpatient admission, or urgent-care clinic visit; and cases of pneumonia or oral candidiasis. Primary and secondary outcomes were evaluated via chart review in CPRS. For secondary outcomes of pneumonia and COPD exacerbation, identification was made by documented diagnosis in CPRS. For continuous data such as age, the mean was calculated.
Results
Pharmacist ICS de-escalation recommendations were made between September 21, 2023, and November 19, 2023, for 106 patients. The mean age was 72 years and 99 (93%) patients were male (Table 1). Forty-one (39%) of the patients used tobacco at the time of the study. FEV1 was available for 69 patients with a mean of 63% (GOLD grade 2).1 Based on FEV1 values, 16 patients had mild COPD (GOLD grade 1), 37 patients had moderate COPD (GOLD grade 2), 14 patients had severe COPD (GOLD grade 3), and 2 patients had very severe COPD (GOLD grade 4).1 Thirty-four patients received LABA + LAMA + ICS, 65 received LABA + ICS, 2 received LAMA + ICS, and 5 received ICS monotherapy. The most common dose of ICS was a moderate dose (Table 2). Only 2 patients had an ICS AE in the previous year.


ICS de-escalation recommendations resulted in ICS de-escalation in 50 (47.2%) and 62 (58.5%) patients at 3 and 6 months, respectively. The 6-month ICS de-escalation rate by ICS dose at baseline was 72.2% (high dose), 60.0% (moderate), and 30.8% (low). De-escalation at 6 months by GOLD grade at baseline was 56.3% (9 of 16 patients, GOLD 1), 64.9% (24 of 37 patients, GOLD 2), 50% (7 of 14 patients, GOLD 3), and 50% (1 of 2 patients, GOLD 4). Six months after the ICS de-escalation recommendation appeared in the CPRS, the percentage of patients on LABA + ICS therapy dropped from 65 patients (61.3%) at baseline to 25 patients (23.6%).
Secondary outcomes were assessed at 3 and 6 months following the recommendation. Most patients with de-escalated ICS had their ICS discontinued and a non-ICS alternative initiated per pharmacist recommendations. At 6 months, 39 patients (36.8%) patients were referred to a patient aligned care team (PACT) pharmacist for de-escalation. Of the 39 patients referred to pharmacists, 69.2% (27 patients) were de-escalated; this compared to 52.2% (35 patients) who were not referred to pharmacists (Table 3).

ICS use increases the risk of pneumonia.1 At 6 months, 11 patients were diagnosed with pneumonia; 3 patients were diagnosed with pneumonia twice, resulting in a total of 14 cases. Ten cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation. One patient had a documented case of oral candidiasis that occurred while on ICS therapy; no patients with discontinued ICS were diagnosed with oral candidiasis. In addition, 10 patients had COPD exacerbations; however no patients had exacerbations both before and after de-escalation. Six patients were on ICS therapy when they experienced an exacerbation, and 4 patients had an exacerbation after ICS de-escalation.
Discussion
More than half of patients receiving the pharmacist intervention achieved the primary outcome of ICS de-escalation at 6 months. Furthermore, a larger percentage of patients referred to pharmacists for the management of ICS de-escalation successfully achieved de-escalation compared to those who were not referred. These outcomes reflect the important role pharmacists can play in identifying appropriate candidates for ICS de-escalation and assisting in the management of ICS de-escalation. Patients referred to pharmacists also received other services such as smoking cessation pharmacotherapy and counseling on inhaler technique and adherence. These interventions can support improved COPD clinical outcomes.
The purpose of de-escalating ICS therapy is to reduce the risk of AEs such as pneumonia and oral candidiasis.1 The secondary outcomes of this study support previous evidence that patients who have de-escalated ICS therapy may have reduced risk of AEs compared to those who remain on ICS therapy.3 Specifically, of the 14 cases of pneumonia that occurred during the study, 10 cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation.
ICS de-escalation may increase risk of increased COPD exacerbations.1 However, the secondary outcomes of this study do not indicate that those with de-escalated ICS had more COPD exacerbations compared to those who continued on ICS. Pharmacists’ recommendations were more effective for patients with less severe COPD based on baseline FEV1.
The previous GOLD Guidelines for COPD suggested LABA + ICS therapy as an option for patients with a high symptom and exacerbation burden (previously known as GOLD Group D). Guidelines no longer recommend LABA + ICS therapy due to the superiority of triple inhaled therapy for exacerbations and the superiority of LAMA + LABA therapy for dyspnea.7 A majority of identified patients in this project were on LABA + ICS therapy alone at baseline. The ICS de-escalation recommendation resulted in a 61.5% reduction in patients on LABA + ICS therapy at 6 months. By decreasing the number of patients on LABA + ICS without LAMA, recommendations increased the number of patients on guideline-directed therapy.
Limitations
This study lacked a control group, and the rate of ICS de-escalation in patients who did not receive a pharmacist recommendation was not assessed. Therefore, it could not be determined whether the pharmacist recommendation is more effective than no recommendation. Another limitation was our inability to access records from non-VA health care facilities. This may have resulted in missed COPD exacerbations, pneumonia, and oral candidiasis prior to or following the pharmacist recommendation.
In addition, the method used to notify PCPs of the pharmacist recommendation was a CPRS alert. Clinicians often receive multiple daily alerts and may not always pay close attention to them due to alert fatigue. Early in the study, some PCPs were unknowingly omitted from the alert of the pharmacist recommendation for 10 patients due to human error. For 8 of these 10 patients, the PCP was notified of the recommendations during the 3-month follow-up period. However, 2 patients had COPD exacerbations during the 3-month follow-up period. In these cases, the PCP was not alerted to de-escalate ICS. The data for these patients were collected at 3 and 6 months in the same manner as all other patients. Also, 7 of 35 patients who were referred to a pharmacist for ICS de-escalation did not have a scheduled appointment. These patients were considered to be lost to follow-up and this may have resulted in an underestimation of the ability of pharmacists to successfully de-escalate ICS in patients with COPD.
Other studies have evaluated the efficacy of a pharmacy-driven ICS de-escalation.8,9 Hegland et al reported ICS de-escalation for 22% of 141 eligible ambulatory patients with COPD on triple inhaled therapy following pharmacist appointments.8 A study by Hahn et al resulted in 63.8% of 58 patients with COPD being maintained off ICS following a pharmacist de-escalation initiative.9 However, these studies relied upon more time-consuming de-escalation interventions, including at least 1 phone, video, or in-person patient visit.8,9
This project used a single chart review and templated progress note to recommend ICS de-escalation and achieved similar or improved de-escalation rates compared to previous studies.8,9 Previous studies were conducted prior to the updated 2023 GOLD guidelines for COPD which no longer recommend LABA + ICS therapy. This project addressed ICS de-escalation in patients on LABA + ICS therapy in addition to those on triple inhaled therapy. Additionally, previous studies did not address rates of moderate to severe COPD exacerbation and adverse events to ICS following the pharmacist intervention.8,9
This study included COPD exacerbations and cases of pneumonia or oral candidiasis as secondary outcomes to assess the safety and efficacy of the ICS de-escalation. It appeared there were similar or lower rates of COPD exacerbations, pneumonia, and oral candidiasis in those with de-escalated ICS therapy in this study. However, these secondary outcomes are exploratory and would need to be confirmed by larger studies powered to address these outcomes.
CONCLUSIONS
Pharmacist-driven ICS de-escalation may be an effective method for reducing ICS usage in veterans as seen in this study. Additional controlled studies are required to evaluate the efficacy and safety of pharmacist-driven ICS de-escalation.

Systemic glucocorticoids play an important role in the treatment of chronic obstructive pulmonary disease (COPD) exacerbations. They are recommended to shorten recovery time and increase forced expiratory volume in 1 second (FEV1) during exacerbations.1 However, the role of the chronic use of inhaled corticosteroids (ICSs) in the treatment of COPD is less clear.
When added to inhaled β-2 agonists and muscarinic antagonists, ICSs can decrease the risk of exacerbations.1 However, not all patients with COPD benefit from ICS therapy. The degree of benefit an ICS can provide has been shown to correlate with eosinophil count—a marker of inflammation. The expected benefit of using an ICS increases as the eosinophil count increases.1 Maximum benefit can be observed with eosinophil counts ≥ 300 cells/µL, and minimal benefit is observed with eosinophil counts < 100 cells/µL. Adverse effects (AEs) of ICSs include a hoarse voice, oral candidiasis, and an increased risk of pneumonia.1 Given the risk of AEs, it is important to limit ICS use in patients who are unlikely to reap any benefits.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest the use of ICSs in patients who experience exacerbations while using long-acting β agonist (LABA) plus long-acting muscarinic antagonist (LAMA) therapy and have an eosinophil count ≥ 100 cells/µL. Switching from LABA or LAMA monotherapy to triple therapy with LAMA/LABA/ICS may be considered if patients have continued exacerbations and an eosinophil count ≥ 300 cells/µL. De-escalation of ICS therapy should be considered if patients do not meet these criteria or if patients experience ICS AEs, such as pneumonia. The patients most likely to have increased exacerbations or decreased FEV1 with ICS withdrawal are those with eosinophil counts ≥ 300 cells/µL.1,2
Several studies have explored the effects of ICS de-escalation in real-world clinical settings. A systematic review of 11 studies indicated that de-escalation of ICS in COPD does not result in increased exacerbations.3 A prospective study by Rossi et al found that in a 6-month period, 141 of 482 patients on ICS therapy (29%) had an exacerbation. In the opposing arm of the study, 88 of 334 patients (26%) with deprescribed ICS experienced an exacerbation. The difference between these 2 groups was not statistically significant.4 The researchers concluded that in real-world practice, ICS withdrawal can be safe in patients at low risk of exacerbation.
About 25% of veterans (1.25 million) have been diagnosed with COPD.5 To address this, the US Department of Veterans Affairs (VA) and US Department of Defense published updated COPD guidelines in 2021 that specify criteria for de-escalation of ICS.6 Guidelines, however, may not be reflected in common clinical practice for several years following publication. The VA Academic Detailing Service (ADS) provides tools to help clinicians identify patients who may benefit from changes in treatment plans. A recent ADS focus was the implementation of a COPD dashboard, which identifies patients with COPD who are candidates for ICS de-escalation based on comorbid diagnoses, exacerbation history, and eosinophil count. VA pharmacists have an expanded role in the management of primary care disease states and are therefore well-positioned to increase adherence to guideline-directed therapy. The objective of this quality improvement project was to determine the impact of pharmacist-driven de-escalation on ICS usage in veterans with COPD.
Methods
This project was conducted in an outpatient clinic at the Robley Rex VA Medical Center beginning September 21, 2023, with a progress note in the Computerized Patient Record System (CPRS). Eligible patients were selected using the COPD Dashboard provided by ADS. The COPD Dashboard defined patients with COPD as those with ≥ 2 outpatient COPD diagnoses in the past 2 years, 1 inpatient discharge COPD diagnosis in the past year, or COPD listed as an active problem. COPD diagnoses were identified using International Statistical Classification of Disease, Tenth Revision (ICD-10) codes
Candidates identified for ICS de-escalation by the dashboard were excluded if they had a history of COPD exacerbation in the previous 2 years. The dashboard identified COPD exacerbations via ICD-10 codes for COPD or acute respiratory failure for inpatient discharges, emergency department (ED) visits, urgent care visits, and community care consults with 1 of the following terms: emergency, inpatient, hospital, urgent, ED (self). The COPD dashboard excluded patients with a diagnosis of asthma.
After patients were selected, they were screened for additional exclusion criteria. Patients were excluded if a pulmonary care practitioner managed their COPD; if identified via an active pulmonary consult in CPRS; if a non-VA clinician prescribed their ICS; or if they were being treated with roflumilast, theophylline, or chronic azithromycin. Individuals taking these 3 drugs were excluded due to potential severe and/or refractory COPD. Patients also were excluded if they: (1) had prior ICS de-escalation failure (defined as a COPD exacerbation following ICS de-escalation that resulted in ICS resumption); (2) had a COPD exacerbation requiring systemic corticosteroids or antibiotics in the previous year; (3) had active lung cancer; (4) did not have any eosinophil levels in CPRS within the previous 2 years; or (5) had any eosinophil levels ≥ 300 cells/µL in the previous year.
Each patient who met the inclusion criteria and was not excluded received a focused medication review by a pharmacist who created a templated progress note, with patient-specific recommendations, that was entered in the CPRS (eAppendix). The recommendations were also attached as an addendum to the patient’s last primary care visit note, and the primary care practitioner (PCP) was alerted via CPRS to consider ICS de-escalation and non-ICS alternatives. Tapering of ICS therapy was offered as an option to de-escalate if abrupt discontinuation was deemed inappropriate. PCPs were also prompted to consider referral to a primary care clinical pharmacy specialist for management and follow-up of ICS de-escalation.
The primary outcome was the number of patients with de-escalated ICS at 3 and 6 months following the recommendation. Secondary outcomes included the number of: patients who were no longer prescribed an ICS or who had a non-ICS alternative initiated at a pharmacist’s recommendation; patients who were referred to a primary care clinical pharmacy specialist for ICS de-escalation; COPD exacerbations requiring systemic steroids or antibiotics, or requiring an ED visit, inpatient admission, or urgent-care clinic visit; and cases of pneumonia or oral candidiasis. Primary and secondary outcomes were evaluated via chart review in CPRS. For secondary outcomes of pneumonia and COPD exacerbation, identification was made by documented diagnosis in CPRS. For continuous data such as age, the mean was calculated.
Results
Pharmacist ICS de-escalation recommendations were made between September 21, 2023, and November 19, 2023, for 106 patients. The mean age was 72 years and 99 (93%) patients were male (Table 1). Forty-one (39%) of the patients used tobacco at the time of the study. FEV1 was available for 69 patients with a mean of 63% (GOLD grade 2).1 Based on FEV1 values, 16 patients had mild COPD (GOLD grade 1), 37 patients had moderate COPD (GOLD grade 2), 14 patients had severe COPD (GOLD grade 3), and 2 patients had very severe COPD (GOLD grade 4).1 Thirty-four patients received LABA + LAMA + ICS, 65 received LABA + ICS, 2 received LAMA + ICS, and 5 received ICS monotherapy. The most common dose of ICS was a moderate dose (Table 2). Only 2 patients had an ICS AE in the previous year.


ICS de-escalation recommendations resulted in ICS de-escalation in 50 (47.2%) and 62 (58.5%) patients at 3 and 6 months, respectively. The 6-month ICS de-escalation rate by ICS dose at baseline was 72.2% (high dose), 60.0% (moderate), and 30.8% (low). De-escalation at 6 months by GOLD grade at baseline was 56.3% (9 of 16 patients, GOLD 1), 64.9% (24 of 37 patients, GOLD 2), 50% (7 of 14 patients, GOLD 3), and 50% (1 of 2 patients, GOLD 4). Six months after the ICS de-escalation recommendation appeared in the CPRS, the percentage of patients on LABA + ICS therapy dropped from 65 patients (61.3%) at baseline to 25 patients (23.6%).
Secondary outcomes were assessed at 3 and 6 months following the recommendation. Most patients with de-escalated ICS had their ICS discontinued and a non-ICS alternative initiated per pharmacist recommendations. At 6 months, 39 patients (36.8%) patients were referred to a patient aligned care team (PACT) pharmacist for de-escalation. Of the 39 patients referred to pharmacists, 69.2% (27 patients) were de-escalated; this compared to 52.2% (35 patients) who were not referred to pharmacists (Table 3).

ICS use increases the risk of pneumonia.1 At 6 months, 11 patients were diagnosed with pneumonia; 3 patients were diagnosed with pneumonia twice, resulting in a total of 14 cases. Ten cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation. One patient had a documented case of oral candidiasis that occurred while on ICS therapy; no patients with discontinued ICS were diagnosed with oral candidiasis. In addition, 10 patients had COPD exacerbations; however no patients had exacerbations both before and after de-escalation. Six patients were on ICS therapy when they experienced an exacerbation, and 4 patients had an exacerbation after ICS de-escalation.
Discussion
More than half of patients receiving the pharmacist intervention achieved the primary outcome of ICS de-escalation at 6 months. Furthermore, a larger percentage of patients referred to pharmacists for the management of ICS de-escalation successfully achieved de-escalation compared to those who were not referred. These outcomes reflect the important role pharmacists can play in identifying appropriate candidates for ICS de-escalation and assisting in the management of ICS de-escalation. Patients referred to pharmacists also received other services such as smoking cessation pharmacotherapy and counseling on inhaler technique and adherence. These interventions can support improved COPD clinical outcomes.
The purpose of de-escalating ICS therapy is to reduce the risk of AEs such as pneumonia and oral candidiasis.1 The secondary outcomes of this study support previous evidence that patients who have de-escalated ICS therapy may have reduced risk of AEs compared to those who remain on ICS therapy.3 Specifically, of the 14 cases of pneumonia that occurred during the study, 10 cases occurred while patients were on ICS and 4 cases occurred following ICS de-escalation.
ICS de-escalation may increase risk of increased COPD exacerbations.1 However, the secondary outcomes of this study do not indicate that those with de-escalated ICS had more COPD exacerbations compared to those who continued on ICS. Pharmacists’ recommendations were more effective for patients with less severe COPD based on baseline FEV1.
The previous GOLD Guidelines for COPD suggested LABA + ICS therapy as an option for patients with a high symptom and exacerbation burden (previously known as GOLD Group D). Guidelines no longer recommend LABA + ICS therapy due to the superiority of triple inhaled therapy for exacerbations and the superiority of LAMA + LABA therapy for dyspnea.7 A majority of identified patients in this project were on LABA + ICS therapy alone at baseline. The ICS de-escalation recommendation resulted in a 61.5% reduction in patients on LABA + ICS therapy at 6 months. By decreasing the number of patients on LABA + ICS without LAMA, recommendations increased the number of patients on guideline-directed therapy.
Limitations
This study lacked a control group, and the rate of ICS de-escalation in patients who did not receive a pharmacist recommendation was not assessed. Therefore, it could not be determined whether the pharmacist recommendation is more effective than no recommendation. Another limitation was our inability to access records from non-VA health care facilities. This may have resulted in missed COPD exacerbations, pneumonia, and oral candidiasis prior to or following the pharmacist recommendation.
In addition, the method used to notify PCPs of the pharmacist recommendation was a CPRS alert. Clinicians often receive multiple daily alerts and may not always pay close attention to them due to alert fatigue. Early in the study, some PCPs were unknowingly omitted from the alert of the pharmacist recommendation for 10 patients due to human error. For 8 of these 10 patients, the PCP was notified of the recommendations during the 3-month follow-up period. However, 2 patients had COPD exacerbations during the 3-month follow-up period. In these cases, the PCP was not alerted to de-escalate ICS. The data for these patients were collected at 3 and 6 months in the same manner as all other patients. Also, 7 of 35 patients who were referred to a pharmacist for ICS de-escalation did not have a scheduled appointment. These patients were considered to be lost to follow-up and this may have resulted in an underestimation of the ability of pharmacists to successfully de-escalate ICS in patients with COPD.
Other studies have evaluated the efficacy of a pharmacy-driven ICS de-escalation.8,9 Hegland et al reported ICS de-escalation for 22% of 141 eligible ambulatory patients with COPD on triple inhaled therapy following pharmacist appointments.8 A study by Hahn et al resulted in 63.8% of 58 patients with COPD being maintained off ICS following a pharmacist de-escalation initiative.9 However, these studies relied upon more time-consuming de-escalation interventions, including at least 1 phone, video, or in-person patient visit.8,9
This project used a single chart review and templated progress note to recommend ICS de-escalation and achieved similar or improved de-escalation rates compared to previous studies.8,9 Previous studies were conducted prior to the updated 2023 GOLD guidelines for COPD which no longer recommend LABA + ICS therapy. This project addressed ICS de-escalation in patients on LABA + ICS therapy in addition to those on triple inhaled therapy. Additionally, previous studies did not address rates of moderate to severe COPD exacerbation and adverse events to ICS following the pharmacist intervention.8,9
This study included COPD exacerbations and cases of pneumonia or oral candidiasis as secondary outcomes to assess the safety and efficacy of the ICS de-escalation. It appeared there were similar or lower rates of COPD exacerbations, pneumonia, and oral candidiasis in those with de-escalated ICS therapy in this study. However, these secondary outcomes are exploratory and would need to be confirmed by larger studies powered to address these outcomes.
CONCLUSIONS
Pharmacist-driven ICS de-escalation may be an effective method for reducing ICS usage in veterans as seen in this study. Additional controlled studies are required to evaluate the efficacy and safety of pharmacist-driven ICS de-escalation.

- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2024 Report). Accessed October 14, 2025. https://goldcopd.org/2024-gold-report/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2025 Report). Accessed November 14, 2025. https://goldcopd.org/2025-gold-report/
- Rogliani P, Ritondo BL, Gabriele M, et al. Optimizing de-escalation of inhaled corticosteroids in COPD: a systematic review of real-world findings. Expert Rev Clin Pharmacol. 2020;13(9):977-990. doi:10.1080/17512433.2020.1817739
- Rossi A, Guerriero M, Corrado A; OPTIMO/AIPO Study Group. Withdrawal of inhaled corticosteroids can be safe in COPD patients at low risk of exacerbation: a real-life study on the appropriateness of treatment in moderate COPD patients (OPTIMO). Respir Res. 2014;15(1):77. doi:10.1186/1465-9921-15-77
- Anderson E, Wiener RS, Resnick K, et al. Care coordination for veterans with COPD: a positive deviance study. Am J Manag Care. 2020;26(2):63-68. doi:10.37765/ajmc.2020.42394
- US Department of Veterans Affairs, US Department of Defense. VA/DoD Clinical Practice Guideline for the Management of Chronic Obstructive Pulmonary Disease. 2021. Accessed October 14, 2025. https://www.healthquality.va.gov/guidelines/CD/copd/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2023 Report). Accessed October 14, 2025. https://goldcopd.org/wp-content/uploads/2023/03/GOLD-2023-ver-1.3-17Feb2023_WMV.pdf
- Hegland AJ, Bolduc J, Jones L, Kunisaki KM, Melzer AC. Pharmacist-driven deprescribing of inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2021;18(4):730-733. doi:10.1513/AnnalsATS.202007-871RL
- Hahn NM, Nagy MW. Implementation of a targeted inhaled corticosteroid de-escalation process in patients with chronic obstructive pulmonary disease in the primary care setting. Innov Pharm. 2022;13(1):10.24926/iip.v13i1.4349. doi:10.24926/iip.v13i1.4349
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2024 Report). Accessed October 14, 2025. https://goldcopd.org/2024-gold-report/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2025 Report). Accessed November 14, 2025. https://goldcopd.org/2025-gold-report/
- Rogliani P, Ritondo BL, Gabriele M, et al. Optimizing de-escalation of inhaled corticosteroids in COPD: a systematic review of real-world findings. Expert Rev Clin Pharmacol. 2020;13(9):977-990. doi:10.1080/17512433.2020.1817739
- Rossi A, Guerriero M, Corrado A; OPTIMO/AIPO Study Group. Withdrawal of inhaled corticosteroids can be safe in COPD patients at low risk of exacerbation: a real-life study on the appropriateness of treatment in moderate COPD patients (OPTIMO). Respir Res. 2014;15(1):77. doi:10.1186/1465-9921-15-77
- Anderson E, Wiener RS, Resnick K, et al. Care coordination for veterans with COPD: a positive deviance study. Am J Manag Care. 2020;26(2):63-68. doi:10.37765/ajmc.2020.42394
- US Department of Veterans Affairs, US Department of Defense. VA/DoD Clinical Practice Guideline for the Management of Chronic Obstructive Pulmonary Disease. 2021. Accessed October 14, 2025. https://www.healthquality.va.gov/guidelines/CD/copd/
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (2023 Report). Accessed October 14, 2025. https://goldcopd.org/wp-content/uploads/2023/03/GOLD-2023-ver-1.3-17Feb2023_WMV.pdf
- Hegland AJ, Bolduc J, Jones L, Kunisaki KM, Melzer AC. Pharmacist-driven deprescribing of inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2021;18(4):730-733. doi:10.1513/AnnalsATS.202007-871RL
- Hahn NM, Nagy MW. Implementation of a targeted inhaled corticosteroid de-escalation process in patients with chronic obstructive pulmonary disease in the primary care setting. Innov Pharm. 2022;13(1):10.24926/iip.v13i1.4349. doi:10.24926/iip.v13i1.4349
Evaluation of Pharmacist-Driven Inhaled Corticosteroid De-escalation in Veterans
Evaluation of Pharmacist-Driven Inhaled Corticosteroid De-escalation in Veterans
Alopecia and Pruritic Rash on the Forehead and Scalp
Alopecia and Pruritic Rash on the Forehead and Scalp
THE DIAGNOSIS: Folliculitis Decalvans
Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.
Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1
Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5
A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.
Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.
- Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
- Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
- Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
- Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
- Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
- Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
- Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
- Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
- Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
- Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
- Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
- Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
- Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
- Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
THE DIAGNOSIS: Folliculitis Decalvans
Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.
Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1
Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5
A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.
Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.
THE DIAGNOSIS: Folliculitis Decalvans
Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.
Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1
Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5
A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.
Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.
- Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
- Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
- Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
- Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
- Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
- Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
- Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
- Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
- Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
- Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
- Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
- Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
- Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
- Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
- Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
- Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
- Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
- Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
- Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
- Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
- Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
- Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
- Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
- Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
- Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
- Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
- Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
- Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
Alopecia and Pruritic Rash on the Forehead and Scalp
Alopecia and Pruritic Rash on the Forehead and Scalp
A 52-year-old woman presented to the dermatology department with an intermittently pruritic rash in a bandlike distribution on the left upper forehead and the frontal and temporal scalp of 4 years’ duration. The rash initially was diagnosed as psoriasis at an outside facility. Treatment over the year prior to presentation included tildrakizumab-asmn; topical crisaborole 2%; and excimer laser, which was complicated by blistering. The patient reported no history of topical or injected steroid use in the involved areas. Physical examination at the current presentation revealed arcuate erythematous plaques with follicular prominence, perifollicular scaling, pustules, and lone hairs. There also were porcelain-white atrophic plaques with loss of follicular ostia that were most prominent over the temporal scalp. A biopsy of the left lateral forehead was performed.

Introduction: Health Professions Education Evaluation and Research (HPEER) Advanced Fellowship Abstracts
The original four HPEER Advanced Fellowship sites were established by the Department of Veterans Affairs (VA) Office of Academic Affiliation in 2014, and expanded in 2020 to include 8 sites and a national coordinating center with leadership shared between VA facilities in Houston and White River Junction. The VA invests heavily in training the nation’s healthcare professionals. The mission of HPEER is to develop leaders who can educate, evaluate, and innovate in Health Professions Education for the VA and the nation. All HPEER sites take part in a nationally coordinated curriculum covering topics in curriculum design, learner assessment, leadership, interprofessional education, as well as scholarship and educational research.
As part of the national HPEER curriculum covering scholarship and educational research, and in concert with Wednesday, May 14, 2025 VA Research Week 2025, HPEER organized a joint conference with the Center for Health Professions Education at the Uniformed Services University of the Health Sciences (USUHS). This interagency online event included poster sessions and oral presentations from HPEER fellows and students in USUHS certificate and graduate degree programs.
Education scholarship is broad, ranging from descriptions of curricular innovations and works in progress to advanced research using techniques drawn from psychology, sociology, anthropology, economics, and other scientific disciplines. The abstracts presented here summarize some of the work being done by HPEER fellows. Dougherty et al (Boston) described a project to create a primer outlining methodology for conducting and interpreting cost-effectiveness evaluations in the context of proposed HPE innovations. Cohen et al (Cleveland) found reduction in potentially problematic orders in the context of life-sustaining treatment following a multifaceted intervention program. Sorenson (Dublin, Georgia) reported an expanded Tai Chi program that included modifications allowing seated positions for veterans with mobility limitations. Young et al (Dublin) described an interprofessional curriculum to strengthen communication between nurses and social workers in their conversations with women veterans living in rural settings. Misedah-Robinson et al (Houston) showed that a new training program strengthened coordinators’ self-reports of preparedness and confidence in their ability to support veterans who have experienced human trafficking. Tovar et al (Salt Lake City) describe a methodology for using data from the VHA Corporate Data Warehouse to optimize schedules of HPE students assigned to VA clinical rotations. Yanez et al (San Francisco) presented initial observations of learner-centered outcomes following participation in a new multidisciplinary integrative health elective. Resto et al (West Haven) reported that implementation of self-serve kiosks increased distribution of substance use harm reduction resources beyond usual clinical care.
A second joint conference between VA HPEER and USUHS is planned for VA Research Week 2026; we look forward to the abstracts that will be produced by this new cohort of fellows, as well as to the future scholarship and contributions to the field that will be made by alumni of the HPEER Advanced Fellowship.
The original four HPEER Advanced Fellowship sites were established by the Department of Veterans Affairs (VA) Office of Academic Affiliation in 2014, and expanded in 2020 to include 8 sites and a national coordinating center with leadership shared between VA facilities in Houston and White River Junction. The VA invests heavily in training the nation’s healthcare professionals. The mission of HPEER is to develop leaders who can educate, evaluate, and innovate in Health Professions Education for the VA and the nation. All HPEER sites take part in a nationally coordinated curriculum covering topics in curriculum design, learner assessment, leadership, interprofessional education, as well as scholarship and educational research.
As part of the national HPEER curriculum covering scholarship and educational research, and in concert with Wednesday, May 14, 2025 VA Research Week 2025, HPEER organized a joint conference with the Center for Health Professions Education at the Uniformed Services University of the Health Sciences (USUHS). This interagency online event included poster sessions and oral presentations from HPEER fellows and students in USUHS certificate and graduate degree programs.
Education scholarship is broad, ranging from descriptions of curricular innovations and works in progress to advanced research using techniques drawn from psychology, sociology, anthropology, economics, and other scientific disciplines. The abstracts presented here summarize some of the work being done by HPEER fellows. Dougherty et al (Boston) described a project to create a primer outlining methodology for conducting and interpreting cost-effectiveness evaluations in the context of proposed HPE innovations. Cohen et al (Cleveland) found reduction in potentially problematic orders in the context of life-sustaining treatment following a multifaceted intervention program. Sorenson (Dublin, Georgia) reported an expanded Tai Chi program that included modifications allowing seated positions for veterans with mobility limitations. Young et al (Dublin) described an interprofessional curriculum to strengthen communication between nurses and social workers in their conversations with women veterans living in rural settings. Misedah-Robinson et al (Houston) showed that a new training program strengthened coordinators’ self-reports of preparedness and confidence in their ability to support veterans who have experienced human trafficking. Tovar et al (Salt Lake City) describe a methodology for using data from the VHA Corporate Data Warehouse to optimize schedules of HPE students assigned to VA clinical rotations. Yanez et al (San Francisco) presented initial observations of learner-centered outcomes following participation in a new multidisciplinary integrative health elective. Resto et al (West Haven) reported that implementation of self-serve kiosks increased distribution of substance use harm reduction resources beyond usual clinical care.
A second joint conference between VA HPEER and USUHS is planned for VA Research Week 2026; we look forward to the abstracts that will be produced by this new cohort of fellows, as well as to the future scholarship and contributions to the field that will be made by alumni of the HPEER Advanced Fellowship.
The original four HPEER Advanced Fellowship sites were established by the Department of Veterans Affairs (VA) Office of Academic Affiliation in 2014, and expanded in 2020 to include 8 sites and a national coordinating center with leadership shared between VA facilities in Houston and White River Junction. The VA invests heavily in training the nation’s healthcare professionals. The mission of HPEER is to develop leaders who can educate, evaluate, and innovate in Health Professions Education for the VA and the nation. All HPEER sites take part in a nationally coordinated curriculum covering topics in curriculum design, learner assessment, leadership, interprofessional education, as well as scholarship and educational research.
As part of the national HPEER curriculum covering scholarship and educational research, and in concert with Wednesday, May 14, 2025 VA Research Week 2025, HPEER organized a joint conference with the Center for Health Professions Education at the Uniformed Services University of the Health Sciences (USUHS). This interagency online event included poster sessions and oral presentations from HPEER fellows and students in USUHS certificate and graduate degree programs.
Education scholarship is broad, ranging from descriptions of curricular innovations and works in progress to advanced research using techniques drawn from psychology, sociology, anthropology, economics, and other scientific disciplines. The abstracts presented here summarize some of the work being done by HPEER fellows. Dougherty et al (Boston) described a project to create a primer outlining methodology for conducting and interpreting cost-effectiveness evaluations in the context of proposed HPE innovations. Cohen et al (Cleveland) found reduction in potentially problematic orders in the context of life-sustaining treatment following a multifaceted intervention program. Sorenson (Dublin, Georgia) reported an expanded Tai Chi program that included modifications allowing seated positions for veterans with mobility limitations. Young et al (Dublin) described an interprofessional curriculum to strengthen communication between nurses and social workers in their conversations with women veterans living in rural settings. Misedah-Robinson et al (Houston) showed that a new training program strengthened coordinators’ self-reports of preparedness and confidence in their ability to support veterans who have experienced human trafficking. Tovar et al (Salt Lake City) describe a methodology for using data from the VHA Corporate Data Warehouse to optimize schedules of HPE students assigned to VA clinical rotations. Yanez et al (San Francisco) presented initial observations of learner-centered outcomes following participation in a new multidisciplinary integrative health elective. Resto et al (West Haven) reported that implementation of self-serve kiosks increased distribution of substance use harm reduction resources beyond usual clinical care.
A second joint conference between VA HPEER and USUHS is planned for VA Research Week 2026; we look forward to the abstracts that will be produced by this new cohort of fellows, as well as to the future scholarship and contributions to the field that will be made by alumni of the HPEER Advanced Fellowship.
Development and Implementation of an Anti-Human Trafficking Education for Veterans and Clinicians
Background
Veterans may have a greater risk of experiencing human trafficking (HT) than the general population because of social aspects of health, including housing insecurity, justice involvement, food insecurity, and adverse childhood events.1-4 Since 2023, the U.S. Department of Veterans Affairs (VA) has explored veterans’ experiences of HT through the Anti-Human Trafficking (AHT) Pilot Project. This quality improvement project evaluated: 1) development of clinician AHT training materials to enhance identification and response to Veterans experiencing HT, and 2) educational resources aimed at raising awareness tailored to veterans and clinicians.
Methods
South Central Mental Illness Research, Education and Clinical Center (SCMIRECC) facilitated two focus group discussions with AHT coordinators implementing the pilot at six sites. Based on discussions and leadership input, SCMIRECC developed a training curriculum, with bi-weekly readings culminating in a two-hour workshop. Training evaluation followed Kirkpatrick’s model using questions adapted from the Provider Responses, Treatment, and Care for Trafficked People (PROTECT) Survey.5,6 Veteran-facing materials, including a brochure and whiteboard video, were reviewed by two Veteran Consumer Advisory Boards (CAB). The brochures, whiteboard video, and awareness modules were developed and revised based on feedback from focus group discussions. VA Central Office cleared all materials.
Results
Coordinators were satisfied with the training (mean, 4.20). After the training, none of the coordinators (n = 6) felt unprepared to assist Veterans (pre-training mean, 2.25; post-training mean, 1.40), and confidence in documentation improved (pre-training mean, 3.00; post-training mean, 3.40). Veteran CAB members recommended simplified language and veteran-centered messaging. The coordinators found the brochures and training useful. Recommendations included adding more representation to brochure covers, advanced training, a list of commonly asked questions, and a simplified screening tool. Barriers included delays in material development due to language guidance under recent executive orders.
Conclusions
The AHT training improved coordinators’ preparedness and confidence in supporting Veterans with trafficking experiences. Feedback emphasized the value of concise, Veteran-centered materials and a practical HT screening tool. These findings support the continued implementation of AHT education across VA settings to enhance identification and response for Veterans at risk of HT.
- US Department of Veterans Affairs, Veterans Health Administration. Annual Report 2023 Veterans Health Administration Homeless Programs Office.
- Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460. doi:10.1016/j.addbeh.2013.02.002
- Wang EA, McGinnis KA, Goulet J, et al. Food insecurity and health: data from the Veterans Aging Cohort Study. Public Health Rep. 2015;130(3):261-268. doi:10.1177/003335491513000313
- Blosnich JR, Garfin DR, Maguen S, et al. Differences in childhood adversity, suicidal ideation, and suicide attempt among veterans and nonveterans. Am Psychol. 2021;76(2):284-299. doi:10.1037/amp0000755
- Kirkpatrick D. Great ideas revisited. Training & Development. 1996;50(1):54-60.
- Ross C, Dimitrova S, Howard LM, Dewey M, Zimmerman C, Oram S. Human trafficking and health: a cross-sectional survey of NHS professionals' contact with victims of human trafficking. BMJ Open. 2015;5(8):e008682. Published 2015 Aug 20. doi:10.1136/bmjopen-2015-008682
Background
Veterans may have a greater risk of experiencing human trafficking (HT) than the general population because of social aspects of health, including housing insecurity, justice involvement, food insecurity, and adverse childhood events.1-4 Since 2023, the U.S. Department of Veterans Affairs (VA) has explored veterans’ experiences of HT through the Anti-Human Trafficking (AHT) Pilot Project. This quality improvement project evaluated: 1) development of clinician AHT training materials to enhance identification and response to Veterans experiencing HT, and 2) educational resources aimed at raising awareness tailored to veterans and clinicians.
Methods
South Central Mental Illness Research, Education and Clinical Center (SCMIRECC) facilitated two focus group discussions with AHT coordinators implementing the pilot at six sites. Based on discussions and leadership input, SCMIRECC developed a training curriculum, with bi-weekly readings culminating in a two-hour workshop. Training evaluation followed Kirkpatrick’s model using questions adapted from the Provider Responses, Treatment, and Care for Trafficked People (PROTECT) Survey.5,6 Veteran-facing materials, including a brochure and whiteboard video, were reviewed by two Veteran Consumer Advisory Boards (CAB). The brochures, whiteboard video, and awareness modules were developed and revised based on feedback from focus group discussions. VA Central Office cleared all materials.
Results
Coordinators were satisfied with the training (mean, 4.20). After the training, none of the coordinators (n = 6) felt unprepared to assist Veterans (pre-training mean, 2.25; post-training mean, 1.40), and confidence in documentation improved (pre-training mean, 3.00; post-training mean, 3.40). Veteran CAB members recommended simplified language and veteran-centered messaging. The coordinators found the brochures and training useful. Recommendations included adding more representation to brochure covers, advanced training, a list of commonly asked questions, and a simplified screening tool. Barriers included delays in material development due to language guidance under recent executive orders.
Conclusions
The AHT training improved coordinators’ preparedness and confidence in supporting Veterans with trafficking experiences. Feedback emphasized the value of concise, Veteran-centered materials and a practical HT screening tool. These findings support the continued implementation of AHT education across VA settings to enhance identification and response for Veterans at risk of HT.
Background
Veterans may have a greater risk of experiencing human trafficking (HT) than the general population because of social aspects of health, including housing insecurity, justice involvement, food insecurity, and adverse childhood events.1-4 Since 2023, the U.S. Department of Veterans Affairs (VA) has explored veterans’ experiences of HT through the Anti-Human Trafficking (AHT) Pilot Project. This quality improvement project evaluated: 1) development of clinician AHT training materials to enhance identification and response to Veterans experiencing HT, and 2) educational resources aimed at raising awareness tailored to veterans and clinicians.
Methods
South Central Mental Illness Research, Education and Clinical Center (SCMIRECC) facilitated two focus group discussions with AHT coordinators implementing the pilot at six sites. Based on discussions and leadership input, SCMIRECC developed a training curriculum, with bi-weekly readings culminating in a two-hour workshop. Training evaluation followed Kirkpatrick’s model using questions adapted from the Provider Responses, Treatment, and Care for Trafficked People (PROTECT) Survey.5,6 Veteran-facing materials, including a brochure and whiteboard video, were reviewed by two Veteran Consumer Advisory Boards (CAB). The brochures, whiteboard video, and awareness modules were developed and revised based on feedback from focus group discussions. VA Central Office cleared all materials.
Results
Coordinators were satisfied with the training (mean, 4.20). After the training, none of the coordinators (n = 6) felt unprepared to assist Veterans (pre-training mean, 2.25; post-training mean, 1.40), and confidence in documentation improved (pre-training mean, 3.00; post-training mean, 3.40). Veteran CAB members recommended simplified language and veteran-centered messaging. The coordinators found the brochures and training useful. Recommendations included adding more representation to brochure covers, advanced training, a list of commonly asked questions, and a simplified screening tool. Barriers included delays in material development due to language guidance under recent executive orders.
Conclusions
The AHT training improved coordinators’ preparedness and confidence in supporting Veterans with trafficking experiences. Feedback emphasized the value of concise, Veteran-centered materials and a practical HT screening tool. These findings support the continued implementation of AHT education across VA settings to enhance identification and response for Veterans at risk of HT.
- US Department of Veterans Affairs, Veterans Health Administration. Annual Report 2023 Veterans Health Administration Homeless Programs Office.
- Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460. doi:10.1016/j.addbeh.2013.02.002
- Wang EA, McGinnis KA, Goulet J, et al. Food insecurity and health: data from the Veterans Aging Cohort Study. Public Health Rep. 2015;130(3):261-268. doi:10.1177/003335491513000313
- Blosnich JR, Garfin DR, Maguen S, et al. Differences in childhood adversity, suicidal ideation, and suicide attempt among veterans and nonveterans. Am Psychol. 2021;76(2):284-299. doi:10.1037/amp0000755
- Kirkpatrick D. Great ideas revisited. Training & Development. 1996;50(1):54-60.
- Ross C, Dimitrova S, Howard LM, Dewey M, Zimmerman C, Oram S. Human trafficking and health: a cross-sectional survey of NHS professionals' contact with victims of human trafficking. BMJ Open. 2015;5(8):e008682. Published 2015 Aug 20. doi:10.1136/bmjopen-2015-008682
- US Department of Veterans Affairs, Veterans Health Administration. Annual Report 2023 Veterans Health Administration Homeless Programs Office.
- Tsai J, Kasprow WJ, Rosenheck RA. Alcohol and drug use disorders among homeless veterans: prevalence and association with supported housing outcomes. Addict Behav. 2014;39(2):455-460. doi:10.1016/j.addbeh.2013.02.002
- Wang EA, McGinnis KA, Goulet J, et al. Food insecurity and health: data from the Veterans Aging Cohort Study. Public Health Rep. 2015;130(3):261-268. doi:10.1177/003335491513000313
- Blosnich JR, Garfin DR, Maguen S, et al. Differences in childhood adversity, suicidal ideation, and suicide attempt among veterans and nonveterans. Am Psychol. 2021;76(2):284-299. doi:10.1037/amp0000755
- Kirkpatrick D. Great ideas revisited. Training & Development. 1996;50(1):54-60.
- Ross C, Dimitrova S, Howard LM, Dewey M, Zimmerman C, Oram S. Human trafficking and health: a cross-sectional survey of NHS professionals' contact with victims of human trafficking. BMJ Open. 2015;5(8):e008682. Published 2015 Aug 20. doi:10.1136/bmjopen-2015-008682
Weekends Off on Clinical Rotations? Examining Clinical Opportunity Trends on Weekdays vs Weekends During Internal Medicine Clerkship Rotations in Veterans Health Administration Inpatient Wards
Background
The Accreditation Council for Graduate Medical Education (ACGME) mandates an 80-hour weekly work limit for residents.1 In contrast, decisions regarding undergraduate medical education (UME) are strongly influenced locally, with individual institutions setting academic policy for students. These differences in oversight reflect fundamental differences in residents’ and students’ roles in patient care, power, and responsibility. Considering rotation schedules, internal medicine (IM) clerkship directors have discussed the relative value of weekend vs weekday duty during inpatient rotations, a scheduling topic of interest to students as well, though these conversations are limited by a lack of knowledge regarding admission patterns. Addressing this information gap would inform policy decisions.
The Veterans Health Administration (VHA) is uniquely positioned to address questions about UME clinical experiences nationwide: annually, over 118,000 students representing 97% of US medical schools train at VHA facilities.2,3 We aim to compare the number and variety of patient encounter opportunities presenting during inpatient VHA IM rotations on weekdays versus weekends to inform policy decisions for UME rotation schedules.
Innovation
The VHA Corporate Data Warehouse will be queried for all admissions, diagnoses, and length of stay on inpatient IM services at the 420 VHA hospitals affiliated with US medical schools from 2016-2026. We will aggregate case data for day of week, floor, hospital, and Veteran Integrated Service Network (VISN), and determine number of admissions by weekday (Monday-Friday) and weekend (Saturday-Sunday). Weekday vs. weekend admission data will be compared using generalized mixed effects models for clustered longitudinal data. Heterogeneity across hospitals and VISNs will be explored to examine unique regional trends.
Results
We have drafted strategies to query and curate relevant datasets, developed a preliminary analysis plan, and await data deployment from VHA data stewards.
Conclusions
We believe this will be the first VHA-wide evaluation of patient encounter trends on IM services to examine potential training experiences for medical students. This will increase understanding of the critical role VHA has in developing the nations’ healthcare workforce, and how patterns of opportunities for clinical education may be distributed over time, informing decisions about rotation schedules to maximize students’ abilities to interact with, learn from, and serve our nation’s veterans
- Dimitris KD, Taylor BC, Fankhauser RA. Resident work-week regulations: historical review and modern perspectives. J Surg Educ. 2008;65(4):290-296. doi:10.1016/j.jsurg.2008.05.011
- Health professions education statistics. Veterans Health Administration. Accessed March 19, 2025. https://www.va.gov/oaa/docs/OAACurrentStats.pdf
- Medical education at VA: It’s all about the Veterans. VA News. Updated August 16, 2021. Accessed March 19, 2025. https://news.va.gov/93370/medical-education-at-va-its-all-about-the-veterans/
Background
The Accreditation Council for Graduate Medical Education (ACGME) mandates an 80-hour weekly work limit for residents.1 In contrast, decisions regarding undergraduate medical education (UME) are strongly influenced locally, with individual institutions setting academic policy for students. These differences in oversight reflect fundamental differences in residents’ and students’ roles in patient care, power, and responsibility. Considering rotation schedules, internal medicine (IM) clerkship directors have discussed the relative value of weekend vs weekday duty during inpatient rotations, a scheduling topic of interest to students as well, though these conversations are limited by a lack of knowledge regarding admission patterns. Addressing this information gap would inform policy decisions.
The Veterans Health Administration (VHA) is uniquely positioned to address questions about UME clinical experiences nationwide: annually, over 118,000 students representing 97% of US medical schools train at VHA facilities.2,3 We aim to compare the number and variety of patient encounter opportunities presenting during inpatient VHA IM rotations on weekdays versus weekends to inform policy decisions for UME rotation schedules.
Innovation
The VHA Corporate Data Warehouse will be queried for all admissions, diagnoses, and length of stay on inpatient IM services at the 420 VHA hospitals affiliated with US medical schools from 2016-2026. We will aggregate case data for day of week, floor, hospital, and Veteran Integrated Service Network (VISN), and determine number of admissions by weekday (Monday-Friday) and weekend (Saturday-Sunday). Weekday vs. weekend admission data will be compared using generalized mixed effects models for clustered longitudinal data. Heterogeneity across hospitals and VISNs will be explored to examine unique regional trends.
Results
We have drafted strategies to query and curate relevant datasets, developed a preliminary analysis plan, and await data deployment from VHA data stewards.
Conclusions
We believe this will be the first VHA-wide evaluation of patient encounter trends on IM services to examine potential training experiences for medical students. This will increase understanding of the critical role VHA has in developing the nations’ healthcare workforce, and how patterns of opportunities for clinical education may be distributed over time, informing decisions about rotation schedules to maximize students’ abilities to interact with, learn from, and serve our nation’s veterans
Background
The Accreditation Council for Graduate Medical Education (ACGME) mandates an 80-hour weekly work limit for residents.1 In contrast, decisions regarding undergraduate medical education (UME) are strongly influenced locally, with individual institutions setting academic policy for students. These differences in oversight reflect fundamental differences in residents’ and students’ roles in patient care, power, and responsibility. Considering rotation schedules, internal medicine (IM) clerkship directors have discussed the relative value of weekend vs weekday duty during inpatient rotations, a scheduling topic of interest to students as well, though these conversations are limited by a lack of knowledge regarding admission patterns. Addressing this information gap would inform policy decisions.
The Veterans Health Administration (VHA) is uniquely positioned to address questions about UME clinical experiences nationwide: annually, over 118,000 students representing 97% of US medical schools train at VHA facilities.2,3 We aim to compare the number and variety of patient encounter opportunities presenting during inpatient VHA IM rotations on weekdays versus weekends to inform policy decisions for UME rotation schedules.
Innovation
The VHA Corporate Data Warehouse will be queried for all admissions, diagnoses, and length of stay on inpatient IM services at the 420 VHA hospitals affiliated with US medical schools from 2016-2026. We will aggregate case data for day of week, floor, hospital, and Veteran Integrated Service Network (VISN), and determine number of admissions by weekday (Monday-Friday) and weekend (Saturday-Sunday). Weekday vs. weekend admission data will be compared using generalized mixed effects models for clustered longitudinal data. Heterogeneity across hospitals and VISNs will be explored to examine unique regional trends.
Results
We have drafted strategies to query and curate relevant datasets, developed a preliminary analysis plan, and await data deployment from VHA data stewards.
Conclusions
We believe this will be the first VHA-wide evaluation of patient encounter trends on IM services to examine potential training experiences for medical students. This will increase understanding of the critical role VHA has in developing the nations’ healthcare workforce, and how patterns of opportunities for clinical education may be distributed over time, informing decisions about rotation schedules to maximize students’ abilities to interact with, learn from, and serve our nation’s veterans
- Dimitris KD, Taylor BC, Fankhauser RA. Resident work-week regulations: historical review and modern perspectives. J Surg Educ. 2008;65(4):290-296. doi:10.1016/j.jsurg.2008.05.011
- Health professions education statistics. Veterans Health Administration. Accessed March 19, 2025. https://www.va.gov/oaa/docs/OAACurrentStats.pdf
- Medical education at VA: It’s all about the Veterans. VA News. Updated August 16, 2021. Accessed March 19, 2025. https://news.va.gov/93370/medical-education-at-va-its-all-about-the-veterans/
- Dimitris KD, Taylor BC, Fankhauser RA. Resident work-week regulations: historical review and modern perspectives. J Surg Educ. 2008;65(4):290-296. doi:10.1016/j.jsurg.2008.05.011
- Health professions education statistics. Veterans Health Administration. Accessed March 19, 2025. https://www.va.gov/oaa/docs/OAACurrentStats.pdf
- Medical education at VA: It’s all about the Veterans. VA News. Updated August 16, 2021. Accessed March 19, 2025. https://news.va.gov/93370/medical-education-at-va-its-all-about-the-veterans/