Article

Background

Germline genetic testing (GGT) is essential in prostate cancer care, informing clinical decisions. The Veterans Affairs National Oncology Program (VA NOP) recommends GGT for patients with specific risk factors in non-metastatic prostate cancer and all patients with metastatic disease. Understanding GGT access helps evaluate care quality and guide improvements. Since 2021, VA NOP has implemented pathway health factor (HF) templates to standardize cancer care documentation, including GGT status, enabling data extraction from the Corporate Data Warehouse (CDW) rather than requiring manual review of clinical notes. This work aims to evaluate Veterans’ access to GGT in prostate cancer care by leveraging pathway HF templates, and to assess the feasibility of using structured electronic health record (EHR) data to monitor adherence to GGT recommendations.

Methods

Process delivery diagrams (PDDs) were used to map data flow from prostate cancer clinical pathways to the VA CDW. We identified and categorized HFs related to prostate cancer GGT through the computerized patient record system (CPRS). Descriptive statistics were used to summarize access, ordering, and consent rates.

Results

We identified 5,744 Veterans with at least one prostate cancer GGT-relevant HF entered between 02/01/2021 and 12/31/2024. Of these, 5,125 (89.2%) had access to GGT, with 4,569 (89.2%) consenting to or having GGT ordered, while 556 (10.8%) declined testing. Among the 619 (10.8%) Veterans without GGT access, providers reported plans to discuss GGT in the future for 528 (85.3%) patients, while 91 (14.7%) were off pathway.

Conclusions

NOP-developed HF templates enabled extraction of GGT information from structured EHR data, eliminating manual extraction from clinical notes. We observed high GGT utilization among Veterans with pathway-entered HFs. However, low overall HF utilization may introduce selection bias. Future work includes developing a Natural Language Processing pipeline using large language models to automatically extract GGT information from clinical notes, with HF data serving as ground truth.

Background

Germline genetic testing (GGT) is essential in prostate cancer care, informing clinical decisions. The Veterans Affairs National Oncology Program (VA NOP) recommends GGT for patients with specific risk factors in non-metastatic prostate cancer and all patients with metastatic disease. Understanding GGT access helps evaluate care quality and guide improvements. Since 2021, VA NOP has implemented pathway health factor (HF) templates to standardize cancer care documentation, including GGT status, enabling data extraction from the Corporate Data Warehouse (CDW) rather than requiring manual review of clinical notes. This work aims to evaluate Veterans’ access to GGT in prostate cancer care by leveraging pathway HF templates, and to assess the feasibility of using structured electronic health record (EHR) data to monitor adherence to GGT recommendations.

Methods

Process delivery diagrams (PDDs) were used to map data flow from prostate cancer clinical pathways to the VA CDW. We identified and categorized HFs related to prostate cancer GGT through the computerized patient record system (CPRS). Descriptive statistics were used to summarize access, ordering, and consent rates.

Results

We identified 5,744 Veterans with at least one prostate cancer GGT-relevant HF entered between 02/01/2021 and 12/31/2024. Of these, 5,125 (89.2%) had access to GGT, with 4,569 (89.2%) consenting to or having GGT ordered, while 556 (10.8%) declined testing. Among the 619 (10.8%) Veterans without GGT access, providers reported plans to discuss GGT in the future for 528 (85.3%) patients, while 91 (14.7%) were off pathway.

Conclusions

NOP-developed HF templates enabled extraction of GGT information from structured EHR data, eliminating manual extraction from clinical notes. We observed high GGT utilization among Veterans with pathway-entered HFs. However, low overall HF utilization may introduce selection bias. Future work includes developing a Natural Language Processing pipeline using large language models to automatically extract GGT information from clinical notes, with HF data serving as ground truth.

Background

Germline genetic testing (GGT) is essential in prostate cancer care, informing clinical decisions. The Veterans Affairs National Oncology Program (VA NOP) recommends GGT for patients with specific risk factors in non-metastatic prostate cancer and all patients with metastatic disease. Understanding GGT access helps evaluate care quality and guide improvements. Since 2021, VA NOP has implemented pathway health factor (HF) templates to standardize cancer care documentation, including GGT status, enabling data extraction from the Corporate Data Warehouse (CDW) rather than requiring manual review of clinical notes. This work aims to evaluate Veterans’ access to GGT in prostate cancer care by leveraging pathway HF templates, and to assess the feasibility of using structured electronic health record (EHR) data to monitor adherence to GGT recommendations.

Methods

Process delivery diagrams (PDDs) were used to map data flow from prostate cancer clinical pathways to the VA CDW. We identified and categorized HFs related to prostate cancer GGT through the computerized patient record system (CPRS). Descriptive statistics were used to summarize access, ordering, and consent rates.

Results

We identified 5,744 Veterans with at least one prostate cancer GGT-relevant HF entered between 02/01/2021 and 12/31/2024. Of these, 5,125 (89.2%) had access to GGT, with 4,569 (89.2%) consenting to or having GGT ordered, while 556 (10.8%) declined testing. Among the 619 (10.8%) Veterans without GGT access, providers reported plans to discuss GGT in the future for 528 (85.3%) patients, while 91 (14.7%) were off pathway.

Conclusions

NOP-developed HF templates enabled extraction of GGT information from structured EHR data, eliminating manual extraction from clinical notes. We observed high GGT utilization among Veterans with pathway-entered HFs. However, low overall HF utilization may introduce selection bias. Future work includes developing a Natural Language Processing pipeline using large language models to automatically extract GGT information from clinical notes, with HF data serving as ground truth.

Purpose

To compare vial utilization and spending between fixed and weight-based dosing of pembrolizumab in Veterans. Promote and assess pembrolizumab extended interval dosing.

Background

FDA approved pembrolizumab label change from weight-based to fixed dosing without evidence of fixed-dosing’s superiority. Retrospective studies demonstrate equivalent outcomes for 2 mg/kg every 3 weeks (Q3W), 200 mg Q3W, 4 mg/kg every 6 weeks (Q6W), and 400 mg Q6W.

Methods

In July 2024 VAAAHS (VA Ann Arbor Healthcare System) initiated an immunotherapy stewardship quality improvement program to deprescribe unnecessary pembrolizumab units and promote extended-interval dosing. Specific interventions included order template modification and targeted outreach to key stakeholders.

Data Analysis

All pembrolizumab doses administered at VAAAHS between July 1, 2024 (launch) and March 31, 2025 (data cutoff) were extracted from EHR. Drug utilization, spending, and healthcare contact hours averted were compared to a fixed-dosing counterfactual.

Results

Sixty-three Veterans received 286 total pembrolizumab doses, of which 107 (37.4%) were Q6W and 179 (62.6%) were Q3W. In total, 741 vials were utilized, against expectation of 786 (5.7% reduction), reflecting approximately $182,000 in savings (annualized, $243,000) and 86.5% of the theoretical maximum savings were captured. Q6W’s share of all doses rose from 27.3% in July 2024 to 53.8% in March 2025. Amongst monotherapy, Q6W’s share rose from 60.0% in July 2024 to 86.7% in March 2025. Q6W adoption saved 381 Veteran-healthcare contact hours, not including travel time.

Conclusions

Stewardship efforts reduced unnecessary pembrolizumab utilization and spending while saving Veterans and VAAAHS providers’ time. Continued provider reinforcement, preparation for Oracle/ Cerner implementation, VISN expansion, refinement of pembrolizumab dose-banding, and development of dose bands for other immunotherapies are underway.

Significance

National implementation would improve Veteran convenience and quality of life, enable reductions in drug and resource costs, and enhance clinic throughput.

Purpose

To compare vial utilization and spending between fixed and weight-based dosing of pembrolizumab in Veterans. Promote and assess pembrolizumab extended interval dosing.

Background

FDA approved pembrolizumab label change from weight-based to fixed dosing without evidence of fixed-dosing’s superiority. Retrospective studies demonstrate equivalent outcomes for 2 mg/kg every 3 weeks (Q3W), 200 mg Q3W, 4 mg/kg every 6 weeks (Q6W), and 400 mg Q6W.

Methods

In July 2024 VAAAHS (VA Ann Arbor Healthcare System) initiated an immunotherapy stewardship quality improvement program to deprescribe unnecessary pembrolizumab units and promote extended-interval dosing. Specific interventions included order template modification and targeted outreach to key stakeholders.

Data Analysis

All pembrolizumab doses administered at VAAAHS between July 1, 2024 (launch) and March 31, 2025 (data cutoff) were extracted from EHR. Drug utilization, spending, and healthcare contact hours averted were compared to a fixed-dosing counterfactual.

Results

Sixty-three Veterans received 286 total pembrolizumab doses, of which 107 (37.4%) were Q6W and 179 (62.6%) were Q3W. In total, 741 vials were utilized, against expectation of 786 (5.7% reduction), reflecting approximately $182,000 in savings (annualized, $243,000) and 86.5% of the theoretical maximum savings were captured. Q6W’s share of all doses rose from 27.3% in July 2024 to 53.8% in March 2025. Amongst monotherapy, Q6W’s share rose from 60.0% in July 2024 to 86.7% in March 2025. Q6W adoption saved 381 Veteran-healthcare contact hours, not including travel time.

Conclusions

Stewardship efforts reduced unnecessary pembrolizumab utilization and spending while saving Veterans and VAAAHS providers’ time. Continued provider reinforcement, preparation for Oracle/ Cerner implementation, VISN expansion, refinement of pembrolizumab dose-banding, and development of dose bands for other immunotherapies are underway.

Significance

National implementation would improve Veteran convenience and quality of life, enable reductions in drug and resource costs, and enhance clinic throughput.

Purpose

To compare vial utilization and spending between fixed and weight-based dosing of pembrolizumab in Veterans. Promote and assess pembrolizumab extended interval dosing.

Background

FDA approved pembrolizumab label change from weight-based to fixed dosing without evidence of fixed-dosing’s superiority. Retrospective studies demonstrate equivalent outcomes for 2 mg/kg every 3 weeks (Q3W), 200 mg Q3W, 4 mg/kg every 6 weeks (Q6W), and 400 mg Q6W.

Methods

In July 2024 VAAAHS (VA Ann Arbor Healthcare System) initiated an immunotherapy stewardship quality improvement program to deprescribe unnecessary pembrolizumab units and promote extended-interval dosing. Specific interventions included order template modification and targeted outreach to key stakeholders.

Data Analysis

All pembrolizumab doses administered at VAAAHS between July 1, 2024 (launch) and March 31, 2025 (data cutoff) were extracted from EHR. Drug utilization, spending, and healthcare contact hours averted were compared to a fixed-dosing counterfactual.

Results

Sixty-three Veterans received 286 total pembrolizumab doses, of which 107 (37.4%) were Q6W and 179 (62.6%) were Q3W. In total, 741 vials were utilized, against expectation of 786 (5.7% reduction), reflecting approximately $182,000 in savings (annualized, $243,000) and 86.5% of the theoretical maximum savings were captured. Q6W’s share of all doses rose from 27.3% in July 2024 to 53.8% in March 2025. Amongst monotherapy, Q6W’s share rose from 60.0% in July 2024 to 86.7% in March 2025. Q6W adoption saved 381 Veteran-healthcare contact hours, not including travel time.

Conclusions

Stewardship efforts reduced unnecessary pembrolizumab utilization and spending while saving Veterans and VAAAHS providers’ time. Continued provider reinforcement, preparation for Oracle/ Cerner implementation, VISN expansion, refinement of pembrolizumab dose-banding, and development of dose bands for other immunotherapies are underway.

Significance

National implementation would improve Veteran convenience and quality of life, enable reductions in drug and resource costs, and enhance clinic throughput.

Background

Addressing cancer-related distress is a critical component of comprehensive oncology care. In alignment with the National Comprehensive Cancer Network (NCCN) guidelines, which advocate for routine distress screening as a standard of care, our institution aimed to enhance a previously underutilized paper-based screening process by implementing a more efficient and accessible solution.

Objective

To improve screening rates and streamline the identification of psychosocial needs of Veterans who have cancer.

Population

This initiative was conducted in an outpatient Hematology/Oncology clinic at a Midwest Federal Healthcare Center.

Methods

The Plan-Do-Study-Act (PDSA) quality improvement model was used to guide the implementation of the electronic screener. The eScreener was integrated into routine clinical workflow and staff received training to facilitate implementation. Veterans self-identified their needs through the screener, which included a range of practical, family/social, physical, religious or emotional concerns. Clinical staff then review the responses, assessed the identified needs, and entered appropriate referrals into the electronic health record. A dedicated certified nursing assistant (CNA) was incorporated into the workflow to support implementation efforts. As part of their role, the CNA was tasked with ensuring that all Veterans completed the distress screener either electronically or on paper during their visit

Results

Between January 2025 and March 2025, a total of 180 distress screens were completed using the newly implement method. During the same period in the previous year, only 60 screens were completed, representing a 200% increase. The new process enabled timely referrals based on identified needs, resulting in 39 referrals to physicians, 32 to psychologists, 10 to social work, 7 to dieticians, 6 to nurses, and 1 to pastoral care. These outcomes reflect a significant improvement in both accessibility and patient engagement.

Conclusions

The implementation of an electronic cancer distress screener, along with a dedicated staff member resulted in a substantial increase in screening completion rates and multidisciplinary referrals. These preliminary finds suggest that digital tools can significantly enhance psychosocial assessment, improve coordination, and support the delivery of timely, patient-centered oncology care.

Background

Addressing cancer-related distress is a critical component of comprehensive oncology care. In alignment with the National Comprehensive Cancer Network (NCCN) guidelines, which advocate for routine distress screening as a standard of care, our institution aimed to enhance a previously underutilized paper-based screening process by implementing a more efficient and accessible solution.

Objective

To improve screening rates and streamline the identification of psychosocial needs of Veterans who have cancer.

Population

This initiative was conducted in an outpatient Hematology/Oncology clinic at a Midwest Federal Healthcare Center.

Methods

The Plan-Do-Study-Act (PDSA) quality improvement model was used to guide the implementation of the electronic screener. The eScreener was integrated into routine clinical workflow and staff received training to facilitate implementation. Veterans self-identified their needs through the screener, which included a range of practical, family/social, physical, religious or emotional concerns. Clinical staff then review the responses, assessed the identified needs, and entered appropriate referrals into the electronic health record. A dedicated certified nursing assistant (CNA) was incorporated into the workflow to support implementation efforts. As part of their role, the CNA was tasked with ensuring that all Veterans completed the distress screener either electronically or on paper during their visit

Results

Between January 2025 and March 2025, a total of 180 distress screens were completed using the newly implement method. During the same period in the previous year, only 60 screens were completed, representing a 200% increase. The new process enabled timely referrals based on identified needs, resulting in 39 referrals to physicians, 32 to psychologists, 10 to social work, 7 to dieticians, 6 to nurses, and 1 to pastoral care. These outcomes reflect a significant improvement in both accessibility and patient engagement.

Conclusions

The implementation of an electronic cancer distress screener, along with a dedicated staff member resulted in a substantial increase in screening completion rates and multidisciplinary referrals. These preliminary finds suggest that digital tools can significantly enhance psychosocial assessment, improve coordination, and support the delivery of timely, patient-centered oncology care.

Background

Addressing cancer-related distress is a critical component of comprehensive oncology care. In alignment with the National Comprehensive Cancer Network (NCCN) guidelines, which advocate for routine distress screening as a standard of care, our institution aimed to enhance a previously underutilized paper-based screening process by implementing a more efficient and accessible solution.

Objective

To improve screening rates and streamline the identification of psychosocial needs of Veterans who have cancer.

Population

This initiative was conducted in an outpatient Hematology/Oncology clinic at a Midwest Federal Healthcare Center.

Methods

The Plan-Do-Study-Act (PDSA) quality improvement model was used to guide the implementation of the electronic screener. The eScreener was integrated into routine clinical workflow and staff received training to facilitate implementation. Veterans self-identified their needs through the screener, which included a range of practical, family/social, physical, religious or emotional concerns. Clinical staff then review the responses, assessed the identified needs, and entered appropriate referrals into the electronic health record. A dedicated certified nursing assistant (CNA) was incorporated into the workflow to support implementation efforts. As part of their role, the CNA was tasked with ensuring that all Veterans completed the distress screener either electronically or on paper during their visit

Results

Between January 2025 and March 2025, a total of 180 distress screens were completed using the newly implement method. During the same period in the previous year, only 60 screens were completed, representing a 200% increase. The new process enabled timely referrals based on identified needs, resulting in 39 referrals to physicians, 32 to psychologists, 10 to social work, 7 to dieticians, 6 to nurses, and 1 to pastoral care. These outcomes reflect a significant improvement in both accessibility and patient engagement.

Conclusions

The implementation of an electronic cancer distress screener, along with a dedicated staff member resulted in a substantial increase in screening completion rates and multidisciplinary referrals. These preliminary finds suggest that digital tools can significantly enhance psychosocial assessment, improve coordination, and support the delivery of timely, patient-centered oncology care.

Background

Autologous stem cell transplant (ASCT) is an important part of the treatment paradigm for patients with multiple myeloma (MM) and remains the standard of care for newly diagnosed patients. Blood product transfusion support in the form of platelets and packed red blood cells (pRBCs) is part of the standard of practice as supportive measures during the severely pancytopenic period. Some MM patients, such as those of Jehovah’s Witness (JW) faith, may have religious beliefs or preferences that preclude acceptance of such blood products. Some transplant centers have developed protocols to allow safe “bloodless” ASCT that allows these patients to receive this important treatment while adhering to their beliefs or preferences.

Case Presentation

A 61-year-old veteran of JW faith with newly diagnosed IgG Kappa Multiple Myeloma was referred to the Tennessee Valley Healthcare System (TVHS) Stem Cell Transplant program for consideration of “bloodless” ASCT. With the assistance and expertise of the academic affiliate, Vanderbilt University Medical Center’s established bloodless ASCT protocol, this same protocol was established at TVHS to optimize the patient’s care pretransplant (use of erythropoiesis stimulating agents, intravenous iron, B12 supplementation) as well as post-transplant (use of antifibrinolytics, close inpatient monitoring). Both Ethics and Legal consultation was obtained, and guidance was provided to create a life sustaining treatment (LST) note in the veteran’s electronic health record that captured the veteran’s blood product preference. Once all protocols and guidance were in place, the TVHS SCT/CT program proceeded to treat the veteran with a myeloablative melphalan ASCT. The patient tolerated the procedure exceptionally well with minimal complications. He achieved full engraftment on day +14 after ASCT as expected and was discharged from the inpatient setting. He was monitored in the outpatient setting until day +30 without further complications.

Conclusions

The TVHS SCT/CT performed the first ever bloodless autologous stem cell transplant within the VA. This pioneering effort to establish such protocols to provide care to all veterans whatever their personal or religious preferences is a testament to commitment of VA to provide care for all veterans and the willingness to innovate to do so.

Background

Autologous stem cell transplant (ASCT) is an important part of the treatment paradigm for patients with multiple myeloma (MM) and remains the standard of care for newly diagnosed patients. Blood product transfusion support in the form of platelets and packed red blood cells (pRBCs) is part of the standard of practice as supportive measures during the severely pancytopenic period. Some MM patients, such as those of Jehovah’s Witness (JW) faith, may have religious beliefs or preferences that preclude acceptance of such blood products. Some transplant centers have developed protocols to allow safe “bloodless” ASCT that allows these patients to receive this important treatment while adhering to their beliefs or preferences.

Case Presentation

A 61-year-old veteran of JW faith with newly diagnosed IgG Kappa Multiple Myeloma was referred to the Tennessee Valley Healthcare System (TVHS) Stem Cell Transplant program for consideration of “bloodless” ASCT. With the assistance and expertise of the academic affiliate, Vanderbilt University Medical Center’s established bloodless ASCT protocol, this same protocol was established at TVHS to optimize the patient’s care pretransplant (use of erythropoiesis stimulating agents, intravenous iron, B12 supplementation) as well as post-transplant (use of antifibrinolytics, close inpatient monitoring). Both Ethics and Legal consultation was obtained, and guidance was provided to create a life sustaining treatment (LST) note in the veteran’s electronic health record that captured the veteran’s blood product preference. Once all protocols and guidance were in place, the TVHS SCT/CT program proceeded to treat the veteran with a myeloablative melphalan ASCT. The patient tolerated the procedure exceptionally well with minimal complications. He achieved full engraftment on day +14 after ASCT as expected and was discharged from the inpatient setting. He was monitored in the outpatient setting until day +30 without further complications.

Conclusions

The TVHS SCT/CT performed the first ever bloodless autologous stem cell transplant within the VA. This pioneering effort to establish such protocols to provide care to all veterans whatever their personal or religious preferences is a testament to commitment of VA to provide care for all veterans and the willingness to innovate to do so.

Background

Autologous stem cell transplant (ASCT) is an important part of the treatment paradigm for patients with multiple myeloma (MM) and remains the standard of care for newly diagnosed patients. Blood product transfusion support in the form of platelets and packed red blood cells (pRBCs) is part of the standard of practice as supportive measures during the severely pancytopenic period. Some MM patients, such as those of Jehovah’s Witness (JW) faith, may have religious beliefs or preferences that preclude acceptance of such blood products. Some transplant centers have developed protocols to allow safe “bloodless” ASCT that allows these patients to receive this important treatment while adhering to their beliefs or preferences.

Case Presentation

A 61-year-old veteran of JW faith with newly diagnosed IgG Kappa Multiple Myeloma was referred to the Tennessee Valley Healthcare System (TVHS) Stem Cell Transplant program for consideration of “bloodless” ASCT. With the assistance and expertise of the academic affiliate, Vanderbilt University Medical Center’s established bloodless ASCT protocol, this same protocol was established at TVHS to optimize the patient’s care pretransplant (use of erythropoiesis stimulating agents, intravenous iron, B12 supplementation) as well as post-transplant (use of antifibrinolytics, close inpatient monitoring). Both Ethics and Legal consultation was obtained, and guidance was provided to create a life sustaining treatment (LST) note in the veteran’s electronic health record that captured the veteran’s blood product preference. Once all protocols and guidance were in place, the TVHS SCT/CT program proceeded to treat the veteran with a myeloablative melphalan ASCT. The patient tolerated the procedure exceptionally well with minimal complications. He achieved full engraftment on day +14 after ASCT as expected and was discharged from the inpatient setting. He was monitored in the outpatient setting until day +30 without further complications.

Conclusions

The TVHS SCT/CT performed the first ever bloodless autologous stem cell transplant within the VA. This pioneering effort to establish such protocols to provide care to all veterans whatever their personal or religious preferences is a testament to commitment of VA to provide care for all veterans and the willingness to innovate to do so.

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

Quality improvement (QI) initiatives within the US Department of Veterans Affairs (VA) play an important role in enhancing health care for veterans.^1,2 While effective QI programs are often developed, veterans benefit only if they receive care at sites where the program is offered.³ It is estimated only 1% to 5% of patients receive benefit from evidence-based programs, limiting the opportunity for widespread impact.^4,5

The Chronic Obstructive Pulmonary Disease (COPD) Coordinated Access to Reduce Exacerbations (CARE) Academy is a national training program designed to promote the adoption of a COPD primary care service.⁶ The Academy was created and iteratively refined by VA staff to include both clinical training emphasizing COPD management and program implementation strategies. Training programs such as COPD CARE are commonly described as a method to support adoption of health care services, but there is no consensus on a universal approach to training design.

This article describes COPD CARE training and implementation strategies (Table). The Academy began as a training program at 1 VA medical center (VAMC) and has expanded to 49 diverse VAMCs. The Academy illustrates how implementation strategies can be leveraged to develop pragmatic and impactful training. Highlights from the Academy's 9-year history are outlined in this article.

COPD CARE

One in 4 veterans have a COPD diagnosis, and the 5-year mortality rate following a COPD flare is ≥ 50%.^7,8 In 2015, a pharmacy resident designed and piloted COPD CARE, a program that used evidence-based practice to optimize management of the disease.^9,10

The COPD CARE program is delivered by interprofessional team members. It includes a postacute care call completed 48 hours postdischarge, a wellness visit (face-to-face or virtual) 1 month postdischarge, and a follow-up visit scheduled 2 months postdischarge. Clinical pharmacist practitioners (CPPs) prescribe and collaborate with the COPD CARE health care team. Evidence-based practices embedded within COPD CARE include treatment optimization, symptom evaluation, severity staging, vaccination promotion, referrals, tobacco treatment, and comorbidity management.^11-16 The initial COPD CARE pilot demonstrated promising results; patients received timely care and high rates of COPD best practices.¹¹

Academy Design and Implementation

Initial COPD CARE training was tailored to the culture, context, and workflow of the William S. Middleton Memorial Veteran’s Hospital in Madison, Wisconsin. Further service expansion required integration of implementation strategies that enable learners to apply and adapt content to fit different processes, staffing, and patient needs.

Formal Implementation Blueprint

A key aspect of the Academy is the integration of a formal implementation blueprint that includes training goals, scope, and key milestones to guide implementation. The Academy blueprint includes 4 phased training workbooks: (1) preimplementation support from local stakeholders; (2) integration of COPD CARE operational infrastructure into workflows; (3) preparing clinical champions; and (4) leading clinical training (Figure 1). Five weekly 1-hour synchronous virtual discussions are used for learning the workbook content that include learning objectives and opportunities to strategize how to overcome implementation barriers.

Promoting and Facilitating Implementation

As clinicians apply content from the Academy to install informatics tools, coordinate clinical training, and build relationships across service lines, implementation barriers may occur. A learning collaborative allows peer-mentorship and shared problem solving. The Academy learning collaborative includes attendees across multiple VAMCs, allowing for diverse perspectives and cross-site learning. Within the field of dissemination and implementation science, this process of shared problem-solving to support individuals is referred to as implementation facilitation.¹⁷ Academy facilitators with prior experience provide a unique perspective and external facilitation from outside local VAMCs. Academy learners form local teams to engage in shared decision-making when applying Academy content. Following Academy completion, learning collaboratives continue to meet monthly to share clinical insights and operational updates.

Local Champions Promote Adaptability

One or more local champions were identified at each VAMC who were focused on the implementation of clinical training content and operational implementation of Academy content.¹⁸ Champions have helped develop adaptations of Academy content, such as integrating telehealth nursing within the COPD CARE referral process, which have become new best practices. Champions attend Academy sessions, which provide an opportunity to share adaptations to meet local needs.¹⁹

Using a Train-The-Trainer Model

Clinical training was designed to be dynamic and included video modeling, such as recorded examples of CPPs conducting COPD CARE visits and video clips highlighting clinical content. Each learner received a clinical workbook summarizing the content. The champion shares discussion questions to relate training content to the local clinical practice setting. The combination of live training, with videos of clinic visits and case-based discussion was intended to address differing learning styles. Clinical training was delivered using a train-the-trainer model led by the local champion, which allows clinicians with expertise to tailor their training. The use of a train-the-trainer model was intended to promote local buy-in and was often completed by frontline clinicians.

Informatics note templates provide clinicians with information needed to deliver training content during clinic visits. Direct hyperlinks to symptomatic scoring tools, resources to promote evidence-based medication optimization, and patient education resources were embedded within the electronic health record note templates. Direct links to consults for COPD referrals services discussed during clinical training were also included to promote ease of care coordination and awareness of referral opportunities. The integration of clinical training with informatics note template support was intentional to directly relate clinical training to clinical care delivery.

Audit and Feedback

To inform COPD CARE practice, the Academy included informatics infrastructure that allowed for timely local quality monitoring. Electronic health record note templates with embedded data fields track COPD CARE service implementation, including timely completion of patient visits, completion of patient medication reviews, appropriate testing, symptom assessment, and interventions made. Champions can organize template installation and integrate templates into COPD CARE clinical training. Data are included on a COPD CARE implementation dashboard.

An audit and feedback process is allows for the review of performance metrics and development of action plans.^20,21 Data reports from note templates are described during the Academy, along with resources to help teams enhance delivery of their program based on performance metrics.

Building a Coalition

Within VA primary care, clinical care delivery is optimized through a team-based coalition of clinicians using the patient aligned care team (PACT) framework. The VA patient-centered team-based care delivery model, patient facilitates coordination of patient referrals, including patient review, scheduling, and completion of patient visits.²²

Partnerships with VA Pharmacy Benefits Manager, VA Diffusion of Excellence, VA Quality Enhancement Research Initiative, VA Office of Pulmonary Medicine, and the VA Office of Rural Health have facilitated COPD CARE successes. Collaborations with VA Centers of Innovation helped benchmark the Academy’s impact. An academic partnership with the University of Wisconsin-Madison was established in 2017 and has provided evaluation expertise and leadership as the Academy has been iteratively developed, and revised.

Preliminary Metrics

COPD CARE has delivered > 2000 visits. CPPs have delivered COPD care, with a mean 9.4 of 10 best practices per patient visit. Improvements in veteran COPD symptoms have also been observed following COPD CARE patient visits.

DISCUSSION

The COPD CARE Academy was developed to promote rapid scale-up of a complex, team-based COPD service delivered during veteran care transitions. The implementation blueprint for the Academy is multifaceted and integrates both clinical-focused and implementation-focused infrastructure to apply training content.²³ A randomized control trial evaluating the efficacy of training modalities found a need to expand implementation blueprints beyond clinical training alone, as training by itself may not be sufficient to change behavior.²⁴ VA staff designed the Academy using clinical- and implementation-focused content within its implementation blueprint. Key components included leveraging clinical champions, using a train-the-trainer approach, and incorporating facilitation strategies to overcome adoption barriers.

Lewis et al emphasize matching implementation strategies to barriers within VA staff who identify care coordination as a key challenge.²³ The informatics infrastructure developed for Academy learners, including standardized note templates, video modeling examples of clinic visits, and data capture for audit and feedback, was designed to complement clinical training and standardize service workflows (Figure 2). There are opportunities to explore how to optimize technology in the Academy.

While Academy clinical training specifically focuses on COPD management, many implementation strategies can be considered to promote care delivery services for other chronic conditions. The Academy blueprint and implementation infrastructure, are strategies that may be considered within and outside the federal health care system. The opportunity for adaptations to Academy training enables clinical champions to promote tailored content to the needs of each unique VAMC. The translation of Academy implementation strategies for new chronic conditions will similarly require adaptations at each VAMC to promote adoption of content.

CONCLUSIONS

COPD CARE Academy is an example of the collaborative spirit within VA, and the opportunity for further advancement of health care programs. The VA is a national leader in Learning Health Systems implementation, in which “science, informatics, incentives and culture are aligned for continuous improvement and innovation.”^25,26 There are many opportunities for VA staff to learn from one another to form partnerships between leaders, clinicians, and scientists to optimize health care delivery and further the VA’s work as a learning health system.

Quality improvement (QI) initiatives within the US Department of Veterans Affairs (VA) play an important role in enhancing health care for veterans.^1,2 While effective QI programs are often developed, veterans benefit only if they receive care at sites where the program is offered.³ It is estimated only 1% to 5% of patients receive benefit from evidence-based programs, limiting the opportunity for widespread impact.^4,5

The Chronic Obstructive Pulmonary Disease (COPD) Coordinated Access to Reduce Exacerbations (CARE) Academy is a national training program designed to promote the adoption of a COPD primary care service.⁶ The Academy was created and iteratively refined by VA staff to include both clinical training emphasizing COPD management and program implementation strategies. Training programs such as COPD CARE are commonly described as a method to support adoption of health care services, but there is no consensus on a universal approach to training design.

This article describes COPD CARE training and implementation strategies (Table). The Academy began as a training program at 1 VA medical center (VAMC) and has expanded to 49 diverse VAMCs. The Academy illustrates how implementation strategies can be leveraged to develop pragmatic and impactful training. Highlights from the Academy's 9-year history are outlined in this article.

COPD CARE

One in 4 veterans have a COPD diagnosis, and the 5-year mortality rate following a COPD flare is ≥ 50%.^7,8 In 2015, a pharmacy resident designed and piloted COPD CARE, a program that used evidence-based practice to optimize management of the disease.^9,10

The COPD CARE program is delivered by interprofessional team members. It includes a postacute care call completed 48 hours postdischarge, a wellness visit (face-to-face or virtual) 1 month postdischarge, and a follow-up visit scheduled 2 months postdischarge. Clinical pharmacist practitioners (CPPs) prescribe and collaborate with the COPD CARE health care team. Evidence-based practices embedded within COPD CARE include treatment optimization, symptom evaluation, severity staging, vaccination promotion, referrals, tobacco treatment, and comorbidity management.^11-16 The initial COPD CARE pilot demonstrated promising results; patients received timely care and high rates of COPD best practices.¹¹

Academy Design and Implementation

Initial COPD CARE training was tailored to the culture, context, and workflow of the William S. Middleton Memorial Veteran’s Hospital in Madison, Wisconsin. Further service expansion required integration of implementation strategies that enable learners to apply and adapt content to fit different processes, staffing, and patient needs.

Formal Implementation Blueprint

A key aspect of the Academy is the integration of a formal implementation blueprint that includes training goals, scope, and key milestones to guide implementation. The Academy blueprint includes 4 phased training workbooks: (1) preimplementation support from local stakeholders; (2) integration of COPD CARE operational infrastructure into workflows; (3) preparing clinical champions; and (4) leading clinical training (Figure 1). Five weekly 1-hour synchronous virtual discussions are used for learning the workbook content that include learning objectives and opportunities to strategize how to overcome implementation barriers.

Promoting and Facilitating Implementation

As clinicians apply content from the Academy to install informatics tools, coordinate clinical training, and build relationships across service lines, implementation barriers may occur. A learning collaborative allows peer-mentorship and shared problem solving. The Academy learning collaborative includes attendees across multiple VAMCs, allowing for diverse perspectives and cross-site learning. Within the field of dissemination and implementation science, this process of shared problem-solving to support individuals is referred to as implementation facilitation.¹⁷ Academy facilitators with prior experience provide a unique perspective and external facilitation from outside local VAMCs. Academy learners form local teams to engage in shared decision-making when applying Academy content. Following Academy completion, learning collaboratives continue to meet monthly to share clinical insights and operational updates.

Local Champions Promote Adaptability

One or more local champions were identified at each VAMC who were focused on the implementation of clinical training content and operational implementation of Academy content.¹⁸ Champions have helped develop adaptations of Academy content, such as integrating telehealth nursing within the COPD CARE referral process, which have become new best practices. Champions attend Academy sessions, which provide an opportunity to share adaptations to meet local needs.¹⁹

Using a Train-The-Trainer Model

Clinical training was designed to be dynamic and included video modeling, such as recorded examples of CPPs conducting COPD CARE visits and video clips highlighting clinical content. Each learner received a clinical workbook summarizing the content. The champion shares discussion questions to relate training content to the local clinical practice setting. The combination of live training, with videos of clinic visits and case-based discussion was intended to address differing learning styles. Clinical training was delivered using a train-the-trainer model led by the local champion, which allows clinicians with expertise to tailor their training. The use of a train-the-trainer model was intended to promote local buy-in and was often completed by frontline clinicians.

Informatics note templates provide clinicians with information needed to deliver training content during clinic visits. Direct hyperlinks to symptomatic scoring tools, resources to promote evidence-based medication optimization, and patient education resources were embedded within the electronic health record note templates. Direct links to consults for COPD referrals services discussed during clinical training were also included to promote ease of care coordination and awareness of referral opportunities. The integration of clinical training with informatics note template support was intentional to directly relate clinical training to clinical care delivery.

Audit and Feedback

To inform COPD CARE practice, the Academy included informatics infrastructure that allowed for timely local quality monitoring. Electronic health record note templates with embedded data fields track COPD CARE service implementation, including timely completion of patient visits, completion of patient medication reviews, appropriate testing, symptom assessment, and interventions made. Champions can organize template installation and integrate templates into COPD CARE clinical training. Data are included on a COPD CARE implementation dashboard.

An audit and feedback process is allows for the review of performance metrics and development of action plans.^20,21 Data reports from note templates are described during the Academy, along with resources to help teams enhance delivery of their program based on performance metrics.

Building a Coalition

Within VA primary care, clinical care delivery is optimized through a team-based coalition of clinicians using the patient aligned care team (PACT) framework. The VA patient-centered team-based care delivery model, patient facilitates coordination of patient referrals, including patient review, scheduling, and completion of patient visits.²²

Partnerships with VA Pharmacy Benefits Manager, VA Diffusion of Excellence, VA Quality Enhancement Research Initiative, VA Office of Pulmonary Medicine, and the VA Office of Rural Health have facilitated COPD CARE successes. Collaborations with VA Centers of Innovation helped benchmark the Academy’s impact. An academic partnership with the University of Wisconsin-Madison was established in 2017 and has provided evaluation expertise and leadership as the Academy has been iteratively developed, and revised.

Preliminary Metrics

COPD CARE has delivered > 2000 visits. CPPs have delivered COPD care, with a mean 9.4 of 10 best practices per patient visit. Improvements in veteran COPD symptoms have also been observed following COPD CARE patient visits.

DISCUSSION

The COPD CARE Academy was developed to promote rapid scale-up of a complex, team-based COPD service delivered during veteran care transitions. The implementation blueprint for the Academy is multifaceted and integrates both clinical-focused and implementation-focused infrastructure to apply training content.²³ A randomized control trial evaluating the efficacy of training modalities found a need to expand implementation blueprints beyond clinical training alone, as training by itself may not be sufficient to change behavior.²⁴ VA staff designed the Academy using clinical- and implementation-focused content within its implementation blueprint. Key components included leveraging clinical champions, using a train-the-trainer approach, and incorporating facilitation strategies to overcome adoption barriers.

Lewis et al emphasize matching implementation strategies to barriers within VA staff who identify care coordination as a key challenge.²³ The informatics infrastructure developed for Academy learners, including standardized note templates, video modeling examples of clinic visits, and data capture for audit and feedback, was designed to complement clinical training and standardize service workflows (Figure 2). There are opportunities to explore how to optimize technology in the Academy.

While Academy clinical training specifically focuses on COPD management, many implementation strategies can be considered to promote care delivery services for other chronic conditions. The Academy blueprint and implementation infrastructure, are strategies that may be considered within and outside the federal health care system. The opportunity for adaptations to Academy training enables clinical champions to promote tailored content to the needs of each unique VAMC. The translation of Academy implementation strategies for new chronic conditions will similarly require adaptations at each VAMC to promote adoption of content.

CONCLUSIONS

COPD CARE Academy is an example of the collaborative spirit within VA, and the opportunity for further advancement of health care programs. The VA is a national leader in Learning Health Systems implementation, in which “science, informatics, incentives and culture are aligned for continuous improvement and innovation.”^25,26 There are many opportunities for VA staff to learn from one another to form partnerships between leaders, clinicians, and scientists to optimize health care delivery and further the VA’s work as a learning health system.

Quality improvement (QI) initiatives within the US Department of Veterans Affairs (VA) play an important role in enhancing health care for veterans.^1,2 While effective QI programs are often developed, veterans benefit only if they receive care at sites where the program is offered.³ It is estimated only 1% to 5% of patients receive benefit from evidence-based programs, limiting the opportunity for widespread impact.^4,5

The Chronic Obstructive Pulmonary Disease (COPD) Coordinated Access to Reduce Exacerbations (CARE) Academy is a national training program designed to promote the adoption of a COPD primary care service.⁶ The Academy was created and iteratively refined by VA staff to include both clinical training emphasizing COPD management and program implementation strategies. Training programs such as COPD CARE are commonly described as a method to support adoption of health care services, but there is no consensus on a universal approach to training design.

This article describes COPD CARE training and implementation strategies (Table). The Academy began as a training program at 1 VA medical center (VAMC) and has expanded to 49 diverse VAMCs. The Academy illustrates how implementation strategies can be leveraged to develop pragmatic and impactful training. Highlights from the Academy's 9-year history are outlined in this article.

COPD CARE

One in 4 veterans have a COPD diagnosis, and the 5-year mortality rate following a COPD flare is ≥ 50%.^7,8 In 2015, a pharmacy resident designed and piloted COPD CARE, a program that used evidence-based practice to optimize management of the disease.^9,10

The COPD CARE program is delivered by interprofessional team members. It includes a postacute care call completed 48 hours postdischarge, a wellness visit (face-to-face or virtual) 1 month postdischarge, and a follow-up visit scheduled 2 months postdischarge. Clinical pharmacist practitioners (CPPs) prescribe and collaborate with the COPD CARE health care team. Evidence-based practices embedded within COPD CARE include treatment optimization, symptom evaluation, severity staging, vaccination promotion, referrals, tobacco treatment, and comorbidity management.^11-16 The initial COPD CARE pilot demonstrated promising results; patients received timely care and high rates of COPD best practices.¹¹

Academy Design and Implementation

Initial COPD CARE training was tailored to the culture, context, and workflow of the William S. Middleton Memorial Veteran’s Hospital in Madison, Wisconsin. Further service expansion required integration of implementation strategies that enable learners to apply and adapt content to fit different processes, staffing, and patient needs.

Formal Implementation Blueprint

A key aspect of the Academy is the integration of a formal implementation blueprint that includes training goals, scope, and key milestones to guide implementation. The Academy blueprint includes 4 phased training workbooks: (1) preimplementation support from local stakeholders; (2) integration of COPD CARE operational infrastructure into workflows; (3) preparing clinical champions; and (4) leading clinical training (Figure 1). Five weekly 1-hour synchronous virtual discussions are used for learning the workbook content that include learning objectives and opportunities to strategize how to overcome implementation barriers.

Promoting and Facilitating Implementation

As clinicians apply content from the Academy to install informatics tools, coordinate clinical training, and build relationships across service lines, implementation barriers may occur. A learning collaborative allows peer-mentorship and shared problem solving. The Academy learning collaborative includes attendees across multiple VAMCs, allowing for diverse perspectives and cross-site learning. Within the field of dissemination and implementation science, this process of shared problem-solving to support individuals is referred to as implementation facilitation.¹⁷ Academy facilitators with prior experience provide a unique perspective and external facilitation from outside local VAMCs. Academy learners form local teams to engage in shared decision-making when applying Academy content. Following Academy completion, learning collaboratives continue to meet monthly to share clinical insights and operational updates.

Local Champions Promote Adaptability

One or more local champions were identified at each VAMC who were focused on the implementation of clinical training content and operational implementation of Academy content.¹⁸ Champions have helped develop adaptations of Academy content, such as integrating telehealth nursing within the COPD CARE referral process, which have become new best practices. Champions attend Academy sessions, which provide an opportunity to share adaptations to meet local needs.¹⁹

Using a Train-The-Trainer Model

Clinical training was designed to be dynamic and included video modeling, such as recorded examples of CPPs conducting COPD CARE visits and video clips highlighting clinical content. Each learner received a clinical workbook summarizing the content. The champion shares discussion questions to relate training content to the local clinical practice setting. The combination of live training, with videos of clinic visits and case-based discussion was intended to address differing learning styles. Clinical training was delivered using a train-the-trainer model led by the local champion, which allows clinicians with expertise to tailor their training. The use of a train-the-trainer model was intended to promote local buy-in and was often completed by frontline clinicians.

Informatics note templates provide clinicians with information needed to deliver training content during clinic visits. Direct hyperlinks to symptomatic scoring tools, resources to promote evidence-based medication optimization, and patient education resources were embedded within the electronic health record note templates. Direct links to consults for COPD referrals services discussed during clinical training were also included to promote ease of care coordination and awareness of referral opportunities. The integration of clinical training with informatics note template support was intentional to directly relate clinical training to clinical care delivery.

Audit and Feedback

To inform COPD CARE practice, the Academy included informatics infrastructure that allowed for timely local quality monitoring. Electronic health record note templates with embedded data fields track COPD CARE service implementation, including timely completion of patient visits, completion of patient medication reviews, appropriate testing, symptom assessment, and interventions made. Champions can organize template installation and integrate templates into COPD CARE clinical training. Data are included on a COPD CARE implementation dashboard.

An audit and feedback process is allows for the review of performance metrics and development of action plans.^20,21 Data reports from note templates are described during the Academy, along with resources to help teams enhance delivery of their program based on performance metrics.

Building a Coalition

Within VA primary care, clinical care delivery is optimized through a team-based coalition of clinicians using the patient aligned care team (PACT) framework. The VA patient-centered team-based care delivery model, patient facilitates coordination of patient referrals, including patient review, scheduling, and completion of patient visits.²²

Partnerships with VA Pharmacy Benefits Manager, VA Diffusion of Excellence, VA Quality Enhancement Research Initiative, VA Office of Pulmonary Medicine, and the VA Office of Rural Health have facilitated COPD CARE successes. Collaborations with VA Centers of Innovation helped benchmark the Academy’s impact. An academic partnership with the University of Wisconsin-Madison was established in 2017 and has provided evaluation expertise and leadership as the Academy has been iteratively developed, and revised.

Preliminary Metrics

COPD CARE has delivered > 2000 visits. CPPs have delivered COPD care, with a mean 9.4 of 10 best practices per patient visit. Improvements in veteran COPD symptoms have also been observed following COPD CARE patient visits.

DISCUSSION

The COPD CARE Academy was developed to promote rapid scale-up of a complex, team-based COPD service delivered during veteran care transitions. The implementation blueprint for the Academy is multifaceted and integrates both clinical-focused and implementation-focused infrastructure to apply training content.²³ A randomized control trial evaluating the efficacy of training modalities found a need to expand implementation blueprints beyond clinical training alone, as training by itself may not be sufficient to change behavior.²⁴ VA staff designed the Academy using clinical- and implementation-focused content within its implementation blueprint. Key components included leveraging clinical champions, using a train-the-trainer approach, and incorporating facilitation strategies to overcome adoption barriers.

Lewis et al emphasize matching implementation strategies to barriers within VA staff who identify care coordination as a key challenge.²³ The informatics infrastructure developed for Academy learners, including standardized note templates, video modeling examples of clinic visits, and data capture for audit and feedback, was designed to complement clinical training and standardize service workflows (Figure 2). There are opportunities to explore how to optimize technology in the Academy.

While Academy clinical training specifically focuses on COPD management, many implementation strategies can be considered to promote care delivery services for other chronic conditions. The Academy blueprint and implementation infrastructure, are strategies that may be considered within and outside the federal health care system. The opportunity for adaptations to Academy training enables clinical champions to promote tailored content to the needs of each unique VAMC. The translation of Academy implementation strategies for new chronic conditions will similarly require adaptations at each VAMC to promote adoption of content.

CONCLUSIONS

COPD CARE Academy is an example of the collaborative spirit within VA, and the opportunity for further advancement of health care programs. The VA is a national leader in Learning Health Systems implementation, in which “science, informatics, incentives and culture are aligned for continuous improvement and innovation.”^25,26 There are many opportunities for VA staff to learn from one another to form partnerships between leaders, clinicians, and scientists to optimize health care delivery and further the VA’s work as a learning health system.

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

At some point, most Americans will experience the anxiety associated with an organizational restructure or a corporate budget cut that leads to job loss. Self-assurances may follow by telling ourselves we will be fine, and we could even start a new position that (if we're lucky) will be better than our previous one. It can be devastating, but is not a life-or-death scenario.

Unless you care for veterans with cancer.

The recent workforce reductions across the US Department of Veterans of Affairs (VA) health care system, whether through voluntary retirements or forced layoffs, is a life-threatening crisis. Every position lost has the potential to directly impact whether a veteran receives the necessary care in their battle with cancer.

Veterans deserve every opportunity, treatment plan, and resource available to ensure their comfort and survival. They are entitled to the specialized, comprehensive, and thorough care they receive through the VA—care that cannot be duplicated in community health care. Because many of the health challenges they face are a direct result of serving our country, we owe it to them to provide the best care available from the most highly-trained and competent clinicians. This level of excellence cannot be achieved in a gutted or chaotic system.

Reducing or eliminating VA health care positions is a decision that demands careful examination. Like any organization, the VA experiences some measure of waste or inefficiency that should be eliminated. But that cannot be done swiftly or in large-scale action.

Consider these examples: the reduction of force resulting in the removal of those deemed to hold unnecessary administrative positions—such as continuing education or physician oversight—has a direct impact on a clinician's ability to provide the most current and precise care. Reduced research funding limits the VA's contribution to health care innovation. The loss of contract positions that appear superfluous on paper represent the staff who schedule appointments, chemotherapy or radiation therapy, and wrap-around services for veterans. Even reducing auxiliary services like laundry may seem like a cost-saving measure—until the hospital can't admit new patients due to lack of sanitized linens.

VA employees know that veterans need specialized care for their complex and unique challenges. That individualized care has led to the VA nearly eliminating disparity gaps experienced in traditional health care. The removal of support positions and opportunities in professional development demands coordination with less-prepared community-based health care; overpopulated work environments will have a lasting impact. Limiting the workforce will make it impossible to provide coordinated and exceptional care.

The Association of VA Hematology/Oncology (AVAHO) is a leader in professional development opportunities for those who care for veterans with cancer. As a nonprofit organization, AVAHO is also a voice for those working with veterans with cancer to ensure they receive the care they deserve. AVAHO is calling on its colleagues, veterans, and those committed to supporting veterans to voice their opposition to reducing critical staff, research, and resources within the VA.

We ask veterans to share stories describing the difference VA care makes. We ask clinicians—including those within the federal system—to explain how a system that is well-staffed, supported, and with ample resources can impact patient care. Americans must stand for the care our veterans have earned.

Most importantly, we call on policymakers to carefully consider the impact each position has on the outcome of excellent, well-coordinated, and state-of-the-art care. The lives of our veterans depend on it.

AVAHO is a 501(c)3 nonprofit organization dedicated to supporting and educating health care providers who serve veterans with cancer and hematological disorders. You can find out more and support their advocacy initiatives at www.avaho.org.

At some point, most Americans will experience the anxiety associated with an organizational restructure or a corporate budget cut that leads to job loss. Self-assurances may follow by telling ourselves we will be fine, and we could even start a new position that (if we're lucky) will be better than our previous one. It can be devastating, but is not a life-or-death scenario.

Unless you care for veterans with cancer.

The recent workforce reductions across the US Department of Veterans of Affairs (VA) health care system, whether through voluntary retirements or forced layoffs, is a life-threatening crisis. Every position lost has the potential to directly impact whether a veteran receives the necessary care in their battle with cancer.

Veterans deserve every opportunity, treatment plan, and resource available to ensure their comfort and survival. They are entitled to the specialized, comprehensive, and thorough care they receive through the VA—care that cannot be duplicated in community health care. Because many of the health challenges they face are a direct result of serving our country, we owe it to them to provide the best care available from the most highly-trained and competent clinicians. This level of excellence cannot be achieved in a gutted or chaotic system.

Reducing or eliminating VA health care positions is a decision that demands careful examination. Like any organization, the VA experiences some measure of waste or inefficiency that should be eliminated. But that cannot be done swiftly or in large-scale action.

Consider these examples: the reduction of force resulting in the removal of those deemed to hold unnecessary administrative positions—such as continuing education or physician oversight—has a direct impact on a clinician's ability to provide the most current and precise care. Reduced research funding limits the VA's contribution to health care innovation. The loss of contract positions that appear superfluous on paper represent the staff who schedule appointments, chemotherapy or radiation therapy, and wrap-around services for veterans. Even reducing auxiliary services like laundry may seem like a cost-saving measure—until the hospital can't admit new patients due to lack of sanitized linens.

VA employees know that veterans need specialized care for their complex and unique challenges. That individualized care has led to the VA nearly eliminating disparity gaps experienced in traditional health care. The removal of support positions and opportunities in professional development demands coordination with less-prepared community-based health care; overpopulated work environments will have a lasting impact. Limiting the workforce will make it impossible to provide coordinated and exceptional care.

The Association of VA Hematology/Oncology (AVAHO) is a leader in professional development opportunities for those who care for veterans with cancer. As a nonprofit organization, AVAHO is also a voice for those working with veterans with cancer to ensure they receive the care they deserve. AVAHO is calling on its colleagues, veterans, and those committed to supporting veterans to voice their opposition to reducing critical staff, research, and resources within the VA.

We ask veterans to share stories describing the difference VA care makes. We ask clinicians—including those within the federal system—to explain how a system that is well-staffed, supported, and with ample resources can impact patient care. Americans must stand for the care our veterans have earned.

Most importantly, we call on policymakers to carefully consider the impact each position has on the outcome of excellent, well-coordinated, and state-of-the-art care. The lives of our veterans depend on it.

AVAHO is a 501(c)3 nonprofit organization dedicated to supporting and educating health care providers who serve veterans with cancer and hematological disorders. You can find out more and support their advocacy initiatives at www.avaho.org.

At some point, most Americans will experience the anxiety associated with an organizational restructure or a corporate budget cut that leads to job loss. Self-assurances may follow by telling ourselves we will be fine, and we could even start a new position that (if we're lucky) will be better than our previous one. It can be devastating, but is not a life-or-death scenario.

Unless you care for veterans with cancer.

The recent workforce reductions across the US Department of Veterans of Affairs (VA) health care system, whether through voluntary retirements or forced layoffs, is a life-threatening crisis. Every position lost has the potential to directly impact whether a veteran receives the necessary care in their battle with cancer.

Veterans deserve every opportunity, treatment plan, and resource available to ensure their comfort and survival. They are entitled to the specialized, comprehensive, and thorough care they receive through the VA—care that cannot be duplicated in community health care. Because many of the health challenges they face are a direct result of serving our country, we owe it to them to provide the best care available from the most highly-trained and competent clinicians. This level of excellence cannot be achieved in a gutted or chaotic system.

Reducing or eliminating VA health care positions is a decision that demands careful examination. Like any organization, the VA experiences some measure of waste or inefficiency that should be eliminated. But that cannot be done swiftly or in large-scale action.

Consider these examples: the reduction of force resulting in the removal of those deemed to hold unnecessary administrative positions—such as continuing education or physician oversight—has a direct impact on a clinician's ability to provide the most current and precise care. Reduced research funding limits the VA's contribution to health care innovation. The loss of contract positions that appear superfluous on paper represent the staff who schedule appointments, chemotherapy or radiation therapy, and wrap-around services for veterans. Even reducing auxiliary services like laundry may seem like a cost-saving measure—until the hospital can't admit new patients due to lack of sanitized linens.

VA employees know that veterans need specialized care for their complex and unique challenges. That individualized care has led to the VA nearly eliminating disparity gaps experienced in traditional health care. The removal of support positions and opportunities in professional development demands coordination with less-prepared community-based health care; overpopulated work environments will have a lasting impact. Limiting the workforce will make it impossible to provide coordinated and exceptional care.

The Association of VA Hematology/Oncology (AVAHO) is a leader in professional development opportunities for those who care for veterans with cancer. As a nonprofit organization, AVAHO is also a voice for those working with veterans with cancer to ensure they receive the care they deserve. AVAHO is calling on its colleagues, veterans, and those committed to supporting veterans to voice their opposition to reducing critical staff, research, and resources within the VA.

We ask veterans to share stories describing the difference VA care makes. We ask clinicians—including those within the federal system—to explain how a system that is well-staffed, supported, and with ample resources can impact patient care. Americans must stand for the care our veterans have earned.

Most importantly, we call on policymakers to carefully consider the impact each position has on the outcome of excellent, well-coordinated, and state-of-the-art care. The lives of our veterans depend on it.

AVAHO is a 501(c)3 nonprofit organization dedicated to supporting and educating health care providers who serve veterans with cancer and hematological disorders. You can find out more and support their advocacy initiatives at www.avaho.org.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.