Commentary

Worldwide, it is estimated that up to 1 in 5 individuals will experience a dermatophyte infection (commonly called ringworm or tinea infection) in their lifetime.¹ Historically, dermatophyte infections have been considered relatively minor conditions usually treated with short courses of topical antifungals.² Oral antifungals historically were needed only for patients with nail or hair shaft infections or extensive cutaneous fungal infections, which typically occurred in immunosuppressed patients.² However, the landscape is changing rapidly due to the global emergence of severe dermatophyte infections that frequently are resistant to first-line antifungal medications.^3-5 In this article, we aimed to review the epidemiology of emerging dermatophyte infections and provide dermatologists with information needed for effective diagnosis and management.

Emergence of Trichophyton indotineae

In recent decades, public health officials and dermatologists have noted with concern the spread of the recently emerged dermatophyte species Trichophyton indotineae in South Asia.^3,6 This species (previously known as Trichophyton mentagrophytes genotype VIII) usually is transmitted from person to person, either through direct skin-to-skin contact or by fomites.^4,6 Potential sexual transmission of T indotineae infections also has been reported,⁷ and it is possible that animals may serve as reservoirs for this pathogen, although there are no known reports of direct spread from animals to humans.^8,9 Major outbreaks of T indotineae are ongoing in South Asia, and cases have been documented in 6 continents.^10-12 In the United States, most but not all cases have occurred in immigrants from or recently returned travelers to South Asia.^6,13 The emergence and spread of T indotineae is hypothesized to be promoted by the misuse and overuse of topical antifungal products, particularly those containing combinations of potent corticosteroids with other antimicrobial drugs.^14,15

Cutaneous manifestations of T indotineae infections tend to cover large body surface areas, recur frequently, and pose substantial treatment challenges.^6,13,16 Several clinical presentations have been documented, including erythematous, scaly concentric plaques; papulosquamous lesions; pustular forms; and corticosteroid-modified disease (Figure 1).^6,16 Affected patients seldom are immunocompromised and often have a history of multiple failed courses of topical or oral antifungals, including oral terbinafine.¹³ Many also have been prescribed topical corticosteroids or have used over-the-counter topical corticosteroids, which worsen the rash.¹⁷

Direct microscopy with potassium hydroxide could be used to confirm the diagnosis of dermatophyte infection, but it does not distinguish T indotineae from other dermatophyte species.^2,6 Importantly, culture-based testing usually will misidentify T indotineae as other Trichophyton species such as the more common T mentagrophytes or Trichophyton interdigitale. Definitive identification of T indotineae requires advanced molecular techniques that are available only at select laboratories.⁶ Unfortunately, availability of such testing is limited (Table), and results may take several weeks; therefore, it is suggested that dermatologists who suspect T indotineae infections based on the patient’s history and clinical presentation begin antifungal treatment after confirmation of dermatophyte infection but not wait for definitive confirmation of the causative organism.¹⁶

Itraconazole is considered the first-line therapy for T indotineae infection, as terbinafine usually is ineffective due to mutations in the squalene epoxidase gene.¹⁶ Dermatologists should be aware that itraconazole is available in different formulations that can affect absorption. The oral solution has greater bioavailability and should be taken on an empty stomach, whereas the capsules are required to be taken with food for effective absorption; the capsules also should be taken with an acidic beverage such as orange juice. Dermatologists should carefully assess for drug-drug interactions when prescribing itraconazole, given its extensive interaction profile with numerous other medications. Patients may require treatment with itraconazole (100 mg/d or 200 mg/d) for a minimum of 6 to 8 weeks until complete clearance has been achieved and ideally a negative potassium hydroxide preparation of skin scrapings has been obtained. A longer treatment period (eg, ≥3 months) frequently is needed, and relapses are common.^6,16,18 Regular follow-up is needed to monitor for infection clearance and recurrences. It is important to note that cases of itraconazole resistance have been reported, although this currently appears to be uncommon.^19,20

Other Emerging Dermatophytes to Watch

Trichophyton rubrum is the most common cause of dermatophyte infections among humans,²¹ and cases of terbinafine-resistant T rubrum infections have been reported increasingly in the United States and Canada.^5,22-24 Onychomycosis caused by terbinafine-resistant T rubrum has been documented, and patients may have infections that do not respond to terbinafine given at the standard dose and duration.^22,23 Case reports have indicated successful treatment using itraconazole 200 mg/d and posaconazole 300 mg/d.^5,23

Trichophyton mentagrophytes genotype VII (TMVII) is an emerging dermatophyte that recently has been reported as a cause of sexually transmitted dermatophyte infections in Europe and the United States primarily affecting men who have sex with men.^25-27 Patients may present with pruritic, annular, scaly patches and plaques involving the trunk, groin, genital region, or face (Figure 2). Although closely related to T indotineae, TMVII differs in that it more often affects the genital region, generally is susceptible to terbinafine, and in the United States and Europe usually is not related to travel or immigration involving South Asia.²⁶ Although TMVII has not been associated with antifungal resistance, awareness among dermatologists is important because patients may experience inflamed, painful, and persistent rashes that can lead to secondary bacterial infection or scarring, and physicians might mistake it for mimics including eczema or psoriasis.^25,26

Importance of Judicious Antifungal Use

Optimizing the use of antifungals is critical to improving patient outcomes and preserving available treatment options.^28,29 A retrospective analysis of commercial health insurance data estimated that topical antifungal prescriptions were potentially unnecessary for more than half of the more than 560,000 patients who were prescribed these medications in 2023. In this study, it also was observed that only 16% of patients prescribed a topical antifungal had received diagnostic testing, with low rates across specialties.³⁰ This is concerning because even among board-certified dermatologists, incorrect diagnosis of suspected fungal skin infections can occur; in one survey-based study of board-certified dermatologists who were presented with dermatomycosis images, respondents categorized cases with greater than 75% accuracy in only 31% (4/13) of instances.³¹ Clotrimazole-betamethasone is among the most commonly prescribed topical antifungals in the United States,^14,32 and 2 recent retrospective analyses highlighted that the majority of patients prescribed this medication did not receive any fungal diagnostic testing.^33,34

Final Thoughts

In an era of emerging antifungal-resistant dermatophyte infections, it is important for dermatologists to educate nondermatologists about the importance of using diagnostic testing for suspected dermatophyte infections.^14,28 Dermatologists also can educate nondermatologist colleagues on the importance of avoiding the use of topical combination antifungal/corticosteroid medications and referring for dermatologic evaluation when diagnoses are uncertain.^33,34 Strategies for education by dermatologists could include giving workshops, creating educational materials, and fostering open communication about optimal treatment practices and referral parameters for suspected dermatophyte infections.

Worldwide, it is estimated that up to 1 in 5 individuals will experience a dermatophyte infection (commonly called ringworm or tinea infection) in their lifetime.¹ Historically, dermatophyte infections have been considered relatively minor conditions usually treated with short courses of topical antifungals.² Oral antifungals historically were needed only for patients with nail or hair shaft infections or extensive cutaneous fungal infections, which typically occurred in immunosuppressed patients.² However, the landscape is changing rapidly due to the global emergence of severe dermatophyte infections that frequently are resistant to first-line antifungal medications.^3-5 In this article, we aimed to review the epidemiology of emerging dermatophyte infections and provide dermatologists with information needed for effective diagnosis and management.

Emergence of Trichophyton indotineae

In recent decades, public health officials and dermatologists have noted with concern the spread of the recently emerged dermatophyte species Trichophyton indotineae in South Asia.^3,6 This species (previously known as Trichophyton mentagrophytes genotype VIII) usually is transmitted from person to person, either through direct skin-to-skin contact or by fomites.^4,6 Potential sexual transmission of T indotineae infections also has been reported,⁷ and it is possible that animals may serve as reservoirs for this pathogen, although there are no known reports of direct spread from animals to humans.^8,9 Major outbreaks of T indotineae are ongoing in South Asia, and cases have been documented in 6 continents.^10-12 In the United States, most but not all cases have occurred in immigrants from or recently returned travelers to South Asia.^6,13 The emergence and spread of T indotineae is hypothesized to be promoted by the misuse and overuse of topical antifungal products, particularly those containing combinations of potent corticosteroids with other antimicrobial drugs.^14,15

Cutaneous manifestations of T indotineae infections tend to cover large body surface areas, recur frequently, and pose substantial treatment challenges.^6,13,16 Several clinical presentations have been documented, including erythematous, scaly concentric plaques; papulosquamous lesions; pustular forms; and corticosteroid-modified disease (Figure 1).^6,16 Affected patients seldom are immunocompromised and often have a history of multiple failed courses of topical or oral antifungals, including oral terbinafine.¹³ Many also have been prescribed topical corticosteroids or have used over-the-counter topical corticosteroids, which worsen the rash.¹⁷

Direct microscopy with potassium hydroxide could be used to confirm the diagnosis of dermatophyte infection, but it does not distinguish T indotineae from other dermatophyte species.^2,6 Importantly, culture-based testing usually will misidentify T indotineae as other Trichophyton species such as the more common T mentagrophytes or Trichophyton interdigitale. Definitive identification of T indotineae requires advanced molecular techniques that are available only at select laboratories.⁶ Unfortunately, availability of such testing is limited (Table), and results may take several weeks; therefore, it is suggested that dermatologists who suspect T indotineae infections based on the patient’s history and clinical presentation begin antifungal treatment after confirmation of dermatophyte infection but not wait for definitive confirmation of the causative organism.¹⁶

Itraconazole is considered the first-line therapy for T indotineae infection, as terbinafine usually is ineffective due to mutations in the squalene epoxidase gene.¹⁶ Dermatologists should be aware that itraconazole is available in different formulations that can affect absorption. The oral solution has greater bioavailability and should be taken on an empty stomach, whereas the capsules are required to be taken with food for effective absorption; the capsules also should be taken with an acidic beverage such as orange juice. Dermatologists should carefully assess for drug-drug interactions when prescribing itraconazole, given its extensive interaction profile with numerous other medications. Patients may require treatment with itraconazole (100 mg/d or 200 mg/d) for a minimum of 6 to 8 weeks until complete clearance has been achieved and ideally a negative potassium hydroxide preparation of skin scrapings has been obtained. A longer treatment period (eg, ≥3 months) frequently is needed, and relapses are common.^6,16,18 Regular follow-up is needed to monitor for infection clearance and recurrences. It is important to note that cases of itraconazole resistance have been reported, although this currently appears to be uncommon.^19,20

Other Emerging Dermatophytes to Watch

Trichophyton rubrum is the most common cause of dermatophyte infections among humans,²¹ and cases of terbinafine-resistant T rubrum infections have been reported increasingly in the United States and Canada.^5,22-24 Onychomycosis caused by terbinafine-resistant T rubrum has been documented, and patients may have infections that do not respond to terbinafine given at the standard dose and duration.^22,23 Case reports have indicated successful treatment using itraconazole 200 mg/d and posaconazole 300 mg/d.^5,23

Trichophyton mentagrophytes genotype VII (TMVII) is an emerging dermatophyte that recently has been reported as a cause of sexually transmitted dermatophyte infections in Europe and the United States primarily affecting men who have sex with men.^25-27 Patients may present with pruritic, annular, scaly patches and plaques involving the trunk, groin, genital region, or face (Figure 2). Although closely related to T indotineae, TMVII differs in that it more often affects the genital region, generally is susceptible to terbinafine, and in the United States and Europe usually is not related to travel or immigration involving South Asia.²⁶ Although TMVII has not been associated with antifungal resistance, awareness among dermatologists is important because patients may experience inflamed, painful, and persistent rashes that can lead to secondary bacterial infection or scarring, and physicians might mistake it for mimics including eczema or psoriasis.^25,26

Importance of Judicious Antifungal Use

Optimizing the use of antifungals is critical to improving patient outcomes and preserving available treatment options.^28,29 A retrospective analysis of commercial health insurance data estimated that topical antifungal prescriptions were potentially unnecessary for more than half of the more than 560,000 patients who were prescribed these medications in 2023. In this study, it also was observed that only 16% of patients prescribed a topical antifungal had received diagnostic testing, with low rates across specialties.³⁰ This is concerning because even among board-certified dermatologists, incorrect diagnosis of suspected fungal skin infections can occur; in one survey-based study of board-certified dermatologists who were presented with dermatomycosis images, respondents categorized cases with greater than 75% accuracy in only 31% (4/13) of instances.³¹ Clotrimazole-betamethasone is among the most commonly prescribed topical antifungals in the United States,^14,32 and 2 recent retrospective analyses highlighted that the majority of patients prescribed this medication did not receive any fungal diagnostic testing.^33,34

Final Thoughts

In an era of emerging antifungal-resistant dermatophyte infections, it is important for dermatologists to educate nondermatologists about the importance of using diagnostic testing for suspected dermatophyte infections.^14,28 Dermatologists also can educate nondermatologist colleagues on the importance of avoiding the use of topical combination antifungal/corticosteroid medications and referring for dermatologic evaluation when diagnoses are uncertain.^33,34 Strategies for education by dermatologists could include giving workshops, creating educational materials, and fostering open communication about optimal treatment practices and referral parameters for suspected dermatophyte infections.

Worldwide, it is estimated that up to 1 in 5 individuals will experience a dermatophyte infection (commonly called ringworm or tinea infection) in their lifetime.¹ Historically, dermatophyte infections have been considered relatively minor conditions usually treated with short courses of topical antifungals.² Oral antifungals historically were needed only for patients with nail or hair shaft infections or extensive cutaneous fungal infections, which typically occurred in immunosuppressed patients.² However, the landscape is changing rapidly due to the global emergence of severe dermatophyte infections that frequently are resistant to first-line antifungal medications.^3-5 In this article, we aimed to review the epidemiology of emerging dermatophyte infections and provide dermatologists with information needed for effective diagnosis and management.

Emergence of Trichophyton indotineae

In recent decades, public health officials and dermatologists have noted with concern the spread of the recently emerged dermatophyte species Trichophyton indotineae in South Asia.^3,6 This species (previously known as Trichophyton mentagrophytes genotype VIII) usually is transmitted from person to person, either through direct skin-to-skin contact or by fomites.^4,6 Potential sexual transmission of T indotineae infections also has been reported,⁷ and it is possible that animals may serve as reservoirs for this pathogen, although there are no known reports of direct spread from animals to humans.^8,9 Major outbreaks of T indotineae are ongoing in South Asia, and cases have been documented in 6 continents.^10-12 In the United States, most but not all cases have occurred in immigrants from or recently returned travelers to South Asia.^6,13 The emergence and spread of T indotineae is hypothesized to be promoted by the misuse and overuse of topical antifungal products, particularly those containing combinations of potent corticosteroids with other antimicrobial drugs.^14,15

Cutaneous manifestations of T indotineae infections tend to cover large body surface areas, recur frequently, and pose substantial treatment challenges.^6,13,16 Several clinical presentations have been documented, including erythematous, scaly concentric plaques; papulosquamous lesions; pustular forms; and corticosteroid-modified disease (Figure 1).^6,16 Affected patients seldom are immunocompromised and often have a history of multiple failed courses of topical or oral antifungals, including oral terbinafine.¹³ Many also have been prescribed topical corticosteroids or have used over-the-counter topical corticosteroids, which worsen the rash.¹⁷

Direct microscopy with potassium hydroxide could be used to confirm the diagnosis of dermatophyte infection, but it does not distinguish T indotineae from other dermatophyte species.^2,6 Importantly, culture-based testing usually will misidentify T indotineae as other Trichophyton species such as the more common T mentagrophytes or Trichophyton interdigitale. Definitive identification of T indotineae requires advanced molecular techniques that are available only at select laboratories.⁶ Unfortunately, availability of such testing is limited (Table), and results may take several weeks; therefore, it is suggested that dermatologists who suspect T indotineae infections based on the patient’s history and clinical presentation begin antifungal treatment after confirmation of dermatophyte infection but not wait for definitive confirmation of the causative organism.¹⁶

Itraconazole is considered the first-line therapy for T indotineae infection, as terbinafine usually is ineffective due to mutations in the squalene epoxidase gene.¹⁶ Dermatologists should be aware that itraconazole is available in different formulations that can affect absorption. The oral solution has greater bioavailability and should be taken on an empty stomach, whereas the capsules are required to be taken with food for effective absorption; the capsules also should be taken with an acidic beverage such as orange juice. Dermatologists should carefully assess for drug-drug interactions when prescribing itraconazole, given its extensive interaction profile with numerous other medications. Patients may require treatment with itraconazole (100 mg/d or 200 mg/d) for a minimum of 6 to 8 weeks until complete clearance has been achieved and ideally a negative potassium hydroxide preparation of skin scrapings has been obtained. A longer treatment period (eg, ≥3 months) frequently is needed, and relapses are common.^6,16,18 Regular follow-up is needed to monitor for infection clearance and recurrences. It is important to note that cases of itraconazole resistance have been reported, although this currently appears to be uncommon.^19,20

Other Emerging Dermatophytes to Watch

Trichophyton rubrum is the most common cause of dermatophyte infections among humans,²¹ and cases of terbinafine-resistant T rubrum infections have been reported increasingly in the United States and Canada.^5,22-24 Onychomycosis caused by terbinafine-resistant T rubrum has been documented, and patients may have infections that do not respond to terbinafine given at the standard dose and duration.^22,23 Case reports have indicated successful treatment using itraconazole 200 mg/d and posaconazole 300 mg/d.^5,23

Trichophyton mentagrophytes genotype VII (TMVII) is an emerging dermatophyte that recently has been reported as a cause of sexually transmitted dermatophyte infections in Europe and the United States primarily affecting men who have sex with men.^25-27 Patients may present with pruritic, annular, scaly patches and plaques involving the trunk, groin, genital region, or face (Figure 2). Although closely related to T indotineae, TMVII differs in that it more often affects the genital region, generally is susceptible to terbinafine, and in the United States and Europe usually is not related to travel or immigration involving South Asia.²⁶ Although TMVII has not been associated with antifungal resistance, awareness among dermatologists is important because patients may experience inflamed, painful, and persistent rashes that can lead to secondary bacterial infection or scarring, and physicians might mistake it for mimics including eczema or psoriasis.^25,26

Importance of Judicious Antifungal Use

Optimizing the use of antifungals is critical to improving patient outcomes and preserving available treatment options.^28,29 A retrospective analysis of commercial health insurance data estimated that topical antifungal prescriptions were potentially unnecessary for more than half of the more than 560,000 patients who were prescribed these medications in 2023. In this study, it also was observed that only 16% of patients prescribed a topical antifungal had received diagnostic testing, with low rates across specialties.³⁰ This is concerning because even among board-certified dermatologists, incorrect diagnosis of suspected fungal skin infections can occur; in one survey-based study of board-certified dermatologists who were presented with dermatomycosis images, respondents categorized cases with greater than 75% accuracy in only 31% (4/13) of instances.³¹ Clotrimazole-betamethasone is among the most commonly prescribed topical antifungals in the United States,^14,32 and 2 recent retrospective analyses highlighted that the majority of patients prescribed this medication did not receive any fungal diagnostic testing.^33,34

Final Thoughts

In an era of emerging antifungal-resistant dermatophyte infections, it is important for dermatologists to educate nondermatologists about the importance of using diagnostic testing for suspected dermatophyte infections.^14,28 Dermatologists also can educate nondermatologist colleagues on the importance of avoiding the use of topical combination antifungal/corticosteroid medications and referring for dermatologic evaluation when diagnoses are uncertain.^33,34 Strategies for education by dermatologists could include giving workshops, creating educational materials, and fostering open communication about optimal treatment practices and referral parameters for suspected dermatophyte infections.

Lifeguards play a crucial role in ensuring water safety, but they also are uniquely positioned to promote skin cancer prevention and proper sunscreen use.^1,2 There are several benefits and challenges to offering skin cancer prevention training for lifeguards.³ We examine the advantages of training, highlight the role lifeguards can play in larger public skin cancer prevention efforts, and address practical techniques for developing lifeguardfocused skin cancer education programs. By providing this knowledge to lifeguards, we can improve community health outcomes and encourage sun-safe behaviors in high-risk outdoor locations.

Benefits of Skin Cancer Prevention Training for Lifeguards

Research has shown that lifeguards are at an elevated risk for basal cell carcinoma, squamous cell carcinoma, and melanoma due to frequent prolonged occupational sun exposure.^1,2,4-6 Therefore, comprehensive education on skin cancer prevention—including instruction on proper sunscreen application techniques and the importance of regular reapplication as well as how to recognize suspicious skin lesions—should be incorporated into lifeguard certification programs. One study evaluating the effectiveness of a skin cancer prevention program for lifeguards found that many of the participants lacked a thorough understanding of the different types of skin cancer.⁵ Another study found that lifeguards at pools in areas where societal norms supporting sun safety are stronger exhibited noticeably more sun protection practices, with regression estimates of 0.22 (95% CI, 0.17-0.26).⁷ Empowering lifeguards with valuable health knowledge during their regular training could potentially reduce their risk for skin cancer,⁴ as they may be more inclined to use sunscreen appropriately and reach out to a dermatologist for regular skin checks and evaluation of suspicious lesions.

Role of Lifeguards in Public Skin Cancer Prevention Efforts

Once trained on skin cancer prevention, lifeguards also can play a pivotal role in promoting sunscreen use among the public. Despite the widespread availability of high-quality sunscreens, many swimmers and beachgoers neglect to regularly apply or reapply sunscreen, especially on commonly exposed areas such as the back, shoulders, and face.⁸ Educating lifeguards on skin cancer prevention could enhance health outcomes by increasing early detection rates and promoting sun-safe behaviors among the general public.⁹ However, additional training requirements might increase the cost and time commitment for lifeguard certification, potentially leading to staffing shortages.^3,7 There also is a risk of lifeguards overstepping their role and providing inaccurate medical advice, which could cause distress or even lead to liability issues.⁷ Balancing these factors will be crucial in developing effective and sustainable skin cancer prevention programs for lifeguards.

Implementing Lifeguard Skin Cancer Training

Implementing skin cancer prevention training programs for lifeguards requires strategic collaboration between dermatologists, and lifeguard training organizations to ensure that the participants receive consistent and comprehensive training.¹⁰ Additionally, public health campaigns can support these efforts by raising awareness about the importance of sun safety and regular skin checks.⁶ Tailored training modules/materials, ongoing technical assistance, and active, multicomponent approaches that account for both individual and environmental factors can increase program implementation in a variety of community settings.

Final Thoughts

Through effective education, lifeguards can potentially have a substantial impact on skin cancer prevention, both among lifeguards themselves and the general public. By promoting proper sunscreen use, lifeguards can help reduce the incidence and mortality associated with skin cancers. Future studies should focus on developing and implementing targeted education initiatives for lifeguards, fostering collaboration between relevant stakeholders, and raising public awareness about the importance of sun safety and early skin cancer detection. These efforts ultimately could lead to improved public health outcomes and reduced skin cancer rates, particularly in high-risk populations that frequently are exposed to UV radiation.

Lifeguards play a crucial role in ensuring water safety, but they also are uniquely positioned to promote skin cancer prevention and proper sunscreen use.^1,2 There are several benefits and challenges to offering skin cancer prevention training for lifeguards.³ We examine the advantages of training, highlight the role lifeguards can play in larger public skin cancer prevention efforts, and address practical techniques for developing lifeguardfocused skin cancer education programs. By providing this knowledge to lifeguards, we can improve community health outcomes and encourage sun-safe behaviors in high-risk outdoor locations.

Benefits of Skin Cancer Prevention Training for Lifeguards

Research has shown that lifeguards are at an elevated risk for basal cell carcinoma, squamous cell carcinoma, and melanoma due to frequent prolonged occupational sun exposure.^1,2,4-6 Therefore, comprehensive education on skin cancer prevention—including instruction on proper sunscreen application techniques and the importance of regular reapplication as well as how to recognize suspicious skin lesions—should be incorporated into lifeguard certification programs. One study evaluating the effectiveness of a skin cancer prevention program for lifeguards found that many of the participants lacked a thorough understanding of the different types of skin cancer.⁵ Another study found that lifeguards at pools in areas where societal norms supporting sun safety are stronger exhibited noticeably more sun protection practices, with regression estimates of 0.22 (95% CI, 0.17-0.26).⁷ Empowering lifeguards with valuable health knowledge during their regular training could potentially reduce their risk for skin cancer,⁴ as they may be more inclined to use sunscreen appropriately and reach out to a dermatologist for regular skin checks and evaluation of suspicious lesions.

Role of Lifeguards in Public Skin Cancer Prevention Efforts

Once trained on skin cancer prevention, lifeguards also can play a pivotal role in promoting sunscreen use among the public. Despite the widespread availability of high-quality sunscreens, many swimmers and beachgoers neglect to regularly apply or reapply sunscreen, especially on commonly exposed areas such as the back, shoulders, and face.⁸ Educating lifeguards on skin cancer prevention could enhance health outcomes by increasing early detection rates and promoting sun-safe behaviors among the general public.⁹ However, additional training requirements might increase the cost and time commitment for lifeguard certification, potentially leading to staffing shortages.^3,7 There also is a risk of lifeguards overstepping their role and providing inaccurate medical advice, which could cause distress or even lead to liability issues.⁷ Balancing these factors will be crucial in developing effective and sustainable skin cancer prevention programs for lifeguards.

Implementing Lifeguard Skin Cancer Training

Implementing skin cancer prevention training programs for lifeguards requires strategic collaboration between dermatologists, and lifeguard training organizations to ensure that the participants receive consistent and comprehensive training.¹⁰ Additionally, public health campaigns can support these efforts by raising awareness about the importance of sun safety and regular skin checks.⁶ Tailored training modules/materials, ongoing technical assistance, and active, multicomponent approaches that account for both individual and environmental factors can increase program implementation in a variety of community settings.

Final Thoughts

Through effective education, lifeguards can potentially have a substantial impact on skin cancer prevention, both among lifeguards themselves and the general public. By promoting proper sunscreen use, lifeguards can help reduce the incidence and mortality associated with skin cancers. Future studies should focus on developing and implementing targeted education initiatives for lifeguards, fostering collaboration between relevant stakeholders, and raising public awareness about the importance of sun safety and early skin cancer detection. These efforts ultimately could lead to improved public health outcomes and reduced skin cancer rates, particularly in high-risk populations that frequently are exposed to UV radiation.

Lifeguards play a crucial role in ensuring water safety, but they also are uniquely positioned to promote skin cancer prevention and proper sunscreen use.^1,2 There are several benefits and challenges to offering skin cancer prevention training for lifeguards.³ We examine the advantages of training, highlight the role lifeguards can play in larger public skin cancer prevention efforts, and address practical techniques for developing lifeguardfocused skin cancer education programs. By providing this knowledge to lifeguards, we can improve community health outcomes and encourage sun-safe behaviors in high-risk outdoor locations.

Benefits of Skin Cancer Prevention Training for Lifeguards

Research has shown that lifeguards are at an elevated risk for basal cell carcinoma, squamous cell carcinoma, and melanoma due to frequent prolonged occupational sun exposure.^1,2,4-6 Therefore, comprehensive education on skin cancer prevention—including instruction on proper sunscreen application techniques and the importance of regular reapplication as well as how to recognize suspicious skin lesions—should be incorporated into lifeguard certification programs. One study evaluating the effectiveness of a skin cancer prevention program for lifeguards found that many of the participants lacked a thorough understanding of the different types of skin cancer.⁵ Another study found that lifeguards at pools in areas where societal norms supporting sun safety are stronger exhibited noticeably more sun protection practices, with regression estimates of 0.22 (95% CI, 0.17-0.26).⁷ Empowering lifeguards with valuable health knowledge during their regular training could potentially reduce their risk for skin cancer,⁴ as they may be more inclined to use sunscreen appropriately and reach out to a dermatologist for regular skin checks and evaluation of suspicious lesions.

Role of Lifeguards in Public Skin Cancer Prevention Efforts

Once trained on skin cancer prevention, lifeguards also can play a pivotal role in promoting sunscreen use among the public. Despite the widespread availability of high-quality sunscreens, many swimmers and beachgoers neglect to regularly apply or reapply sunscreen, especially on commonly exposed areas such as the back, shoulders, and face.⁸ Educating lifeguards on skin cancer prevention could enhance health outcomes by increasing early detection rates and promoting sun-safe behaviors among the general public.⁹ However, additional training requirements might increase the cost and time commitment for lifeguard certification, potentially leading to staffing shortages.^3,7 There also is a risk of lifeguards overstepping their role and providing inaccurate medical advice, which could cause distress or even lead to liability issues.⁷ Balancing these factors will be crucial in developing effective and sustainable skin cancer prevention programs for lifeguards.

Implementing Lifeguard Skin Cancer Training

Implementing skin cancer prevention training programs for lifeguards requires strategic collaboration between dermatologists, and lifeguard training organizations to ensure that the participants receive consistent and comprehensive training.¹⁰ Additionally, public health campaigns can support these efforts by raising awareness about the importance of sun safety and regular skin checks.⁶ Tailored training modules/materials, ongoing technical assistance, and active, multicomponent approaches that account for both individual and environmental factors can increase program implementation in a variety of community settings.

Final Thoughts

Through effective education, lifeguards can potentially have a substantial impact on skin cancer prevention, both among lifeguards themselves and the general public. By promoting proper sunscreen use, lifeguards can help reduce the incidence and mortality associated with skin cancers. Future studies should focus on developing and implementing targeted education initiatives for lifeguards, fostering collaboration between relevant stakeholders, and raising public awareness about the importance of sun safety and early skin cancer detection. These efforts ultimately could lead to improved public health outcomes and reduced skin cancer rates, particularly in high-risk populations that frequently are exposed to UV radiation.

Eosinophilic esophagitis (EoE) can be considered a “young” disease, with initial case series reported only about 30 years ago. Since that time, it has become a commonly encountered condition in both emergency and clinic settings. The most recent prevalence study estimates that 1 in 700 people in the U.S. have EoE,¹ the volume of EoE-associated ED visits tripped between 2009 and 2019 and is projected to double again by 3030,² and “new” gastroenterologists undoubtedly have learned about and seen this condition. As a chronic disease, EoE necessitates longitudinal follow-up and optimization of care to prevent complications. With increasing diagnostic delay, EoE progresses in most, but not all, patients from an inflammatory- to fibrostenotic-predominant condition.³This article will review a practical approach to diagnosing EoE, including common scenarios where it can be picked-up, as well as treatment and monitoring approaches.

Diagnosis of EoE

The most likely area that you will encounter EoE is during an emergent middle-of-the-night endoscopy for food impaction. If called in for this, EoE will be the cause in more than 50% of patients.⁴ However, the diagnosis can only be made if esophageal biopsies are obtained at the time of the procedure. This is a critical time to decrease diagnostic delay, as half of patients are lost to follow-up after a food impaction.⁵ Unfortunately, although taking biopsies during index food impaction is guideline-recommended, a quality metric, and safe to obtain after the food bolus is cleared, this is infrequently done in practice.^{6, 7}

The next most likely area for EoE detection is in the endoscopy suite where 15-23% of patients with dysphagia and 5-7% of patients undergoing upper endoscopy for any indication will have EoE.⁴ Sometimes EoE will be detected “incidentally” during an open-access case (for example, in a patient with diarrhea undergoing evaluation for celiac). In these cases, it is important to perform a careful history (as noted below) as subtle EoE symptoms can frequently be identified. Finally, when patients are seen in clinic for solid food dysphagia, EoE is clearly on the differential. A few percent of patients with refractory heartburn or chest pain will have EoE causing the symptoms rather than reflux,⁴ and all patients under consideration for antireflux surgery should have an endoscopy to assess for EoE.

When talking to patients with known or suspected EoE, the history must go beyond general questions about dysphagia or trouble swallowing. Many patients with EoE have overtly or subconsciously modified their eating behaviors over many years to minimize symptoms, may have adapted to chronic dysphagia, and will answer “no” when asked if they have trouble swallowing. Instead, use the acronym “IMPACT” to delve deeper into possible symptoms.⁸ Do they “Imbibe” fluids or liquids between each bite to help get food down? Do they “Modify” the way they eat (cut food into small bites; puree foods)? Do they “Prolong” mealtimes? Do they “Avoid” certain foods that stick? Do they “Chew’ until their food is a mush to get it down? And do they “Turn away” tablets or pills? Pill dysphagia is often a subtle symptom, and sometimes the only symptom elicited.

Additionally, it may be important to ask a partner or family member (if present) about their observations. They may provide insight (e.g. “yes – he chokes with every bite but never says it bothers him”) that the patient might not otherwise provide. The suspicion for EoE should also be increased in patients with concomitant atopic diseases and in those with a family history of dysphagia or who have family members needing esophageal dilation. It is important to remember that EoE can be seen across all ages, sexes, and races/ethnicities.

Diagnosis of EoE is based on the AGREE consensus,⁹ which is also echoed in the recently updated American College of Gastroenterology (ACG) guidelines.¹⁰ Diagnosis requires three steps. First, symptoms of esophageal dysfunction must be present. This will most typically be dysphagia in adolescents and adults, but symptoms are non-specific in children (e.g. poor growth and feeding, abdominal pain, vomiting, regurgitation, heartburn).

Second, at least 15 eosinophils per high-power field (eos/hpf) are required on esophageal biopsy, which implies that an endoscopy be performed. A high-quality endoscopic exam in EoE is of the utmost importance. The approach has been described elsewhere,¹¹ but enough time on insertion should be taken to fully insufflate and examine the esophagus, including the areas of the gastroesophageal junction and upper esophageal sphincter where strictures can be missed, to gently wash debris, and to assess the endoscopic findings of EoE. Endoscopic findings should be reported using the validated EoE Endoscopy Reference Score (EREFS),¹² which grades five key features. EREFS is reproducible, is responsive to treatment, and is guideline-recommended (see Figure 1).^{6, 10} The features are edema (present=1), rings (mild=1; moderate=2; severe=3), exudates (mild=1; severe=2), furrows (mild=1; severe=2), and stricture (present=1; also estimate diameter in mm) and are incorporated into many endoscopic reporting programs. Additionally, diffuse luminal narrowing and mucosal fragility (“crepe-paper” mucosa) should be assessed.

After this, biopsies should be obtained with at least 6 biopsy fragments from different locations in the esophagus. Any visible endoscopic abnormalities should be targeted (the highest yield is in exudates and furrows). The rationale is that EoE is patchy and at least 6 biopsies will maximize diagnostic yield.¹⁰ Ideally the initial endoscopy for EoE should be done off of treatments (like PPI or diet restriction) as these could mask the diagnosis. If a patient with suspected EoE has an endoscopy while on PPI, and the endoscopy is normal, a diagnosis of EoE cannot be made. In this case, consideration should be given as to stopping the PPI, allowing a wash out period (at least 1-2 months), and then repeating the endoscopy to confirm the diagnosis. This is important as EoE is a chronic condition necessitating life-long treatment and monitoring, so a definitive diagnosis is critical.

The third and final step in diagnosis is assessing for other conditions that could cause esophageal eosinophilia.⁹ The most common differential diagnosis is gastroesophageal reflux disease (GERD). In some cases, EoE and GERD overlap or can have a complex relationship.¹³ Unfortunately the location of the eosinophilia (i.e. distal only) and the level of the eosinophil counts are not useful in making this distinction, so all clinical features (symptoms, presence of erosive esophagitis, or a hiatal hernia endoscopically), and ancillary reflex testing when indicated may be required prior to a formal EoE diagnosis. After the diagnosis is established, there should be direct communication with the patient to review the diagnosis and select treatments. While it is possible to convey results electronically in a messaging portal or with a letter, a more formal interaction, such as a clinic visit, is recommended because this is a new diagnosis of a chronic condition. Similarly, a new diagnosis of inflammatory bowel disease would never be made in a pathology follow-up letter alone. 

 

Treatment of EoE

When it comes to treatment, the new guidelines emphasize several points.¹⁰ First, there is the concept that anti-inflammatory treatment should be paired with assessment of fibrostenosis and esophageal dilation; to do either in isolation is incomplete treatment. It is safe to perform dilation both prior to anti-inflammatory treatment (for example, with a critical stricture in a patient with dysphagia) and after anti-inflammatory treatment has been prescribed (for example, during an endoscopy to assess treatment response).

Second, proton pump inhibitors (PPIs), swallowed topical corticosteroids (tCS), or dietary elimination are all acceptable first-line treatment options for EoE. A shared decision-making framework should be used for this discussion. If dietary elimination is selected,¹⁴ based on new clinical trial data, guidelines recommend using empiric elimination and starting with a less restrictive diet (either a one-food elimination diet with dairy alone or a two-food elimination with dairy and wheat elimination). If PPIs are selected, the dose should be double the standard reflux dose. Data are mixed as to whether to use twice daily dosing (i.e., omeprazole 20 mg twice daily) or once a day dosing (i.e., omeprazole 40 mg daily), but total dose and adherence may be more important than frequency.¹⁰

For tCS use, either budesonide or fluticasone can be selected, but budesonide oral suspension is the only FDA-approved tCS for EoE.¹⁵ Initial treatment length is usually 6-8 weeks for diet elimination and, 12 weeks for PPI and tCS. In general, it is best to pick a single treatment to start, and reserve combining therapies for patients who do not have a complete response to a single modality as there are few data to support combination therapy.

After initial treatment, it is critical to assess for treatment response.¹⁶ Goals of EoE treatment include improvement in symptoms, but also improvement in endoscopic and histologic features to prevent complications. Symptoms in EoE do not always correlate with underlying biologic disease activity: patients can minimize symptoms with careful eating; they may perceive no difference in symptoms despite histologic improvement if a stricture persists; and they may have minimal symptoms after esophageal dilation despite ongoing inflammation. Because of this, performing a follow-up endoscopy after initial treatment is guideline-recommended.^{10, 17} This allows assessing for endoscopic improvement, re-assessing for fibrostenosis and performing dilation if indicated, and obtaining esophageal biopsies. If there is non-response, options include switching between other first line treatments or considering “stepping-up” to dupilumab which is also an FDA-approved option for EoE that is recommended in the guidelines.^{10, 18} In some cases where patients have multiple severe atopic conditions such as asthma or eczema that would warrant dupilumab use, or if patients are intolerant to PPIs or tCS, dupilumab could be considered as an earlier treatment for EoE.

 

Long-Term Maintenance

If a patient has a good response (for example, improved symptoms, improved endoscopic features, and <15 eos/hpf on biopsy), treatment can be maintained long-term. In almost all cases, if treatment is stopped, EoE disease activity recurs.¹⁹ Patients could be seen back in clinic in 6-12 months, and then a discussion can be conducted about a follow-up endoscopy, with timing to be determined based on their individual disease features and severity.¹⁷

Patients with more severe strictures, however, may have to be seen in endoscopy for serial dilations. Continued follow-up is essential for optimal care. Just as patients can progress in their disease course with diagnostic delay, there are data that show they can also progress after diagnosis when there are gaps in care without regular follow-up.²⁰ Unlike other chronic esophageal disorders such as GERD and Barrett’s esophagus and other chronic GI inflammatory conditions like inflammatory bowel disease, however, EoE is not associated with an increased risk of esophageal cancer.^{21, 22}

Given its increasing frequency, EoE will be commonly encountered by gastroenterologists both new and established. Having a systematic approach for diagnosis, understanding how to elicit subtle symptoms, implementing a shared decision-making framework for treatment with a structured algorithm for assessing response, performing follow-up, maintaining treatment, and monitoring patients long-term will allow the large majority of EoE patients to be successfully managed.

Dr. Dellon is based at the Center for Esophageal Diseases and Swallowing, Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill. He disclosed research funding, consultant fees, and educational grants from multiple companies.

References

1. Thel HL, et al. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.09.031.

2. Lam AY, et al. Epidemiologic Burden and Projections for Eosinophilic Esophagitis-Associated Emergency Department Visits in the United States: 2009-2030. Clin Gastroenterol Hepatol. 2023 Nov. doi: 10.1016/j.cgh.2023.04.028.

3. Schoepfer AM, et al. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology. 2013 Dec. doi: 10.1053/j.gastro.2013.08.015.

4. Dellon ES, Hirano I. Epidemiology and Natural History of Eosinophilic Esophagitis. Gastroenterology. 2018 Jan. doi: 10.1053/j.gastro.2017.06.067.

5. Chang JW, et al. Loss to follow-up after food impaction among patients with and without eosinophilic esophagitis. Dis Esophagus. 2019 Dec. doi: 10.1093/dote/doz056.

6. Aceves SS, et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest Endosc. 2022 Aug. doi: 10.1016/j.gie.2022.05.013.

7. Leiman DA, et al. Quality Indicators for the Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2023 Jun. doi: 10.14309/ajg.0000000000002138.

8. Hirano I, Furuta GT. Approaches and Challenges to Management of Pediatric and Adult Patients With Eosinophilic Esophagitis. Gastroenterology. 2020 Mar. doi: 10.1053/j.gastro.2019.09.052.

9. Dellon ES, et al. Updated international consensus diagnostic criteria for eosinophilic esophagitis: Proceedings of the AGREE conference. Gastroenterology. 2018 Oct. doi: 10.1053/j.gastro.2018.07.009.

10. Dellon ES, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2025 Jan. doi: 10.14309/ajg.0000000000003194.

11. Dellon ES. Optimizing the Endoscopic Examination in Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2021 Dec. doi: 10.1016/j.cgh.2021.07.011.

12. Hirano I, et al. Endoscopic assessment of the oesophageal features of eosinophilic oesophagitis: validation of a novel classification and grading system. Gut. 2012 May. doi: 10.1136/gutjnl-2011-301817.

13. Spechler SJ, et al. Thoughts on the complex relationship between gastroesophageal reflux disease and eosinophilic esophagitis. Am J Gastroenterol. 2007 Jun. doi: 10.1111/j.1572-0241.2007.01179.x.

14. Chang JW, et al. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2023 Jul. doi: 10.1016/j.cgh.2023.03.006.

15. Hirano I, et al. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022 Mar. doi: 10.1016/j.cgh.2021.04.022.

16. Dellon ES, Gupta SK. A conceptual approach to understanding treatment response in eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2019 Oct. doi: 10.1016/j.cgh.2019.01.030.

17. von Arnim U, et al. Monitoring Patients With Eosinophilic Esophagitis in Routine Clinical Practice - International Expert Recommendations. Clin Gastroenterol Hepatol. 2023 Sep. doi: 10.1016/j.cgh.2022.12.018.

18. Dellon ES, et al. Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis. N Engl J Med. 2022 Dec. doi: 10.1056/NEJMoa220598.

19. Dellon ES, et al. Rapid Recurrence of Eosinophilic Esophagitis Activity After Successful Treatment in the Observation Phase of a Randomized, Double-Blind, Double-Dummy Trial. Clin Gastroenterol Hepatol. 2020 Jun. doi: 10.1016/j.cgh.2019.08.050.

20. Chang NC, et al. A Gap in Care Leads to Progression of Fibrosis in Eosinophilic Esophagitis Patients. Clin Gastroenterol Hepatol. 2022 Aug. doi: 10.1016/j.cgh.2021.10.028.

21. Syed A, et al. The relationship between eosinophilic esophagitis and esophageal cancer. Dis Esophagus. 2017 Jul. doi: 10.1093/dote/dox050.

22. Albaneze N, et al. No Association Between Eosinophilic Oesophagitis and Oesophageal Cancer in US Adults: A Case-Control Study. Aliment Pharmacol Ther. 2025 Jan. doi: 10.1111/apt.18431.







 

Eosinophilic esophagitis (EoE) can be considered a “young” disease, with initial case series reported only about 30 years ago. Since that time, it has become a commonly encountered condition in both emergency and clinic settings. The most recent prevalence study estimates that 1 in 700 people in the U.S. have EoE,¹ the volume of EoE-associated ED visits tripped between 2009 and 2019 and is projected to double again by 3030,² and “new” gastroenterologists undoubtedly have learned about and seen this condition. As a chronic disease, EoE necessitates longitudinal follow-up and optimization of care to prevent complications. With increasing diagnostic delay, EoE progresses in most, but not all, patients from an inflammatory- to fibrostenotic-predominant condition.³This article will review a practical approach to diagnosing EoE, including common scenarios where it can be picked-up, as well as treatment and monitoring approaches.

Diagnosis of EoE

The most likely area that you will encounter EoE is during an emergent middle-of-the-night endoscopy for food impaction. If called in for this, EoE will be the cause in more than 50% of patients.⁴ However, the diagnosis can only be made if esophageal biopsies are obtained at the time of the procedure. This is a critical time to decrease diagnostic delay, as half of patients are lost to follow-up after a food impaction.⁵ Unfortunately, although taking biopsies during index food impaction is guideline-recommended, a quality metric, and safe to obtain after the food bolus is cleared, this is infrequently done in practice.^{6, 7}

The next most likely area for EoE detection is in the endoscopy suite where 15-23% of patients with dysphagia and 5-7% of patients undergoing upper endoscopy for any indication will have EoE.⁴ Sometimes EoE will be detected “incidentally” during an open-access case (for example, in a patient with diarrhea undergoing evaluation for celiac). In these cases, it is important to perform a careful history (as noted below) as subtle EoE symptoms can frequently be identified. Finally, when patients are seen in clinic for solid food dysphagia, EoE is clearly on the differential. A few percent of patients with refractory heartburn or chest pain will have EoE causing the symptoms rather than reflux,⁴ and all patients under consideration for antireflux surgery should have an endoscopy to assess for EoE.

When talking to patients with known or suspected EoE, the history must go beyond general questions about dysphagia or trouble swallowing. Many patients with EoE have overtly or subconsciously modified their eating behaviors over many years to minimize symptoms, may have adapted to chronic dysphagia, and will answer “no” when asked if they have trouble swallowing. Instead, use the acronym “IMPACT” to delve deeper into possible symptoms.⁸ Do they “Imbibe” fluids or liquids between each bite to help get food down? Do they “Modify” the way they eat (cut food into small bites; puree foods)? Do they “Prolong” mealtimes? Do they “Avoid” certain foods that stick? Do they “Chew’ until their food is a mush to get it down? And do they “Turn away” tablets or pills? Pill dysphagia is often a subtle symptom, and sometimes the only symptom elicited.

Additionally, it may be important to ask a partner or family member (if present) about their observations. They may provide insight (e.g. “yes – he chokes with every bite but never says it bothers him”) that the patient might not otherwise provide. The suspicion for EoE should also be increased in patients with concomitant atopic diseases and in those with a family history of dysphagia or who have family members needing esophageal dilation. It is important to remember that EoE can be seen across all ages, sexes, and races/ethnicities.

Diagnosis of EoE is based on the AGREE consensus,⁹ which is also echoed in the recently updated American College of Gastroenterology (ACG) guidelines.¹⁰ Diagnosis requires three steps. First, symptoms of esophageal dysfunction must be present. This will most typically be dysphagia in adolescents and adults, but symptoms are non-specific in children (e.g. poor growth and feeding, abdominal pain, vomiting, regurgitation, heartburn).

Second, at least 15 eosinophils per high-power field (eos/hpf) are required on esophageal biopsy, which implies that an endoscopy be performed. A high-quality endoscopic exam in EoE is of the utmost importance. The approach has been described elsewhere,¹¹ but enough time on insertion should be taken to fully insufflate and examine the esophagus, including the areas of the gastroesophageal junction and upper esophageal sphincter where strictures can be missed, to gently wash debris, and to assess the endoscopic findings of EoE. Endoscopic findings should be reported using the validated EoE Endoscopy Reference Score (EREFS),¹² which grades five key features. EREFS is reproducible, is responsive to treatment, and is guideline-recommended (see Figure 1).^{6, 10} The features are edema (present=1), rings (mild=1; moderate=2; severe=3), exudates (mild=1; severe=2), furrows (mild=1; severe=2), and stricture (present=1; also estimate diameter in mm) and are incorporated into many endoscopic reporting programs. Additionally, diffuse luminal narrowing and mucosal fragility (“crepe-paper” mucosa) should be assessed.

After this, biopsies should be obtained with at least 6 biopsy fragments from different locations in the esophagus. Any visible endoscopic abnormalities should be targeted (the highest yield is in exudates and furrows). The rationale is that EoE is patchy and at least 6 biopsies will maximize diagnostic yield.¹⁰ Ideally the initial endoscopy for EoE should be done off of treatments (like PPI or diet restriction) as these could mask the diagnosis. If a patient with suspected EoE has an endoscopy while on PPI, and the endoscopy is normal, a diagnosis of EoE cannot be made. In this case, consideration should be given as to stopping the PPI, allowing a wash out period (at least 1-2 months), and then repeating the endoscopy to confirm the diagnosis. This is important as EoE is a chronic condition necessitating life-long treatment and monitoring, so a definitive diagnosis is critical.

The third and final step in diagnosis is assessing for other conditions that could cause esophageal eosinophilia.⁹ The most common differential diagnosis is gastroesophageal reflux disease (GERD). In some cases, EoE and GERD overlap or can have a complex relationship.¹³ Unfortunately the location of the eosinophilia (i.e. distal only) and the level of the eosinophil counts are not useful in making this distinction, so all clinical features (symptoms, presence of erosive esophagitis, or a hiatal hernia endoscopically), and ancillary reflex testing when indicated may be required prior to a formal EoE diagnosis. After the diagnosis is established, there should be direct communication with the patient to review the diagnosis and select treatments. While it is possible to convey results electronically in a messaging portal or with a letter, a more formal interaction, such as a clinic visit, is recommended because this is a new diagnosis of a chronic condition. Similarly, a new diagnosis of inflammatory bowel disease would never be made in a pathology follow-up letter alone. 

 

Treatment of EoE

When it comes to treatment, the new guidelines emphasize several points.¹⁰ First, there is the concept that anti-inflammatory treatment should be paired with assessment of fibrostenosis and esophageal dilation; to do either in isolation is incomplete treatment. It is safe to perform dilation both prior to anti-inflammatory treatment (for example, with a critical stricture in a patient with dysphagia) and after anti-inflammatory treatment has been prescribed (for example, during an endoscopy to assess treatment response).

Second, proton pump inhibitors (PPIs), swallowed topical corticosteroids (tCS), or dietary elimination are all acceptable first-line treatment options for EoE. A shared decision-making framework should be used for this discussion. If dietary elimination is selected,¹⁴ based on new clinical trial data, guidelines recommend using empiric elimination and starting with a less restrictive diet (either a one-food elimination diet with dairy alone or a two-food elimination with dairy and wheat elimination). If PPIs are selected, the dose should be double the standard reflux dose. Data are mixed as to whether to use twice daily dosing (i.e., omeprazole 20 mg twice daily) or once a day dosing (i.e., omeprazole 40 mg daily), but total dose and adherence may be more important than frequency.¹⁰

For tCS use, either budesonide or fluticasone can be selected, but budesonide oral suspension is the only FDA-approved tCS for EoE.¹⁵ Initial treatment length is usually 6-8 weeks for diet elimination and, 12 weeks for PPI and tCS. In general, it is best to pick a single treatment to start, and reserve combining therapies for patients who do not have a complete response to a single modality as there are few data to support combination therapy.

After initial treatment, it is critical to assess for treatment response.¹⁶ Goals of EoE treatment include improvement in symptoms, but also improvement in endoscopic and histologic features to prevent complications. Symptoms in EoE do not always correlate with underlying biologic disease activity: patients can minimize symptoms with careful eating; they may perceive no difference in symptoms despite histologic improvement if a stricture persists; and they may have minimal symptoms after esophageal dilation despite ongoing inflammation. Because of this, performing a follow-up endoscopy after initial treatment is guideline-recommended.^{10, 17} This allows assessing for endoscopic improvement, re-assessing for fibrostenosis and performing dilation if indicated, and obtaining esophageal biopsies. If there is non-response, options include switching between other first line treatments or considering “stepping-up” to dupilumab which is also an FDA-approved option for EoE that is recommended in the guidelines.^{10, 18} In some cases where patients have multiple severe atopic conditions such as asthma or eczema that would warrant dupilumab use, or if patients are intolerant to PPIs or tCS, dupilumab could be considered as an earlier treatment for EoE.

 

Long-Term Maintenance

If a patient has a good response (for example, improved symptoms, improved endoscopic features, and <15 eos/hpf on biopsy), treatment can be maintained long-term. In almost all cases, if treatment is stopped, EoE disease activity recurs.¹⁹ Patients could be seen back in clinic in 6-12 months, and then a discussion can be conducted about a follow-up endoscopy, with timing to be determined based on their individual disease features and severity.¹⁷

Patients with more severe strictures, however, may have to be seen in endoscopy for serial dilations. Continued follow-up is essential for optimal care. Just as patients can progress in their disease course with diagnostic delay, there are data that show they can also progress after diagnosis when there are gaps in care without regular follow-up.²⁰ Unlike other chronic esophageal disorders such as GERD and Barrett’s esophagus and other chronic GI inflammatory conditions like inflammatory bowel disease, however, EoE is not associated with an increased risk of esophageal cancer.^{21, 22}

Given its increasing frequency, EoE will be commonly encountered by gastroenterologists both new and established. Having a systematic approach for diagnosis, understanding how to elicit subtle symptoms, implementing a shared decision-making framework for treatment with a structured algorithm for assessing response, performing follow-up, maintaining treatment, and monitoring patients long-term will allow the large majority of EoE patients to be successfully managed.

Dr. Dellon is based at the Center for Esophageal Diseases and Swallowing, Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill. He disclosed research funding, consultant fees, and educational grants from multiple companies.

References

1. Thel HL, et al. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.09.031.

2. Lam AY, et al. Epidemiologic Burden and Projections for Eosinophilic Esophagitis-Associated Emergency Department Visits in the United States: 2009-2030. Clin Gastroenterol Hepatol. 2023 Nov. doi: 10.1016/j.cgh.2023.04.028.

3. Schoepfer AM, et al. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology. 2013 Dec. doi: 10.1053/j.gastro.2013.08.015.

4. Dellon ES, Hirano I. Epidemiology and Natural History of Eosinophilic Esophagitis. Gastroenterology. 2018 Jan. doi: 10.1053/j.gastro.2017.06.067.

5. Chang JW, et al. Loss to follow-up after food impaction among patients with and without eosinophilic esophagitis. Dis Esophagus. 2019 Dec. doi: 10.1093/dote/doz056.

6. Aceves SS, et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest Endosc. 2022 Aug. doi: 10.1016/j.gie.2022.05.013.

7. Leiman DA, et al. Quality Indicators for the Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2023 Jun. doi: 10.14309/ajg.0000000000002138.

8. Hirano I, Furuta GT. Approaches and Challenges to Management of Pediatric and Adult Patients With Eosinophilic Esophagitis. Gastroenterology. 2020 Mar. doi: 10.1053/j.gastro.2019.09.052.

9. Dellon ES, et al. Updated international consensus diagnostic criteria for eosinophilic esophagitis: Proceedings of the AGREE conference. Gastroenterology. 2018 Oct. doi: 10.1053/j.gastro.2018.07.009.

10. Dellon ES, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2025 Jan. doi: 10.14309/ajg.0000000000003194.

11. Dellon ES. Optimizing the Endoscopic Examination in Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2021 Dec. doi: 10.1016/j.cgh.2021.07.011.

12. Hirano I, et al. Endoscopic assessment of the oesophageal features of eosinophilic oesophagitis: validation of a novel classification and grading system. Gut. 2012 May. doi: 10.1136/gutjnl-2011-301817.

13. Spechler SJ, et al. Thoughts on the complex relationship between gastroesophageal reflux disease and eosinophilic esophagitis. Am J Gastroenterol. 2007 Jun. doi: 10.1111/j.1572-0241.2007.01179.x.

14. Chang JW, et al. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2023 Jul. doi: 10.1016/j.cgh.2023.03.006.

15. Hirano I, et al. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022 Mar. doi: 10.1016/j.cgh.2021.04.022.

16. Dellon ES, Gupta SK. A conceptual approach to understanding treatment response in eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2019 Oct. doi: 10.1016/j.cgh.2019.01.030.

17. von Arnim U, et al. Monitoring Patients With Eosinophilic Esophagitis in Routine Clinical Practice - International Expert Recommendations. Clin Gastroenterol Hepatol. 2023 Sep. doi: 10.1016/j.cgh.2022.12.018.

18. Dellon ES, et al. Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis. N Engl J Med. 2022 Dec. doi: 10.1056/NEJMoa220598.

19. Dellon ES, et al. Rapid Recurrence of Eosinophilic Esophagitis Activity After Successful Treatment in the Observation Phase of a Randomized, Double-Blind, Double-Dummy Trial. Clin Gastroenterol Hepatol. 2020 Jun. doi: 10.1016/j.cgh.2019.08.050.

20. Chang NC, et al. A Gap in Care Leads to Progression of Fibrosis in Eosinophilic Esophagitis Patients. Clin Gastroenterol Hepatol. 2022 Aug. doi: 10.1016/j.cgh.2021.10.028.

21. Syed A, et al. The relationship between eosinophilic esophagitis and esophageal cancer. Dis Esophagus. 2017 Jul. doi: 10.1093/dote/dox050.

22. Albaneze N, et al. No Association Between Eosinophilic Oesophagitis and Oesophageal Cancer in US Adults: A Case-Control Study. Aliment Pharmacol Ther. 2025 Jan. doi: 10.1111/apt.18431.







 

Eosinophilic esophagitis (EoE) can be considered a “young” disease, with initial case series reported only about 30 years ago. Since that time, it has become a commonly encountered condition in both emergency and clinic settings. The most recent prevalence study estimates that 1 in 700 people in the U.S. have EoE,¹ the volume of EoE-associated ED visits tripped between 2009 and 2019 and is projected to double again by 3030,² and “new” gastroenterologists undoubtedly have learned about and seen this condition. As a chronic disease, EoE necessitates longitudinal follow-up and optimization of care to prevent complications. With increasing diagnostic delay, EoE progresses in most, but not all, patients from an inflammatory- to fibrostenotic-predominant condition.³This article will review a practical approach to diagnosing EoE, including common scenarios where it can be picked-up, as well as treatment and monitoring approaches.

Diagnosis of EoE

The most likely area that you will encounter EoE is during an emergent middle-of-the-night endoscopy for food impaction. If called in for this, EoE will be the cause in more than 50% of patients.⁴ However, the diagnosis can only be made if esophageal biopsies are obtained at the time of the procedure. This is a critical time to decrease diagnostic delay, as half of patients are lost to follow-up after a food impaction.⁵ Unfortunately, although taking biopsies during index food impaction is guideline-recommended, a quality metric, and safe to obtain after the food bolus is cleared, this is infrequently done in practice.^{6, 7}

The next most likely area for EoE detection is in the endoscopy suite where 15-23% of patients with dysphagia and 5-7% of patients undergoing upper endoscopy for any indication will have EoE.⁴ Sometimes EoE will be detected “incidentally” during an open-access case (for example, in a patient with diarrhea undergoing evaluation for celiac). In these cases, it is important to perform a careful history (as noted below) as subtle EoE symptoms can frequently be identified. Finally, when patients are seen in clinic for solid food dysphagia, EoE is clearly on the differential. A few percent of patients with refractory heartburn or chest pain will have EoE causing the symptoms rather than reflux,⁴ and all patients under consideration for antireflux surgery should have an endoscopy to assess for EoE.

When talking to patients with known or suspected EoE, the history must go beyond general questions about dysphagia or trouble swallowing. Many patients with EoE have overtly or subconsciously modified their eating behaviors over many years to minimize symptoms, may have adapted to chronic dysphagia, and will answer “no” when asked if they have trouble swallowing. Instead, use the acronym “IMPACT” to delve deeper into possible symptoms.⁸ Do they “Imbibe” fluids or liquids between each bite to help get food down? Do they “Modify” the way they eat (cut food into small bites; puree foods)? Do they “Prolong” mealtimes? Do they “Avoid” certain foods that stick? Do they “Chew’ until their food is a mush to get it down? And do they “Turn away” tablets or pills? Pill dysphagia is often a subtle symptom, and sometimes the only symptom elicited.

Additionally, it may be important to ask a partner or family member (if present) about their observations. They may provide insight (e.g. “yes – he chokes with every bite but never says it bothers him”) that the patient might not otherwise provide. The suspicion for EoE should also be increased in patients with concomitant atopic diseases and in those with a family history of dysphagia or who have family members needing esophageal dilation. It is important to remember that EoE can be seen across all ages, sexes, and races/ethnicities.

Diagnosis of EoE is based on the AGREE consensus,⁹ which is also echoed in the recently updated American College of Gastroenterology (ACG) guidelines.¹⁰ Diagnosis requires three steps. First, symptoms of esophageal dysfunction must be present. This will most typically be dysphagia in adolescents and adults, but symptoms are non-specific in children (e.g. poor growth and feeding, abdominal pain, vomiting, regurgitation, heartburn).

Second, at least 15 eosinophils per high-power field (eos/hpf) are required on esophageal biopsy, which implies that an endoscopy be performed. A high-quality endoscopic exam in EoE is of the utmost importance. The approach has been described elsewhere,¹¹ but enough time on insertion should be taken to fully insufflate and examine the esophagus, including the areas of the gastroesophageal junction and upper esophageal sphincter where strictures can be missed, to gently wash debris, and to assess the endoscopic findings of EoE. Endoscopic findings should be reported using the validated EoE Endoscopy Reference Score (EREFS),¹² which grades five key features. EREFS is reproducible, is responsive to treatment, and is guideline-recommended (see Figure 1).^{6, 10} The features are edema (present=1), rings (mild=1; moderate=2; severe=3), exudates (mild=1; severe=2), furrows (mild=1; severe=2), and stricture (present=1; also estimate diameter in mm) and are incorporated into many endoscopic reporting programs. Additionally, diffuse luminal narrowing and mucosal fragility (“crepe-paper” mucosa) should be assessed.

After this, biopsies should be obtained with at least 6 biopsy fragments from different locations in the esophagus. Any visible endoscopic abnormalities should be targeted (the highest yield is in exudates and furrows). The rationale is that EoE is patchy and at least 6 biopsies will maximize diagnostic yield.¹⁰ Ideally the initial endoscopy for EoE should be done off of treatments (like PPI or diet restriction) as these could mask the diagnosis. If a patient with suspected EoE has an endoscopy while on PPI, and the endoscopy is normal, a diagnosis of EoE cannot be made. In this case, consideration should be given as to stopping the PPI, allowing a wash out period (at least 1-2 months), and then repeating the endoscopy to confirm the diagnosis. This is important as EoE is a chronic condition necessitating life-long treatment and monitoring, so a definitive diagnosis is critical.

The third and final step in diagnosis is assessing for other conditions that could cause esophageal eosinophilia.⁹ The most common differential diagnosis is gastroesophageal reflux disease (GERD). In some cases, EoE and GERD overlap or can have a complex relationship.¹³ Unfortunately the location of the eosinophilia (i.e. distal only) and the level of the eosinophil counts are not useful in making this distinction, so all clinical features (symptoms, presence of erosive esophagitis, or a hiatal hernia endoscopically), and ancillary reflex testing when indicated may be required prior to a formal EoE diagnosis. After the diagnosis is established, there should be direct communication with the patient to review the diagnosis and select treatments. While it is possible to convey results electronically in a messaging portal or with a letter, a more formal interaction, such as a clinic visit, is recommended because this is a new diagnosis of a chronic condition. Similarly, a new diagnosis of inflammatory bowel disease would never be made in a pathology follow-up letter alone. 

 

Treatment of EoE

When it comes to treatment, the new guidelines emphasize several points.¹⁰ First, there is the concept that anti-inflammatory treatment should be paired with assessment of fibrostenosis and esophageal dilation; to do either in isolation is incomplete treatment. It is safe to perform dilation both prior to anti-inflammatory treatment (for example, with a critical stricture in a patient with dysphagia) and after anti-inflammatory treatment has been prescribed (for example, during an endoscopy to assess treatment response).

Second, proton pump inhibitors (PPIs), swallowed topical corticosteroids (tCS), or dietary elimination are all acceptable first-line treatment options for EoE. A shared decision-making framework should be used for this discussion. If dietary elimination is selected,¹⁴ based on new clinical trial data, guidelines recommend using empiric elimination and starting with a less restrictive diet (either a one-food elimination diet with dairy alone or a two-food elimination with dairy and wheat elimination). If PPIs are selected, the dose should be double the standard reflux dose. Data are mixed as to whether to use twice daily dosing (i.e., omeprazole 20 mg twice daily) or once a day dosing (i.e., omeprazole 40 mg daily), but total dose and adherence may be more important than frequency.¹⁰

For tCS use, either budesonide or fluticasone can be selected, but budesonide oral suspension is the only FDA-approved tCS for EoE.¹⁵ Initial treatment length is usually 6-8 weeks for diet elimination and, 12 weeks for PPI and tCS. In general, it is best to pick a single treatment to start, and reserve combining therapies for patients who do not have a complete response to a single modality as there are few data to support combination therapy.

After initial treatment, it is critical to assess for treatment response.¹⁶ Goals of EoE treatment include improvement in symptoms, but also improvement in endoscopic and histologic features to prevent complications. Symptoms in EoE do not always correlate with underlying biologic disease activity: patients can minimize symptoms with careful eating; they may perceive no difference in symptoms despite histologic improvement if a stricture persists; and they may have minimal symptoms after esophageal dilation despite ongoing inflammation. Because of this, performing a follow-up endoscopy after initial treatment is guideline-recommended.^{10, 17} This allows assessing for endoscopic improvement, re-assessing for fibrostenosis and performing dilation if indicated, and obtaining esophageal biopsies. If there is non-response, options include switching between other first line treatments or considering “stepping-up” to dupilumab which is also an FDA-approved option for EoE that is recommended in the guidelines.^{10, 18} In some cases where patients have multiple severe atopic conditions such as asthma or eczema that would warrant dupilumab use, or if patients are intolerant to PPIs or tCS, dupilumab could be considered as an earlier treatment for EoE.

 

Long-Term Maintenance

If a patient has a good response (for example, improved symptoms, improved endoscopic features, and <15 eos/hpf on biopsy), treatment can be maintained long-term. In almost all cases, if treatment is stopped, EoE disease activity recurs.¹⁹ Patients could be seen back in clinic in 6-12 months, and then a discussion can be conducted about a follow-up endoscopy, with timing to be determined based on their individual disease features and severity.¹⁷

Patients with more severe strictures, however, may have to be seen in endoscopy for serial dilations. Continued follow-up is essential for optimal care. Just as patients can progress in their disease course with diagnostic delay, there are data that show they can also progress after diagnosis when there are gaps in care without regular follow-up.²⁰ Unlike other chronic esophageal disorders such as GERD and Barrett’s esophagus and other chronic GI inflammatory conditions like inflammatory bowel disease, however, EoE is not associated with an increased risk of esophageal cancer.^{21, 22}

Given its increasing frequency, EoE will be commonly encountered by gastroenterologists both new and established. Having a systematic approach for diagnosis, understanding how to elicit subtle symptoms, implementing a shared decision-making framework for treatment with a structured algorithm for assessing response, performing follow-up, maintaining treatment, and monitoring patients long-term will allow the large majority of EoE patients to be successfully managed.

Dr. Dellon is based at the Center for Esophageal Diseases and Swallowing, Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill. He disclosed research funding, consultant fees, and educational grants from multiple companies.

References

1. Thel HL, et al. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.09.031.

2. Lam AY, et al. Epidemiologic Burden and Projections for Eosinophilic Esophagitis-Associated Emergency Department Visits in the United States: 2009-2030. Clin Gastroenterol Hepatol. 2023 Nov. doi: 10.1016/j.cgh.2023.04.028.

3. Schoepfer AM, et al. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology. 2013 Dec. doi: 10.1053/j.gastro.2013.08.015.

4. Dellon ES, Hirano I. Epidemiology and Natural History of Eosinophilic Esophagitis. Gastroenterology. 2018 Jan. doi: 10.1053/j.gastro.2017.06.067.

5. Chang JW, et al. Loss to follow-up after food impaction among patients with and without eosinophilic esophagitis. Dis Esophagus. 2019 Dec. doi: 10.1093/dote/doz056.

6. Aceves SS, et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest Endosc. 2022 Aug. doi: 10.1016/j.gie.2022.05.013.

7. Leiman DA, et al. Quality Indicators for the Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2023 Jun. doi: 10.14309/ajg.0000000000002138.

8. Hirano I, Furuta GT. Approaches and Challenges to Management of Pediatric and Adult Patients With Eosinophilic Esophagitis. Gastroenterology. 2020 Mar. doi: 10.1053/j.gastro.2019.09.052.

9. Dellon ES, et al. Updated international consensus diagnostic criteria for eosinophilic esophagitis: Proceedings of the AGREE conference. Gastroenterology. 2018 Oct. doi: 10.1053/j.gastro.2018.07.009.

10. Dellon ES, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2025 Jan. doi: 10.14309/ajg.0000000000003194.

11. Dellon ES. Optimizing the Endoscopic Examination in Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2021 Dec. doi: 10.1016/j.cgh.2021.07.011.

12. Hirano I, et al. Endoscopic assessment of the oesophageal features of eosinophilic oesophagitis: validation of a novel classification and grading system. Gut. 2012 May. doi: 10.1136/gutjnl-2011-301817.

13. Spechler SJ, et al. Thoughts on the complex relationship between gastroesophageal reflux disease and eosinophilic esophagitis. Am J Gastroenterol. 2007 Jun. doi: 10.1111/j.1572-0241.2007.01179.x.

14. Chang JW, et al. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2023 Jul. doi: 10.1016/j.cgh.2023.03.006.

15. Hirano I, et al. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022 Mar. doi: 10.1016/j.cgh.2021.04.022.

16. Dellon ES, Gupta SK. A conceptual approach to understanding treatment response in eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2019 Oct. doi: 10.1016/j.cgh.2019.01.030.

17. von Arnim U, et al. Monitoring Patients With Eosinophilic Esophagitis in Routine Clinical Practice - International Expert Recommendations. Clin Gastroenterol Hepatol. 2023 Sep. doi: 10.1016/j.cgh.2022.12.018.

18. Dellon ES, et al. Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis. N Engl J Med. 2022 Dec. doi: 10.1056/NEJMoa220598.

19. Dellon ES, et al. Rapid Recurrence of Eosinophilic Esophagitis Activity After Successful Treatment in the Observation Phase of a Randomized, Double-Blind, Double-Dummy Trial. Clin Gastroenterol Hepatol. 2020 Jun. doi: 10.1016/j.cgh.2019.08.050.

20. Chang NC, et al. A Gap in Care Leads to Progression of Fibrosis in Eosinophilic Esophagitis Patients. Clin Gastroenterol Hepatol. 2022 Aug. doi: 10.1016/j.cgh.2021.10.028.

21. Syed A, et al. The relationship between eosinophilic esophagitis and esophageal cancer. Dis Esophagus. 2017 Jul. doi: 10.1093/dote/dox050.

22. Albaneze N, et al. No Association Between Eosinophilic Oesophagitis and Oesophageal Cancer in US Adults: A Case-Control Study. Aliment Pharmacol Ther. 2025 Jan. doi: 10.1111/apt.18431.







 

In this video, Lisa Mathew, MD, of South Denver Gastroenterology in Denver, Colorado, and Raja Taunk, MD, of Anne Arundel Gastroenterology Associates, in Annapolis, Maryland, share insights on private practice gastroenterology and offer tips on building your practice – specifically improving your referral base.

In this video, Lisa Mathew, MD, of South Denver Gastroenterology in Denver, Colorado, and Raja Taunk, MD, of Anne Arundel Gastroenterology Associates, in Annapolis, Maryland, share insights on private practice gastroenterology and offer tips on building your practice – specifically improving your referral base.

In this video, Lisa Mathew, MD, of South Denver Gastroenterology in Denver, Colorado, and Raja Taunk, MD, of Anne Arundel Gastroenterology Associates, in Annapolis, Maryland, share insights on private practice gastroenterology and offer tips on building your practice – specifically improving your referral base.

The United States boasts one of the premier health care systems for medical education in the world. Indeed, institutions such as Johns Hopkins, Harvard, and the Mayo Clinic have storied reputations and are recognized names the world over. The United States also stands as a country of remarkable discovery in medicine with an abundance of enormously talented and productive medical scientists. This reputation draws physicians from every corner of the world who dream of studying medicine in our country.

Unfortunately, many US medical institutions, particularly the most prestigious medical centers, lean heavily toward preferential acceptance of US medical school graduates as an indicator of the highest-quality trainees. This historical bias is being further compounded by our current government’s pejorative view of immigrants in general. Will this affect the pool of tomorrow’s stars who will change the course of American medicine?

 

A glance at the list of recent AGA Presidents may yield some insight; over the past 10 years, three of our presidents trained internationally at universities in Malta, Libya, and Germany. This is a small snapshot of the multitude of international graduates in gastroenterology and hepatology who have served as division chiefs, AGA award winners, and journal editors, all now US citizens. This is not to mention the influence of varied insights and talents native to international study and culture that enhance our practice of medicine and biomedical research. 

We live in time when “immigrant” has been assigned a negative and almost subhuman connotation, and diversity has become something to be demonized rather than celebrated. Yet, intuitively, should a top US medical graduate be any more intelligent or driven than a top graduate from the United Kingdom, India, China, or Syria? As American medical physicians, we place the utmost value on our traditions and high standards. We boast an unmatched depth of medical talent spread across our GI divisions and practices and take pride in the way we teach medicine, like no other nation. Now, more than ever, is a time to attract the best and brightest international graduates not to compete with but to complement our remarkable US students. American medicine benefits from their talent and they inspire us to remember and care for diseases in our field that affect the world’s population, not just ours. 

Over 100 years ago, Dr. William Mayo stated “American practice is too broad to be national. It had the scientific spirit, and science knows no country.” Dr. Mayo also said, “Democracy is safe only so long as culture is in the ascendancy.” These lessons apply more than ever today.

David Katzka, MD

Associate Editor

The United States boasts one of the premier health care systems for medical education in the world. Indeed, institutions such as Johns Hopkins, Harvard, and the Mayo Clinic have storied reputations and are recognized names the world over. The United States also stands as a country of remarkable discovery in medicine with an abundance of enormously talented and productive medical scientists. This reputation draws physicians from every corner of the world who dream of studying medicine in our country.

Unfortunately, many US medical institutions, particularly the most prestigious medical centers, lean heavily toward preferential acceptance of US medical school graduates as an indicator of the highest-quality trainees. This historical bias is being further compounded by our current government’s pejorative view of immigrants in general. Will this affect the pool of tomorrow’s stars who will change the course of American medicine?

 

A glance at the list of recent AGA Presidents may yield some insight; over the past 10 years, three of our presidents trained internationally at universities in Malta, Libya, and Germany. This is a small snapshot of the multitude of international graduates in gastroenterology and hepatology who have served as division chiefs, AGA award winners, and journal editors, all now US citizens. This is not to mention the influence of varied insights and talents native to international study and culture that enhance our practice of medicine and biomedical research. 

We live in time when “immigrant” has been assigned a negative and almost subhuman connotation, and diversity has become something to be demonized rather than celebrated. Yet, intuitively, should a top US medical graduate be any more intelligent or driven than a top graduate from the United Kingdom, India, China, or Syria? As American medical physicians, we place the utmost value on our traditions and high standards. We boast an unmatched depth of medical talent spread across our GI divisions and practices and take pride in the way we teach medicine, like no other nation. Now, more than ever, is a time to attract the best and brightest international graduates not to compete with but to complement our remarkable US students. American medicine benefits from their talent and they inspire us to remember and care for diseases in our field that affect the world’s population, not just ours. 

Over 100 years ago, Dr. William Mayo stated “American practice is too broad to be national. It had the scientific spirit, and science knows no country.” Dr. Mayo also said, “Democracy is safe only so long as culture is in the ascendancy.” These lessons apply more than ever today.

David Katzka, MD

Associate Editor

The United States boasts one of the premier health care systems for medical education in the world. Indeed, institutions such as Johns Hopkins, Harvard, and the Mayo Clinic have storied reputations and are recognized names the world over. The United States also stands as a country of remarkable discovery in medicine with an abundance of enormously talented and productive medical scientists. This reputation draws physicians from every corner of the world who dream of studying medicine in our country.

Unfortunately, many US medical institutions, particularly the most prestigious medical centers, lean heavily toward preferential acceptance of US medical school graduates as an indicator of the highest-quality trainees. This historical bias is being further compounded by our current government’s pejorative view of immigrants in general. Will this affect the pool of tomorrow’s stars who will change the course of American medicine?

 

A glance at the list of recent AGA Presidents may yield some insight; over the past 10 years, three of our presidents trained internationally at universities in Malta, Libya, and Germany. This is a small snapshot of the multitude of international graduates in gastroenterology and hepatology who have served as division chiefs, AGA award winners, and journal editors, all now US citizens. This is not to mention the influence of varied insights and talents native to international study and culture that enhance our practice of medicine and biomedical research. 

We live in time when “immigrant” has been assigned a negative and almost subhuman connotation, and diversity has become something to be demonized rather than celebrated. Yet, intuitively, should a top US medical graduate be any more intelligent or driven than a top graduate from the United Kingdom, India, China, or Syria? As American medical physicians, we place the utmost value on our traditions and high standards. We boast an unmatched depth of medical talent spread across our GI divisions and practices and take pride in the way we teach medicine, like no other nation. Now, more than ever, is a time to attract the best and brightest international graduates not to compete with but to complement our remarkable US students. American medicine benefits from their talent and they inspire us to remember and care for diseases in our field that affect the world’s population, not just ours. 

Over 100 years ago, Dr. William Mayo stated “American practice is too broad to be national. It had the scientific spirit, and science knows no country.” Dr. Mayo also said, “Democracy is safe only so long as culture is in the ascendancy.” These lessons apply more than ever today.

David Katzka, MD

Associate Editor

Worldwide, health care is becoming increasingly complex as a result of greater clinical workforce demands, expanded roles and responsibilities, health care system mergers, stakeholder calls for new capabilities, and digital transformation. ^1,2These increasing demands has prompted many health care institutions to place greater focus on the psychological safety of their workforce, particularly in high reliability organizations (HROs). Building a robust foundation for high reliability in health care requires the presence of psychological safety—that is, staff members at all levels of the organization must feel comfortable speaking up when they have questions or concerns.^3,4 Psychological safety can improve the safety and quality of patient care but has not reached its full potential in health care.^5,6 However, there are strategies that promote the widespread implementation of psychological safety in health care organizations.^3-6

PSYCHOLOGICAL SAFETY

The concept of psychological safety in organizational behavior originated in 1965 when Edgar Schein and Warren Bennis, leaders in organizational psychology and management, published their reflections on the importance of psychological safety in helping individuals feel secure in the work environment.^5-7 Psychological safety in the workplace is foundational to staff members feeling comfortable asking questions or expressing concerns without fear of negative consequences.^8,9 It supports both individual and team efforts to raise safety concerns and report near misses and adverse events so that similar events can be averted in the future.⁹ Patients aren’t the only ones who benefit; psychological safety has also been found to promote job satisfaction and employee well-being.¹⁰

THE VETERANS HEALTH ADMINISTRATION JOURNEY

Achieving psychological safety is by no means an easy or comfortable process. As with any organizational change, a multipronged approach offers the best chance of success.^6,9 When the Veterans Health Administration (VHA) began its incremental, enterprise-wide journey to high reliability in 2019, 3 cohorts were identified. In February 2019, 18 US Department of Veterans Affairs (VA) medical centers (VAMCs) (cohort 1) began the process of becoming HROs. Cohort 2 followed in October 2020 and included 54 VAMC. Finally, in October 2021, 67 additional VAMCs (cohort 3) started the process.² During cohort 2, the VA Providence Healthcare System (VAPHCS) decided to emphasize psychological safety at the start of the journey to becoming an HRO. This system is part of the VA New England Healthcare System (VISN 1), which includes VAMCs and clinics in Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, and Vermont.¹¹ Soon thereafter, the VA Bedford Healthcare System and the VA Connecticut Healthcare System adopted similar strategies. Since then, other VAMCs have also adopted this approach. These collective experiences identified 4 useful strategies for achieving psychological safety: leadership engagement, open communication, education and training, and accountability.

Leadership Engagement

Health care organization leaders play a critical role in making psychological safety happen—especially in complex and constantly changing environments, such as HROs.⁴ Leaders behaviors are consistently linked to the perception of psychological safety at the individual, team, and organizational levels.⁸ It is especially important to have leaders who recognize the views of individuals and team members and encourage staff participation in discussions to gain additional perspectives.^7,8,12 Psychological safety can also be facilitated when leaders are visible, approachable, and communicative.^4,7-9

Organizational practices, policies, and processes (eg, reporting adverse events without the fear of negative consequences) are also important ways that leaders can establish and sustain psychological safety. On a more granular level, leaders can enhance psychological safety by promoting and acknowledging individuals who speak up, regularly asking staff about safety concerns, highlighting “good catches” when harm is avoided, and using staff feedback to initiate improvements.^4,7,13Finally, in the authors’ experience, psychological safety requires clear commitment from leaders at all levels of an organization. Communication should be bidirectional, and leaders should close the proverbial “loop” with feedback and timely follow-up. This encourages and reinforces staff engagement and speaking up behaviors.^2,4,7,13

Open Communication

Promoting an environment of open communication, where all individuals and teams feel empowered to speak up with questions, concerns, and recommendations—regardless of position within the organization—is critical to psychological safety.^4,6,9 Open communication is especially critical when processes and systems are constantly changing and advancing as a result of new information and technology.⁹ Promoting open, bidirectional communication during the delivery of patient care can be accomplished with huddles, tiered safety huddles, leader rounding for high reliability, and time-outs.^2,4,6 These opportunities allow team members to discuss concerns, identify resources that support safe, high-quality care; reflect on successes and opportunities for improvement; and circle back on concerns.^2,6 Open communication in psychologically safe environments empowers staff to raise patient care concerns and is instrumental for improving patient safety, increasing staff job satisfaction, and decreasing turnover.^6,14

Education and Training

Education and training for all staff—from the frontline to the executive level—are essential to successfully implementing the principles and practices of psychological safety.^5-7 VHA training covers many topics, including the origins, benefits, and implementation strategies of psychological safety (Table). Role-playing simulation is an effective teaching format, providing staff with opportunities to practice techniques for raising concerns or share feedback in a controlled environment.⁶ In addition, education should be ongoing; it helps leaders and staff members feel competent and confident when implementing psychological safety across the health care organization.^6,10

Accountability

The final critical strategy for achieving psychological safety is accountability. It is the responsibility of all leadership—from senior leaders to clinical and nonclinical managers—to create a culture of shared accountability.⁵ But first, expectations must be set. Leadership must establish well-defined behavioral expectations that align with the organization’s values. Understanding behavioral expectations will help to ensure that employees know what achievement looks like, as well as how they are being held accountable for their individual actions.^4,5,7 In practical terms, this means ensuring that staff members have the skills and resources to achieve goals and expectations, providing performance feedback in a timely manner, and including expectations in annual performance evaluations (as they are in the VHA).

Consistency is key. Accountability should be the expectation across all levels and services of the health care organization. No staff member should be exempt from promoting a psychologically safe work environment. Compliance with behavioral expectations should be monitored and if a person’s actions are not consistent with expectations, the situation will need to be addressed. Interventions will depend on the type, severity, and frequency of the problematic behaviors. Depending on an organization’s policies and practices, courses of action can range from feedback counseling to employment termination.⁵

A practical matter in ensuring accountability is implementing a psychologically safe process for reporting concerns. Staff members must feel comfortable reporting behavioral concerns without fear of retaliation, negative judgment, or consequences from peers and supervisors. One method for doing this is to create a confidential, centralized process for reporting concerns.⁵

First-Hand Results

VAPHCS has seen the results of implementing the strategies outlined here. For example, VAPHCS has observed a 45% increase in the use of the patient safety reporting system that logs medical errors and near-misses. In addition, there have been improvements in levels of psychological safety and patient safety reported in the annual VHA All Employee Survey, which is conducted annually to gauge workplace satisfaction, culture, climate, turnover, supervisory behaviors, and general workplace perceptions. VAPHCS has shown consistent improvements in 12 patient safety elements scored on a 5-point scale (1, very dissatisfied; 5, very satisfied) (Figure). Notably, employee ratings of error prevention discussed increased from 4.0 in 2022 to 4.3 in 2024. Data collection and analysis are ongoing; more comprehensive findings will be published in the future.

CONCLUSIONS

Health care organizations are increasingly recognizing the importance of psychologically safe workplaces in order to provide safe, high-quality patient care. Psychological safety is a critical tool for empowering staff to raise concerns, ask tough questions, challenge the status quo, and share new ideas for providing health care services. While psychological safety has been slowly adopted in health care, it’s clear that evidence-based strategies can make psychological safety a reality.

Worldwide, health care is becoming increasingly complex as a result of greater clinical workforce demands, expanded roles and responsibilities, health care system mergers, stakeholder calls for new capabilities, and digital transformation. ^1,2These increasing demands has prompted many health care institutions to place greater focus on the psychological safety of their workforce, particularly in high reliability organizations (HROs). Building a robust foundation for high reliability in health care requires the presence of psychological safety—that is, staff members at all levels of the organization must feel comfortable speaking up when they have questions or concerns.^3,4 Psychological safety can improve the safety and quality of patient care but has not reached its full potential in health care.^5,6 However, there are strategies that promote the widespread implementation of psychological safety in health care organizations.^3-6

PSYCHOLOGICAL SAFETY

The concept of psychological safety in organizational behavior originated in 1965 when Edgar Schein and Warren Bennis, leaders in organizational psychology and management, published their reflections on the importance of psychological safety in helping individuals feel secure in the work environment.^5-7 Psychological safety in the workplace is foundational to staff members feeling comfortable asking questions or expressing concerns without fear of negative consequences.^8,9 It supports both individual and team efforts to raise safety concerns and report near misses and adverse events so that similar events can be averted in the future.⁹ Patients aren’t the only ones who benefit; psychological safety has also been found to promote job satisfaction and employee well-being.¹⁰

THE VETERANS HEALTH ADMINISTRATION JOURNEY

Achieving psychological safety is by no means an easy or comfortable process. As with any organizational change, a multipronged approach offers the best chance of success.^6,9 When the Veterans Health Administration (VHA) began its incremental, enterprise-wide journey to high reliability in 2019, 3 cohorts were identified. In February 2019, 18 US Department of Veterans Affairs (VA) medical centers (VAMCs) (cohort 1) began the process of becoming HROs. Cohort 2 followed in October 2020 and included 54 VAMC. Finally, in October 2021, 67 additional VAMCs (cohort 3) started the process.² During cohort 2, the VA Providence Healthcare System (VAPHCS) decided to emphasize psychological safety at the start of the journey to becoming an HRO. This system is part of the VA New England Healthcare System (VISN 1), which includes VAMCs and clinics in Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, and Vermont.¹¹ Soon thereafter, the VA Bedford Healthcare System and the VA Connecticut Healthcare System adopted similar strategies. Since then, other VAMCs have also adopted this approach. These collective experiences identified 4 useful strategies for achieving psychological safety: leadership engagement, open communication, education and training, and accountability.

Leadership Engagement

Health care organization leaders play a critical role in making psychological safety happen—especially in complex and constantly changing environments, such as HROs.⁴ Leaders behaviors are consistently linked to the perception of psychological safety at the individual, team, and organizational levels.⁸ It is especially important to have leaders who recognize the views of individuals and team members and encourage staff participation in discussions to gain additional perspectives.^7,8,12 Psychological safety can also be facilitated when leaders are visible, approachable, and communicative.^4,7-9

Organizational practices, policies, and processes (eg, reporting adverse events without the fear of negative consequences) are also important ways that leaders can establish and sustain psychological safety. On a more granular level, leaders can enhance psychological safety by promoting and acknowledging individuals who speak up, regularly asking staff about safety concerns, highlighting “good catches” when harm is avoided, and using staff feedback to initiate improvements.^4,7,13Finally, in the authors’ experience, psychological safety requires clear commitment from leaders at all levels of an organization. Communication should be bidirectional, and leaders should close the proverbial “loop” with feedback and timely follow-up. This encourages and reinforces staff engagement and speaking up behaviors.^2,4,7,13

Open Communication

Promoting an environment of open communication, where all individuals and teams feel empowered to speak up with questions, concerns, and recommendations—regardless of position within the organization—is critical to psychological safety.^4,6,9 Open communication is especially critical when processes and systems are constantly changing and advancing as a result of new information and technology.⁹ Promoting open, bidirectional communication during the delivery of patient care can be accomplished with huddles, tiered safety huddles, leader rounding for high reliability, and time-outs.^2,4,6 These opportunities allow team members to discuss concerns, identify resources that support safe, high-quality care; reflect on successes and opportunities for improvement; and circle back on concerns.^2,6 Open communication in psychologically safe environments empowers staff to raise patient care concerns and is instrumental for improving patient safety, increasing staff job satisfaction, and decreasing turnover.^6,14

Education and Training

Education and training for all staff—from the frontline to the executive level—are essential to successfully implementing the principles and practices of psychological safety.^5-7 VHA training covers many topics, including the origins, benefits, and implementation strategies of psychological safety (Table). Role-playing simulation is an effective teaching format, providing staff with opportunities to practice techniques for raising concerns or share feedback in a controlled environment.⁶ In addition, education should be ongoing; it helps leaders and staff members feel competent and confident when implementing psychological safety across the health care organization.^6,10

Accountability

The final critical strategy for achieving psychological safety is accountability. It is the responsibility of all leadership—from senior leaders to clinical and nonclinical managers—to create a culture of shared accountability.⁵ But first, expectations must be set. Leadership must establish well-defined behavioral expectations that align with the organization’s values. Understanding behavioral expectations will help to ensure that employees know what achievement looks like, as well as how they are being held accountable for their individual actions.^4,5,7 In practical terms, this means ensuring that staff members have the skills and resources to achieve goals and expectations, providing performance feedback in a timely manner, and including expectations in annual performance evaluations (as they are in the VHA).

Consistency is key. Accountability should be the expectation across all levels and services of the health care organization. No staff member should be exempt from promoting a psychologically safe work environment. Compliance with behavioral expectations should be monitored and if a person’s actions are not consistent with expectations, the situation will need to be addressed. Interventions will depend on the type, severity, and frequency of the problematic behaviors. Depending on an organization’s policies and practices, courses of action can range from feedback counseling to employment termination.⁵

A practical matter in ensuring accountability is implementing a psychologically safe process for reporting concerns. Staff members must feel comfortable reporting behavioral concerns without fear of retaliation, negative judgment, or consequences from peers and supervisors. One method for doing this is to create a confidential, centralized process for reporting concerns.⁵

First-Hand Results

VAPHCS has seen the results of implementing the strategies outlined here. For example, VAPHCS has observed a 45% increase in the use of the patient safety reporting system that logs medical errors and near-misses. In addition, there have been improvements in levels of psychological safety and patient safety reported in the annual VHA All Employee Survey, which is conducted annually to gauge workplace satisfaction, culture, climate, turnover, supervisory behaviors, and general workplace perceptions. VAPHCS has shown consistent improvements in 12 patient safety elements scored on a 5-point scale (1, very dissatisfied; 5, very satisfied) (Figure). Notably, employee ratings of error prevention discussed increased from 4.0 in 2022 to 4.3 in 2024. Data collection and analysis are ongoing; more comprehensive findings will be published in the future.

CONCLUSIONS

Health care organizations are increasingly recognizing the importance of psychologically safe workplaces in order to provide safe, high-quality patient care. Psychological safety is a critical tool for empowering staff to raise concerns, ask tough questions, challenge the status quo, and share new ideas for providing health care services. While psychological safety has been slowly adopted in health care, it’s clear that evidence-based strategies can make psychological safety a reality.

Worldwide, health care is becoming increasingly complex as a result of greater clinical workforce demands, expanded roles and responsibilities, health care system mergers, stakeholder calls for new capabilities, and digital transformation. ^1,2These increasing demands has prompted many health care institutions to place greater focus on the psychological safety of their workforce, particularly in high reliability organizations (HROs). Building a robust foundation for high reliability in health care requires the presence of psychological safety—that is, staff members at all levels of the organization must feel comfortable speaking up when they have questions or concerns.^3,4 Psychological safety can improve the safety and quality of patient care but has not reached its full potential in health care.^5,6 However, there are strategies that promote the widespread implementation of psychological safety in health care organizations.^3-6

PSYCHOLOGICAL SAFETY

The concept of psychological safety in organizational behavior originated in 1965 when Edgar Schein and Warren Bennis, leaders in organizational psychology and management, published their reflections on the importance of psychological safety in helping individuals feel secure in the work environment.^5-7 Psychological safety in the workplace is foundational to staff members feeling comfortable asking questions or expressing concerns without fear of negative consequences.^8,9 It supports both individual and team efforts to raise safety concerns and report near misses and adverse events so that similar events can be averted in the future.⁹ Patients aren’t the only ones who benefit; psychological safety has also been found to promote job satisfaction and employee well-being.¹⁰

THE VETERANS HEALTH ADMINISTRATION JOURNEY

Achieving psychological safety is by no means an easy or comfortable process. As with any organizational change, a multipronged approach offers the best chance of success.^6,9 When the Veterans Health Administration (VHA) began its incremental, enterprise-wide journey to high reliability in 2019, 3 cohorts were identified. In February 2019, 18 US Department of Veterans Affairs (VA) medical centers (VAMCs) (cohort 1) began the process of becoming HROs. Cohort 2 followed in October 2020 and included 54 VAMC. Finally, in October 2021, 67 additional VAMCs (cohort 3) started the process.² During cohort 2, the VA Providence Healthcare System (VAPHCS) decided to emphasize psychological safety at the start of the journey to becoming an HRO. This system is part of the VA New England Healthcare System (VISN 1), which includes VAMCs and clinics in Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, and Vermont.¹¹ Soon thereafter, the VA Bedford Healthcare System and the VA Connecticut Healthcare System adopted similar strategies. Since then, other VAMCs have also adopted this approach. These collective experiences identified 4 useful strategies for achieving psychological safety: leadership engagement, open communication, education and training, and accountability.

Leadership Engagement

Health care organization leaders play a critical role in making psychological safety happen—especially in complex and constantly changing environments, such as HROs.⁴ Leaders behaviors are consistently linked to the perception of psychological safety at the individual, team, and organizational levels.⁸ It is especially important to have leaders who recognize the views of individuals and team members and encourage staff participation in discussions to gain additional perspectives.^7,8,12 Psychological safety can also be facilitated when leaders are visible, approachable, and communicative.^4,7-9

Organizational practices, policies, and processes (eg, reporting adverse events without the fear of negative consequences) are also important ways that leaders can establish and sustain psychological safety. On a more granular level, leaders can enhance psychological safety by promoting and acknowledging individuals who speak up, regularly asking staff about safety concerns, highlighting “good catches” when harm is avoided, and using staff feedback to initiate improvements.^4,7,13Finally, in the authors’ experience, psychological safety requires clear commitment from leaders at all levels of an organization. Communication should be bidirectional, and leaders should close the proverbial “loop” with feedback and timely follow-up. This encourages and reinforces staff engagement and speaking up behaviors.^2,4,7,13

Open Communication

Promoting an environment of open communication, where all individuals and teams feel empowered to speak up with questions, concerns, and recommendations—regardless of position within the organization—is critical to psychological safety.^4,6,9 Open communication is especially critical when processes and systems are constantly changing and advancing as a result of new information and technology.⁹ Promoting open, bidirectional communication during the delivery of patient care can be accomplished with huddles, tiered safety huddles, leader rounding for high reliability, and time-outs.^2,4,6 These opportunities allow team members to discuss concerns, identify resources that support safe, high-quality care; reflect on successes and opportunities for improvement; and circle back on concerns.^2,6 Open communication in psychologically safe environments empowers staff to raise patient care concerns and is instrumental for improving patient safety, increasing staff job satisfaction, and decreasing turnover.^6,14

Education and Training

Education and training for all staff—from the frontline to the executive level—are essential to successfully implementing the principles and practices of psychological safety.^5-7 VHA training covers many topics, including the origins, benefits, and implementation strategies of psychological safety (Table). Role-playing simulation is an effective teaching format, providing staff with opportunities to practice techniques for raising concerns or share feedback in a controlled environment.⁶ In addition, education should be ongoing; it helps leaders and staff members feel competent and confident when implementing psychological safety across the health care organization.^6,10

Accountability

The final critical strategy for achieving psychological safety is accountability. It is the responsibility of all leadership—from senior leaders to clinical and nonclinical managers—to create a culture of shared accountability.⁵ But first, expectations must be set. Leadership must establish well-defined behavioral expectations that align with the organization’s values. Understanding behavioral expectations will help to ensure that employees know what achievement looks like, as well as how they are being held accountable for their individual actions.^4,5,7 In practical terms, this means ensuring that staff members have the skills and resources to achieve goals and expectations, providing performance feedback in a timely manner, and including expectations in annual performance evaluations (as they are in the VHA).

Consistency is key. Accountability should be the expectation across all levels and services of the health care organization. No staff member should be exempt from promoting a psychologically safe work environment. Compliance with behavioral expectations should be monitored and if a person’s actions are not consistent with expectations, the situation will need to be addressed. Interventions will depend on the type, severity, and frequency of the problematic behaviors. Depending on an organization’s policies and practices, courses of action can range from feedback counseling to employment termination.⁵

A practical matter in ensuring accountability is implementing a psychologically safe process for reporting concerns. Staff members must feel comfortable reporting behavioral concerns without fear of retaliation, negative judgment, or consequences from peers and supervisors. One method for doing this is to create a confidential, centralized process for reporting concerns.⁵

First-Hand Results

VAPHCS has seen the results of implementing the strategies outlined here. For example, VAPHCS has observed a 45% increase in the use of the patient safety reporting system that logs medical errors and near-misses. In addition, there have been improvements in levels of psychological safety and patient safety reported in the annual VHA All Employee Survey, which is conducted annually to gauge workplace satisfaction, culture, climate, turnover, supervisory behaviors, and general workplace perceptions. VAPHCS has shown consistent improvements in 12 patient safety elements scored on a 5-point scale (1, very dissatisfied; 5, very satisfied) (Figure). Notably, employee ratings of error prevention discussed increased from 4.0 in 2022 to 4.3 in 2024. Data collection and analysis are ongoing; more comprehensive findings will be published in the future.

CONCLUSIONS

Health care organizations are increasingly recognizing the importance of psychologically safe workplaces in order to provide safe, high-quality patient care. Psychological safety is a critical tool for empowering staff to raise concerns, ask tough questions, challenge the status quo, and share new ideas for providing health care services. While psychological safety has been slowly adopted in health care, it’s clear that evidence-based strategies can make psychological safety a reality.

April is the cruellest month, breeding
Lilacs out of the dead land, mixing
Memory and desire, stirring
Dull roots with spring rain.
T.S. Eliot¹

The epigraph for this column is from The Waste Land, T.S. Eliot’s postmodern poem that, in part, reflects his experience of the destruction of an entire way of living and a generation of young men in the wake of the First World War. The terrible contemporary toll suicide has taken on veterans and the active-duty military makes it easy to forget that suicide is an inveterate and disturbing aftermath of all wars.²

There is a profound and elemental connection in the human mind between Spring and renewal. In almost every culture and religion, across nearly every historical epoch and location, Spring is associated with themes of growth, returning life, light, and hope. On a more prosaic modern level, almost all of us—us—especially those in Northern climates—look forward to warmer weather, more time spent outdoors, and the simple joys of seeing perennials return in the garden and birds nest in blooming trees.

It is a paradox of human life that suicide is more common in the season of rebirth than in the season of decline. The bare trees, freezing temperatures, and icy darkness that accompany winter in much of the world inherently lead us to contemplate our mortality. The counterintuitive finding that individuals, many of them veterans, take their own lives more often in Spring creates a cognitive dissonance to be explored in this editorial.

As a layperson, I too assumed there were more suicides in winter, especially around the holidays when the expectation of belonging, privilege, and pleasure painfully reminds the alienated, lonely, homeless, and ailing of all they lack and all they have lost. As a psychiatric intern, I anticipated that the inpatient US Department of Veterans Affairs (VA) ward where I was training would empty with the arrival of nicer weather. Instead, I was mystified when the opposite occurred and the unit was overflowing with manic and suicidal patients.

The Centers for Disease Control and Prevention National Center for Health Statistics ranked suicide by month from 1999 to 2010. Contrary to popular belief, more suicides occurred in late Spring and Summer than any other season.³ A 2023 study of systematic reviews of seasonal variation in mood disorders, suicide risk, and health care utilization found that suicide was 11% to 23% higher, suicide attempts resulting in emergency department visits showed an increase of 1.2% to 1.7%, and hospital admissions for mania rose 7.4% to 16.0% in Spring and Summer, compared with Fall and Winter.⁴ This general population finding is also seen in veteran and military cohorts. A recent study analyzed VA and US Department of Defense (DoD) data from 133,867 veteran suicides from 2001 to 2021. Results showed that veteran suicides were highest in Summer.⁵

The rise of suicide in the Spring was first observed in the 17th century and has been the object of scientific study for at least 3 decades. That research has produced several different hypotheses from a variety of disciplines, none of which are conclusive as of this writing. Cho and Lee note that the phrase “Spring fever” is a much more serious illness for those with a predisposition or diagnosis of unipolar or bipolar disorder than the quotidian irritant that afflicts those without affective disorders.⁶ In residency, I learned that longer exposure to light in Spring led to an imbalance in neurotransmitters that triggered manias. This is a simplistic version of the complex circadian interactions of temperature, climate, light, and other environmental variables causing dysregulation or misalignment of our natural biological cycles and those of nature proposed by chronobiologists.⁷

Sociological and criminal justice scholars underscore that an increase in temperature may exacerbate violent tendencies, especially in older males—a demographic profile more frequently found in veterans—and those already prone to acting out their frustrations with firearms.⁸ Psychologists have hypothesized that individuals with depressions persevere through Winter by telling themselves they will feel relief in the Spring. Too often the coming of Spring brings not reprieve but a deadly combination of deeper mental desperation coupled with the release from winter lassitude that energizes the now hopeless person to put ideation into action.^4,9 The elevation of suicide rates in Spring is likely multidetermined with all these putative causes contributing in different variations to every individual who tragically dies by suicide.

Yet despite decades of public education, this dangerous fiction stubbornly persists in the educated public and even among many health care professionals, in part due to misguided media. For years, the Annenberg Public Policy Center (APPC) has made busting this myth of holiday suicides in the media an organizational initiative. A 2023 APPC survey found that 4 of 5 Americans picked December as the month when suicide rates were highest. The organization has been analyzing holiday—related media reports for decades; those results show some improvement, with the most recent analysis of media reports somewhat better and 40% communicating erroneous information. ¹⁰

APPC believes the opinion that suicide is more common around the holidays will persuade those struggling with an exacerbation of a mental health condition or an acute crisis to attempt or die by suicide, believing it to be a reasonable social response. While recognizing there is a real risk of such contagion behavior, I believe the reverse problem is more concerning. As I observed during my internship, the acceptance of the fiction that everyone is happy in Spring may even blind health care professionals from detecting clues that patients and even our loved ones are contemplating suicide. Our relief that Winter has passed and enjoyment of Spring activities can fool us into believing everyone else is also feeling fine and doing well and miss an opportunity to intervene and treat mania or depression to save a life—the medical manifestation of renewal.

April is the cruellest month, breeding
Lilacs out of the dead land, mixing
Memory and desire, stirring
Dull roots with spring rain.
T.S. Eliot¹

The epigraph for this column is from The Waste Land, T.S. Eliot’s postmodern poem that, in part, reflects his experience of the destruction of an entire way of living and a generation of young men in the wake of the First World War. The terrible contemporary toll suicide has taken on veterans and the active-duty military makes it easy to forget that suicide is an inveterate and disturbing aftermath of all wars.²

There is a profound and elemental connection in the human mind between Spring and renewal. In almost every culture and religion, across nearly every historical epoch and location, Spring is associated with themes of growth, returning life, light, and hope. On a more prosaic modern level, almost all of us—us—especially those in Northern climates—look forward to warmer weather, more time spent outdoors, and the simple joys of seeing perennials return in the garden and birds nest in blooming trees.

It is a paradox of human life that suicide is more common in the season of rebirth than in the season of decline. The bare trees, freezing temperatures, and icy darkness that accompany winter in much of the world inherently lead us to contemplate our mortality. The counterintuitive finding that individuals, many of them veterans, take their own lives more often in Spring creates a cognitive dissonance to be explored in this editorial.

As a layperson, I too assumed there were more suicides in winter, especially around the holidays when the expectation of belonging, privilege, and pleasure painfully reminds the alienated, lonely, homeless, and ailing of all they lack and all they have lost. As a psychiatric intern, I anticipated that the inpatient US Department of Veterans Affairs (VA) ward where I was training would empty with the arrival of nicer weather. Instead, I was mystified when the opposite occurred and the unit was overflowing with manic and suicidal patients.

The Centers for Disease Control and Prevention National Center for Health Statistics ranked suicide by month from 1999 to 2010. Contrary to popular belief, more suicides occurred in late Spring and Summer than any other season.³ A 2023 study of systematic reviews of seasonal variation in mood disorders, suicide risk, and health care utilization found that suicide was 11% to 23% higher, suicide attempts resulting in emergency department visits showed an increase of 1.2% to 1.7%, and hospital admissions for mania rose 7.4% to 16.0% in Spring and Summer, compared with Fall and Winter.⁴ This general population finding is also seen in veteran and military cohorts. A recent study analyzed VA and US Department of Defense (DoD) data from 133,867 veteran suicides from 2001 to 2021. Results showed that veteran suicides were highest in Summer.⁵

The rise of suicide in the Spring was first observed in the 17th century and has been the object of scientific study for at least 3 decades. That research has produced several different hypotheses from a variety of disciplines, none of which are conclusive as of this writing. Cho and Lee note that the phrase “Spring fever” is a much more serious illness for those with a predisposition or diagnosis of unipolar or bipolar disorder than the quotidian irritant that afflicts those without affective disorders.⁶ In residency, I learned that longer exposure to light in Spring led to an imbalance in neurotransmitters that triggered manias. This is a simplistic version of the complex circadian interactions of temperature, climate, light, and other environmental variables causing dysregulation or misalignment of our natural biological cycles and those of nature proposed by chronobiologists.⁷

Sociological and criminal justice scholars underscore that an increase in temperature may exacerbate violent tendencies, especially in older males—a demographic profile more frequently found in veterans—and those already prone to acting out their frustrations with firearms.⁸ Psychologists have hypothesized that individuals with depressions persevere through Winter by telling themselves they will feel relief in the Spring. Too often the coming of Spring brings not reprieve but a deadly combination of deeper mental desperation coupled with the release from winter lassitude that energizes the now hopeless person to put ideation into action.^4,9 The elevation of suicide rates in Spring is likely multidetermined with all these putative causes contributing in different variations to every individual who tragically dies by suicide.

Yet despite decades of public education, this dangerous fiction stubbornly persists in the educated public and even among many health care professionals, in part due to misguided media. For years, the Annenberg Public Policy Center (APPC) has made busting this myth of holiday suicides in the media an organizational initiative. A 2023 APPC survey found that 4 of 5 Americans picked December as the month when suicide rates were highest. The organization has been analyzing holiday—related media reports for decades; those results show some improvement, with the most recent analysis of media reports somewhat better and 40% communicating erroneous information. ¹⁰

APPC believes the opinion that suicide is more common around the holidays will persuade those struggling with an exacerbation of a mental health condition or an acute crisis to attempt or die by suicide, believing it to be a reasonable social response. While recognizing there is a real risk of such contagion behavior, I believe the reverse problem is more concerning. As I observed during my internship, the acceptance of the fiction that everyone is happy in Spring may even blind health care professionals from detecting clues that patients and even our loved ones are contemplating suicide. Our relief that Winter has passed and enjoyment of Spring activities can fool us into believing everyone else is also feeling fine and doing well and miss an opportunity to intervene and treat mania or depression to save a life—the medical manifestation of renewal.

April is the cruellest month, breeding
Lilacs out of the dead land, mixing
Memory and desire, stirring
Dull roots with spring rain.
T.S. Eliot¹

The epigraph for this column is from The Waste Land, T.S. Eliot’s postmodern poem that, in part, reflects his experience of the destruction of an entire way of living and a generation of young men in the wake of the First World War. The terrible contemporary toll suicide has taken on veterans and the active-duty military makes it easy to forget that suicide is an inveterate and disturbing aftermath of all wars.²

There is a profound and elemental connection in the human mind between Spring and renewal. In almost every culture and religion, across nearly every historical epoch and location, Spring is associated with themes of growth, returning life, light, and hope. On a more prosaic modern level, almost all of us—us—especially those in Northern climates—look forward to warmer weather, more time spent outdoors, and the simple joys of seeing perennials return in the garden and birds nest in blooming trees.

It is a paradox of human life that suicide is more common in the season of rebirth than in the season of decline. The bare trees, freezing temperatures, and icy darkness that accompany winter in much of the world inherently lead us to contemplate our mortality. The counterintuitive finding that individuals, many of them veterans, take their own lives more often in Spring creates a cognitive dissonance to be explored in this editorial.

As a layperson, I too assumed there were more suicides in winter, especially around the holidays when the expectation of belonging, privilege, and pleasure painfully reminds the alienated, lonely, homeless, and ailing of all they lack and all they have lost. As a psychiatric intern, I anticipated that the inpatient US Department of Veterans Affairs (VA) ward where I was training would empty with the arrival of nicer weather. Instead, I was mystified when the opposite occurred and the unit was overflowing with manic and suicidal patients.

The Centers for Disease Control and Prevention National Center for Health Statistics ranked suicide by month from 1999 to 2010. Contrary to popular belief, more suicides occurred in late Spring and Summer than any other season.³ A 2023 study of systematic reviews of seasonal variation in mood disorders, suicide risk, and health care utilization found that suicide was 11% to 23% higher, suicide attempts resulting in emergency department visits showed an increase of 1.2% to 1.7%, and hospital admissions for mania rose 7.4% to 16.0% in Spring and Summer, compared with Fall and Winter.⁴ This general population finding is also seen in veteran and military cohorts. A recent study analyzed VA and US Department of Defense (DoD) data from 133,867 veteran suicides from 2001 to 2021. Results showed that veteran suicides were highest in Summer.⁵

The rise of suicide in the Spring was first observed in the 17th century and has been the object of scientific study for at least 3 decades. That research has produced several different hypotheses from a variety of disciplines, none of which are conclusive as of this writing. Cho and Lee note that the phrase “Spring fever” is a much more serious illness for those with a predisposition or diagnosis of unipolar or bipolar disorder than the quotidian irritant that afflicts those without affective disorders.⁶ In residency, I learned that longer exposure to light in Spring led to an imbalance in neurotransmitters that triggered manias. This is a simplistic version of the complex circadian interactions of temperature, climate, light, and other environmental variables causing dysregulation or misalignment of our natural biological cycles and those of nature proposed by chronobiologists.⁷

Sociological and criminal justice scholars underscore that an increase in temperature may exacerbate violent tendencies, especially in older males—a demographic profile more frequently found in veterans—and those already prone to acting out their frustrations with firearms.⁸ Psychologists have hypothesized that individuals with depressions persevere through Winter by telling themselves they will feel relief in the Spring. Too often the coming of Spring brings not reprieve but a deadly combination of deeper mental desperation coupled with the release from winter lassitude that energizes the now hopeless person to put ideation into action.^4,9 The elevation of suicide rates in Spring is likely multidetermined with all these putative causes contributing in different variations to every individual who tragically dies by suicide.

Yet despite decades of public education, this dangerous fiction stubbornly persists in the educated public and even among many health care professionals, in part due to misguided media. For years, the Annenberg Public Policy Center (APPC) has made busting this myth of holiday suicides in the media an organizational initiative. A 2023 APPC survey found that 4 of 5 Americans picked December as the month when suicide rates were highest. The organization has been analyzing holiday—related media reports for decades; those results show some improvement, with the most recent analysis of media reports somewhat better and 40% communicating erroneous information. ¹⁰

APPC believes the opinion that suicide is more common around the holidays will persuade those struggling with an exacerbation of a mental health condition or an acute crisis to attempt or die by suicide, believing it to be a reasonable social response. While recognizing there is a real risk of such contagion behavior, I believe the reverse problem is more concerning. As I observed during my internship, the acceptance of the fiction that everyone is happy in Spring may even blind health care professionals from detecting clues that patients and even our loved ones are contemplating suicide. Our relief that Winter has passed and enjoyment of Spring activities can fool us into believing everyone else is also feeling fine and doing well and miss an opportunity to intervene and treat mania or depression to save a life—the medical manifestation of renewal.