Article

Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,¹ are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.² Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.³ Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.⁴ Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.⁵

Cutaneous Manifestations

Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.⁶ The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.³ A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.⁷

When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.² Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.⁸ Rare reports of nephrotic syndrome also have appeared in the literature.⁹ Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.⁶

Nomenclature

Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,⁶ derived from the Greek words toxikos (poison) and dendron (tree).¹⁰

Distribution

Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.^6,11

Identifying Features

Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.

As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”¹²

Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.⁶

Dermatitis-Inducing Plant Parts

The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.^2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.¹⁴

Allergens

The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.¹⁵ The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).¹²

Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.⁵

Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.¹⁶ Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.^5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4⁺ T cells.⁶ These cells then expand to form circulating activated T-effector and T-memory lymphocytes.¹⁸

The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.¹⁹ In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.² The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.²⁰

Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.^14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.² Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.²²

Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.²³ One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.²⁴

Treatment

After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.^25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.^27,28

Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.^29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.^31,32

Clinical Uses

Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin³³ reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues³⁴ in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.²

Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.

Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,¹ are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.² Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.³ Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.⁴ Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.⁵

Cutaneous Manifestations

Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.⁶ The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.³ A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.⁷

When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.² Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.⁸ Rare reports of nephrotic syndrome also have appeared in the literature.⁹ Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.⁶

Nomenclature

Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,⁶ derived from the Greek words toxikos (poison) and dendron (tree).¹⁰

Distribution

Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.^6,11

Identifying Features

Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.

As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”¹²

Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.⁶

Dermatitis-Inducing Plant Parts

The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.^2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.¹⁴

Allergens

The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.¹⁵ The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).¹²

Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.⁵

Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.¹⁶ Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.^5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4⁺ T cells.⁶ These cells then expand to form circulating activated T-effector and T-memory lymphocytes.¹⁸

The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.¹⁹ In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.² The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.²⁰

Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.^14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.² Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.²²

Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.²³ One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.²⁴

Treatment

After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.^25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.^27,28

Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.^29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.^31,32

Clinical Uses

Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin³³ reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues³⁴ in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.²

Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.

Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,¹ are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.² Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.³ Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.⁴ Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.⁵

Cutaneous Manifestations

Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.⁶ The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.³ A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.⁷

When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.² Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.⁸ Rare reports of nephrotic syndrome also have appeared in the literature.⁹ Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.⁶

Nomenclature

Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,⁶ derived from the Greek words toxikos (poison) and dendron (tree).¹⁰

Distribution

Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.^6,11

Identifying Features

Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.

As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”¹²

Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.⁶

Dermatitis-Inducing Plant Parts

The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.^2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.¹⁴

Allergens

The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.¹⁵ The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).¹²

Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.⁵

Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.¹⁶ Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.^5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4⁺ T cells.⁶ These cells then expand to form circulating activated T-effector and T-memory lymphocytes.¹⁸

The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.¹⁹ In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.² The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.²⁰

Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.^14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.² Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.²²

Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.²³ One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.²⁴

Treatment

After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.^25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.^27,28

Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.^29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.^31,32

Clinical Uses

Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin³³ reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues³⁴ in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.²

Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.

It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.¹ For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.² The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.³ As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.⁴ It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.^5,6

Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”⁷ Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.

No Easy Answers

A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).⁸ Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”⁸ The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing. 

The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.⁹ Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.

The Labyrinth of Testing for Food Allergies

Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.¹⁰ Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.

The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.¹¹ 

To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.¹²

 

 

Classification of Food Allergies

It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.³ The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.^13,14 

A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.¹⁵ Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,¹⁵ which is an important finding.

A recent retrospective review of 372 children with AD reported similar results.⁴ The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.⁴ 

There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.^16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.

Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.^18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin²⁰ illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.²⁰

 

 

Navigating the Complexity of Dietary Restrictions

This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.³ In particular, there are major concerns for iatrogenic harm. 

First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.²¹ Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.²² 

Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.²³

It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself. 

Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD. 

Final Thoughts

Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”³ With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD. 

It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.¹ For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.² The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.³ As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.⁴ It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.^5,6

Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”⁷ Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.

No Easy Answers

A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).⁸ Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”⁸ The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing. 

The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.⁹ Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.

The Labyrinth of Testing for Food Allergies

Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.¹⁰ Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.

The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.¹¹ 

To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.¹²

 

 

Classification of Food Allergies

It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.³ The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.^13,14 

A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.¹⁵ Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,¹⁵ which is an important finding.

A recent retrospective review of 372 children with AD reported similar results.⁴ The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.⁴ 

There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.^16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.

Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.^18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin²⁰ illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.²⁰

 

 

Navigating the Complexity of Dietary Restrictions

This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.³ In particular, there are major concerns for iatrogenic harm. 

First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.²¹ Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.²² 

Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.²³

It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself. 

Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD. 

Final Thoughts

Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”³ With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD. 

It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.¹ For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.² The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.³ As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.⁴ It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.^5,6

Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”⁷ Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.

No Easy Answers

A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).⁸ Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”⁸ The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing. 

The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.⁹ Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.

The Labyrinth of Testing for Food Allergies

Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.¹⁰ Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.

The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.¹¹ 

To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.¹²

 

 

Classification of Food Allergies

It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.³ The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.^13,14 

A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.¹⁵ Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,¹⁵ which is an important finding.

A recent retrospective review of 372 children with AD reported similar results.⁴ The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.⁴ 

There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.^16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.

Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.^18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin²⁰ illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.²⁰

 

 

Navigating the Complexity of Dietary Restrictions

This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.³ In particular, there are major concerns for iatrogenic harm. 

First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.²¹ Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.²² 

Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.²³

It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself. 

Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD. 

Final Thoughts

Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”³ With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD. 

In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,^1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines⁹ do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).

Resident Safety and Wellness

Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.^4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.^4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.⁹ Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.^10,11

Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.^2-4,12,13

Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.^3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.¹⁴

Resident Education

Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.⁴ In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.¹⁰

Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.¹⁵ Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.

Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.^2,4,5

Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.⁷

Patient Care

Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.¹¹ Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.¹² If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.

In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.¹⁶ Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.⁷ If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.^7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.⁷

Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.¹⁷

Final Thoughts

Disasters often are unpredictable. Dermatology residency programs will not be immune to the future impacts of climate change, violent threats, or emerging pandemics. Lessons from prior natural disasters and the COVID-19 pandemic have made it clear that program directors need to be adaptable. If they plan proactively, comprehensive disaster preparedness can help to maintain high-quality training of dermatology residents in the face of extraordinary and challenging circumstances, promoting the resiliency and sustainability of graduate medical education.

In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,^1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines⁹ do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).

Resident Safety and Wellness

Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.^4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.^4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.⁹ Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.^10,11

Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.^2-4,12,13

Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.^3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.¹⁴

Resident Education

Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.⁴ In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.¹⁰

Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.¹⁵ Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.

Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.^2,4,5

Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.⁷

Patient Care

Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.¹¹ Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.¹² If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.

In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.¹⁶ Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.⁷ If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.^7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.⁷

Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.¹⁷

Final Thoughts

Disasters often are unpredictable. Dermatology residency programs will not be immune to the future impacts of climate change, violent threats, or emerging pandemics. Lessons from prior natural disasters and the COVID-19 pandemic have made it clear that program directors need to be adaptable. If they plan proactively, comprehensive disaster preparedness can help to maintain high-quality training of dermatology residents in the face of extraordinary and challenging circumstances, promoting the resiliency and sustainability of graduate medical education.

In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,^1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines⁹ do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).

Resident Safety and Wellness

Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.^4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.^4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.⁹ Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.^10,11

Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.^2-4,12,13

Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.^3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.¹⁴

Resident Education

Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.⁴ In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.¹⁰

Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.¹⁵ Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.

Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.^2,4,5

Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.⁷

Patient Care

Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.¹¹ Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.¹² If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.

In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.¹⁶ Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.⁷ If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.^7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.⁷

Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.¹⁷

Final Thoughts

Disasters often are unpredictable. Dermatology residency programs will not be immune to the future impacts of climate change, violent threats, or emerging pandemics. Lessons from prior natural disasters and the COVID-19 pandemic have made it clear that program directors need to be adaptable. If they plan proactively, comprehensive disaster preparedness can help to maintain high-quality training of dermatology residents in the face of extraordinary and challenging circumstances, promoting the resiliency and sustainability of graduate medical education.

Practice Gap

A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.

This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:

• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.

• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.

Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).

Technique

In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.¹

For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.

To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.

Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.

Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.

The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.

The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.

Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.

Practice Implications

Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.

The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.

Practice Gap

A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.

This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:

• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.

• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.

Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).

Technique

In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.¹

For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.

To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.

Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.

Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.

The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.

The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.

Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.

Practice Implications

Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.

The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.

Practice Gap

A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.

This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:

• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.

• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.

Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).

Technique

In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.¹

For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.

To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.

Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.

Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.

The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.

The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.

Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.

Practice Implications

Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.

The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.

Click to view more from Gastroenterology Data Trends 2022.

Click to view more from Gastroenterology Data Trends 2022.

Click to view more from Gastroenterology Data Trends 2022.