What’s Eating You? Bedbugs

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What’s Eating You? Bedbugs

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.1 The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.2 Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

Figure 1. Several pink, ill-defined papules coalescing into a 10-cm patch on the posterior right arm. Sutures show the punch biopsy location.

 

Figure 2. A, A 4-mm punch biopsy showed a dense superficial and deep infiltrate (H&E, original magnification ×2). B, A perivascular infiltrate of lymphocytes and sporadic eosinophils without epidermal change also was noted (H&E, original magnification ×20).

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Figure 3. The patient’s office chair showed bedbugs protruding through the mesh backing.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.6 Females lay more than 200 eggs that hatch in approximately 6 to 10 days.7 Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.6

Figure 4. Cimex lectularius (bedbug) taking a blood meal. Photograph by Harold J. Harlan, PhD (Crownsville, Maryland).

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.3 Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.4 Additionally, they frequently move around to find a suitable host.5 As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.8 Other presentations include purpuric macules, bullae, and papular urticaria.8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.11

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.12 The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.4 It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.12



Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.8 Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.8 The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

 

 

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.2 Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

References

1. Ralph N, Jones HE, Thorpe LE. Self-reported bed bug infestation among New York City residents: prevalence and risk factors. J Environ Health; 2013;76:38-45.

2. US Environmental Protection Agency. Bed Bugs are public health pests. EPA website. https://www.epa.gov/bedbugs/bed-bugs-are-public-health-pests. Accessed December 6, 2018.

3. Potter MF, Haynes KF, Fredericks J. Bed bugs across America: 2015 Bugs Without Borders survey. Pestworld. 2015:4-14. https://www.npmapestworld.org/default/assets/File/newsroom/magazine/2015/nov-dec_2015.pdf. Accessed December 6, 2018.

4. Pinto LJ, Cooper R, Kraft SK. Bed bugs in office buildings: the ultimate challenge? MGK website. http://giecdn.blob.core.windows.net/fileuploads/file/bedbugs-office-buildings.pdf. Accessed December 6, 2018.

5. Baumblatt JA, Dunn JR, Schaffner W, et al. An outbreak of bed bug infestation in an office building. J Environ Health. 2014;76:16-19.

6. Parasites: bed bugs. Centers for Disease Control and Prevention website. www.cdc.gov/parasites/bedbugs/biology.html. Updated March 17, 2015. Accessed September 21, 2018.

7. Bed bugs. University of Minnesota Extension website. https://www.extension.umn.edu/garden/insects/find/bed-bugs-in-residences. Accessed September 21, 2018.

8. Goddard J, deShazo R. Bed bugs (Cimex lectularius) and clinical consequences of their bites. JAMA. 2009;301:1358-1366.

9. Scarupa, MD, Economides A. Bedbug bites masquerading as urticaria. J Allergy Clin Immunol. 2006;117:1508-1509.

10. Abdel-Naser MB, Lotfy RA, Al-Sherbiny MM, et al. Patients with papular urticaria have IgG antibodies to bedbug (Cimex lectularius) antigens. Parasitol Res. 2006;98:550-556.

11. Lai O, Ho D, Glick S, et al. Bed bugs and possible transmission of human pathogens: a systematic review. Arch Dermatol Res. 2016;308:531-538.

12. Vaidyanathan R, Feldlaufer MF. Bed bug detection: current technologies and future directions. Am J Trop Med Hyg. 2013;88:619-625.

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Author and Disclosure Information

Mr. Chittoor is from Midwestern University Chicago College of Osteopathic Medicine, Downers Grove, Illinois. Drs. Wilkison and McNally are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Texas.

The authors report no conflicts of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, 59 MDSP/SGMD/Dermatology, 1100 Wilford Hall Loop, Bldg 4554, JBSA-Lackland, TX 78236 ([email protected]).

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Mr. Chittoor is from Midwestern University Chicago College of Osteopathic Medicine, Downers Grove, Illinois. Drs. Wilkison and McNally are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Texas.

The authors report no conflicts of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, 59 MDSP/SGMD/Dermatology, 1100 Wilford Hall Loop, Bldg 4554, JBSA-Lackland, TX 78236 ([email protected]).

Author and Disclosure Information

Mr. Chittoor is from Midwestern University Chicago College of Osteopathic Medicine, Downers Grove, Illinois. Drs. Wilkison and McNally are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Texas.

The authors report no conflicts of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, 59 MDSP/SGMD/Dermatology, 1100 Wilford Hall Loop, Bldg 4554, JBSA-Lackland, TX 78236 ([email protected]).

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Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.1 The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.2 Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

Figure 1. Several pink, ill-defined papules coalescing into a 10-cm patch on the posterior right arm. Sutures show the punch biopsy location.

 

Figure 2. A, A 4-mm punch biopsy showed a dense superficial and deep infiltrate (H&E, original magnification ×2). B, A perivascular infiltrate of lymphocytes and sporadic eosinophils without epidermal change also was noted (H&E, original magnification ×20).

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Figure 3. The patient’s office chair showed bedbugs protruding through the mesh backing.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.6 Females lay more than 200 eggs that hatch in approximately 6 to 10 days.7 Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.6

Figure 4. Cimex lectularius (bedbug) taking a blood meal. Photograph by Harold J. Harlan, PhD (Crownsville, Maryland).

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.3 Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.4 Additionally, they frequently move around to find a suitable host.5 As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.8 Other presentations include purpuric macules, bullae, and papular urticaria.8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.11

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.12 The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.4 It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.12



Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.8 Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.8 The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

 

 

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.2 Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.1 The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.2 Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

Figure 1. Several pink, ill-defined papules coalescing into a 10-cm patch on the posterior right arm. Sutures show the punch biopsy location.

 

Figure 2. A, A 4-mm punch biopsy showed a dense superficial and deep infiltrate (H&E, original magnification ×2). B, A perivascular infiltrate of lymphocytes and sporadic eosinophils without epidermal change also was noted (H&E, original magnification ×20).

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

Figure 3. The patient’s office chair showed bedbugs protruding through the mesh backing.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.6 Females lay more than 200 eggs that hatch in approximately 6 to 10 days.7 Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.6

Figure 4. Cimex lectularius (bedbug) taking a blood meal. Photograph by Harold J. Harlan, PhD (Crownsville, Maryland).

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.3 Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.4 Additionally, they frequently move around to find a suitable host.5 As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.8 Other presentations include purpuric macules, bullae, and papular urticaria.8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.11

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.12 The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.4 It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.12



Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.8 Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.8 The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

 

 

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.2 Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

References

1. Ralph N, Jones HE, Thorpe LE. Self-reported bed bug infestation among New York City residents: prevalence and risk factors. J Environ Health; 2013;76:38-45.

2. US Environmental Protection Agency. Bed Bugs are public health pests. EPA website. https://www.epa.gov/bedbugs/bed-bugs-are-public-health-pests. Accessed December 6, 2018.

3. Potter MF, Haynes KF, Fredericks J. Bed bugs across America: 2015 Bugs Without Borders survey. Pestworld. 2015:4-14. https://www.npmapestworld.org/default/assets/File/newsroom/magazine/2015/nov-dec_2015.pdf. Accessed December 6, 2018.

4. Pinto LJ, Cooper R, Kraft SK. Bed bugs in office buildings: the ultimate challenge? MGK website. http://giecdn.blob.core.windows.net/fileuploads/file/bedbugs-office-buildings.pdf. Accessed December 6, 2018.

5. Baumblatt JA, Dunn JR, Schaffner W, et al. An outbreak of bed bug infestation in an office building. J Environ Health. 2014;76:16-19.

6. Parasites: bed bugs. Centers for Disease Control and Prevention website. www.cdc.gov/parasites/bedbugs/biology.html. Updated March 17, 2015. Accessed September 21, 2018.

7. Bed bugs. University of Minnesota Extension website. https://www.extension.umn.edu/garden/insects/find/bed-bugs-in-residences. Accessed September 21, 2018.

8. Goddard J, deShazo R. Bed bugs (Cimex lectularius) and clinical consequences of their bites. JAMA. 2009;301:1358-1366.

9. Scarupa, MD, Economides A. Bedbug bites masquerading as urticaria. J Allergy Clin Immunol. 2006;117:1508-1509.

10. Abdel-Naser MB, Lotfy RA, Al-Sherbiny MM, et al. Patients with papular urticaria have IgG antibodies to bedbug (Cimex lectularius) antigens. Parasitol Res. 2006;98:550-556.

11. Lai O, Ho D, Glick S, et al. Bed bugs and possible transmission of human pathogens: a systematic review. Arch Dermatol Res. 2016;308:531-538.

12. Vaidyanathan R, Feldlaufer MF. Bed bug detection: current technologies and future directions. Am J Trop Med Hyg. 2013;88:619-625.

References

1. Ralph N, Jones HE, Thorpe LE. Self-reported bed bug infestation among New York City residents: prevalence and risk factors. J Environ Health; 2013;76:38-45.

2. US Environmental Protection Agency. Bed Bugs are public health pests. EPA website. https://www.epa.gov/bedbugs/bed-bugs-are-public-health-pests. Accessed December 6, 2018.

3. Potter MF, Haynes KF, Fredericks J. Bed bugs across America: 2015 Bugs Without Borders survey. Pestworld. 2015:4-14. https://www.npmapestworld.org/default/assets/File/newsroom/magazine/2015/nov-dec_2015.pdf. Accessed December 6, 2018.

4. Pinto LJ, Cooper R, Kraft SK. Bed bugs in office buildings: the ultimate challenge? MGK website. http://giecdn.blob.core.windows.net/fileuploads/file/bedbugs-office-buildings.pdf. Accessed December 6, 2018.

5. Baumblatt JA, Dunn JR, Schaffner W, et al. An outbreak of bed bug infestation in an office building. J Environ Health. 2014;76:16-19.

6. Parasites: bed bugs. Centers for Disease Control and Prevention website. www.cdc.gov/parasites/bedbugs/biology.html. Updated March 17, 2015. Accessed September 21, 2018.

7. Bed bugs. University of Minnesota Extension website. https://www.extension.umn.edu/garden/insects/find/bed-bugs-in-residences. Accessed September 21, 2018.

8. Goddard J, deShazo R. Bed bugs (Cimex lectularius) and clinical consequences of their bites. JAMA. 2009;301:1358-1366.

9. Scarupa, MD, Economides A. Bedbug bites masquerading as urticaria. J Allergy Clin Immunol. 2006;117:1508-1509.

10. Abdel-Naser MB, Lotfy RA, Al-Sherbiny MM, et al. Patients with papular urticaria have IgG antibodies to bedbug (Cimex lectularius) antigens. Parasitol Res. 2006;98:550-556.

11. Lai O, Ho D, Glick S, et al. Bed bugs and possible transmission of human pathogens: a systematic review. Arch Dermatol Res. 2016;308:531-538.

12. Vaidyanathan R, Feldlaufer MF. Bed bug detection: current technologies and future directions. Am J Trop Med Hyg. 2013;88:619-625.

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  • Bedbug exposures in the workplace are on the rise.
  • High clinical suspicion is required when atypical dermatoses are not responding to therapy and histology suggests arthropod exposure.
  • Once detected, partnership with occupational health and pest management experts is critical to eradicate bedbugs.
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Skin Cancer in Military Pilots: A Special Population With Special Risk Factors

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Skin Cancer in Military Pilots: A Special Population With Special Risk Factors
In partnership with the Association of Military Dermatologists

Military dermatologists are charged with caring for a diverse population of active-duty members, civilian dependents, and military retirees. Although certain risk factors for cutaneous malignancies are common in all of these groups, the active-duty population experiences unique exposures to be considered when determining their risk for skin cancer. One subset that may be at a higher risk is military pilots who fly at high altitudes on irregular schedules in austere environments. Through the unparalleled comradeship inherent in many military units, pilots “hear” from their fellow pilots that they are at increased risk for skin cancer. Do their occupational exposures translate into increased risk for cutaneous malignancy? This article will survey the literature pertaining to pilots and skin cancer so that all dermatologists may better care for this unique population.

Epidemiology

Anecdotally, we have observed basal cell carcinoma in pilots in their 20s and early 30s, earlier than would be expected in an otherwise healthy prescreened military population.1 Woolley and Hughes2 published a case report of skin cancer in a young military aviator. The patient was a 32-year-old male helicopter pilot with Fitzpatrick skin type II and no personal or family history of skin cancer who was diagnosed with a periocular nodular basal cell carcinoma. He deployed to locations with high UV radiation (UVR) indices, and his vacation time also was spent in such areas.2 UV radiation exposure and Fitzpatrick skin type are known risk factors across occupations, but are there special exposures that come with military aviation service?

To better understand the risk for malignancy in this special population, the US Air Force examined the rates of all cancer types among a cohort of flying versus nonflying officers.3 Aviation personnel showed increased incidence of testicular, bladder, and all-site cancers combined. Noticeably absent was a statistically significant increased risk for malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Other epidemiological studies examined the incidence rates of MM in the US Armed Forces compared with age- and race-matched civilian populations and showed mixed results: 2 studies showed increased risk,4,5 while a third showed decreased risk.6 Despite finding opposite results of MM rates in military members versus the civilian population, 2 of these studies showed US Air Force members to have higher rates of MM than those in the US Army or Navy.4,6 Interestingly, the air force has the highest number of pilots among all the services, with 4000 more pilots than the army and navy.7 Further studies are needed to determine if the higher air force MM rates occur in pilots.

Although there are mixed and limited data pertaining to military flight crews, there is more robust literature concerning civilian flight personnel. One meta-analysis pooled studies related to cancer risk in cabin crews and civil and military pilots.8 In military pilots, they found a standardized incidence ratio (SIR) of 1.43 (95% confidence interval [CI], 1.09-1.87) for MM and 1.80 (95% CI, 1.25-2.80) for NMSC. The SIRs were higher for male cabin attendants (3.42 and 7.46, respectively) and civil pilots (2.18 and 1.88, respectively). They also found the most common cause of mortality in civilian cabin crews was AIDS, possibly explaining the higher SIRs for all types of malignancy in that population.8 In the United States, many civilian pilots previously were military pilots9 who likely served in the military for at least 10 years.10 A 2015 meta-analysis of 19 studies of more than 266,000 civil pilots and aircrew members found an SIR for MM of 2.22 (95% CI, 1.67-2.93) for civil pilots and 2.09 (95% CI, 1.67-2.62) for aircrews, stating the risk for MM is at least twice that of the general population.11

 

 

Risk Factors

UV Radiation
These studies suggest flight duties increase the risk for cutaneous malignancy. UV radiation is a known risk factor for skin cancer.12 The main body of the aircraft may protect the cabin’s crew and passengers from UVR, but pilots are exposed to more UVR, especially in aircraft with larger windshields. A government study in 2007 examined the transmittance of UVR through windscreens of 8 aircraft: 3 commercial jets, 2 commercial propeller planes, 1 private jet, and 2 small propeller planes.13 UVB was attenuated by all the windscreens (<1% transmittance), but 43% to 54% of UVA was transmitted, with plastic windshields attenuating more than glass. Sanlorenzo et al14 measured UVA irradiance at the pilot’s seat of a turboprop aircraft at 30,000-ft altitude. They compared this exposure to a UVA tanning bed and estimated that 57 minutes of flight at 30,000-ft altitude was equivalent to 20 minutes inside a UVA tanning booth, a startling finding.14

Cosmic Radiation
Cosmic radiation consists of neutrons and gamma rays that originate outside Earth’s atmosphere. Pilots are exposed to higher doses of cosmic radiation than nonpilots, but the health effects are difficult to study. Boice et al15 described how factors such as altitude, latitude, and flight time determine pilots’ cumulative exposure. With longer flight times at higher altitudes, a pilot’s exposure to cosmic radiation is increasing over the years.15 A 2012 review found that aircrews have low-level cosmic radiation exposure. Despite increases in MM and NMSC in pilots and increased rates of breast cancer in female aircrew, overall cancer-related mortality was lower in flying versus nonflying controls.16 Thus, cosmic radiation may not be as onerous of an occupational hazard for pilots as has been postulated.

Altered Circadian Rhythms
Aviation duties, especially in the military, require irregular work schedules that repeatedly interfere with normal sleep-wake cycles, disrupt circadian rhythms, and lead to reduced melatonin levels.8 Evidence suggests that low levels of melatonin could increase the risk for breast and prostate cancer—both cancers that occur more frequently in female aircrew and male pilots, respectively—by reducing melatonin’s natural protective role in such malignancies.17,18 A World Health Organization working group categorized shift work as “probably carcinogenic” and cited alterations of melatonin levels, changes in other circadian rhythm–related gene pathways, and relative immunosuppression as likely causative factors.19 In a 2011 study, exposing mice to UVR during times when nucleotide excision repair mechanisms were at their lowest activity caused an increased rate of skin cancers.20 A 2014 review discussed how epidemiological studies of shift workers such as nurses, firefighters, pilots, and flight crews found contradictory data, but molecular studies show that circadian rhythm–linked repair and tumorigenesis mechanisms are altered by aberrations in the normal sleep-wake cycle.21

Cockpit Instrumentation
Electromagnetic energy from the flight instruments in the cockpit also could influence malignancy risk. Nicholas et al22 found magnetic field measurements within the cockpit to be 2 to 10 times that experienced within the home or office. However, no studies examining the health effects of cockpit flight instruments and magnetic fields were found.

Final Thoughts

It is important to counsel pilots on the generally recognized, nonaviation-specific risk factors of family history, skin type, and UVR exposure in the development of skin cancer. Additionally, it is important to explain the possible role of exposure to UVR at higher altitudes, cosmic radiation, and electromagnetic energy from cockpit instruments, as well as altered sleep-wake cycles. A pilot’s risk for MM may be twice that of matched controls, and the risk for NMSC could be higher.8,11 Although the literature lacks specific recommendations for pilots, it is reasonable to screen pilots once per year to better assess their individual risk and encourage diligent use of sunscreen and sun-protective measures when flying. It also may be important to advocate for the development of engineering controls that decrease UVR transmittance through windscreens, particularly for aircraft flying at higher altitudes for longer flights. More research is needed to determine if changes in circadian rhythm and decreases in melatonin increase skin cancer risk, which could impact how pilots’ schedules are managed. Together, we can ensure adequate surveillance, diagnosis, and treatment in this at-risk population.

References
  1. Roewert‐Huber J, Lange-Asschenfeldt B, Stockfleth E, et al. Epidemiology and aetiology of basal cell carcinoma. Br J Dermatol. 2007;157(suppl 2):47-51.
  2. Woolley SD, Hughes C. A young military pilot presents with a periocular basal cell carcinoma: a case report. Travel Med Infect Dis. 2013;11:435-437.
  3. Grayson JK, Lyons TJ. Cancer incidence in United States Air Force aircrew, 1975-89. Aviat Space Environ Med. 1996;67:101-104.
  4. Lea CS, Efird JT, Toland AE, et al. Melanoma incidence rates in active duty military personnel compared with a population-based registry in the United States, 2000-2007. Mil Med. 2014;179:247-253.
  5. Garland FC, White MR, Garland CF, et al. Occupational sunlight exposure and melanoma in the US Navy. Arc Environ Health. 1990;45:261-267.
  6. Zhou J, Enewold L, Zahm SH, et al. Melanoma incidence rates among whites in the US military. Cancer Epidemiol Biomarkers Prev. 2011;20:318-323.
  7. Active Duty Master Personnel File: Active Duty Tactical Operations Officers. Seaside, CA: Defense Manpower Data Center; August 31, 2017. Accessed September 22, 2017.
  8. Buja A, Lange JH, Perissinotto E, et al. Cancer incidence among male military and civil pilots and flight attendants: an analysis on published data. Toxicol Ind Health. 2005;21:273-282.
  9. Jansen HS, Oster CV, eds. Taking Flight: Education and Training for Aviation Careers. Washington, DC: National Academy Press; 1997.
  10. About AFROTC Service Commitment. US Air Force ROTC website. https://www.afrotc.com/about/service. Accessed September 20, 2017.
  11. Sanlorenzo M, Wehner MR, Linos E, et al. The risk of melanoma in airline pilots and cabin crew: a meta-analysis. JAMA Dermatol. 2015;151:51-58.
  12. Ananthaswamy HN, Pierceall WE. Molecular mechanisms of ultraviolet radiation carcinogenesis. Photochem Photobiol. 1990;52:1119-1136.
  13. Nakagawara VB, Montgomery RW, Marshall WJ. Optical Radiation Transmittance of Aircraft Windscreens and Pilot Vision. Oklahoma City, OK: Federal Aviation Administration; 2007.
  14. Sanlorenzo M, Vujic I, Posch C, et al. The risk of melanoma in pilots and cabin crew: UV measurements in flying airplanes. JAMA Dermatol. 2015;151:450-452.
  15. Boice JD, Blettner M, Auvinen A. Epidemiologic studies of pilots and aircrew. Health Phys. 2000;79:576-584.
  16. Zeeb H, Hammer GP, Blettner M. Epidemiological investigations of aircrew: an occupational group with low-level cosmic radiation exposure [published online March 6, 2012]. J Radiol Prot. 2012;32:N15-N19.
  17. Stevens RG. Circadian disruption and breast cancer: from melatonin to clock genes. Epidemiology. 2005;16:254-258.
  18. Siu SW, Lau KW, Tam PC, et al. Melatonin and prostate cancer cell proliferation: interplay with castration, epidermal growth factor, and androgen sensitivity. Prostate. 2002;52:106-122.
  19. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. Lyon, France: World Health Organization International Agency for Research on Cancer; 2010.
  20. Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci. 2011;108:18790-18795.
  21. Markova-Car EP, Jurišic´ D, Ilic´ N, et al. Running for time: circadian rhythms and melanoma. Tumour Biol. 2014;35:8359-8368.
  22. Nicholas JS, Lackland DT, Butler GC, et al. Cosmic radiation and magnetic field exposure to airline flight crews. Am J Ind Med. 1998;34:574-580.
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Author and Disclosure Information

Dr. Wilkison is from Wilford Hall Ambulatory Surgical Center, San Antonio, Texas. Dr. Wong is from the University of Colorado, Aurora.

The authors report no conflict of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Department of the Army, the Department of the Air Force, or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, Department of Dermatology, 2200 Bergquist Dr, San Antonio, TX 78236 ([email protected]).

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Author and Disclosure Information

Dr. Wilkison is from Wilford Hall Ambulatory Surgical Center, San Antonio, Texas. Dr. Wong is from the University of Colorado, Aurora.

The authors report no conflict of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Department of the Army, the Department of the Air Force, or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, Department of Dermatology, 2200 Bergquist Dr, San Antonio, TX 78236 ([email protected]).

Author and Disclosure Information

Dr. Wilkison is from Wilford Hall Ambulatory Surgical Center, San Antonio, Texas. Dr. Wong is from the University of Colorado, Aurora.

The authors report no conflict of interest.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Department of the Army, the Department of the Air Force, or the Department of Defense.

Correspondence: Bart D. Wilkison, MD, Department of Dermatology, 2200 Bergquist Dr, San Antonio, TX 78236 ([email protected]).

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Related Articles
In partnership with the Association of Military Dermatologists
In partnership with the Association of Military Dermatologists

Military dermatologists are charged with caring for a diverse population of active-duty members, civilian dependents, and military retirees. Although certain risk factors for cutaneous malignancies are common in all of these groups, the active-duty population experiences unique exposures to be considered when determining their risk for skin cancer. One subset that may be at a higher risk is military pilots who fly at high altitudes on irregular schedules in austere environments. Through the unparalleled comradeship inherent in many military units, pilots “hear” from their fellow pilots that they are at increased risk for skin cancer. Do their occupational exposures translate into increased risk for cutaneous malignancy? This article will survey the literature pertaining to pilots and skin cancer so that all dermatologists may better care for this unique population.

Epidemiology

Anecdotally, we have observed basal cell carcinoma in pilots in their 20s and early 30s, earlier than would be expected in an otherwise healthy prescreened military population.1 Woolley and Hughes2 published a case report of skin cancer in a young military aviator. The patient was a 32-year-old male helicopter pilot with Fitzpatrick skin type II and no personal or family history of skin cancer who was diagnosed with a periocular nodular basal cell carcinoma. He deployed to locations with high UV radiation (UVR) indices, and his vacation time also was spent in such areas.2 UV radiation exposure and Fitzpatrick skin type are known risk factors across occupations, but are there special exposures that come with military aviation service?

To better understand the risk for malignancy in this special population, the US Air Force examined the rates of all cancer types among a cohort of flying versus nonflying officers.3 Aviation personnel showed increased incidence of testicular, bladder, and all-site cancers combined. Noticeably absent was a statistically significant increased risk for malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Other epidemiological studies examined the incidence rates of MM in the US Armed Forces compared with age- and race-matched civilian populations and showed mixed results: 2 studies showed increased risk,4,5 while a third showed decreased risk.6 Despite finding opposite results of MM rates in military members versus the civilian population, 2 of these studies showed US Air Force members to have higher rates of MM than those in the US Army or Navy.4,6 Interestingly, the air force has the highest number of pilots among all the services, with 4000 more pilots than the army and navy.7 Further studies are needed to determine if the higher air force MM rates occur in pilots.

Although there are mixed and limited data pertaining to military flight crews, there is more robust literature concerning civilian flight personnel. One meta-analysis pooled studies related to cancer risk in cabin crews and civil and military pilots.8 In military pilots, they found a standardized incidence ratio (SIR) of 1.43 (95% confidence interval [CI], 1.09-1.87) for MM and 1.80 (95% CI, 1.25-2.80) for NMSC. The SIRs were higher for male cabin attendants (3.42 and 7.46, respectively) and civil pilots (2.18 and 1.88, respectively). They also found the most common cause of mortality in civilian cabin crews was AIDS, possibly explaining the higher SIRs for all types of malignancy in that population.8 In the United States, many civilian pilots previously were military pilots9 who likely served in the military for at least 10 years.10 A 2015 meta-analysis of 19 studies of more than 266,000 civil pilots and aircrew members found an SIR for MM of 2.22 (95% CI, 1.67-2.93) for civil pilots and 2.09 (95% CI, 1.67-2.62) for aircrews, stating the risk for MM is at least twice that of the general population.11

 

 

Risk Factors

UV Radiation
These studies suggest flight duties increase the risk for cutaneous malignancy. UV radiation is a known risk factor for skin cancer.12 The main body of the aircraft may protect the cabin’s crew and passengers from UVR, but pilots are exposed to more UVR, especially in aircraft with larger windshields. A government study in 2007 examined the transmittance of UVR through windscreens of 8 aircraft: 3 commercial jets, 2 commercial propeller planes, 1 private jet, and 2 small propeller planes.13 UVB was attenuated by all the windscreens (<1% transmittance), but 43% to 54% of UVA was transmitted, with plastic windshields attenuating more than glass. Sanlorenzo et al14 measured UVA irradiance at the pilot’s seat of a turboprop aircraft at 30,000-ft altitude. They compared this exposure to a UVA tanning bed and estimated that 57 minutes of flight at 30,000-ft altitude was equivalent to 20 minutes inside a UVA tanning booth, a startling finding.14

Cosmic Radiation
Cosmic radiation consists of neutrons and gamma rays that originate outside Earth’s atmosphere. Pilots are exposed to higher doses of cosmic radiation than nonpilots, but the health effects are difficult to study. Boice et al15 described how factors such as altitude, latitude, and flight time determine pilots’ cumulative exposure. With longer flight times at higher altitudes, a pilot’s exposure to cosmic radiation is increasing over the years.15 A 2012 review found that aircrews have low-level cosmic radiation exposure. Despite increases in MM and NMSC in pilots and increased rates of breast cancer in female aircrew, overall cancer-related mortality was lower in flying versus nonflying controls.16 Thus, cosmic radiation may not be as onerous of an occupational hazard for pilots as has been postulated.

Altered Circadian Rhythms
Aviation duties, especially in the military, require irregular work schedules that repeatedly interfere with normal sleep-wake cycles, disrupt circadian rhythms, and lead to reduced melatonin levels.8 Evidence suggests that low levels of melatonin could increase the risk for breast and prostate cancer—both cancers that occur more frequently in female aircrew and male pilots, respectively—by reducing melatonin’s natural protective role in such malignancies.17,18 A World Health Organization working group categorized shift work as “probably carcinogenic” and cited alterations of melatonin levels, changes in other circadian rhythm–related gene pathways, and relative immunosuppression as likely causative factors.19 In a 2011 study, exposing mice to UVR during times when nucleotide excision repair mechanisms were at their lowest activity caused an increased rate of skin cancers.20 A 2014 review discussed how epidemiological studies of shift workers such as nurses, firefighters, pilots, and flight crews found contradictory data, but molecular studies show that circadian rhythm–linked repair and tumorigenesis mechanisms are altered by aberrations in the normal sleep-wake cycle.21

Cockpit Instrumentation
Electromagnetic energy from the flight instruments in the cockpit also could influence malignancy risk. Nicholas et al22 found magnetic field measurements within the cockpit to be 2 to 10 times that experienced within the home or office. However, no studies examining the health effects of cockpit flight instruments and magnetic fields were found.

Final Thoughts

It is important to counsel pilots on the generally recognized, nonaviation-specific risk factors of family history, skin type, and UVR exposure in the development of skin cancer. Additionally, it is important to explain the possible role of exposure to UVR at higher altitudes, cosmic radiation, and electromagnetic energy from cockpit instruments, as well as altered sleep-wake cycles. A pilot’s risk for MM may be twice that of matched controls, and the risk for NMSC could be higher.8,11 Although the literature lacks specific recommendations for pilots, it is reasonable to screen pilots once per year to better assess their individual risk and encourage diligent use of sunscreen and sun-protective measures when flying. It also may be important to advocate for the development of engineering controls that decrease UVR transmittance through windscreens, particularly for aircraft flying at higher altitudes for longer flights. More research is needed to determine if changes in circadian rhythm and decreases in melatonin increase skin cancer risk, which could impact how pilots’ schedules are managed. Together, we can ensure adequate surveillance, diagnosis, and treatment in this at-risk population.

Military dermatologists are charged with caring for a diverse population of active-duty members, civilian dependents, and military retirees. Although certain risk factors for cutaneous malignancies are common in all of these groups, the active-duty population experiences unique exposures to be considered when determining their risk for skin cancer. One subset that may be at a higher risk is military pilots who fly at high altitudes on irregular schedules in austere environments. Through the unparalleled comradeship inherent in many military units, pilots “hear” from their fellow pilots that they are at increased risk for skin cancer. Do their occupational exposures translate into increased risk for cutaneous malignancy? This article will survey the literature pertaining to pilots and skin cancer so that all dermatologists may better care for this unique population.

Epidemiology

Anecdotally, we have observed basal cell carcinoma in pilots in their 20s and early 30s, earlier than would be expected in an otherwise healthy prescreened military population.1 Woolley and Hughes2 published a case report of skin cancer in a young military aviator. The patient was a 32-year-old male helicopter pilot with Fitzpatrick skin type II and no personal or family history of skin cancer who was diagnosed with a periocular nodular basal cell carcinoma. He deployed to locations with high UV radiation (UVR) indices, and his vacation time also was spent in such areas.2 UV radiation exposure and Fitzpatrick skin type are known risk factors across occupations, but are there special exposures that come with military aviation service?

To better understand the risk for malignancy in this special population, the US Air Force examined the rates of all cancer types among a cohort of flying versus nonflying officers.3 Aviation personnel showed increased incidence of testicular, bladder, and all-site cancers combined. Noticeably absent was a statistically significant increased risk for malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Other epidemiological studies examined the incidence rates of MM in the US Armed Forces compared with age- and race-matched civilian populations and showed mixed results: 2 studies showed increased risk,4,5 while a third showed decreased risk.6 Despite finding opposite results of MM rates in military members versus the civilian population, 2 of these studies showed US Air Force members to have higher rates of MM than those in the US Army or Navy.4,6 Interestingly, the air force has the highest number of pilots among all the services, with 4000 more pilots than the army and navy.7 Further studies are needed to determine if the higher air force MM rates occur in pilots.

Although there are mixed and limited data pertaining to military flight crews, there is more robust literature concerning civilian flight personnel. One meta-analysis pooled studies related to cancer risk in cabin crews and civil and military pilots.8 In military pilots, they found a standardized incidence ratio (SIR) of 1.43 (95% confidence interval [CI], 1.09-1.87) for MM and 1.80 (95% CI, 1.25-2.80) for NMSC. The SIRs were higher for male cabin attendants (3.42 and 7.46, respectively) and civil pilots (2.18 and 1.88, respectively). They also found the most common cause of mortality in civilian cabin crews was AIDS, possibly explaining the higher SIRs for all types of malignancy in that population.8 In the United States, many civilian pilots previously were military pilots9 who likely served in the military for at least 10 years.10 A 2015 meta-analysis of 19 studies of more than 266,000 civil pilots and aircrew members found an SIR for MM of 2.22 (95% CI, 1.67-2.93) for civil pilots and 2.09 (95% CI, 1.67-2.62) for aircrews, stating the risk for MM is at least twice that of the general population.11

 

 

Risk Factors

UV Radiation
These studies suggest flight duties increase the risk for cutaneous malignancy. UV radiation is a known risk factor for skin cancer.12 The main body of the aircraft may protect the cabin’s crew and passengers from UVR, but pilots are exposed to more UVR, especially in aircraft with larger windshields. A government study in 2007 examined the transmittance of UVR through windscreens of 8 aircraft: 3 commercial jets, 2 commercial propeller planes, 1 private jet, and 2 small propeller planes.13 UVB was attenuated by all the windscreens (<1% transmittance), but 43% to 54% of UVA was transmitted, with plastic windshields attenuating more than glass. Sanlorenzo et al14 measured UVA irradiance at the pilot’s seat of a turboprop aircraft at 30,000-ft altitude. They compared this exposure to a UVA tanning bed and estimated that 57 minutes of flight at 30,000-ft altitude was equivalent to 20 minutes inside a UVA tanning booth, a startling finding.14

Cosmic Radiation
Cosmic radiation consists of neutrons and gamma rays that originate outside Earth’s atmosphere. Pilots are exposed to higher doses of cosmic radiation than nonpilots, but the health effects are difficult to study. Boice et al15 described how factors such as altitude, latitude, and flight time determine pilots’ cumulative exposure. With longer flight times at higher altitudes, a pilot’s exposure to cosmic radiation is increasing over the years.15 A 2012 review found that aircrews have low-level cosmic radiation exposure. Despite increases in MM and NMSC in pilots and increased rates of breast cancer in female aircrew, overall cancer-related mortality was lower in flying versus nonflying controls.16 Thus, cosmic radiation may not be as onerous of an occupational hazard for pilots as has been postulated.

Altered Circadian Rhythms
Aviation duties, especially in the military, require irregular work schedules that repeatedly interfere with normal sleep-wake cycles, disrupt circadian rhythms, and lead to reduced melatonin levels.8 Evidence suggests that low levels of melatonin could increase the risk for breast and prostate cancer—both cancers that occur more frequently in female aircrew and male pilots, respectively—by reducing melatonin’s natural protective role in such malignancies.17,18 A World Health Organization working group categorized shift work as “probably carcinogenic” and cited alterations of melatonin levels, changes in other circadian rhythm–related gene pathways, and relative immunosuppression as likely causative factors.19 In a 2011 study, exposing mice to UVR during times when nucleotide excision repair mechanisms were at their lowest activity caused an increased rate of skin cancers.20 A 2014 review discussed how epidemiological studies of shift workers such as nurses, firefighters, pilots, and flight crews found contradictory data, but molecular studies show that circadian rhythm–linked repair and tumorigenesis mechanisms are altered by aberrations in the normal sleep-wake cycle.21

Cockpit Instrumentation
Electromagnetic energy from the flight instruments in the cockpit also could influence malignancy risk. Nicholas et al22 found magnetic field measurements within the cockpit to be 2 to 10 times that experienced within the home or office. However, no studies examining the health effects of cockpit flight instruments and magnetic fields were found.

Final Thoughts

It is important to counsel pilots on the generally recognized, nonaviation-specific risk factors of family history, skin type, and UVR exposure in the development of skin cancer. Additionally, it is important to explain the possible role of exposure to UVR at higher altitudes, cosmic radiation, and electromagnetic energy from cockpit instruments, as well as altered sleep-wake cycles. A pilot’s risk for MM may be twice that of matched controls, and the risk for NMSC could be higher.8,11 Although the literature lacks specific recommendations for pilots, it is reasonable to screen pilots once per year to better assess their individual risk and encourage diligent use of sunscreen and sun-protective measures when flying. It also may be important to advocate for the development of engineering controls that decrease UVR transmittance through windscreens, particularly for aircraft flying at higher altitudes for longer flights. More research is needed to determine if changes in circadian rhythm and decreases in melatonin increase skin cancer risk, which could impact how pilots’ schedules are managed. Together, we can ensure adequate surveillance, diagnosis, and treatment in this at-risk population.

References
  1. Roewert‐Huber J, Lange-Asschenfeldt B, Stockfleth E, et al. Epidemiology and aetiology of basal cell carcinoma. Br J Dermatol. 2007;157(suppl 2):47-51.
  2. Woolley SD, Hughes C. A young military pilot presents with a periocular basal cell carcinoma: a case report. Travel Med Infect Dis. 2013;11:435-437.
  3. Grayson JK, Lyons TJ. Cancer incidence in United States Air Force aircrew, 1975-89. Aviat Space Environ Med. 1996;67:101-104.
  4. Lea CS, Efird JT, Toland AE, et al. Melanoma incidence rates in active duty military personnel compared with a population-based registry in the United States, 2000-2007. Mil Med. 2014;179:247-253.
  5. Garland FC, White MR, Garland CF, et al. Occupational sunlight exposure and melanoma in the US Navy. Arc Environ Health. 1990;45:261-267.
  6. Zhou J, Enewold L, Zahm SH, et al. Melanoma incidence rates among whites in the US military. Cancer Epidemiol Biomarkers Prev. 2011;20:318-323.
  7. Active Duty Master Personnel File: Active Duty Tactical Operations Officers. Seaside, CA: Defense Manpower Data Center; August 31, 2017. Accessed September 22, 2017.
  8. Buja A, Lange JH, Perissinotto E, et al. Cancer incidence among male military and civil pilots and flight attendants: an analysis on published data. Toxicol Ind Health. 2005;21:273-282.
  9. Jansen HS, Oster CV, eds. Taking Flight: Education and Training for Aviation Careers. Washington, DC: National Academy Press; 1997.
  10. About AFROTC Service Commitment. US Air Force ROTC website. https://www.afrotc.com/about/service. Accessed September 20, 2017.
  11. Sanlorenzo M, Wehner MR, Linos E, et al. The risk of melanoma in airline pilots and cabin crew: a meta-analysis. JAMA Dermatol. 2015;151:51-58.
  12. Ananthaswamy HN, Pierceall WE. Molecular mechanisms of ultraviolet radiation carcinogenesis. Photochem Photobiol. 1990;52:1119-1136.
  13. Nakagawara VB, Montgomery RW, Marshall WJ. Optical Radiation Transmittance of Aircraft Windscreens and Pilot Vision. Oklahoma City, OK: Federal Aviation Administration; 2007.
  14. Sanlorenzo M, Vujic I, Posch C, et al. The risk of melanoma in pilots and cabin crew: UV measurements in flying airplanes. JAMA Dermatol. 2015;151:450-452.
  15. Boice JD, Blettner M, Auvinen A. Epidemiologic studies of pilots and aircrew. Health Phys. 2000;79:576-584.
  16. Zeeb H, Hammer GP, Blettner M. Epidemiological investigations of aircrew: an occupational group with low-level cosmic radiation exposure [published online March 6, 2012]. J Radiol Prot. 2012;32:N15-N19.
  17. Stevens RG. Circadian disruption and breast cancer: from melatonin to clock genes. Epidemiology. 2005;16:254-258.
  18. Siu SW, Lau KW, Tam PC, et al. Melatonin and prostate cancer cell proliferation: interplay with castration, epidermal growth factor, and androgen sensitivity. Prostate. 2002;52:106-122.
  19. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. Lyon, France: World Health Organization International Agency for Research on Cancer; 2010.
  20. Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci. 2011;108:18790-18795.
  21. Markova-Car EP, Jurišic´ D, Ilic´ N, et al. Running for time: circadian rhythms and melanoma. Tumour Biol. 2014;35:8359-8368.
  22. Nicholas JS, Lackland DT, Butler GC, et al. Cosmic radiation and magnetic field exposure to airline flight crews. Am J Ind Med. 1998;34:574-580.
References
  1. Roewert‐Huber J, Lange-Asschenfeldt B, Stockfleth E, et al. Epidemiology and aetiology of basal cell carcinoma. Br J Dermatol. 2007;157(suppl 2):47-51.
  2. Woolley SD, Hughes C. A young military pilot presents with a periocular basal cell carcinoma: a case report. Travel Med Infect Dis. 2013;11:435-437.
  3. Grayson JK, Lyons TJ. Cancer incidence in United States Air Force aircrew, 1975-89. Aviat Space Environ Med. 1996;67:101-104.
  4. Lea CS, Efird JT, Toland AE, et al. Melanoma incidence rates in active duty military personnel compared with a population-based registry in the United States, 2000-2007. Mil Med. 2014;179:247-253.
  5. Garland FC, White MR, Garland CF, et al. Occupational sunlight exposure and melanoma in the US Navy. Arc Environ Health. 1990;45:261-267.
  6. Zhou J, Enewold L, Zahm SH, et al. Melanoma incidence rates among whites in the US military. Cancer Epidemiol Biomarkers Prev. 2011;20:318-323.
  7. Active Duty Master Personnel File: Active Duty Tactical Operations Officers. Seaside, CA: Defense Manpower Data Center; August 31, 2017. Accessed September 22, 2017.
  8. Buja A, Lange JH, Perissinotto E, et al. Cancer incidence among male military and civil pilots and flight attendants: an analysis on published data. Toxicol Ind Health. 2005;21:273-282.
  9. Jansen HS, Oster CV, eds. Taking Flight: Education and Training for Aviation Careers. Washington, DC: National Academy Press; 1997.
  10. About AFROTC Service Commitment. US Air Force ROTC website. https://www.afrotc.com/about/service. Accessed September 20, 2017.
  11. Sanlorenzo M, Wehner MR, Linos E, et al. The risk of melanoma in airline pilots and cabin crew: a meta-analysis. JAMA Dermatol. 2015;151:51-58.
  12. Ananthaswamy HN, Pierceall WE. Molecular mechanisms of ultraviolet radiation carcinogenesis. Photochem Photobiol. 1990;52:1119-1136.
  13. Nakagawara VB, Montgomery RW, Marshall WJ. Optical Radiation Transmittance of Aircraft Windscreens and Pilot Vision. Oklahoma City, OK: Federal Aviation Administration; 2007.
  14. Sanlorenzo M, Vujic I, Posch C, et al. The risk of melanoma in pilots and cabin crew: UV measurements in flying airplanes. JAMA Dermatol. 2015;151:450-452.
  15. Boice JD, Blettner M, Auvinen A. Epidemiologic studies of pilots and aircrew. Health Phys. 2000;79:576-584.
  16. Zeeb H, Hammer GP, Blettner M. Epidemiological investigations of aircrew: an occupational group with low-level cosmic radiation exposure [published online March 6, 2012]. J Radiol Prot. 2012;32:N15-N19.
  17. Stevens RG. Circadian disruption and breast cancer: from melatonin to clock genes. Epidemiology. 2005;16:254-258.
  18. Siu SW, Lau KW, Tam PC, et al. Melatonin and prostate cancer cell proliferation: interplay with castration, epidermal growth factor, and androgen sensitivity. Prostate. 2002;52:106-122.
  19. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. Lyon, France: World Health Organization International Agency for Research on Cancer; 2010.
  20. Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci. 2011;108:18790-18795.
  21. Markova-Car EP, Jurišic´ D, Ilic´ N, et al. Running for time: circadian rhythms and melanoma. Tumour Biol. 2014;35:8359-8368.
  22. Nicholas JS, Lackland DT, Butler GC, et al. Cosmic radiation and magnetic field exposure to airline flight crews. Am J Ind Med. 1998;34:574-580.
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  • Military and civilian pilots have an increased risk for melanoma and nonmelanoma skin cancer, likely due to unique occupational exposures.
  • We recommend annual skin cancer screening for all pilots to help assess their individual risk.
  • Pilots should be educated on their increased risk for skin cancer and encouraged to use sun-protective measures during their flying duties and leisure activities.
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How to Teach the Potassium Hydroxide Preparation: A Disappearing Clinical Art Form

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How to Teach the Potassium Hydroxide Preparation: A Disappearing Clinical Art Form

Potassium hydroxide (KOH) preparations remain an important bedside test for prompt and accurate diagnosis of superficial fungal infections known as dermatophytoses. This tool has been used for at least 100 years, with early terminology referring to it as potash; for the last century, it has largely been a technique passed down as a skill from master technician to learning apprentice. The original pioneer of the KOH preparation remains a mystery.1

Variations on techniques for performing the KOH preparation exist, and tips and tricks on the use of this test are a hot topic among dermatologists.2 Although primary care and dermatology-specific publications espouse the importance of the KOH preparation,3,4 it has unfortunately been identified and labeled as one of the forgotten diagnostic tools.5

It is incumbent on dermatologists to educate medical students and residents using a simple and specific method to ensure that this simple and effective technique, with sensitivity reported between 87% and 91% depending on the expertise of the examiner,6 remains part of the clinical armamentarium. One concern in the instruction of large groups of students and clinicians is the ready accessibility or availability of viable skin samples. This article describes a method of collecting and storing skin samples that will allow educators to train large groups of students on performing KOH preparations without having to repeatedly seek skin samples or patients with superficial skin infections. A detailed description of the pedagogy used to teach the preparation and interpretation of KOH slides to a large group of students also is reviewed.

Specimen Collection

The first step in teaching the KOH preparation to a large group is the collection of a suitable number of skin scrapings from patients with a superficial fungal skin infection (eg, tinea corporis, tinea versicolor). A common technique for obtaining skin samples is to use a no. 15 scalpel blade (Figure 1) to scrape the scale of the lesion at its scaly border once the area is moistened with an alcohol pad or soap and water.7 The moisture from the alcohol pad allows the scale to stick to the no. 15 blade, facilitating collection. Once a suitable amount of scale is collected, it is placed on a glass microscope slide by smearing the scale from the blade onto the slide. This process has been modified to facilitate a larger quantity of specimen as follows: dermatophyte-infected plaques with scale are rubbed with the no. 15 blade and the free scale drops into a standard urine specimen cup. This process is repeated multiple times from different sites to capture the displaced scale with the dermatophyte. We have found that as long as the specimen cups are sealed tightly and stored in a relatively dry and cool environment (room temperature), the samples can be used to construct KOH teaching slides for at least 3 years. We have not used them beyond 3 years but suspect that they would continue to be viable after this time.

 

Figure 1. Scraping at leading edge of lesion with a no. 15 scalpel blade after cleaning the area with an alcohol pad.

Preparation of Slides

Given that time for teaching often is limited, it is beneficial to fix many skin scrapings on a large number of glass slides prior to the session, which enables students to simply add KOH to the slides on the teaching day. To prepare the slides in advance, it is necessary to gather the following materials: a specimen cup with skin samples, glass slides, pickups or tweezers, a small pipette, a cup of water, protective gloves, and a pencil. After donning protective gloves, the pickups or tweezers are used to retrieve a few flakes of scale from the specimen cup and place them on the center of a glass slide. Using the pipette, 1 or 2 drops of water are added to the scale, and the slide is then allowed to dry. The slides are marked with the pencil to indicate the “up” side to prevent the students from applying KOH solution to the wrong side of the slide. The skin scale is fixed in place on the slide as the water evaporates and may be stored until needed for use in a standard slide box or folder.

Performing the KOH Preparation

On the day of teaching, it is helpful to engage the entire group of students with an introductory lecture on the purpose and use of the KOH preparation. Upon completion, students move to a workstation with all of the materials needed to prepare the slide. Additional items needed at this time are 10% KOH solution, coverslips, and a heating device (eg, lighter, Bunsen burner, match)(optional). Students are instructed to place 1 or 2 skin scales onto a glass slide or retrieve a slide with skin scales already fixed, and then add 1 drop of 10% KOH solution directly to the sample (Figure 2). Next, they should place a slide coverslip onto the KOH drop and skin sample using a side-to-side technique that will move the scale into a thin layer within the KOH solution and push away any excess solution to the periphery (Figure 3). Large amounts of excess KOH solution should be cleared away with a paper towel, lens paper, or tissue. The heat source can be used to gently heat the underside of the glass slide (Figure 4), but it often is sufficient to simply wait 3 to 5 minutes for the KOH solution to take effect. The heat accelerates the maceration of the scale and makes it easier to see the hyphae among the keratinocytes. Some physicians advocate the use of dimethyl sulfoxide in lieu of heating,8 but this solution may not be available in all primary care settings.

 

 

 

Figure 2. Adding 10% potassium hydroxide solution to skin samples.
  
Figure 3. Placing the slide coverslip.

 

Figure 4. Applying gentle heat to the potassium hydroxide preparations.

Microscopic Examination

Prior to examining the slides under the microscope, students may complete a self-guided tutorial (eg, digital or paper slide show) on the various features seen through the microscope that are indicative of dermatophytes, including branching hyphae and yeast buds. They also should be educated about the common appearance of artifacts that may resemble hyphae. Once the students have completed the tutorial, they may proceed to microscopic examination.

 While the students are viewing their slides under the microscope, we find it helpful to have at least 1 experienced faculty member for every group of 10 students. This instructor should encourage the students to lower the microscope condenser all the way to facilitate better observation. Students should start with low power (×4 or red band) and scan for areas that are rich in skin scale. Once a collection of scale is found, the student can switch to higher power (×10 or yellow band) and start scanning for hyphae. Students should be reminded to search for filamentous and branching tubes that are refractile. The term refractile may be confusing to some students, so we explain that shifting the focus up or down will show the hyphae to change in brightness and may reveal a greenish tint. Another helpful indicator to point out is the feature that hyphae will cross the border of epidermal skin cells, whereas artifacts will not  (Figure 5). Once the students have identified evidence of a dermatophyte infection, they must call the instructor to their station to verify the presence of hyphae or yeast buds, which helps confirm their understanding of the procedure. Once the  student accurately identifies these items, the session is complete.

 

Figure 5. Example of hyphum crossing epithelial cell borders. Figure 5. Example of hyphum crossing epithelial cell borders.
Figure 5. Example of hyphum crossing epithelial cell borders.

Comment

The use of a KOH preparation is a fast, simple, accurate, and cost-effective way to diagnose superficial fungal infections; however, because of insufficient familiarity with this tool, the technique often is replaced by initiation of empiric antifungal therapy in patients with suspected dermatophytosis. This empiric treatment has the potential to delay appropriate diagnosis and treatment (eg, in a patient with nummular dermatitis, which can clinically mimic tinea corporis). One way to encourage the use of the KOH preparation in the primary care and dermatologic setting is to educate large groups of next-generation physicians while in medical training. This article describes a teaching technique that allows for long-term storage of positive skin samples and a detailed description of the pedagogy used to train and educate a large group of students in a relatively short period of time.

All KOH preparations fall under the US federal government’s Clinical Laboratory Improvement Amendments and require proficiency testing.9 Although the teaching method presented here is designed for teaching medical students, it may be utilized to educate or refamiliarize experienced physicians with the procedure in an effort to improve proficiency in point-of-care testing programs used in many health care systems to comply with the Clinical Laboratories Improvement Amendments. Future analyses could assess whether the method described here improves provider performance on such proficiency measures and whether it ultimately helps ensure quality patient care.

References

 

1. Dasgupta T, Sahu J. Origins of the KOH technique. Clin Dermatol. 2012;2:238-242.

2. Stone S. Editor’s commentary. Clin Dermatol. 2012;2:241-242.

3. Monroe JR. The diagnostic value of a KOH. JAAPA. 2001;4:50-51.

4. Hainer BL. Dermatophyte infections. Am Fam Physician. 2003;1:101-109.

5. Ponka D, Baddar F. Microscopic potassium hydroxide preparation. Can Fam Physician. 2014;60:57.

6. Lilly KK, Koshnick RL, Grill JP, et al. Cost-effectiveness of diagnostic tests for toenail onychomycosis: a repeated-measure, single-blinded, cross-sectional evaluation of  7 diagnostic tests. J Am Acad Dermatol. 2006;4:620-626.

7. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012.

8. James WD, Berger T, Elston D. Andrew’s Diseases of the Skin: Clinical Dermatology. 11th ed. New York, NY: Elsevier Saunders; 2011.

9. Clinical Laboratory Improvement Amendments (CLIA). Centers for Medicare & Medicaid Services Web site. https://www.cms.gov/Regulations-and-Guidance/Legislation/CLIA/index.html?redirect=/clia/. Updated June 6, 2015. Accessed July 21, 2015.

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Bart D. Wilkison, MD; Leonard C. Sperling, MD; Anne P. Spillane, MD; Jon H. Meyerle, MD

Dr. Wilkison is from Brooke Army Medical Center, San Antonio, Texas. Drs. Sperling and Meyerle are from the Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Dr. Spillane is from Kimbrough Ambulatory Care Clinic, Fort Meade, Maryland.

The authors report no conflict of interest.

The opinions expressed in this article are solely those of the authors and do not necessarily reflect the official policy or position of the US Army or the US Department of Defense.

Correspondence: Jon H. Meyerle, MD, Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd, Bethesda, MD 20814 ([email protected]).

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Dr. Wilkison is from Brooke Army Medical Center, San Antonio, Texas. Drs. Sperling and Meyerle are from the Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Dr. Spillane is from Kimbrough Ambulatory Care Clinic, Fort Meade, Maryland.

The authors report no conflict of interest.

The opinions expressed in this article are solely those of the authors and do not necessarily reflect the official policy or position of the US Army or the US Department of Defense.

Correspondence: Jon H. Meyerle, MD, Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd, Bethesda, MD 20814 ([email protected]).

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Bart D. Wilkison, MD; Leonard C. Sperling, MD; Anne P. Spillane, MD; Jon H. Meyerle, MD

Dr. Wilkison is from Brooke Army Medical Center, San Antonio, Texas. Drs. Sperling and Meyerle are from the Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Dr. Spillane is from Kimbrough Ambulatory Care Clinic, Fort Meade, Maryland.

The authors report no conflict of interest.

The opinions expressed in this article are solely those of the authors and do not necessarily reflect the official policy or position of the US Army or the US Department of Defense.

Correspondence: Jon H. Meyerle, MD, Department of Dermatology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd, Bethesda, MD 20814 ([email protected]).

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Potassium hydroxide (KOH) preparations remain an important bedside test for prompt and accurate diagnosis of superficial fungal infections known as dermatophytoses. This tool has been used for at least 100 years, with early terminology referring to it as potash; for the last century, it has largely been a technique passed down as a skill from master technician to learning apprentice. The original pioneer of the KOH preparation remains a mystery.1

Variations on techniques for performing the KOH preparation exist, and tips and tricks on the use of this test are a hot topic among dermatologists.2 Although primary care and dermatology-specific publications espouse the importance of the KOH preparation,3,4 it has unfortunately been identified and labeled as one of the forgotten diagnostic tools.5

It is incumbent on dermatologists to educate medical students and residents using a simple and specific method to ensure that this simple and effective technique, with sensitivity reported between 87% and 91% depending on the expertise of the examiner,6 remains part of the clinical armamentarium. One concern in the instruction of large groups of students and clinicians is the ready accessibility or availability of viable skin samples. This article describes a method of collecting and storing skin samples that will allow educators to train large groups of students on performing KOH preparations without having to repeatedly seek skin samples or patients with superficial skin infections. A detailed description of the pedagogy used to teach the preparation and interpretation of KOH slides to a large group of students also is reviewed.

Specimen Collection

The first step in teaching the KOH preparation to a large group is the collection of a suitable number of skin scrapings from patients with a superficial fungal skin infection (eg, tinea corporis, tinea versicolor). A common technique for obtaining skin samples is to use a no. 15 scalpel blade (Figure 1) to scrape the scale of the lesion at its scaly border once the area is moistened with an alcohol pad or soap and water.7 The moisture from the alcohol pad allows the scale to stick to the no. 15 blade, facilitating collection. Once a suitable amount of scale is collected, it is placed on a glass microscope slide by smearing the scale from the blade onto the slide. This process has been modified to facilitate a larger quantity of specimen as follows: dermatophyte-infected plaques with scale are rubbed with the no. 15 blade and the free scale drops into a standard urine specimen cup. This process is repeated multiple times from different sites to capture the displaced scale with the dermatophyte. We have found that as long as the specimen cups are sealed tightly and stored in a relatively dry and cool environment (room temperature), the samples can be used to construct KOH teaching slides for at least 3 years. We have not used them beyond 3 years but suspect that they would continue to be viable after this time.

 

Figure 1. Scraping at leading edge of lesion with a no. 15 scalpel blade after cleaning the area with an alcohol pad.

Preparation of Slides

Given that time for teaching often is limited, it is beneficial to fix many skin scrapings on a large number of glass slides prior to the session, which enables students to simply add KOH to the slides on the teaching day. To prepare the slides in advance, it is necessary to gather the following materials: a specimen cup with skin samples, glass slides, pickups or tweezers, a small pipette, a cup of water, protective gloves, and a pencil. After donning protective gloves, the pickups or tweezers are used to retrieve a few flakes of scale from the specimen cup and place them on the center of a glass slide. Using the pipette, 1 or 2 drops of water are added to the scale, and the slide is then allowed to dry. The slides are marked with the pencil to indicate the “up” side to prevent the students from applying KOH solution to the wrong side of the slide. The skin scale is fixed in place on the slide as the water evaporates and may be stored until needed for use in a standard slide box or folder.

Performing the KOH Preparation

On the day of teaching, it is helpful to engage the entire group of students with an introductory lecture on the purpose and use of the KOH preparation. Upon completion, students move to a workstation with all of the materials needed to prepare the slide. Additional items needed at this time are 10% KOH solution, coverslips, and a heating device (eg, lighter, Bunsen burner, match)(optional). Students are instructed to place 1 or 2 skin scales onto a glass slide or retrieve a slide with skin scales already fixed, and then add 1 drop of 10% KOH solution directly to the sample (Figure 2). Next, they should place a slide coverslip onto the KOH drop and skin sample using a side-to-side technique that will move the scale into a thin layer within the KOH solution and push away any excess solution to the periphery (Figure 3). Large amounts of excess KOH solution should be cleared away with a paper towel, lens paper, or tissue. The heat source can be used to gently heat the underside of the glass slide (Figure 4), but it often is sufficient to simply wait 3 to 5 minutes for the KOH solution to take effect. The heat accelerates the maceration of the scale and makes it easier to see the hyphae among the keratinocytes. Some physicians advocate the use of dimethyl sulfoxide in lieu of heating,8 but this solution may not be available in all primary care settings.

 

 

 

Figure 2. Adding 10% potassium hydroxide solution to skin samples.
  
Figure 3. Placing the slide coverslip.

 

Figure 4. Applying gentle heat to the potassium hydroxide preparations.

Microscopic Examination

Prior to examining the slides under the microscope, students may complete a self-guided tutorial (eg, digital or paper slide show) on the various features seen through the microscope that are indicative of dermatophytes, including branching hyphae and yeast buds. They also should be educated about the common appearance of artifacts that may resemble hyphae. Once the students have completed the tutorial, they may proceed to microscopic examination.

 While the students are viewing their slides under the microscope, we find it helpful to have at least 1 experienced faculty member for every group of 10 students. This instructor should encourage the students to lower the microscope condenser all the way to facilitate better observation. Students should start with low power (×4 or red band) and scan for areas that are rich in skin scale. Once a collection of scale is found, the student can switch to higher power (×10 or yellow band) and start scanning for hyphae. Students should be reminded to search for filamentous and branching tubes that are refractile. The term refractile may be confusing to some students, so we explain that shifting the focus up or down will show the hyphae to change in brightness and may reveal a greenish tint. Another helpful indicator to point out is the feature that hyphae will cross the border of epidermal skin cells, whereas artifacts will not  (Figure 5). Once the students have identified evidence of a dermatophyte infection, they must call the instructor to their station to verify the presence of hyphae or yeast buds, which helps confirm their understanding of the procedure. Once the  student accurately identifies these items, the session is complete.

 

Figure 5. Example of hyphum crossing epithelial cell borders. Figure 5. Example of hyphum crossing epithelial cell borders.
Figure 5. Example of hyphum crossing epithelial cell borders.

Comment

The use of a KOH preparation is a fast, simple, accurate, and cost-effective way to diagnose superficial fungal infections; however, because of insufficient familiarity with this tool, the technique often is replaced by initiation of empiric antifungal therapy in patients with suspected dermatophytosis. This empiric treatment has the potential to delay appropriate diagnosis and treatment (eg, in a patient with nummular dermatitis, which can clinically mimic tinea corporis). One way to encourage the use of the KOH preparation in the primary care and dermatologic setting is to educate large groups of next-generation physicians while in medical training. This article describes a teaching technique that allows for long-term storage of positive skin samples and a detailed description of the pedagogy used to train and educate a large group of students in a relatively short period of time.

All KOH preparations fall under the US federal government’s Clinical Laboratory Improvement Amendments and require proficiency testing.9 Although the teaching method presented here is designed for teaching medical students, it may be utilized to educate or refamiliarize experienced physicians with the procedure in an effort to improve proficiency in point-of-care testing programs used in many health care systems to comply with the Clinical Laboratories Improvement Amendments. Future analyses could assess whether the method described here improves provider performance on such proficiency measures and whether it ultimately helps ensure quality patient care.

Potassium hydroxide (KOH) preparations remain an important bedside test for prompt and accurate diagnosis of superficial fungal infections known as dermatophytoses. This tool has been used for at least 100 years, with early terminology referring to it as potash; for the last century, it has largely been a technique passed down as a skill from master technician to learning apprentice. The original pioneer of the KOH preparation remains a mystery.1

Variations on techniques for performing the KOH preparation exist, and tips and tricks on the use of this test are a hot topic among dermatologists.2 Although primary care and dermatology-specific publications espouse the importance of the KOH preparation,3,4 it has unfortunately been identified and labeled as one of the forgotten diagnostic tools.5

It is incumbent on dermatologists to educate medical students and residents using a simple and specific method to ensure that this simple and effective technique, with sensitivity reported between 87% and 91% depending on the expertise of the examiner,6 remains part of the clinical armamentarium. One concern in the instruction of large groups of students and clinicians is the ready accessibility or availability of viable skin samples. This article describes a method of collecting and storing skin samples that will allow educators to train large groups of students on performing KOH preparations without having to repeatedly seek skin samples or patients with superficial skin infections. A detailed description of the pedagogy used to teach the preparation and interpretation of KOH slides to a large group of students also is reviewed.

Specimen Collection

The first step in teaching the KOH preparation to a large group is the collection of a suitable number of skin scrapings from patients with a superficial fungal skin infection (eg, tinea corporis, tinea versicolor). A common technique for obtaining skin samples is to use a no. 15 scalpel blade (Figure 1) to scrape the scale of the lesion at its scaly border once the area is moistened with an alcohol pad or soap and water.7 The moisture from the alcohol pad allows the scale to stick to the no. 15 blade, facilitating collection. Once a suitable amount of scale is collected, it is placed on a glass microscope slide by smearing the scale from the blade onto the slide. This process has been modified to facilitate a larger quantity of specimen as follows: dermatophyte-infected plaques with scale are rubbed with the no. 15 blade and the free scale drops into a standard urine specimen cup. This process is repeated multiple times from different sites to capture the displaced scale with the dermatophyte. We have found that as long as the specimen cups are sealed tightly and stored in a relatively dry and cool environment (room temperature), the samples can be used to construct KOH teaching slides for at least 3 years. We have not used them beyond 3 years but suspect that they would continue to be viable after this time.

 

Figure 1. Scraping at leading edge of lesion with a no. 15 scalpel blade after cleaning the area with an alcohol pad.

Preparation of Slides

Given that time for teaching often is limited, it is beneficial to fix many skin scrapings on a large number of glass slides prior to the session, which enables students to simply add KOH to the slides on the teaching day. To prepare the slides in advance, it is necessary to gather the following materials: a specimen cup with skin samples, glass slides, pickups or tweezers, a small pipette, a cup of water, protective gloves, and a pencil. After donning protective gloves, the pickups or tweezers are used to retrieve a few flakes of scale from the specimen cup and place them on the center of a glass slide. Using the pipette, 1 or 2 drops of water are added to the scale, and the slide is then allowed to dry. The slides are marked with the pencil to indicate the “up” side to prevent the students from applying KOH solution to the wrong side of the slide. The skin scale is fixed in place on the slide as the water evaporates and may be stored until needed for use in a standard slide box or folder.

Performing the KOH Preparation

On the day of teaching, it is helpful to engage the entire group of students with an introductory lecture on the purpose and use of the KOH preparation. Upon completion, students move to a workstation with all of the materials needed to prepare the slide. Additional items needed at this time are 10% KOH solution, coverslips, and a heating device (eg, lighter, Bunsen burner, match)(optional). Students are instructed to place 1 or 2 skin scales onto a glass slide or retrieve a slide with skin scales already fixed, and then add 1 drop of 10% KOH solution directly to the sample (Figure 2). Next, they should place a slide coverslip onto the KOH drop and skin sample using a side-to-side technique that will move the scale into a thin layer within the KOH solution and push away any excess solution to the periphery (Figure 3). Large amounts of excess KOH solution should be cleared away with a paper towel, lens paper, or tissue. The heat source can be used to gently heat the underside of the glass slide (Figure 4), but it often is sufficient to simply wait 3 to 5 minutes for the KOH solution to take effect. The heat accelerates the maceration of the scale and makes it easier to see the hyphae among the keratinocytes. Some physicians advocate the use of dimethyl sulfoxide in lieu of heating,8 but this solution may not be available in all primary care settings.

 

 

 

Figure 2. Adding 10% potassium hydroxide solution to skin samples.
  
Figure 3. Placing the slide coverslip.

 

Figure 4. Applying gentle heat to the potassium hydroxide preparations.

Microscopic Examination

Prior to examining the slides under the microscope, students may complete a self-guided tutorial (eg, digital or paper slide show) on the various features seen through the microscope that are indicative of dermatophytes, including branching hyphae and yeast buds. They also should be educated about the common appearance of artifacts that may resemble hyphae. Once the students have completed the tutorial, they may proceed to microscopic examination.

 While the students are viewing their slides under the microscope, we find it helpful to have at least 1 experienced faculty member for every group of 10 students. This instructor should encourage the students to lower the microscope condenser all the way to facilitate better observation. Students should start with low power (×4 or red band) and scan for areas that are rich in skin scale. Once a collection of scale is found, the student can switch to higher power (×10 or yellow band) and start scanning for hyphae. Students should be reminded to search for filamentous and branching tubes that are refractile. The term refractile may be confusing to some students, so we explain that shifting the focus up or down will show the hyphae to change in brightness and may reveal a greenish tint. Another helpful indicator to point out is the feature that hyphae will cross the border of epidermal skin cells, whereas artifacts will not  (Figure 5). Once the students have identified evidence of a dermatophyte infection, they must call the instructor to their station to verify the presence of hyphae or yeast buds, which helps confirm their understanding of the procedure. Once the  student accurately identifies these items, the session is complete.

 

Figure 5. Example of hyphum crossing epithelial cell borders. Figure 5. Example of hyphum crossing epithelial cell borders.
Figure 5. Example of hyphum crossing epithelial cell borders.

Comment

The use of a KOH preparation is a fast, simple, accurate, and cost-effective way to diagnose superficial fungal infections; however, because of insufficient familiarity with this tool, the technique often is replaced by initiation of empiric antifungal therapy in patients with suspected dermatophytosis. This empiric treatment has the potential to delay appropriate diagnosis and treatment (eg, in a patient with nummular dermatitis, which can clinically mimic tinea corporis). One way to encourage the use of the KOH preparation in the primary care and dermatologic setting is to educate large groups of next-generation physicians while in medical training. This article describes a teaching technique that allows for long-term storage of positive skin samples and a detailed description of the pedagogy used to train and educate a large group of students in a relatively short period of time.

All KOH preparations fall under the US federal government’s Clinical Laboratory Improvement Amendments and require proficiency testing.9 Although the teaching method presented here is designed for teaching medical students, it may be utilized to educate or refamiliarize experienced physicians with the procedure in an effort to improve proficiency in point-of-care testing programs used in many health care systems to comply with the Clinical Laboratories Improvement Amendments. Future analyses could assess whether the method described here improves provider performance on such proficiency measures and whether it ultimately helps ensure quality patient care.

References

 

1. Dasgupta T, Sahu J. Origins of the KOH technique. Clin Dermatol. 2012;2:238-242.

2. Stone S. Editor’s commentary. Clin Dermatol. 2012;2:241-242.

3. Monroe JR. The diagnostic value of a KOH. JAAPA. 2001;4:50-51.

4. Hainer BL. Dermatophyte infections. Am Fam Physician. 2003;1:101-109.

5. Ponka D, Baddar F. Microscopic potassium hydroxide preparation. Can Fam Physician. 2014;60:57.

6. Lilly KK, Koshnick RL, Grill JP, et al. Cost-effectiveness of diagnostic tests for toenail onychomycosis: a repeated-measure, single-blinded, cross-sectional evaluation of  7 diagnostic tests. J Am Acad Dermatol. 2006;4:620-626.

7. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012.

8. James WD, Berger T, Elston D. Andrew’s Diseases of the Skin: Clinical Dermatology. 11th ed. New York, NY: Elsevier Saunders; 2011.

9. Clinical Laboratory Improvement Amendments (CLIA). Centers for Medicare & Medicaid Services Web site. https://www.cms.gov/Regulations-and-Guidance/Legislation/CLIA/index.html?redirect=/clia/. Updated June 6, 2015. Accessed July 21, 2015.

References

 

1. Dasgupta T, Sahu J. Origins of the KOH technique. Clin Dermatol. 2012;2:238-242.

2. Stone S. Editor’s commentary. Clin Dermatol. 2012;2:241-242.

3. Monroe JR. The diagnostic value of a KOH. JAAPA. 2001;4:50-51.

4. Hainer BL. Dermatophyte infections. Am Fam Physician. 2003;1:101-109.

5. Ponka D, Baddar F. Microscopic potassium hydroxide preparation. Can Fam Physician. 2014;60:57.

6. Lilly KK, Koshnick RL, Grill JP, et al. Cost-effectiveness of diagnostic tests for toenail onychomycosis: a repeated-measure, single-blinded, cross-sectional evaluation of  7 diagnostic tests. J Am Acad Dermatol. 2006;4:620-626.

7. Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012.

8. James WD, Berger T, Elston D. Andrew’s Diseases of the Skin: Clinical Dermatology. 11th ed. New York, NY: Elsevier Saunders; 2011.

9. Clinical Laboratory Improvement Amendments (CLIA). Centers for Medicare & Medicaid Services Web site. https://www.cms.gov/Regulations-and-Guidance/Legislation/CLIA/index.html?redirect=/clia/. Updated June 6, 2015. Accessed July 21, 2015.

Issue
Cutis - 96(2)
Issue
Cutis - 96(2)
Page Number
109-112
Page Number
109-112
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Publications
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How to Teach the Potassium Hydroxide Preparation: A Disappearing Clinical Art Form
Display Headline
How to Teach the Potassium Hydroxide Preparation: A Disappearing Clinical Art Form
Legacy Keywords
KOH preparation, potassium hydroxide, medical education, point of care testing
Legacy Keywords
KOH preparation, potassium hydroxide, medical education, point of care testing
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    Practice Points

 

  • Potassium hydroxide (KOH) preparations can lead to diagnostic confidence and direct appropriate therapy.
  • Refreshing the basics of this simple technique can lead to better patient outcomes in the primary care setting and in the dermatology specialty clinic.
  • Teaching the KOH preparation to the next generation of physicians will ensure its longevity and assure future benefit to patients.
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