Sneak Peek: Journal of Hospital Medicine – Oct. 2017

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Sound and light levels are similarly disruptive in ICU and non-ICU wards

 

BACKGROUND: Hospitalized patients frequently report poor sleep, partly due to the inpatient environment. In-hospital sound and light levels are not well described on non–intensive care unit (non-ICU) wards. Although non-ICU wards may have lower average and peak noise levels, sound level changes (SLCs), which are important in disrupting sleep, may still be a substantial problem.

OBJECTIVE: To compare ambient sound and light levels, including SLCs, in ICU and non-ICU environments.

DESIGN: Observational study.

SETTING: Tertiary-care hospital.

MEASUREMENTS: Sound measurements of 0.5 Hz were analyzed to provide average hourly sound levels, sound peaks, and SLCs greater than or equal to 17.5 decibels (dB). For light data, measurements taken at 2-minute intervals provided average and maximum light levels.

RESULTS: The ICU rooms were louder than non-ICU wards; hourly averages ranged from 56.1 plus or minus 1.3 dB to 60.3 plus or minus 1.7 dB in the ICU, 47.3 plus or minus 3.7 dB to 55.1 plus or minus 3.7 dB on the telemetry floor, and 44.6 plus or minus 2.1 dB to 53.7 plus or minus 3.6 dB on the general ward. However, SLCs greater than or equal to 17.5 dB were not statistically different (ICU, 203.9 plus or minus 28.8 times; non-ICU, 270.9 plus or minus 39.5; P = 0.11). In both ICU and non-ICU wards, average daytime light levels were less than 250 lux, and peak light levels occurred in the afternoon and early evening.

CONCLUSIONS: While quieter, non-ICU wards have as many SLCs as ICUs do, which has implications for quality improvement measurements. Efforts to further reduce average noise levels might be counterproductive. Light levels in the hospital (ICU and non-ICU) may not be optimal for maintenance of a normal circadian rhythm for most people.

Read the entire article in the Journal of Hospital Medicine.
 

Also in JHM this month

Associations of physician empathy with patient anxiety and ratings of communication in hospital admission encounters

AUTHORS: Rachel Weiss, MD, Eric Vittinghoff, PhD, MPH, Margaret C. Fang, MD, MPH, Jenica E. W. Cimino, Kristen Adams Chasteen, MD, Robert M. Arnold, MD, Andrew D. Auerbach, MD, Wendy G. Anderson, MD, MS


A concise tool for measuring care coordination from the provider’s perspective in the hospital setting

AUTHORS: Christine M. Weston, PhD, and Sehyo Yune, MD, Eric B. Bass, MD, MPH, Scott A. Berkowitz, MD, MBA, Daniel J. Brotman, MD, Amy Deutschendorf, MS, RN, ACNS-BC, Eric E. Howell, MD, Melissa B. Richardson, MBA Carol Sylvester, RN, MS, Albert W. Wu, MD, MPH


Post–intensive care unit psychiatric comorbidity and quality of life

AUTHORS: Sophia Wang, MD, and Chris Mosher, MD, Anthony J. Perkins, MS, Sujuan Gao, PhD, Sue Lasiter, RN, PhD, Sikandar Khan, MD, Malaz Boustani, MD, MPH, Babar Khan, MD, MS


An opportunity to improve Medicare’s planned readmissions measure

AUTHORS: Chad Ellimoottil, MD, MS, Roger K. Khouri Jr., MD, Apoorv Dhir, BA, Hechuan Hou, MS, David C. Miller, MD, MPH, James M. Dupree, MD, MPH


Against medical advice discharges

AUTHORS: David Alfandre, MD, MSPH, Jay Brenner, MD, Eberechukwu Onukwugha, MS, PhD

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Sound and light levels are similarly disruptive in ICU and non-ICU wards
Sound and light levels are similarly disruptive in ICU and non-ICU wards

 

BACKGROUND: Hospitalized patients frequently report poor sleep, partly due to the inpatient environment. In-hospital sound and light levels are not well described on non–intensive care unit (non-ICU) wards. Although non-ICU wards may have lower average and peak noise levels, sound level changes (SLCs), which are important in disrupting sleep, may still be a substantial problem.

OBJECTIVE: To compare ambient sound and light levels, including SLCs, in ICU and non-ICU environments.

DESIGN: Observational study.

SETTING: Tertiary-care hospital.

MEASUREMENTS: Sound measurements of 0.5 Hz were analyzed to provide average hourly sound levels, sound peaks, and SLCs greater than or equal to 17.5 decibels (dB). For light data, measurements taken at 2-minute intervals provided average and maximum light levels.

RESULTS: The ICU rooms were louder than non-ICU wards; hourly averages ranged from 56.1 plus or minus 1.3 dB to 60.3 plus or minus 1.7 dB in the ICU, 47.3 plus or minus 3.7 dB to 55.1 plus or minus 3.7 dB on the telemetry floor, and 44.6 plus or minus 2.1 dB to 53.7 plus or minus 3.6 dB on the general ward. However, SLCs greater than or equal to 17.5 dB were not statistically different (ICU, 203.9 plus or minus 28.8 times; non-ICU, 270.9 plus or minus 39.5; P = 0.11). In both ICU and non-ICU wards, average daytime light levels were less than 250 lux, and peak light levels occurred in the afternoon and early evening.

CONCLUSIONS: While quieter, non-ICU wards have as many SLCs as ICUs do, which has implications for quality improvement measurements. Efforts to further reduce average noise levels might be counterproductive. Light levels in the hospital (ICU and non-ICU) may not be optimal for maintenance of a normal circadian rhythm for most people.

Read the entire article in the Journal of Hospital Medicine.
 

Also in JHM this month

Associations of physician empathy with patient anxiety and ratings of communication in hospital admission encounters

AUTHORS: Rachel Weiss, MD, Eric Vittinghoff, PhD, MPH, Margaret C. Fang, MD, MPH, Jenica E. W. Cimino, Kristen Adams Chasteen, MD, Robert M. Arnold, MD, Andrew D. Auerbach, MD, Wendy G. Anderson, MD, MS


A concise tool for measuring care coordination from the provider’s perspective in the hospital setting

AUTHORS: Christine M. Weston, PhD, and Sehyo Yune, MD, Eric B. Bass, MD, MPH, Scott A. Berkowitz, MD, MBA, Daniel J. Brotman, MD, Amy Deutschendorf, MS, RN, ACNS-BC, Eric E. Howell, MD, Melissa B. Richardson, MBA Carol Sylvester, RN, MS, Albert W. Wu, MD, MPH


Post–intensive care unit psychiatric comorbidity and quality of life

AUTHORS: Sophia Wang, MD, and Chris Mosher, MD, Anthony J. Perkins, MS, Sujuan Gao, PhD, Sue Lasiter, RN, PhD, Sikandar Khan, MD, Malaz Boustani, MD, MPH, Babar Khan, MD, MS


An opportunity to improve Medicare’s planned readmissions measure

AUTHORS: Chad Ellimoottil, MD, MS, Roger K. Khouri Jr., MD, Apoorv Dhir, BA, Hechuan Hou, MS, David C. Miller, MD, MPH, James M. Dupree, MD, MPH


Against medical advice discharges

AUTHORS: David Alfandre, MD, MSPH, Jay Brenner, MD, Eberechukwu Onukwugha, MS, PhD

 

BACKGROUND: Hospitalized patients frequently report poor sleep, partly due to the inpatient environment. In-hospital sound and light levels are not well described on non–intensive care unit (non-ICU) wards. Although non-ICU wards may have lower average and peak noise levels, sound level changes (SLCs), which are important in disrupting sleep, may still be a substantial problem.

OBJECTIVE: To compare ambient sound and light levels, including SLCs, in ICU and non-ICU environments.

DESIGN: Observational study.

SETTING: Tertiary-care hospital.

MEASUREMENTS: Sound measurements of 0.5 Hz were analyzed to provide average hourly sound levels, sound peaks, and SLCs greater than or equal to 17.5 decibels (dB). For light data, measurements taken at 2-minute intervals provided average and maximum light levels.

RESULTS: The ICU rooms were louder than non-ICU wards; hourly averages ranged from 56.1 plus or minus 1.3 dB to 60.3 plus or minus 1.7 dB in the ICU, 47.3 plus or minus 3.7 dB to 55.1 plus or minus 3.7 dB on the telemetry floor, and 44.6 plus or minus 2.1 dB to 53.7 plus or minus 3.6 dB on the general ward. However, SLCs greater than or equal to 17.5 dB were not statistically different (ICU, 203.9 plus or minus 28.8 times; non-ICU, 270.9 plus or minus 39.5; P = 0.11). In both ICU and non-ICU wards, average daytime light levels were less than 250 lux, and peak light levels occurred in the afternoon and early evening.

CONCLUSIONS: While quieter, non-ICU wards have as many SLCs as ICUs do, which has implications for quality improvement measurements. Efforts to further reduce average noise levels might be counterproductive. Light levels in the hospital (ICU and non-ICU) may not be optimal for maintenance of a normal circadian rhythm for most people.

Read the entire article in the Journal of Hospital Medicine.
 

Also in JHM this month

Associations of physician empathy with patient anxiety and ratings of communication in hospital admission encounters

AUTHORS: Rachel Weiss, MD, Eric Vittinghoff, PhD, MPH, Margaret C. Fang, MD, MPH, Jenica E. W. Cimino, Kristen Adams Chasteen, MD, Robert M. Arnold, MD, Andrew D. Auerbach, MD, Wendy G. Anderson, MD, MS


A concise tool for measuring care coordination from the provider’s perspective in the hospital setting

AUTHORS: Christine M. Weston, PhD, and Sehyo Yune, MD, Eric B. Bass, MD, MPH, Scott A. Berkowitz, MD, MBA, Daniel J. Brotman, MD, Amy Deutschendorf, MS, RN, ACNS-BC, Eric E. Howell, MD, Melissa B. Richardson, MBA Carol Sylvester, RN, MS, Albert W. Wu, MD, MPH


Post–intensive care unit psychiatric comorbidity and quality of life

AUTHORS: Sophia Wang, MD, and Chris Mosher, MD, Anthony J. Perkins, MS, Sujuan Gao, PhD, Sue Lasiter, RN, PhD, Sikandar Khan, MD, Malaz Boustani, MD, MPH, Babar Khan, MD, MS


An opportunity to improve Medicare’s planned readmissions measure

AUTHORS: Chad Ellimoottil, MD, MS, Roger K. Khouri Jr., MD, Apoorv Dhir, BA, Hechuan Hou, MS, David C. Miller, MD, MPH, James M. Dupree, MD, MPH


Against medical advice discharges

AUTHORS: David Alfandre, MD, MSPH, Jay Brenner, MD, Eberechukwu Onukwugha, MS, PhD

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Verrucoid Lesion on the Eyelid

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Verrucoid Lesion on the Eyelid

The Diagnosis: Inverted Follicular Keratosis

The differential diagnosis for endophytic squamous neoplasms encompasses benign and malignant entities. The histologic findings of our patient's lesion were compatible with the diagnosis of inverted follicular keratosis (IFK), a benign neoplasm that usually presents as a keratotic papule on the head or neck. Histologically, IFK is characterized by an endophytic growth pattern with squamous eddies (quiz images). Inverted follicular keratosis may represent an irritated seborrheic keratosis or a distinct neoplasm derived from the infundibular portion of the hair follicle; the exact etiology is uncertain.1,2 No relationship between IFK and human papillomavirus (HPV) has been established.3 Inverted follicular keratosis can mimic squamous cell carcinoma (SCC). Important clues to the diagnosis of IFK are the presence of squamous eddies and the lack of squamous pearls or cytologic atypia.4 Squamous eddies consist of whorled keratinocytes without keratinization or atypia. Superficial shave biopsies may fail to demonstrate the characteristic well-circumscribed architecture and may lead to an erroneous diagnosis.

Acantholytic SCC is characterized by atypical keratinocytes that have lost cohesive properties, resulting in acantholysis (Figure 1).5 This histologic variant was once categorized as an aggressive variant of SCC, but studies have failed to support this assertion.5,6 Acantholytic SCC has a discohesive nature producing a pseudoglandular appearance sometimes mistaken for adenosquamous carcinoma or metastatic carcinoma. Recent literature has suggested that acantholytic SCCs, similar to IFKs, are derived from the follicular infundibulum.5,6 Also similar to IFKs, acantholytic SCCs often are located on the face. The invasive architecture and atypical cytology of acantholytic SCCs can differentiate them from IFKs. Acantholytic SCCs can contain keratin pearls with concentric keratinocytes showing incomplete keratinization centrally, often with retained nuclei, but rare to no squamous eddies unless irritated.

Figure 1. Acantholytic squamous cell carcinoma showing keratin pearl and atypia (H&E, original magnification ×40 [inset, original magnification ×600]).

Trichilemmoma is an endophytic benign neoplasm derived from the outer sheath of the pilosebaceous follicle characterized by lobules of clear cells hanging from the epidermis.7 A study investigating the relationship between HPV and trichilemmomas failed to definitively detect HPV in trichilemmomas and this relationship remains unclear.8 Desmoplastic trichilemmoma is a subtype histologically characterized by jagged islands of epithelial cells separated by dense pink stroma and encased in a glassy basement membrane (Figure 2). The presence of desmoplasia and a jagged growth pattern can mimic invasive SCC, but the absence of cytologic atypia and the surrounding basement membrane differs from SCC.4,7 Trichilemmomas typically are solitary, but multiple lesions are associated with Cowden syndrome. Cowden syndrome is a rare autosomal-dominant condition characterized by the presence of benign hamartomas and a predisposition to the development of malignancies including breast, endometrial, and thyroid cancers.9,10 There is no such association with desmoplastic trichilemmomas.11

Figure 2. Desmoplastic trichilemmomas (A)(H&E, original magnification ×40) with a smooth outline, clear cells, and central jagged islands in a dense pink stroma (B)(H&E, original magnification ×100).

Pilar sheath acanthoma is a benign neoplasm that clinically presents as a solitary flesh-colored nodule with a central pore containing keratin.12 Histologically, pilar sheath acanthoma is similar to a dilated pore of Winer with the addition of acanthotic epidermal projections (Figure 3).

Figure 3. Pilar sheath acanthoma with acanthotic epidermal projections (H&E, original magnification ×20).

Warty dyskeratoma (WD) is a benign endophytic neoplasm traditionally seen as a solitary lesion histologically similar to Darier disease. Warty dyskeratomas are known to occur both on the skin and oral mucosa.13 Histologically, WD is characterized as a cup-shaped lesion with numerous villi at the base of the lesion along with acantholysis and dyskeratosis (Figure 4). The dyskeratotic cells in WD consist of corps ronds, which are cells with abundant pink cytoplasm, and small nuclei along with grains, which are flattened basophilic cells. These dyskeratotic cells help differentiate WD from IFK. Although they are endophytic neoplasms, WDs are well circumscribed and should not be confused with SCC. Despite this entity's name and histologic similarity to verrucae, no relationship with HPV has been established.14

Figure 4. Warty dyskeratoma (A)(H&E, original magnification ×100) showing acantholytic dyskeratosis (B)(H&E, original magnification ×200).

References
  1. Ruhoy SM, Thomas D, Nuovo GJ. Multiple inverted follicular keratoses as a presenting sign of Cowden's syndrome: case report with human papillomavirus studies. J Am Acad Dermatol. 2004;51:411-415.
  2. Lever WF. Inverted follicular keratosis is an irritated seborrheic keratosis. Am J Dermatopathol. 1983;5:474.
  3. Kambiz KH, Kaveh D, Maede D, et al. Human papillomavirus deoxyribonucleic acid may not be detected in non-genital benign papillomatous skin lesions by polymerase chain reaction. Indian J Dermatol. 2014;59:334-338.
  4. Tan KB, Tan SH, Aw DC, et al. Simulators of squamous cell carcinoma of the skin: diagnostic challenges on small biopsies and clinicopathological correlation [published online June 25, 2013]. J Skin Cancer. 2013;2013:752864.
  5. Ogawa T, Kiuru M, Konia TH, et al. Acantholytic squamous cell carcinoma is usually associated with hair follicles, not acantholytic actinic keratosis, and is not "high risk": diagnosis, management, and clinical outcomes in a series of 115 cases. J Am Acad Dermatol. 2017;76:327-333.
  6. Motaparthi K, Kapil JP, Velazquez EF. Cutaneous squamous cell carcinoma: review of the eighth edition of the American Joint Committee on Cancer staging guidelines, prognostic factors, and histopathologic variants. Adv Anat Pathol. 2017;24:171-194.
  7. Sano DT, Yang JJ, Tebcherani AJ, et al. A rare clinical presentation of desmoplastic trichilemmoma mimicking invasive carcinoma. An Bras Dermatol. 2014;89:796-798.
  8. Stierman S, Chen S, Nuovo G, et al. Detection of human papillomavirus infection in trichilemmomas and verrucae using in situ hybridization. J Cutan Pathol. 2010;37:75-80.
  9. Ngeow J, Eng C. PTEN hamartoma tumor syndrome: clinical risk assessment and management protocol [published online October 22, 2014]. Methods. 2015;77-78:11-19.
  10. Molvi M, Sharma YK, Dash K. Cowden syndrome: case report, update and proposed diagnostic and surveillance routines. Indian J Dermatol. 2015;60:255-259.
  11. Jin M, Hampel H, Pilarski R, et al. Phosphatase and tensin homolog immunohistochemical staining and clinical criteria for Cowden syndrome in patients with trichilemmoma or associated lesions. Am J Dermatopathol. 2013;35:637-640.
  12. Mehregan AH, Brownstein MH. Pilar sheath acanthoma. Arch Dermatol. 1978;114:1495-1497.
  13. Newland JR, Leventon GS. Warty dyskeratoma of the oral mucosa. correlated light and electron microscopic study. Oral Surg Oral Med Oral Pathol. 1984;58:176-183.
  14. Kaddu S, Dong H, Mayer G, et al. Warty dyskeratoma--"follicular dyskeratoma": analysis of clinicopathologic features of a distinctive follicular adnexal neoplasm. J Am Acad Dermatol. 2002;47:423-428.
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Dr. Ullman is from the University of Alabama at Birmingham. Drs. DiCarlo and Ferringer are from Geisinger Medical Center, Danville, Pennsylvania.

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Correspondence: David Ullman, MD ([email protected]).

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Dr. Ullman is from the University of Alabama at Birmingham. Drs. DiCarlo and Ferringer are from Geisinger Medical Center, Danville, Pennsylvania.

The authors report no conflict of interest.

Correspondence: David Ullman, MD ([email protected]).

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Correspondence: David Ullman, MD ([email protected]).

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The Diagnosis: Inverted Follicular Keratosis

The differential diagnosis for endophytic squamous neoplasms encompasses benign and malignant entities. The histologic findings of our patient's lesion were compatible with the diagnosis of inverted follicular keratosis (IFK), a benign neoplasm that usually presents as a keratotic papule on the head or neck. Histologically, IFK is characterized by an endophytic growth pattern with squamous eddies (quiz images). Inverted follicular keratosis may represent an irritated seborrheic keratosis or a distinct neoplasm derived from the infundibular portion of the hair follicle; the exact etiology is uncertain.1,2 No relationship between IFK and human papillomavirus (HPV) has been established.3 Inverted follicular keratosis can mimic squamous cell carcinoma (SCC). Important clues to the diagnosis of IFK are the presence of squamous eddies and the lack of squamous pearls or cytologic atypia.4 Squamous eddies consist of whorled keratinocytes without keratinization or atypia. Superficial shave biopsies may fail to demonstrate the characteristic well-circumscribed architecture and may lead to an erroneous diagnosis.

Acantholytic SCC is characterized by atypical keratinocytes that have lost cohesive properties, resulting in acantholysis (Figure 1).5 This histologic variant was once categorized as an aggressive variant of SCC, but studies have failed to support this assertion.5,6 Acantholytic SCC has a discohesive nature producing a pseudoglandular appearance sometimes mistaken for adenosquamous carcinoma or metastatic carcinoma. Recent literature has suggested that acantholytic SCCs, similar to IFKs, are derived from the follicular infundibulum.5,6 Also similar to IFKs, acantholytic SCCs often are located on the face. The invasive architecture and atypical cytology of acantholytic SCCs can differentiate them from IFKs. Acantholytic SCCs can contain keratin pearls with concentric keratinocytes showing incomplete keratinization centrally, often with retained nuclei, but rare to no squamous eddies unless irritated.

Figure 1. Acantholytic squamous cell carcinoma showing keratin pearl and atypia (H&E, original magnification ×40 [inset, original magnification ×600]).

Trichilemmoma is an endophytic benign neoplasm derived from the outer sheath of the pilosebaceous follicle characterized by lobules of clear cells hanging from the epidermis.7 A study investigating the relationship between HPV and trichilemmomas failed to definitively detect HPV in trichilemmomas and this relationship remains unclear.8 Desmoplastic trichilemmoma is a subtype histologically characterized by jagged islands of epithelial cells separated by dense pink stroma and encased in a glassy basement membrane (Figure 2). The presence of desmoplasia and a jagged growth pattern can mimic invasive SCC, but the absence of cytologic atypia and the surrounding basement membrane differs from SCC.4,7 Trichilemmomas typically are solitary, but multiple lesions are associated with Cowden syndrome. Cowden syndrome is a rare autosomal-dominant condition characterized by the presence of benign hamartomas and a predisposition to the development of malignancies including breast, endometrial, and thyroid cancers.9,10 There is no such association with desmoplastic trichilemmomas.11

Figure 2. Desmoplastic trichilemmomas (A)(H&E, original magnification ×40) with a smooth outline, clear cells, and central jagged islands in a dense pink stroma (B)(H&E, original magnification ×100).

Pilar sheath acanthoma is a benign neoplasm that clinically presents as a solitary flesh-colored nodule with a central pore containing keratin.12 Histologically, pilar sheath acanthoma is similar to a dilated pore of Winer with the addition of acanthotic epidermal projections (Figure 3).

Figure 3. Pilar sheath acanthoma with acanthotic epidermal projections (H&E, original magnification ×20).

Warty dyskeratoma (WD) is a benign endophytic neoplasm traditionally seen as a solitary lesion histologically similar to Darier disease. Warty dyskeratomas are known to occur both on the skin and oral mucosa.13 Histologically, WD is characterized as a cup-shaped lesion with numerous villi at the base of the lesion along with acantholysis and dyskeratosis (Figure 4). The dyskeratotic cells in WD consist of corps ronds, which are cells with abundant pink cytoplasm, and small nuclei along with grains, which are flattened basophilic cells. These dyskeratotic cells help differentiate WD from IFK. Although they are endophytic neoplasms, WDs are well circumscribed and should not be confused with SCC. Despite this entity's name and histologic similarity to verrucae, no relationship with HPV has been established.14

Figure 4. Warty dyskeratoma (A)(H&E, original magnification ×100) showing acantholytic dyskeratosis (B)(H&E, original magnification ×200).

The Diagnosis: Inverted Follicular Keratosis

The differential diagnosis for endophytic squamous neoplasms encompasses benign and malignant entities. The histologic findings of our patient's lesion were compatible with the diagnosis of inverted follicular keratosis (IFK), a benign neoplasm that usually presents as a keratotic papule on the head or neck. Histologically, IFK is characterized by an endophytic growth pattern with squamous eddies (quiz images). Inverted follicular keratosis may represent an irritated seborrheic keratosis or a distinct neoplasm derived from the infundibular portion of the hair follicle; the exact etiology is uncertain.1,2 No relationship between IFK and human papillomavirus (HPV) has been established.3 Inverted follicular keratosis can mimic squamous cell carcinoma (SCC). Important clues to the diagnosis of IFK are the presence of squamous eddies and the lack of squamous pearls or cytologic atypia.4 Squamous eddies consist of whorled keratinocytes without keratinization or atypia. Superficial shave biopsies may fail to demonstrate the characteristic well-circumscribed architecture and may lead to an erroneous diagnosis.

Acantholytic SCC is characterized by atypical keratinocytes that have lost cohesive properties, resulting in acantholysis (Figure 1).5 This histologic variant was once categorized as an aggressive variant of SCC, but studies have failed to support this assertion.5,6 Acantholytic SCC has a discohesive nature producing a pseudoglandular appearance sometimes mistaken for adenosquamous carcinoma or metastatic carcinoma. Recent literature has suggested that acantholytic SCCs, similar to IFKs, are derived from the follicular infundibulum.5,6 Also similar to IFKs, acantholytic SCCs often are located on the face. The invasive architecture and atypical cytology of acantholytic SCCs can differentiate them from IFKs. Acantholytic SCCs can contain keratin pearls with concentric keratinocytes showing incomplete keratinization centrally, often with retained nuclei, but rare to no squamous eddies unless irritated.

Figure 1. Acantholytic squamous cell carcinoma showing keratin pearl and atypia (H&E, original magnification ×40 [inset, original magnification ×600]).

Trichilemmoma is an endophytic benign neoplasm derived from the outer sheath of the pilosebaceous follicle characterized by lobules of clear cells hanging from the epidermis.7 A study investigating the relationship between HPV and trichilemmomas failed to definitively detect HPV in trichilemmomas and this relationship remains unclear.8 Desmoplastic trichilemmoma is a subtype histologically characterized by jagged islands of epithelial cells separated by dense pink stroma and encased in a glassy basement membrane (Figure 2). The presence of desmoplasia and a jagged growth pattern can mimic invasive SCC, but the absence of cytologic atypia and the surrounding basement membrane differs from SCC.4,7 Trichilemmomas typically are solitary, but multiple lesions are associated with Cowden syndrome. Cowden syndrome is a rare autosomal-dominant condition characterized by the presence of benign hamartomas and a predisposition to the development of malignancies including breast, endometrial, and thyroid cancers.9,10 There is no such association with desmoplastic trichilemmomas.11

Figure 2. Desmoplastic trichilemmomas (A)(H&E, original magnification ×40) with a smooth outline, clear cells, and central jagged islands in a dense pink stroma (B)(H&E, original magnification ×100).

Pilar sheath acanthoma is a benign neoplasm that clinically presents as a solitary flesh-colored nodule with a central pore containing keratin.12 Histologically, pilar sheath acanthoma is similar to a dilated pore of Winer with the addition of acanthotic epidermal projections (Figure 3).

Figure 3. Pilar sheath acanthoma with acanthotic epidermal projections (H&E, original magnification ×20).

Warty dyskeratoma (WD) is a benign endophytic neoplasm traditionally seen as a solitary lesion histologically similar to Darier disease. Warty dyskeratomas are known to occur both on the skin and oral mucosa.13 Histologically, WD is characterized as a cup-shaped lesion with numerous villi at the base of the lesion along with acantholysis and dyskeratosis (Figure 4). The dyskeratotic cells in WD consist of corps ronds, which are cells with abundant pink cytoplasm, and small nuclei along with grains, which are flattened basophilic cells. These dyskeratotic cells help differentiate WD from IFK. Although they are endophytic neoplasms, WDs are well circumscribed and should not be confused with SCC. Despite this entity's name and histologic similarity to verrucae, no relationship with HPV has been established.14

Figure 4. Warty dyskeratoma (A)(H&E, original magnification ×100) showing acantholytic dyskeratosis (B)(H&E, original magnification ×200).

References
  1. Ruhoy SM, Thomas D, Nuovo GJ. Multiple inverted follicular keratoses as a presenting sign of Cowden's syndrome: case report with human papillomavirus studies. J Am Acad Dermatol. 2004;51:411-415.
  2. Lever WF. Inverted follicular keratosis is an irritated seborrheic keratosis. Am J Dermatopathol. 1983;5:474.
  3. Kambiz KH, Kaveh D, Maede D, et al. Human papillomavirus deoxyribonucleic acid may not be detected in non-genital benign papillomatous skin lesions by polymerase chain reaction. Indian J Dermatol. 2014;59:334-338.
  4. Tan KB, Tan SH, Aw DC, et al. Simulators of squamous cell carcinoma of the skin: diagnostic challenges on small biopsies and clinicopathological correlation [published online June 25, 2013]. J Skin Cancer. 2013;2013:752864.
  5. Ogawa T, Kiuru M, Konia TH, et al. Acantholytic squamous cell carcinoma is usually associated with hair follicles, not acantholytic actinic keratosis, and is not "high risk": diagnosis, management, and clinical outcomes in a series of 115 cases. J Am Acad Dermatol. 2017;76:327-333.
  6. Motaparthi K, Kapil JP, Velazquez EF. Cutaneous squamous cell carcinoma: review of the eighth edition of the American Joint Committee on Cancer staging guidelines, prognostic factors, and histopathologic variants. Adv Anat Pathol. 2017;24:171-194.
  7. Sano DT, Yang JJ, Tebcherani AJ, et al. A rare clinical presentation of desmoplastic trichilemmoma mimicking invasive carcinoma. An Bras Dermatol. 2014;89:796-798.
  8. Stierman S, Chen S, Nuovo G, et al. Detection of human papillomavirus infection in trichilemmomas and verrucae using in situ hybridization. J Cutan Pathol. 2010;37:75-80.
  9. Ngeow J, Eng C. PTEN hamartoma tumor syndrome: clinical risk assessment and management protocol [published online October 22, 2014]. Methods. 2015;77-78:11-19.
  10. Molvi M, Sharma YK, Dash K. Cowden syndrome: case report, update and proposed diagnostic and surveillance routines. Indian J Dermatol. 2015;60:255-259.
  11. Jin M, Hampel H, Pilarski R, et al. Phosphatase and tensin homolog immunohistochemical staining and clinical criteria for Cowden syndrome in patients with trichilemmoma or associated lesions. Am J Dermatopathol. 2013;35:637-640.
  12. Mehregan AH, Brownstein MH. Pilar sheath acanthoma. Arch Dermatol. 1978;114:1495-1497.
  13. Newland JR, Leventon GS. Warty dyskeratoma of the oral mucosa. correlated light and electron microscopic study. Oral Surg Oral Med Oral Pathol. 1984;58:176-183.
  14. Kaddu S, Dong H, Mayer G, et al. Warty dyskeratoma--"follicular dyskeratoma": analysis of clinicopathologic features of a distinctive follicular adnexal neoplasm. J Am Acad Dermatol. 2002;47:423-428.
References
  1. Ruhoy SM, Thomas D, Nuovo GJ. Multiple inverted follicular keratoses as a presenting sign of Cowden's syndrome: case report with human papillomavirus studies. J Am Acad Dermatol. 2004;51:411-415.
  2. Lever WF. Inverted follicular keratosis is an irritated seborrheic keratosis. Am J Dermatopathol. 1983;5:474.
  3. Kambiz KH, Kaveh D, Maede D, et al. Human papillomavirus deoxyribonucleic acid may not be detected in non-genital benign papillomatous skin lesions by polymerase chain reaction. Indian J Dermatol. 2014;59:334-338.
  4. Tan KB, Tan SH, Aw DC, et al. Simulators of squamous cell carcinoma of the skin: diagnostic challenges on small biopsies and clinicopathological correlation [published online June 25, 2013]. J Skin Cancer. 2013;2013:752864.
  5. Ogawa T, Kiuru M, Konia TH, et al. Acantholytic squamous cell carcinoma is usually associated with hair follicles, not acantholytic actinic keratosis, and is not "high risk": diagnosis, management, and clinical outcomes in a series of 115 cases. J Am Acad Dermatol. 2017;76:327-333.
  6. Motaparthi K, Kapil JP, Velazquez EF. Cutaneous squamous cell carcinoma: review of the eighth edition of the American Joint Committee on Cancer staging guidelines, prognostic factors, and histopathologic variants. Adv Anat Pathol. 2017;24:171-194.
  7. Sano DT, Yang JJ, Tebcherani AJ, et al. A rare clinical presentation of desmoplastic trichilemmoma mimicking invasive carcinoma. An Bras Dermatol. 2014;89:796-798.
  8. Stierman S, Chen S, Nuovo G, et al. Detection of human papillomavirus infection in trichilemmomas and verrucae using in situ hybridization. J Cutan Pathol. 2010;37:75-80.
  9. Ngeow J, Eng C. PTEN hamartoma tumor syndrome: clinical risk assessment and management protocol [published online October 22, 2014]. Methods. 2015;77-78:11-19.
  10. Molvi M, Sharma YK, Dash K. Cowden syndrome: case report, update and proposed diagnostic and surveillance routines. Indian J Dermatol. 2015;60:255-259.
  11. Jin M, Hampel H, Pilarski R, et al. Phosphatase and tensin homolog immunohistochemical staining and clinical criteria for Cowden syndrome in patients with trichilemmoma or associated lesions. Am J Dermatopathol. 2013;35:637-640.
  12. Mehregan AH, Brownstein MH. Pilar sheath acanthoma. Arch Dermatol. 1978;114:1495-1497.
  13. Newland JR, Leventon GS. Warty dyskeratoma of the oral mucosa. correlated light and electron microscopic study. Oral Surg Oral Med Oral Pathol. 1984;58:176-183.
  14. Kaddu S, Dong H, Mayer G, et al. Warty dyskeratoma--"follicular dyskeratoma": analysis of clinicopathologic features of a distinctive follicular adnexal neoplasm. J Am Acad Dermatol. 2002;47:423-428.
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A 60-year-old man presented with a 3-mm verrucous papule on the right upper eyelid of 2 years' duration.

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The Diagnosis: Antiphospholipid Antibody Syndrome

A  biopsy demonstrated scattered intravascular thrombi in the dermis and subcutis, intact vascular walls, and scant lymphocytic inflammation in a background of stasis (Figure 1). A periodic acid-Schiff stain was negative for fungal elements and highlighted the intravascular thrombi. Histologic findings were consistent with thrombotic vasculopathy. On further laboratory workup, lupus anticoagulant studies, including a mixing study, diluted Russell viper venom test, and hexagonal phase phospholipid neutralization test, were abnormal. Titers of anticardiolipin and β2-glycoprotein I antibodies were elevated (anticardiolipin IgG, 137.7 calculated units [normal, <15 calculated units]; β2-glycoprotein I IgG, 256.4 calculated units [normal, <20 calculated units]). Tissue cultures showed no growth of microorganisms and studies for cryoglobulinemia were negative.

Figure 1. In a background of stasis (A), there are deep intravascular thrombi with intact vascular walls and scant lymphocytic inflammation (B and C)(all H&E; original magnifications ×4, ×20, and ×40, respectively).

The patient was diagnosed with primary antiphospholipid syndrome (APS). He remained on anticoagulation therapy with fondaparinux as an inpatient and was treated with pulse-dose intravenous (IV) corticosteroids followed by a slow oral taper, daily plasmapheresis for 1 week, IV immunoglobulin (0.5 g/kg) for 3 doses, and 4 weekly doses of rituximab (375 mg/m2). His cutaneous findings slowly improved over the next several weeks (Figure 2).

Figure 2. Clinical improvement after treatment showing resolved livedo reticularis and gangrene of the fifth toe at 15-week follow-up.

Antiphospholipid syndrome is an autoimmune disorder characterized by thrombotic events and the presence of autoantibodies. The syndrome is defined by 2 major criteria: (1) the occurrence of at least 1 clinical feature of either an episode of vascular thrombosis or pregnancy morbidity such as unexplained fetal death beyond 10 weeks of gestation or recurrent unexplained pregnancy losses; and (2) the presence of at least 1 type of autoantibody, including lupus anticoagulant, anticardiolipin, or β2-glycoprotein antibodies, on 2 separate occasions at least 12 weeks apart.1 Antiphospholipid syndrome can either be primary with no identifiable associated rheumatologic disease or secondary to another autoimmune disease such as systemic lupus erythematosus. Cutaneous manifestations are common and frequently are the first sign of disease in 30% to 40% of patients.2 The most common skin finding is persistent livedo reticularis, which can be seen in 20% to 25% of patients. Patients also may develop skin necrosis, ulcerations, digital gangrene, splinter hemorrhages, and livedoid vasculopathy.2 Systemic manifestations of APS include thrombocytopenia, nephropathy, cognitive dysfunction, and cardiac valve abnormalities. 

The exact pathogenesis of APS remains unknown. It is thought to be due to the combination of an inflammatory stimulus that has yet to be characterized in conjunction with autoantibodies that affect multiple target cells including monocytes, platelets, and endothelial cells, which results in activation of the complement system and clotting cascade.3 In rare cases, the disorder can progress to catastrophic antiphospholipid syndrome (CAPS), which requires fulfillment of 4 criteria: (1) evidence of involvement of 3 organs, tissues, or systems; (2) development of manifestations simultaneously or in less than 1 week; (3) laboratory confirmation of the presence of antiphospholipid antibodies; and (4) confirmation by histopathology of small vessel occlusion.4 Probable CAPS is diagnosed when 3 of 4 criteria are present. Our patient met criteria for probable CAPS, as his antibody titers remained elevated 15 weeks after initial presentation. Precipitating factors that can lead to CAPS are thought to include infection, surgical procedures, medications, or discontinuation of anticoagulation drugs.2 Although the mainstay of management of APS is anticoagulation therapy with warfarin and antiplatelet agents such as aspirin, first-line treatment of CAPS involves high-dose systemic glucocorticoids and plasma exchange. Intravenous immunoglobulin also may be employed in treatment. Data from the CAPS registry demonstrate a role for rituximab, an anti-CD20 antibody, at 375 mg/m2 weekly for 4 weeks (the regimen described in our case) or 1 g every 14 days for 2 sessions.5 A majority of the registry patients treated with rituximab recovered (75% [15/20]) and had no recurrent thrombosis (87% [13/15]) at follow-up.5 Data also are emerging on the role of eculizumab, an anti-C5 antibody that inhibits the terminal complement cascade, as a therapy in difficult-to-treat or refractory CAPS.6-8 The prognosis for CAPS patients without treatment is poor, and mortality has been reported in up to 44% of patients. However, with intervention mortality is reduced by more than 2-fold.9,10

It is important to recognize that acral cyanosis with persistent livedo reticularis and digital gangrene can be a presenting manifestation of APS. These cutaneous manifestations should prompt histologic evaluation for thrombotic vasculopathy in addition to serologic tests for APS autoantibodies. Although APS may be treated with anticoagulants and antiplatelet agents, CAPS may require more aggressive therapy with systemic steroids, plasma exchange, IV immunoglobulin, rituximab, and/or eculizumab.

References
  1. Wilson WA, Gharavi AE, Koike T, et al. International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop. Arthritis Rheum. 1999;42:1309-1311.
  2. Pinto-Almeida T, Caetano M, Sanches M, et al. Cutaneous manifestations of antiphospholipid syndrome: a review of the clinical features, diagnosis and management. Acta Reumatol Port. 2013;38:10-18.
  3. Meroni PL, Chighizola CB, Rovelli F, et al. Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers. Arthritis Res Ther. 2014;16:209.
  4. Asherson RA, Cervera R, de Grott PG, et al; Catastrophic Antiphospholipid Syndrome Registry Project Group. Catastrophic antiphospholipid syndrome: international consensus statement on classification criteria and treatment guidelines. Lupus. 2003;12:530-534.
  5. Berman H, Rodríguez-Pintó I, Cervera R, et al. Rituximab use in the catastrophic antiphospholipid syndrome: descriptive analysis of the CAPS registry patients receiving rituximab [published online June 15, 2013]. Autoimmun Rev. 2013;12:1085-1090.
  6. Shapira I, Andrade D, Allen SL, et al. Brief report: induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab. Arthritis Rheum. 2012;64:2719-2723.
  7. Strakhan M, Hurtado-Sbordoni M, Galeas N, et al. 36-year-old female with catastrophic antiphospholipid syndrome treated with eculizumab: a case report and review of literature. Case Rep Hematol. 2014;2014:704371.
  8. Lonze BE, Zachary AA, Magro CM, et al. Eculizumab prevents recurrent antiphospholipid antibody syndrome and enables successful renal transplantation. Am J Transplant. 2014;14:459-465.
  9. Bucciarelli S, Espinosa G, Cervera R, et al. Mortality in the catastrophic antiphospholipid syndrome: causes of death and prognostic factors in a series of 250 patients. Arthritis Rheum. 2006;54:2568-2576.
  10. Asherson RA, Cervera R, Piette JC, et al. Catastrophic antiphospholipid syndrome. clinical and laboratory features of 50 patients. Medicine (Baltimore). 1998;77:195-207.
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From Yale School of Medicine, New Haven, Connecticut. Drs. Shi, Leventhal, Galan, and Choate are from the Department of Dermatology. Dr. Mensah is from the Department of Internal Medicine, Section of Rheumatology. Drs. Galan and Choate also are from the Department of Pathology. Dr. Choate also is from the Department of Genetics.

The authors report no conflict of interest.

Correspondence: Jonathan S. Leventhal, MD, 15 York St, LMP 5040, New Haven, CT 06510 ([email protected]).

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From Yale School of Medicine, New Haven, Connecticut. Drs. Shi, Leventhal, Galan, and Choate are from the Department of Dermatology. Dr. Mensah is from the Department of Internal Medicine, Section of Rheumatology. Drs. Galan and Choate also are from the Department of Pathology. Dr. Choate also is from the Department of Genetics.

The authors report no conflict of interest.

Correspondence: Jonathan S. Leventhal, MD, 15 York St, LMP 5040, New Haven, CT 06510 ([email protected]).

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The Diagnosis: Antiphospholipid Antibody Syndrome

A  biopsy demonstrated scattered intravascular thrombi in the dermis and subcutis, intact vascular walls, and scant lymphocytic inflammation in a background of stasis (Figure 1). A periodic acid-Schiff stain was negative for fungal elements and highlighted the intravascular thrombi. Histologic findings were consistent with thrombotic vasculopathy. On further laboratory workup, lupus anticoagulant studies, including a mixing study, diluted Russell viper venom test, and hexagonal phase phospholipid neutralization test, were abnormal. Titers of anticardiolipin and β2-glycoprotein I antibodies were elevated (anticardiolipin IgG, 137.7 calculated units [normal, <15 calculated units]; β2-glycoprotein I IgG, 256.4 calculated units [normal, <20 calculated units]). Tissue cultures showed no growth of microorganisms and studies for cryoglobulinemia were negative.

Figure 1. In a background of stasis (A), there are deep intravascular thrombi with intact vascular walls and scant lymphocytic inflammation (B and C)(all H&E; original magnifications ×4, ×20, and ×40, respectively).

The patient was diagnosed with primary antiphospholipid syndrome (APS). He remained on anticoagulation therapy with fondaparinux as an inpatient and was treated with pulse-dose intravenous (IV) corticosteroids followed by a slow oral taper, daily plasmapheresis for 1 week, IV immunoglobulin (0.5 g/kg) for 3 doses, and 4 weekly doses of rituximab (375 mg/m2). His cutaneous findings slowly improved over the next several weeks (Figure 2).

Figure 2. Clinical improvement after treatment showing resolved livedo reticularis and gangrene of the fifth toe at 15-week follow-up.

Antiphospholipid syndrome is an autoimmune disorder characterized by thrombotic events and the presence of autoantibodies. The syndrome is defined by 2 major criteria: (1) the occurrence of at least 1 clinical feature of either an episode of vascular thrombosis or pregnancy morbidity such as unexplained fetal death beyond 10 weeks of gestation or recurrent unexplained pregnancy losses; and (2) the presence of at least 1 type of autoantibody, including lupus anticoagulant, anticardiolipin, or β2-glycoprotein antibodies, on 2 separate occasions at least 12 weeks apart.1 Antiphospholipid syndrome can either be primary with no identifiable associated rheumatologic disease or secondary to another autoimmune disease such as systemic lupus erythematosus. Cutaneous manifestations are common and frequently are the first sign of disease in 30% to 40% of patients.2 The most common skin finding is persistent livedo reticularis, which can be seen in 20% to 25% of patients. Patients also may develop skin necrosis, ulcerations, digital gangrene, splinter hemorrhages, and livedoid vasculopathy.2 Systemic manifestations of APS include thrombocytopenia, nephropathy, cognitive dysfunction, and cardiac valve abnormalities. 

The exact pathogenesis of APS remains unknown. It is thought to be due to the combination of an inflammatory stimulus that has yet to be characterized in conjunction with autoantibodies that affect multiple target cells including monocytes, platelets, and endothelial cells, which results in activation of the complement system and clotting cascade.3 In rare cases, the disorder can progress to catastrophic antiphospholipid syndrome (CAPS), which requires fulfillment of 4 criteria: (1) evidence of involvement of 3 organs, tissues, or systems; (2) development of manifestations simultaneously or in less than 1 week; (3) laboratory confirmation of the presence of antiphospholipid antibodies; and (4) confirmation by histopathology of small vessel occlusion.4 Probable CAPS is diagnosed when 3 of 4 criteria are present. Our patient met criteria for probable CAPS, as his antibody titers remained elevated 15 weeks after initial presentation. Precipitating factors that can lead to CAPS are thought to include infection, surgical procedures, medications, or discontinuation of anticoagulation drugs.2 Although the mainstay of management of APS is anticoagulation therapy with warfarin and antiplatelet agents such as aspirin, first-line treatment of CAPS involves high-dose systemic glucocorticoids and plasma exchange. Intravenous immunoglobulin also may be employed in treatment. Data from the CAPS registry demonstrate a role for rituximab, an anti-CD20 antibody, at 375 mg/m2 weekly for 4 weeks (the regimen described in our case) or 1 g every 14 days for 2 sessions.5 A majority of the registry patients treated with rituximab recovered (75% [15/20]) and had no recurrent thrombosis (87% [13/15]) at follow-up.5 Data also are emerging on the role of eculizumab, an anti-C5 antibody that inhibits the terminal complement cascade, as a therapy in difficult-to-treat or refractory CAPS.6-8 The prognosis for CAPS patients without treatment is poor, and mortality has been reported in up to 44% of patients. However, with intervention mortality is reduced by more than 2-fold.9,10

It is important to recognize that acral cyanosis with persistent livedo reticularis and digital gangrene can be a presenting manifestation of APS. These cutaneous manifestations should prompt histologic evaluation for thrombotic vasculopathy in addition to serologic tests for APS autoantibodies. Although APS may be treated with anticoagulants and antiplatelet agents, CAPS may require more aggressive therapy with systemic steroids, plasma exchange, IV immunoglobulin, rituximab, and/or eculizumab.

The Diagnosis: Antiphospholipid Antibody Syndrome

A  biopsy demonstrated scattered intravascular thrombi in the dermis and subcutis, intact vascular walls, and scant lymphocytic inflammation in a background of stasis (Figure 1). A periodic acid-Schiff stain was negative for fungal elements and highlighted the intravascular thrombi. Histologic findings were consistent with thrombotic vasculopathy. On further laboratory workup, lupus anticoagulant studies, including a mixing study, diluted Russell viper venom test, and hexagonal phase phospholipid neutralization test, were abnormal. Titers of anticardiolipin and β2-glycoprotein I antibodies were elevated (anticardiolipin IgG, 137.7 calculated units [normal, <15 calculated units]; β2-glycoprotein I IgG, 256.4 calculated units [normal, <20 calculated units]). Tissue cultures showed no growth of microorganisms and studies for cryoglobulinemia were negative.

Figure 1. In a background of stasis (A), there are deep intravascular thrombi with intact vascular walls and scant lymphocytic inflammation (B and C)(all H&E; original magnifications ×4, ×20, and ×40, respectively).

The patient was diagnosed with primary antiphospholipid syndrome (APS). He remained on anticoagulation therapy with fondaparinux as an inpatient and was treated with pulse-dose intravenous (IV) corticosteroids followed by a slow oral taper, daily plasmapheresis for 1 week, IV immunoglobulin (0.5 g/kg) for 3 doses, and 4 weekly doses of rituximab (375 mg/m2). His cutaneous findings slowly improved over the next several weeks (Figure 2).

Figure 2. Clinical improvement after treatment showing resolved livedo reticularis and gangrene of the fifth toe at 15-week follow-up.

Antiphospholipid syndrome is an autoimmune disorder characterized by thrombotic events and the presence of autoantibodies. The syndrome is defined by 2 major criteria: (1) the occurrence of at least 1 clinical feature of either an episode of vascular thrombosis or pregnancy morbidity such as unexplained fetal death beyond 10 weeks of gestation or recurrent unexplained pregnancy losses; and (2) the presence of at least 1 type of autoantibody, including lupus anticoagulant, anticardiolipin, or β2-glycoprotein antibodies, on 2 separate occasions at least 12 weeks apart.1 Antiphospholipid syndrome can either be primary with no identifiable associated rheumatologic disease or secondary to another autoimmune disease such as systemic lupus erythematosus. Cutaneous manifestations are common and frequently are the first sign of disease in 30% to 40% of patients.2 The most common skin finding is persistent livedo reticularis, which can be seen in 20% to 25% of patients. Patients also may develop skin necrosis, ulcerations, digital gangrene, splinter hemorrhages, and livedoid vasculopathy.2 Systemic manifestations of APS include thrombocytopenia, nephropathy, cognitive dysfunction, and cardiac valve abnormalities. 

The exact pathogenesis of APS remains unknown. It is thought to be due to the combination of an inflammatory stimulus that has yet to be characterized in conjunction with autoantibodies that affect multiple target cells including monocytes, platelets, and endothelial cells, which results in activation of the complement system and clotting cascade.3 In rare cases, the disorder can progress to catastrophic antiphospholipid syndrome (CAPS), which requires fulfillment of 4 criteria: (1) evidence of involvement of 3 organs, tissues, or systems; (2) development of manifestations simultaneously or in less than 1 week; (3) laboratory confirmation of the presence of antiphospholipid antibodies; and (4) confirmation by histopathology of small vessel occlusion.4 Probable CAPS is diagnosed when 3 of 4 criteria are present. Our patient met criteria for probable CAPS, as his antibody titers remained elevated 15 weeks after initial presentation. Precipitating factors that can lead to CAPS are thought to include infection, surgical procedures, medications, or discontinuation of anticoagulation drugs.2 Although the mainstay of management of APS is anticoagulation therapy with warfarin and antiplatelet agents such as aspirin, first-line treatment of CAPS involves high-dose systemic glucocorticoids and plasma exchange. Intravenous immunoglobulin also may be employed in treatment. Data from the CAPS registry demonstrate a role for rituximab, an anti-CD20 antibody, at 375 mg/m2 weekly for 4 weeks (the regimen described in our case) or 1 g every 14 days for 2 sessions.5 A majority of the registry patients treated with rituximab recovered (75% [15/20]) and had no recurrent thrombosis (87% [13/15]) at follow-up.5 Data also are emerging on the role of eculizumab, an anti-C5 antibody that inhibits the terminal complement cascade, as a therapy in difficult-to-treat or refractory CAPS.6-8 The prognosis for CAPS patients without treatment is poor, and mortality has been reported in up to 44% of patients. However, with intervention mortality is reduced by more than 2-fold.9,10

It is important to recognize that acral cyanosis with persistent livedo reticularis and digital gangrene can be a presenting manifestation of APS. These cutaneous manifestations should prompt histologic evaluation for thrombotic vasculopathy in addition to serologic tests for APS autoantibodies. Although APS may be treated with anticoagulants and antiplatelet agents, CAPS may require more aggressive therapy with systemic steroids, plasma exchange, IV immunoglobulin, rituximab, and/or eculizumab.

References
  1. Wilson WA, Gharavi AE, Koike T, et al. International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop. Arthritis Rheum. 1999;42:1309-1311.
  2. Pinto-Almeida T, Caetano M, Sanches M, et al. Cutaneous manifestations of antiphospholipid syndrome: a review of the clinical features, diagnosis and management. Acta Reumatol Port. 2013;38:10-18.
  3. Meroni PL, Chighizola CB, Rovelli F, et al. Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers. Arthritis Res Ther. 2014;16:209.
  4. Asherson RA, Cervera R, de Grott PG, et al; Catastrophic Antiphospholipid Syndrome Registry Project Group. Catastrophic antiphospholipid syndrome: international consensus statement on classification criteria and treatment guidelines. Lupus. 2003;12:530-534.
  5. Berman H, Rodríguez-Pintó I, Cervera R, et al. Rituximab use in the catastrophic antiphospholipid syndrome: descriptive analysis of the CAPS registry patients receiving rituximab [published online June 15, 2013]. Autoimmun Rev. 2013;12:1085-1090.
  6. Shapira I, Andrade D, Allen SL, et al. Brief report: induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab. Arthritis Rheum. 2012;64:2719-2723.
  7. Strakhan M, Hurtado-Sbordoni M, Galeas N, et al. 36-year-old female with catastrophic antiphospholipid syndrome treated with eculizumab: a case report and review of literature. Case Rep Hematol. 2014;2014:704371.
  8. Lonze BE, Zachary AA, Magro CM, et al. Eculizumab prevents recurrent antiphospholipid antibody syndrome and enables successful renal transplantation. Am J Transplant. 2014;14:459-465.
  9. Bucciarelli S, Espinosa G, Cervera R, et al. Mortality in the catastrophic antiphospholipid syndrome: causes of death and prognostic factors in a series of 250 patients. Arthritis Rheum. 2006;54:2568-2576.
  10. Asherson RA, Cervera R, Piette JC, et al. Catastrophic antiphospholipid syndrome. clinical and laboratory features of 50 patients. Medicine (Baltimore). 1998;77:195-207.
References
  1. Wilson WA, Gharavi AE, Koike T, et al. International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop. Arthritis Rheum. 1999;42:1309-1311.
  2. Pinto-Almeida T, Caetano M, Sanches M, et al. Cutaneous manifestations of antiphospholipid syndrome: a review of the clinical features, diagnosis and management. Acta Reumatol Port. 2013;38:10-18.
  3. Meroni PL, Chighizola CB, Rovelli F, et al. Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers. Arthritis Res Ther. 2014;16:209.
  4. Asherson RA, Cervera R, de Grott PG, et al; Catastrophic Antiphospholipid Syndrome Registry Project Group. Catastrophic antiphospholipid syndrome: international consensus statement on classification criteria and treatment guidelines. Lupus. 2003;12:530-534.
  5. Berman H, Rodríguez-Pintó I, Cervera R, et al. Rituximab use in the catastrophic antiphospholipid syndrome: descriptive analysis of the CAPS registry patients receiving rituximab [published online June 15, 2013]. Autoimmun Rev. 2013;12:1085-1090.
  6. Shapira I, Andrade D, Allen SL, et al. Brief report: induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab. Arthritis Rheum. 2012;64:2719-2723.
  7. Strakhan M, Hurtado-Sbordoni M, Galeas N, et al. 36-year-old female with catastrophic antiphospholipid syndrome treated with eculizumab: a case report and review of literature. Case Rep Hematol. 2014;2014:704371.
  8. Lonze BE, Zachary AA, Magro CM, et al. Eculizumab prevents recurrent antiphospholipid antibody syndrome and enables successful renal transplantation. Am J Transplant. 2014;14:459-465.
  9. Bucciarelli S, Espinosa G, Cervera R, et al. Mortality in the catastrophic antiphospholipid syndrome: causes of death and prognostic factors in a series of 250 patients. Arthritis Rheum. 2006;54:2568-2576.
  10. Asherson RA, Cervera R, Piette JC, et al. Catastrophic antiphospholipid syndrome. clinical and laboratory features of 50 patients. Medicine (Baltimore). 1998;77:195-207.
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A man in his 50s with a medical history of arterial thrombosis of the right arm, multiple deep vein thromboses (DVTs) of the legs on long-term warfarin, ischemic stroke, atrial fibrillation, and peripheral arterial disease presented with discoloration of the right foot and increasing tenderness of 1 month's duration. There was no history of trauma or recent change in outpatient medications. A family history was notable for an aunt and 2 cousins with DVTs and protein S deficiency. Physical examination revealed livedo reticularis on the sole and lateral aspect of the right foot. There was violaceous discoloration of the volar aspects of all 5 toes and a focal area of ulceration on the fifth toe. Pulses were palpable bilaterally. Initial laboratory evaluation was notable for thrombocytopenia, and preliminary blood cultures revealed no growth of bacterial or fungal organisms. Imaging studies revealed increased arterial stenosis of the right leg as well as DVT of the right great saphenous vein. A punch biopsy of the right medial foot was performed for hematoxylin and eosin stain as well as tissue culture.  

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Don't let the federal government keep money -- in the form of Medicare reimbursements -- to which you are entitled!

Learn all about coding and reimbursement, from the essentials to modifiers to future initiatives, at the SVS Coding and Reimbursement Workshop, Oct. 13-14, in Chicago. Cost is $880 for an SVS member or staff, $955 for a non-member and $250 for residents and trainees. Cost for an optional session is $100 for an SVS member or staff, $215 for a non-member and $50 for residents and trainees.

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Read about the Foundation’s expanded mission, emphasizing disease prevent and patient education along with the core commitment to fund basic and clinical research. Read why Michael C. Dalsing, MD, gives and how Ulka Sachdev, MD, has utilized her Foundation awards to try to unlock the suffering caused by chronic venous insufficiency. Read about this year’s grant recipients, Foundation financial details, lists of donors to not only the Foundation but also the new Alexander Clowes Lecture Fund, award opportunities and how every gift helps. Read, and donate today.

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The SVS Foundation highlights innovation and the connection between research bench and patient bedside in its just-published 2017 Annual Report, now available online.

Read about the Foundation’s expanded mission, emphasizing disease prevent and patient education along with the core commitment to fund basic and clinical research. Read why Michael C. Dalsing, MD, gives and how Ulka Sachdev, MD, has utilized her Foundation awards to try to unlock the suffering caused by chronic venous insufficiency. Read about this year’s grant recipients, Foundation financial details, lists of donors to not only the Foundation but also the new Alexander Clowes Lecture Fund, award opportunities and how every gift helps. Read, and donate today.

The SVS Foundation highlights innovation and the connection between research bench and patient bedside in its just-published 2017 Annual Report, now available online.

Read about the Foundation’s expanded mission, emphasizing disease prevent and patient education along with the core commitment to fund basic and clinical research. Read why Michael C. Dalsing, MD, gives and how Ulka Sachdev, MD, has utilized her Foundation awards to try to unlock the suffering caused by chronic venous insufficiency. Read about this year’s grant recipients, Foundation financial details, lists of donors to not only the Foundation but also the new Alexander Clowes Lecture Fund, award opportunities and how every gift helps. Read, and donate today.

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The fourth edition – which will soon include a mobile app (Apple products only) for off-line – launched just two months ago. Besides the app, VESAP4 also offers syncing between the companion app and desktop version; expanded bookmarking and annotation, easier navigation and simplified tracking of CME/MOC certificates.

Costs is $450 for candidates, $550 for members and $650 for non-members. A total of 75 CME (7.5 for each of the 10 sections) will be available. For information, email [email protected] or call 800-258-7188. 

 

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Don’t forget how valuable the Vascular Educational and Self-Assessment Program can be in keeping with all things vascular-related.

The fourth edition – which will soon include a mobile app (Apple products only) for off-line – launched just two months ago. Besides the app, VESAP4 also offers syncing between the companion app and desktop version; expanded bookmarking and annotation, easier navigation and simplified tracking of CME/MOC certificates.

Costs is $450 for candidates, $550 for members and $650 for non-members. A total of 75 CME (7.5 for each of the 10 sections) will be available. For information, email [email protected] or call 800-258-7188. 

 

Don’t forget how valuable the Vascular Educational and Self-Assessment Program can be in keeping with all things vascular-related.

The fourth edition – which will soon include a mobile app (Apple products only) for off-line – launched just two months ago. Besides the app, VESAP4 also offers syncing between the companion app and desktop version; expanded bookmarking and annotation, easier navigation and simplified tracking of CME/MOC certificates.

Costs is $450 for candidates, $550 for members and $650 for non-members. A total of 75 CME (7.5 for each of the 10 sections) will be available. For information, email [email protected] or call 800-258-7188. 

 

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Assessing the Effectiveness of Knowledge-Based Interventions in Increasing Skin Cancer Awareness, Knowledge, and Protective Behaviors in Skin of Color Populations

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Assessing the Effectiveness of Knowledge-Based Interventions in Increasing Skin Cancer Awareness, Knowledge, and Protective Behaviors in Skin of Color Populations
In Collaboration with the Skin of Color Society

Malignant melanoma, basal cell carcinoma, and squamous cell carcinoma account for approximately 40% of all neoplasms among the white population in the United States. Skin cancer is the most common malignancy in the United States.1 However, despite this occurrence, there are limited data regarding skin cancer in individuals with skin of color (SOC). The 5-year survival rates for melanoma are 58.2% for black individuals, 69.7% for Hispanics, and 70.9% for Asians compared to 79.8% for white individuals in the United States.2 Even though SOC populations have lower incidences of skin cancer—melanoma, basal cell carcinoma, and squamous cell carcinoma—they exhibit higher death rates.3-7 Nonetheless, no specific guidelines exist to address sun exposure and safety habits in SOC populations.6,8 Furthermore, current demographics suggest that by the year 2050, approximately half of the US population will be nonwhite.4 Paradoxically, despite having increased sun protection from greater amounts of melanin in their skin, black individuals are more likely to present with advanced-stage melanoma (eg, stage III/IV) compared to white individuals.8-12 Furthermore, those of nonwhite populations are more likely to present with more advanced stages of acral lentiginous melanomas than white individuals.13,14 Hispanics also face an increasing incidence of more invasive acral lentiginous melanomas.15 Overall, SOC patients have the poorest skin cancer prognosis, and the data suggest that the reason for this paradox is delayed diagnosis.1

Although skin cancer is largely a preventable condition, the literature suggests that lack of awareness of melanoma among ethnic minorities is one of the main reasons for their poor skin cancer prognosis.16 This lack of awareness decreases the likelihood that an SOC patient would be alert to early detection of cancerous changes.17 Because educating at-risk SOC populations is key to decreasing skin cancer risk, this study focused on determining the efficacy of major knowledge-based interventions conducted to date.1 Overall, we sought to answer the question, do knowledge-based interventions increase skin cancer awareness, knowledge, and protective behavior among people of color?

Methods

For this review, the Cochrane method of analysis was used to conduct a thorough search of PubMed articles indexed for MEDLINE (1994-2016), as well as a search of CINAHL (1997-2016), PsycINFO (1999-2016), and Web of Science (1965-2016), using a combination of more than 100 search terms including but not limited to skin cancer, skin of color, intervention, and ethnic skin. The search yielded a total of 52 articles (Figure). Following review, only 8 articles met inclusion criteria, which were as follows: (1) study was related to skin cancer in SOC patients, which included an intervention to increase skin cancer awareness and knowledge; (2) study included adult participants or adolescents aged 12 to 18 years; (3) study was written in English; and (4) study was published in a peer-reviewed journal. Of the remaining 8 articles, 4 were excluded due to the following criteria: (1) study failed to provide both preintervention and postintervention data, (2) study failed to provide quantitative data, and (3) study included participants who worked as health care professionals or ancillary staff. As a result, a total of 4 articles were analyzed and discussed in this review (Table).

Data collection flowchart of the total number of articles yielded in the literature search.

Results

Robinson et al18 conducted 12 focus groups with 120 total participants (40 black, 40 Asian, and 40 Hispanic patients). Participants engaged in a 2-hour tape-recorded focus group with a moderator guide on melanoma and skin cancer. Furthermore, they also were asked to assess skin cancer risk in 5 celebrities with different skin tones. The statistically significant preintervention results of the study (χ2=4.6, P<.001) were as follows: only 2%, 4%, and 14% correctly reported that celebrities with a very fair skin type, a fair skin type, and very dark skin type, respectively, could get sunburn, compared to 75%, 76%, and 62% post-intervention. Additionally, prior to intervention, 14% of the study population believed that dark brown skin type could get sunburn compared to 62% of the same group postintervention. This study demonstrated that the intervention helped SOC patients better identify their ability to get sunburn and identify their skin cancer risk.18

Hernandez et al19 used a video-based intervention in a Hispanic community, which was in contrast to the multiracial focus group intervention conducted by Robinson et al.18 Eighty Hispanic individuals were recruited from beauty salons to participate in the study. Participants watched two 3-minute videos in Spanish and completed a preintervention and postintervention survey. The first video emphasized the photoaging benefits of sun protection, while the second focused on skin cancer prevention. Preintervention surveys indicated that only 54 (68%) participants believed that fair-skinned Hispanics were at risk for skin cancer, which improved to 72 (90%) participants postintervention. Furthermore, initially only 44 (55%) participants thought those with darker skin types could develop skin cancer, but this number increased to 69 (86%) postintervention. For both questions regarding fair and dark skin, the agreement proportion was significantly different between the preeducation and posteducation videos (P<.0002 for the fair skin question and P<.0001 for the dark skin question). This study greatly increased awareness of skin cancer risk among Hispanics,19 similar to the Robinson et al18 study.

In contrast to 2-hour focus groups or 3-minute video–based interventions, a study by Kundu et al17 employed a 20-minute educational class-based intervention with both verbal and visual instruction. This study assessed the efficacy of an educational tutorial on improving awareness and early detection of melanoma in SOC individuals. Photographs were used to help participants recognize the ABCDEs of melanoma and to show examples of acral lentiginous melanomas in white individuals. A total of 71 participants completed a preintervention questionnaire, participated in a 20-minute class, and completed a postintervention questionnaire immediately after and 3 months following the class. The study population included 44 black, 15 Asian, 10 Hispanic, and 2 multiethnic participants. Knowledge that melanoma is a skin cancer increased from 83.9% to 100% immediately postintervention (P=.0001) and 97.2% at 3 months postintervention (P=.0075). Additionally, knowledge that people of color are at risk for melanoma increased from 48.4% preintervention to 82.8% immediately postintervention (P<.0001). However, only 40.8% of participants retained this knowledge at 3 months postintervention. Because only 1 participant reported a family history of skin cancer, the authors hypothesized that the reason for this loss of knowledge was that most participants were not personally affected by friends or family members with melanoma. A future study with an appropriate control group would be needed to support this claim. This study shed light on the potential of class-based interventions to increase both awareness and knowledge of skin cancer in SOC populations.17

A study by Chapman et al20 examined the effects of a sun protection educational program on increasing awareness of skin cancer in Hispanic and black middle school students in southern Los Angeles, California. It was the only study we reviewed that focused primarily on adolescents. Furthermore, it included the largest sample size (N=148) analyzed here. Students were given a preintervention questionnaire to evaluate their awareness of skin cancer and current sun-protection practices. Based on these results, the investigators devised a set of learning goals and incorporated them into an educational pamphlet. The intervention, called “Skin Teaching Day,” was a 1-day program discussing skin cancer and the importance of sun protection. Prior to the intervention, 68% of participants reported that they used sunscreen. Three months after completing the program, 80% of participants reported sunscreen use, an increase of 12% prior to the intervention. The results of this study demonstrated the unique effectiveness and potential of pamphlets in increasing sunscreen use.20

 

 

Comment

Overall, various methods of interventions such as focus groups, videos, pamphlets, and lectures improved knowledge of skin cancer risk and sun-protection behaviors in SOC populations. Furthermore, the unique differences of each study provided important insights into the successful design of an intervention.

An important characteristic of the Robinson et al18 study was the addition of photographs, which allowed participants not only to visualize different skin tones but also provided them with the opportunity to relate themselves to the photographs; by doing so, participants could effectively pick out the skin tone that best suited them. Written SOC scales are limited to mere descriptions and thus make it more difficult for participants to accurately identify the tone that best fits them. Kundu et al17 used photographs to teach skin self-examination and ABCDEs for detection of melanoma. Additionally, both studies used photographs to demonstrate examples of skin cancer.17,18 Recent evidence suggests the use of visuals can be efficacious for improving skin cancer knowledge and awareness; a study in 16 SOC kidney transplant recipients found that the addition of photographs of squamous cell carcinoma in various skin tones to a sun-protection educational pamphlet was more effective than the original pamphlet without photographs.21

In contrast to the Robinson et al18 study and Hernandez et al19 study, the Kundu et al17 study showed photographs of acral lentiginous melanomas in white patients rather than SOC patients. However, SOC populations may be less likely to relate to or identify skin changes in skin types that are different from their own. This technique was still beneficial, as acral lentiginous melanoma is the most common type of melanoma in SOC populations. Another benefit of the study was that it was the only study reviewed that included a follow-up postintervention questionnaire. Such data is useful, as it demonstrates how muchinformation is retained by participants and may be more likely to predict compliance with skin cancer protective behaviors.17

The Hernandez et al19 study is unique in that it was the only one to include an educational intervention entirely in Spanish, which is important to consider, as language may be a hindrance to participants’ understanding in the other studies, particularly Hispanics, possibly leading to a lack of information retention regarding sun-protective behaviors. Furthermore, it also was the only study to utilize videos as a method for interventions. The 3-minute videos demonstrated that interventions could be efficient as compared to the 2-hour in-class intervention used by Robinson et al18 and the 20-minute intervention used by Kundu et al.17 Additionally, videos also could be more cost-effective, as incentives for large focus groups would no longer be needed. Furthermore, in the Hernandez et al19 study, there was minimal to no disruption in the participants’ daily routine, as the participants were getting cosmetic services while watching the videos, perhaps allowing them to be more attentive. In contrast, both the Robinson et al18 and Kundu et al17 studies required time out from the participants’ daily schedules. In addition, these studies were notably longer than the Hernandez et al19 study. The 8-hour intervention in the Chapman et al20 study also may not be feasible for the general population because of its excessive length. However, the intervention was successful among the adolescent participants, which suggested that shorter durations are effective in the adult population and longer interventions may be more appropriate for adolescents because they benefit from peer activity.

Despite the success of the educational interventions as outlined in the 4 studies described here, a major epidemiologic flaw is that these interventions included only a small percentage of the target population. The largest total number of adults surveyed and undergoing an intervention in any of the populations was only 120.17 By failing to reach a substantial proportion of the population at risk, the number of preventable deaths likely will not decrease. The authors believe a larger-scale intervention would provide meaningful change. Australia’s SunSmart campaign to increase skin cancer awareness in the Australian population is an example of one such large-scale national intervention. The campaign focused on massive television advertisements in the summer to educate participants about the dangers of skin cancer and the importance of protective behaviors. Telephone surveys conducted from 1987 to 2011 demonstrated that more exposure to the advertisements in the SunSmart campaign meant that individuals were more likely to use sunscreen and avoid sun exposure.22 In the United States, a similar intervention would be of great benefit in educating SOC populations regarding skin cancer risk. Additionally, dermatology residents need to be adequately trained to educate patients of color about the risk for skin cancer, as survey data indicated more than 80% of Australian dermatologists desired more SOC teaching during their training and 50% indicated that they would have time to learn it during their training if offered.23 Furthermore, one study suggested that future interventions must include primary-, secondary-, and tertiary-prevention methods to effectively reduce skin cancer risk among patients of color.24 Primary prevention involves sun avoidance, secondary prevention involves detecting cancerous lesions, and tertiary prevention involves undergoing treatment of skin malignancies. However, increased knowledge does not necessarily mean increased preventative action will be employed (eg, sunscreen use, wearing sun-protective clothing and sunglasses, avoiding tanning beds and excessive sun exposure). Additional studies that demonstrate a notable increase in sun-protective behaviors related to increased knowledge are needed.

Because retention of skin cancer knowledge decreased in several postintervention surveys, there also is a dire need for continuing skin cancer education in patients of color, which may be accomplished through a combination effort of television advertisement campaigns, pamphlets, social media, community health departments, or even community members. For example, a pilot program found that Hispanic lay health workers who are educated about skin cancer may serve as a bridge between medical providers and the Hispanic community by encouraging individuals in this population to get regular skin examinations from a physician.25 Overall, there are currently gaps in the understanding and treatment of skin cancer in people of color.26 Identifying the advantages and disadvantages of all relevant skin cancer interventions conducted in the SOC population will hopefully guide future studies to help close these gaps by allowing others to design the best possible intervention. By doing so, researchers can generate an intervention that is precise, well-informed, and effective in decreasing mortality rates from skin cancer among SOC populations.

 

 

Conclusion

All of the studies reviewed demonstrated that instructional and educational interventions are promising methods for improving either knowledge, awareness, or safe skin practices and sun-protective behaviors in SOC populations to differing degrees (Table). Although each of the 4 interventions employed their own methods, they all increased 1 or more of the 3 aforementioned concepts—knowledge, awareness, or safe skin practices and sun-protective behaviors—when comparing postsurvey to presurvey data. However, the critically important message derived from this research is that there is a tremendous need for a substantial large-scale educational intervention to increase knowledge regarding skin cancer in SOC populations.

References
  1. Agbai ON, Buster K, Sanchez M, et al. Skin cancer and photoprotection in people of color: a review and recommendations for physicians and the public. J Am Acad Dermatol. 2014;70:748-762.
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914.
  3. Gloster HM Jr, Neal K. Skin cancer in skin of color. J Am Acad Dermatol. 2006;55:741-760.
  4. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  5. Byrd KM, Wilson DC, Hoyler SS, et al. Advanced presentation of melanoma in African Americans. J Am Acad Dermatol. 2004;50:21-24.
  6. Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
  7. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5, suppl 1):S26-S37.
  8. Byrd-Miles K, Toombs EL, Peck GL. Skin cancer in individuals of African, Asian, Latin-American, and American-Indian descent: differences in incidence, clinical presentation, and survival compared to Caucasians. J Drugs Dermatol. 2007;6:10-16.
  9. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708.
  10. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;5:1031-1032.
  11. Bellows CF, Belafsky P, Fortgang IS, et al. Melanoma in African-Americans: trends in biological behavior and clinical characteristics over two decades. J Surg Oncol. 2001;78:10-16.
  12. Pritchett EN, Doyle A, Shaver CM, et al. Nonmelanoma skin cancer in nonwhite organ transplant recipients. JAMA Dermatol. 2016;152:1348-1353.
  13. Shin S, Palis BE, Phillips JL, et al. Cutaneous melanoma in Asian-Americans. J Surg Oncol. 2009;99:114-118.
  14. Stubblefield J, Kelly B. Melanoma in non-caucasian populations. Surg Clin North Am. 2014;94:1115-1126.
  15. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  16. Pichon LC, Corral I, Landrine H, et al. Perceived skin cancer risk and sunscreen use among African American adults. J Health Psychol. 2010;15:1181-1189.
  17. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784.
  18. Robinson JK, Joshi KM, Ortiz S, et al. Melanoma knowledge, perception, and awareness in ethnic minorities in Chicago: recommendations regarding education. Psychooncology. 2010;20:313-320.
  19. Hernandez C, Wang S, Abraham I, et al. Evaluation of educational videos to increase skin cancer risk awareness and sun safe behaviors among adult Hispanics. J Cancer Educ. 2014;29:563-569.
  20. Chapman LW, Ochoa A, Tenconi F, et al. Dermatologic health literacy in underserved communities: a case report of south Los Angeles middle schools. Dermatol Online J. 2015;21. pii:13030/qt8671p40n.
  21. Yanina G, Gaber R, Clayman ML, et al. Sun protection education for diverse audiences: need for skin cancer pictures. J Cancer Educ. 2015;30:187-189.
  22. Dobbinson SJ, Volkov A, Wakefield MA. Continued impact of sunsmart advertising on youth and adults’ behaviors. Am J Prev Med. 2015;49:20-28.
  23. Rodrigues MA, Ross AL, Gilmore S, et al. Australian dermatologists’ perspective on skin of colour: results of a national survey [published online December 9, 2016]. Australas J Dermatol. doi:10.1111/ajd.12556.
  24. Jacobsen A, Galvan A, Lachapelle CC, et al. Defining the need for skin cancer prevention education in uninsured, minority, and immigrant communities. JAMA Dermatol. 2016;152:1342-1347.
  25. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345.
  26. Kailas A, Solomon JA, Mostow EN, et al. Gaps in the understanding and treatment of skin cancer in people of color. J Am Acad Dermatol. 2016;74:144-149.
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Mr. Kailas and Mr. Botwin are from the University of Central Florida College of Medicine, Orlando. Drs. Pritchett and Jackson-Richards are from the Multicultural Dermatology Center, Henry Ford Medical Center, Detroit, Michigan. Drs. Lewis and Sadhwani are from the Department of Dermatology, University of South Florida, Tampa. Dr. Desai is from the Department of Dermatology, University of Texas Southwestern Medical Center, Dallas. Dr. Taylor is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

The authors report no conflict of interest.

Correspondence: Ajay Kailas, BS, UCF College of Medicine, 6850 Lake Nona Blvd, Orlando, FL 32827 ([email protected]).

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The authors report no conflict of interest.

Correspondence: Ajay Kailas, BS, UCF College of Medicine, 6850 Lake Nona Blvd, Orlando, FL 32827 ([email protected]).

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Mr. Kailas and Mr. Botwin are from the University of Central Florida College of Medicine, Orlando. Drs. Pritchett and Jackson-Richards are from the Multicultural Dermatology Center, Henry Ford Medical Center, Detroit, Michigan. Drs. Lewis and Sadhwani are from the Department of Dermatology, University of South Florida, Tampa. Dr. Desai is from the Department of Dermatology, University of Texas Southwestern Medical Center, Dallas. Dr. Taylor is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

The authors report no conflict of interest.

Correspondence: Ajay Kailas, BS, UCF College of Medicine, 6850 Lake Nona Blvd, Orlando, FL 32827 ([email protected]).

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In Collaboration with the Skin of Color Society
In Collaboration with the Skin of Color Society

Malignant melanoma, basal cell carcinoma, and squamous cell carcinoma account for approximately 40% of all neoplasms among the white population in the United States. Skin cancer is the most common malignancy in the United States.1 However, despite this occurrence, there are limited data regarding skin cancer in individuals with skin of color (SOC). The 5-year survival rates for melanoma are 58.2% for black individuals, 69.7% for Hispanics, and 70.9% for Asians compared to 79.8% for white individuals in the United States.2 Even though SOC populations have lower incidences of skin cancer—melanoma, basal cell carcinoma, and squamous cell carcinoma—they exhibit higher death rates.3-7 Nonetheless, no specific guidelines exist to address sun exposure and safety habits in SOC populations.6,8 Furthermore, current demographics suggest that by the year 2050, approximately half of the US population will be nonwhite.4 Paradoxically, despite having increased sun protection from greater amounts of melanin in their skin, black individuals are more likely to present with advanced-stage melanoma (eg, stage III/IV) compared to white individuals.8-12 Furthermore, those of nonwhite populations are more likely to present with more advanced stages of acral lentiginous melanomas than white individuals.13,14 Hispanics also face an increasing incidence of more invasive acral lentiginous melanomas.15 Overall, SOC patients have the poorest skin cancer prognosis, and the data suggest that the reason for this paradox is delayed diagnosis.1

Although skin cancer is largely a preventable condition, the literature suggests that lack of awareness of melanoma among ethnic minorities is one of the main reasons for their poor skin cancer prognosis.16 This lack of awareness decreases the likelihood that an SOC patient would be alert to early detection of cancerous changes.17 Because educating at-risk SOC populations is key to decreasing skin cancer risk, this study focused on determining the efficacy of major knowledge-based interventions conducted to date.1 Overall, we sought to answer the question, do knowledge-based interventions increase skin cancer awareness, knowledge, and protective behavior among people of color?

Methods

For this review, the Cochrane method of analysis was used to conduct a thorough search of PubMed articles indexed for MEDLINE (1994-2016), as well as a search of CINAHL (1997-2016), PsycINFO (1999-2016), and Web of Science (1965-2016), using a combination of more than 100 search terms including but not limited to skin cancer, skin of color, intervention, and ethnic skin. The search yielded a total of 52 articles (Figure). Following review, only 8 articles met inclusion criteria, which were as follows: (1) study was related to skin cancer in SOC patients, which included an intervention to increase skin cancer awareness and knowledge; (2) study included adult participants or adolescents aged 12 to 18 years; (3) study was written in English; and (4) study was published in a peer-reviewed journal. Of the remaining 8 articles, 4 were excluded due to the following criteria: (1) study failed to provide both preintervention and postintervention data, (2) study failed to provide quantitative data, and (3) study included participants who worked as health care professionals or ancillary staff. As a result, a total of 4 articles were analyzed and discussed in this review (Table).

Data collection flowchart of the total number of articles yielded in the literature search.

Results

Robinson et al18 conducted 12 focus groups with 120 total participants (40 black, 40 Asian, and 40 Hispanic patients). Participants engaged in a 2-hour tape-recorded focus group with a moderator guide on melanoma and skin cancer. Furthermore, they also were asked to assess skin cancer risk in 5 celebrities with different skin tones. The statistically significant preintervention results of the study (χ2=4.6, P<.001) were as follows: only 2%, 4%, and 14% correctly reported that celebrities with a very fair skin type, a fair skin type, and very dark skin type, respectively, could get sunburn, compared to 75%, 76%, and 62% post-intervention. Additionally, prior to intervention, 14% of the study population believed that dark brown skin type could get sunburn compared to 62% of the same group postintervention. This study demonstrated that the intervention helped SOC patients better identify their ability to get sunburn and identify their skin cancer risk.18

Hernandez et al19 used a video-based intervention in a Hispanic community, which was in contrast to the multiracial focus group intervention conducted by Robinson et al.18 Eighty Hispanic individuals were recruited from beauty salons to participate in the study. Participants watched two 3-minute videos in Spanish and completed a preintervention and postintervention survey. The first video emphasized the photoaging benefits of sun protection, while the second focused on skin cancer prevention. Preintervention surveys indicated that only 54 (68%) participants believed that fair-skinned Hispanics were at risk for skin cancer, which improved to 72 (90%) participants postintervention. Furthermore, initially only 44 (55%) participants thought those with darker skin types could develop skin cancer, but this number increased to 69 (86%) postintervention. For both questions regarding fair and dark skin, the agreement proportion was significantly different between the preeducation and posteducation videos (P<.0002 for the fair skin question and P<.0001 for the dark skin question). This study greatly increased awareness of skin cancer risk among Hispanics,19 similar to the Robinson et al18 study.

In contrast to 2-hour focus groups or 3-minute video–based interventions, a study by Kundu et al17 employed a 20-minute educational class-based intervention with both verbal and visual instruction. This study assessed the efficacy of an educational tutorial on improving awareness and early detection of melanoma in SOC individuals. Photographs were used to help participants recognize the ABCDEs of melanoma and to show examples of acral lentiginous melanomas in white individuals. A total of 71 participants completed a preintervention questionnaire, participated in a 20-minute class, and completed a postintervention questionnaire immediately after and 3 months following the class. The study population included 44 black, 15 Asian, 10 Hispanic, and 2 multiethnic participants. Knowledge that melanoma is a skin cancer increased from 83.9% to 100% immediately postintervention (P=.0001) and 97.2% at 3 months postintervention (P=.0075). Additionally, knowledge that people of color are at risk for melanoma increased from 48.4% preintervention to 82.8% immediately postintervention (P<.0001). However, only 40.8% of participants retained this knowledge at 3 months postintervention. Because only 1 participant reported a family history of skin cancer, the authors hypothesized that the reason for this loss of knowledge was that most participants were not personally affected by friends or family members with melanoma. A future study with an appropriate control group would be needed to support this claim. This study shed light on the potential of class-based interventions to increase both awareness and knowledge of skin cancer in SOC populations.17

A study by Chapman et al20 examined the effects of a sun protection educational program on increasing awareness of skin cancer in Hispanic and black middle school students in southern Los Angeles, California. It was the only study we reviewed that focused primarily on adolescents. Furthermore, it included the largest sample size (N=148) analyzed here. Students were given a preintervention questionnaire to evaluate their awareness of skin cancer and current sun-protection practices. Based on these results, the investigators devised a set of learning goals and incorporated them into an educational pamphlet. The intervention, called “Skin Teaching Day,” was a 1-day program discussing skin cancer and the importance of sun protection. Prior to the intervention, 68% of participants reported that they used sunscreen. Three months after completing the program, 80% of participants reported sunscreen use, an increase of 12% prior to the intervention. The results of this study demonstrated the unique effectiveness and potential of pamphlets in increasing sunscreen use.20

 

 

Comment

Overall, various methods of interventions such as focus groups, videos, pamphlets, and lectures improved knowledge of skin cancer risk and sun-protection behaviors in SOC populations. Furthermore, the unique differences of each study provided important insights into the successful design of an intervention.

An important characteristic of the Robinson et al18 study was the addition of photographs, which allowed participants not only to visualize different skin tones but also provided them with the opportunity to relate themselves to the photographs; by doing so, participants could effectively pick out the skin tone that best suited them. Written SOC scales are limited to mere descriptions and thus make it more difficult for participants to accurately identify the tone that best fits them. Kundu et al17 used photographs to teach skin self-examination and ABCDEs for detection of melanoma. Additionally, both studies used photographs to demonstrate examples of skin cancer.17,18 Recent evidence suggests the use of visuals can be efficacious for improving skin cancer knowledge and awareness; a study in 16 SOC kidney transplant recipients found that the addition of photographs of squamous cell carcinoma in various skin tones to a sun-protection educational pamphlet was more effective than the original pamphlet without photographs.21

In contrast to the Robinson et al18 study and Hernandez et al19 study, the Kundu et al17 study showed photographs of acral lentiginous melanomas in white patients rather than SOC patients. However, SOC populations may be less likely to relate to or identify skin changes in skin types that are different from their own. This technique was still beneficial, as acral lentiginous melanoma is the most common type of melanoma in SOC populations. Another benefit of the study was that it was the only study reviewed that included a follow-up postintervention questionnaire. Such data is useful, as it demonstrates how muchinformation is retained by participants and may be more likely to predict compliance with skin cancer protective behaviors.17

The Hernandez et al19 study is unique in that it was the only one to include an educational intervention entirely in Spanish, which is important to consider, as language may be a hindrance to participants’ understanding in the other studies, particularly Hispanics, possibly leading to a lack of information retention regarding sun-protective behaviors. Furthermore, it also was the only study to utilize videos as a method for interventions. The 3-minute videos demonstrated that interventions could be efficient as compared to the 2-hour in-class intervention used by Robinson et al18 and the 20-minute intervention used by Kundu et al.17 Additionally, videos also could be more cost-effective, as incentives for large focus groups would no longer be needed. Furthermore, in the Hernandez et al19 study, there was minimal to no disruption in the participants’ daily routine, as the participants were getting cosmetic services while watching the videos, perhaps allowing them to be more attentive. In contrast, both the Robinson et al18 and Kundu et al17 studies required time out from the participants’ daily schedules. In addition, these studies were notably longer than the Hernandez et al19 study. The 8-hour intervention in the Chapman et al20 study also may not be feasible for the general population because of its excessive length. However, the intervention was successful among the adolescent participants, which suggested that shorter durations are effective in the adult population and longer interventions may be more appropriate for adolescents because they benefit from peer activity.

Despite the success of the educational interventions as outlined in the 4 studies described here, a major epidemiologic flaw is that these interventions included only a small percentage of the target population. The largest total number of adults surveyed and undergoing an intervention in any of the populations was only 120.17 By failing to reach a substantial proportion of the population at risk, the number of preventable deaths likely will not decrease. The authors believe a larger-scale intervention would provide meaningful change. Australia’s SunSmart campaign to increase skin cancer awareness in the Australian population is an example of one such large-scale national intervention. The campaign focused on massive television advertisements in the summer to educate participants about the dangers of skin cancer and the importance of protective behaviors. Telephone surveys conducted from 1987 to 2011 demonstrated that more exposure to the advertisements in the SunSmart campaign meant that individuals were more likely to use sunscreen and avoid sun exposure.22 In the United States, a similar intervention would be of great benefit in educating SOC populations regarding skin cancer risk. Additionally, dermatology residents need to be adequately trained to educate patients of color about the risk for skin cancer, as survey data indicated more than 80% of Australian dermatologists desired more SOC teaching during their training and 50% indicated that they would have time to learn it during their training if offered.23 Furthermore, one study suggested that future interventions must include primary-, secondary-, and tertiary-prevention methods to effectively reduce skin cancer risk among patients of color.24 Primary prevention involves sun avoidance, secondary prevention involves detecting cancerous lesions, and tertiary prevention involves undergoing treatment of skin malignancies. However, increased knowledge does not necessarily mean increased preventative action will be employed (eg, sunscreen use, wearing sun-protective clothing and sunglasses, avoiding tanning beds and excessive sun exposure). Additional studies that demonstrate a notable increase in sun-protective behaviors related to increased knowledge are needed.

Because retention of skin cancer knowledge decreased in several postintervention surveys, there also is a dire need for continuing skin cancer education in patients of color, which may be accomplished through a combination effort of television advertisement campaigns, pamphlets, social media, community health departments, or even community members. For example, a pilot program found that Hispanic lay health workers who are educated about skin cancer may serve as a bridge between medical providers and the Hispanic community by encouraging individuals in this population to get regular skin examinations from a physician.25 Overall, there are currently gaps in the understanding and treatment of skin cancer in people of color.26 Identifying the advantages and disadvantages of all relevant skin cancer interventions conducted in the SOC population will hopefully guide future studies to help close these gaps by allowing others to design the best possible intervention. By doing so, researchers can generate an intervention that is precise, well-informed, and effective in decreasing mortality rates from skin cancer among SOC populations.

 

 

Conclusion

All of the studies reviewed demonstrated that instructional and educational interventions are promising methods for improving either knowledge, awareness, or safe skin practices and sun-protective behaviors in SOC populations to differing degrees (Table). Although each of the 4 interventions employed their own methods, they all increased 1 or more of the 3 aforementioned concepts—knowledge, awareness, or safe skin practices and sun-protective behaviors—when comparing postsurvey to presurvey data. However, the critically important message derived from this research is that there is a tremendous need for a substantial large-scale educational intervention to increase knowledge regarding skin cancer in SOC populations.

Malignant melanoma, basal cell carcinoma, and squamous cell carcinoma account for approximately 40% of all neoplasms among the white population in the United States. Skin cancer is the most common malignancy in the United States.1 However, despite this occurrence, there are limited data regarding skin cancer in individuals with skin of color (SOC). The 5-year survival rates for melanoma are 58.2% for black individuals, 69.7% for Hispanics, and 70.9% for Asians compared to 79.8% for white individuals in the United States.2 Even though SOC populations have lower incidences of skin cancer—melanoma, basal cell carcinoma, and squamous cell carcinoma—they exhibit higher death rates.3-7 Nonetheless, no specific guidelines exist to address sun exposure and safety habits in SOC populations.6,8 Furthermore, current demographics suggest that by the year 2050, approximately half of the US population will be nonwhite.4 Paradoxically, despite having increased sun protection from greater amounts of melanin in their skin, black individuals are more likely to present with advanced-stage melanoma (eg, stage III/IV) compared to white individuals.8-12 Furthermore, those of nonwhite populations are more likely to present with more advanced stages of acral lentiginous melanomas than white individuals.13,14 Hispanics also face an increasing incidence of more invasive acral lentiginous melanomas.15 Overall, SOC patients have the poorest skin cancer prognosis, and the data suggest that the reason for this paradox is delayed diagnosis.1

Although skin cancer is largely a preventable condition, the literature suggests that lack of awareness of melanoma among ethnic minorities is one of the main reasons for their poor skin cancer prognosis.16 This lack of awareness decreases the likelihood that an SOC patient would be alert to early detection of cancerous changes.17 Because educating at-risk SOC populations is key to decreasing skin cancer risk, this study focused on determining the efficacy of major knowledge-based interventions conducted to date.1 Overall, we sought to answer the question, do knowledge-based interventions increase skin cancer awareness, knowledge, and protective behavior among people of color?

Methods

For this review, the Cochrane method of analysis was used to conduct a thorough search of PubMed articles indexed for MEDLINE (1994-2016), as well as a search of CINAHL (1997-2016), PsycINFO (1999-2016), and Web of Science (1965-2016), using a combination of more than 100 search terms including but not limited to skin cancer, skin of color, intervention, and ethnic skin. The search yielded a total of 52 articles (Figure). Following review, only 8 articles met inclusion criteria, which were as follows: (1) study was related to skin cancer in SOC patients, which included an intervention to increase skin cancer awareness and knowledge; (2) study included adult participants or adolescents aged 12 to 18 years; (3) study was written in English; and (4) study was published in a peer-reviewed journal. Of the remaining 8 articles, 4 were excluded due to the following criteria: (1) study failed to provide both preintervention and postintervention data, (2) study failed to provide quantitative data, and (3) study included participants who worked as health care professionals or ancillary staff. As a result, a total of 4 articles were analyzed and discussed in this review (Table).

Data collection flowchart of the total number of articles yielded in the literature search.

Results

Robinson et al18 conducted 12 focus groups with 120 total participants (40 black, 40 Asian, and 40 Hispanic patients). Participants engaged in a 2-hour tape-recorded focus group with a moderator guide on melanoma and skin cancer. Furthermore, they also were asked to assess skin cancer risk in 5 celebrities with different skin tones. The statistically significant preintervention results of the study (χ2=4.6, P<.001) were as follows: only 2%, 4%, and 14% correctly reported that celebrities with a very fair skin type, a fair skin type, and very dark skin type, respectively, could get sunburn, compared to 75%, 76%, and 62% post-intervention. Additionally, prior to intervention, 14% of the study population believed that dark brown skin type could get sunburn compared to 62% of the same group postintervention. This study demonstrated that the intervention helped SOC patients better identify their ability to get sunburn and identify their skin cancer risk.18

Hernandez et al19 used a video-based intervention in a Hispanic community, which was in contrast to the multiracial focus group intervention conducted by Robinson et al.18 Eighty Hispanic individuals were recruited from beauty salons to participate in the study. Participants watched two 3-minute videos in Spanish and completed a preintervention and postintervention survey. The first video emphasized the photoaging benefits of sun protection, while the second focused on skin cancer prevention. Preintervention surveys indicated that only 54 (68%) participants believed that fair-skinned Hispanics were at risk for skin cancer, which improved to 72 (90%) participants postintervention. Furthermore, initially only 44 (55%) participants thought those with darker skin types could develop skin cancer, but this number increased to 69 (86%) postintervention. For both questions regarding fair and dark skin, the agreement proportion was significantly different between the preeducation and posteducation videos (P<.0002 for the fair skin question and P<.0001 for the dark skin question). This study greatly increased awareness of skin cancer risk among Hispanics,19 similar to the Robinson et al18 study.

In contrast to 2-hour focus groups or 3-minute video–based interventions, a study by Kundu et al17 employed a 20-minute educational class-based intervention with both verbal and visual instruction. This study assessed the efficacy of an educational tutorial on improving awareness and early detection of melanoma in SOC individuals. Photographs were used to help participants recognize the ABCDEs of melanoma and to show examples of acral lentiginous melanomas in white individuals. A total of 71 participants completed a preintervention questionnaire, participated in a 20-minute class, and completed a postintervention questionnaire immediately after and 3 months following the class. The study population included 44 black, 15 Asian, 10 Hispanic, and 2 multiethnic participants. Knowledge that melanoma is a skin cancer increased from 83.9% to 100% immediately postintervention (P=.0001) and 97.2% at 3 months postintervention (P=.0075). Additionally, knowledge that people of color are at risk for melanoma increased from 48.4% preintervention to 82.8% immediately postintervention (P<.0001). However, only 40.8% of participants retained this knowledge at 3 months postintervention. Because only 1 participant reported a family history of skin cancer, the authors hypothesized that the reason for this loss of knowledge was that most participants were not personally affected by friends or family members with melanoma. A future study with an appropriate control group would be needed to support this claim. This study shed light on the potential of class-based interventions to increase both awareness and knowledge of skin cancer in SOC populations.17

A study by Chapman et al20 examined the effects of a sun protection educational program on increasing awareness of skin cancer in Hispanic and black middle school students in southern Los Angeles, California. It was the only study we reviewed that focused primarily on adolescents. Furthermore, it included the largest sample size (N=148) analyzed here. Students were given a preintervention questionnaire to evaluate their awareness of skin cancer and current sun-protection practices. Based on these results, the investigators devised a set of learning goals and incorporated them into an educational pamphlet. The intervention, called “Skin Teaching Day,” was a 1-day program discussing skin cancer and the importance of sun protection. Prior to the intervention, 68% of participants reported that they used sunscreen. Three months after completing the program, 80% of participants reported sunscreen use, an increase of 12% prior to the intervention. The results of this study demonstrated the unique effectiveness and potential of pamphlets in increasing sunscreen use.20

 

 

Comment

Overall, various methods of interventions such as focus groups, videos, pamphlets, and lectures improved knowledge of skin cancer risk and sun-protection behaviors in SOC populations. Furthermore, the unique differences of each study provided important insights into the successful design of an intervention.

An important characteristic of the Robinson et al18 study was the addition of photographs, which allowed participants not only to visualize different skin tones but also provided them with the opportunity to relate themselves to the photographs; by doing so, participants could effectively pick out the skin tone that best suited them. Written SOC scales are limited to mere descriptions and thus make it more difficult for participants to accurately identify the tone that best fits them. Kundu et al17 used photographs to teach skin self-examination and ABCDEs for detection of melanoma. Additionally, both studies used photographs to demonstrate examples of skin cancer.17,18 Recent evidence suggests the use of visuals can be efficacious for improving skin cancer knowledge and awareness; a study in 16 SOC kidney transplant recipients found that the addition of photographs of squamous cell carcinoma in various skin tones to a sun-protection educational pamphlet was more effective than the original pamphlet without photographs.21

In contrast to the Robinson et al18 study and Hernandez et al19 study, the Kundu et al17 study showed photographs of acral lentiginous melanomas in white patients rather than SOC patients. However, SOC populations may be less likely to relate to or identify skin changes in skin types that are different from their own. This technique was still beneficial, as acral lentiginous melanoma is the most common type of melanoma in SOC populations. Another benefit of the study was that it was the only study reviewed that included a follow-up postintervention questionnaire. Such data is useful, as it demonstrates how muchinformation is retained by participants and may be more likely to predict compliance with skin cancer protective behaviors.17

The Hernandez et al19 study is unique in that it was the only one to include an educational intervention entirely in Spanish, which is important to consider, as language may be a hindrance to participants’ understanding in the other studies, particularly Hispanics, possibly leading to a lack of information retention regarding sun-protective behaviors. Furthermore, it also was the only study to utilize videos as a method for interventions. The 3-minute videos demonstrated that interventions could be efficient as compared to the 2-hour in-class intervention used by Robinson et al18 and the 20-minute intervention used by Kundu et al.17 Additionally, videos also could be more cost-effective, as incentives for large focus groups would no longer be needed. Furthermore, in the Hernandez et al19 study, there was minimal to no disruption in the participants’ daily routine, as the participants were getting cosmetic services while watching the videos, perhaps allowing them to be more attentive. In contrast, both the Robinson et al18 and Kundu et al17 studies required time out from the participants’ daily schedules. In addition, these studies were notably longer than the Hernandez et al19 study. The 8-hour intervention in the Chapman et al20 study also may not be feasible for the general population because of its excessive length. However, the intervention was successful among the adolescent participants, which suggested that shorter durations are effective in the adult population and longer interventions may be more appropriate for adolescents because they benefit from peer activity.

Despite the success of the educational interventions as outlined in the 4 studies described here, a major epidemiologic flaw is that these interventions included only a small percentage of the target population. The largest total number of adults surveyed and undergoing an intervention in any of the populations was only 120.17 By failing to reach a substantial proportion of the population at risk, the number of preventable deaths likely will not decrease. The authors believe a larger-scale intervention would provide meaningful change. Australia’s SunSmart campaign to increase skin cancer awareness in the Australian population is an example of one such large-scale national intervention. The campaign focused on massive television advertisements in the summer to educate participants about the dangers of skin cancer and the importance of protective behaviors. Telephone surveys conducted from 1987 to 2011 demonstrated that more exposure to the advertisements in the SunSmart campaign meant that individuals were more likely to use sunscreen and avoid sun exposure.22 In the United States, a similar intervention would be of great benefit in educating SOC populations regarding skin cancer risk. Additionally, dermatology residents need to be adequately trained to educate patients of color about the risk for skin cancer, as survey data indicated more than 80% of Australian dermatologists desired more SOC teaching during their training and 50% indicated that they would have time to learn it during their training if offered.23 Furthermore, one study suggested that future interventions must include primary-, secondary-, and tertiary-prevention methods to effectively reduce skin cancer risk among patients of color.24 Primary prevention involves sun avoidance, secondary prevention involves detecting cancerous lesions, and tertiary prevention involves undergoing treatment of skin malignancies. However, increased knowledge does not necessarily mean increased preventative action will be employed (eg, sunscreen use, wearing sun-protective clothing and sunglasses, avoiding tanning beds and excessive sun exposure). Additional studies that demonstrate a notable increase in sun-protective behaviors related to increased knowledge are needed.

Because retention of skin cancer knowledge decreased in several postintervention surveys, there also is a dire need for continuing skin cancer education in patients of color, which may be accomplished through a combination effort of television advertisement campaigns, pamphlets, social media, community health departments, or even community members. For example, a pilot program found that Hispanic lay health workers who are educated about skin cancer may serve as a bridge between medical providers and the Hispanic community by encouraging individuals in this population to get regular skin examinations from a physician.25 Overall, there are currently gaps in the understanding and treatment of skin cancer in people of color.26 Identifying the advantages and disadvantages of all relevant skin cancer interventions conducted in the SOC population will hopefully guide future studies to help close these gaps by allowing others to design the best possible intervention. By doing so, researchers can generate an intervention that is precise, well-informed, and effective in decreasing mortality rates from skin cancer among SOC populations.

 

 

Conclusion

All of the studies reviewed demonstrated that instructional and educational interventions are promising methods for improving either knowledge, awareness, or safe skin practices and sun-protective behaviors in SOC populations to differing degrees (Table). Although each of the 4 interventions employed their own methods, they all increased 1 or more of the 3 aforementioned concepts—knowledge, awareness, or safe skin practices and sun-protective behaviors—when comparing postsurvey to presurvey data. However, the critically important message derived from this research is that there is a tremendous need for a substantial large-scale educational intervention to increase knowledge regarding skin cancer in SOC populations.

References
  1. Agbai ON, Buster K, Sanchez M, et al. Skin cancer and photoprotection in people of color: a review and recommendations for physicians and the public. J Am Acad Dermatol. 2014;70:748-762.
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914.
  3. Gloster HM Jr, Neal K. Skin cancer in skin of color. J Am Acad Dermatol. 2006;55:741-760.
  4. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  5. Byrd KM, Wilson DC, Hoyler SS, et al. Advanced presentation of melanoma in African Americans. J Am Acad Dermatol. 2004;50:21-24.
  6. Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
  7. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5, suppl 1):S26-S37.
  8. Byrd-Miles K, Toombs EL, Peck GL. Skin cancer in individuals of African, Asian, Latin-American, and American-Indian descent: differences in incidence, clinical presentation, and survival compared to Caucasians. J Drugs Dermatol. 2007;6:10-16.
  9. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708.
  10. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;5:1031-1032.
  11. Bellows CF, Belafsky P, Fortgang IS, et al. Melanoma in African-Americans: trends in biological behavior and clinical characteristics over two decades. J Surg Oncol. 2001;78:10-16.
  12. Pritchett EN, Doyle A, Shaver CM, et al. Nonmelanoma skin cancer in nonwhite organ transplant recipients. JAMA Dermatol. 2016;152:1348-1353.
  13. Shin S, Palis BE, Phillips JL, et al. Cutaneous melanoma in Asian-Americans. J Surg Oncol. 2009;99:114-118.
  14. Stubblefield J, Kelly B. Melanoma in non-caucasian populations. Surg Clin North Am. 2014;94:1115-1126.
  15. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  16. Pichon LC, Corral I, Landrine H, et al. Perceived skin cancer risk and sunscreen use among African American adults. J Health Psychol. 2010;15:1181-1189.
  17. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784.
  18. Robinson JK, Joshi KM, Ortiz S, et al. Melanoma knowledge, perception, and awareness in ethnic minorities in Chicago: recommendations regarding education. Psychooncology. 2010;20:313-320.
  19. Hernandez C, Wang S, Abraham I, et al. Evaluation of educational videos to increase skin cancer risk awareness and sun safe behaviors among adult Hispanics. J Cancer Educ. 2014;29:563-569.
  20. Chapman LW, Ochoa A, Tenconi F, et al. Dermatologic health literacy in underserved communities: a case report of south Los Angeles middle schools. Dermatol Online J. 2015;21. pii:13030/qt8671p40n.
  21. Yanina G, Gaber R, Clayman ML, et al. Sun protection education for diverse audiences: need for skin cancer pictures. J Cancer Educ. 2015;30:187-189.
  22. Dobbinson SJ, Volkov A, Wakefield MA. Continued impact of sunsmart advertising on youth and adults’ behaviors. Am J Prev Med. 2015;49:20-28.
  23. Rodrigues MA, Ross AL, Gilmore S, et al. Australian dermatologists’ perspective on skin of colour: results of a national survey [published online December 9, 2016]. Australas J Dermatol. doi:10.1111/ajd.12556.
  24. Jacobsen A, Galvan A, Lachapelle CC, et al. Defining the need for skin cancer prevention education in uninsured, minority, and immigrant communities. JAMA Dermatol. 2016;152:1342-1347.
  25. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345.
  26. Kailas A, Solomon JA, Mostow EN, et al. Gaps in the understanding and treatment of skin cancer in people of color. J Am Acad Dermatol. 2016;74:144-149.
References
  1. Agbai ON, Buster K, Sanchez M, et al. Skin cancer and photoprotection in people of color: a review and recommendations for physicians and the public. J Am Acad Dermatol. 2014;70:748-762.
  2. Cormier JN, Xing Y, Ding M, et al. Ethnic differences among patients with cutaneous melanoma. Arch Intern Med. 2006;166:1907-1914.
  3. Gloster HM Jr, Neal K. Skin cancer in skin of color. J Am Acad Dermatol. 2006;55:741-760.
  4. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  5. Byrd KM, Wilson DC, Hoyler SS, et al. Advanced presentation of melanoma in African Americans. J Am Acad Dermatol. 2004;50:21-24.
  6. Hu S, Parmet Y, Allen G, et al. Disparity in melanoma: a trend analysis of melanoma incidence and stage at diagnosis among whites, Hispanics, and blacks in Florida. Arch Dermatol. 2009;145:1369-1374.
  7. Wu XC, Eide MJ, King J, et al. Racial and ethnic variations in incidence and survival of cutaneous melanoma in the United States, 1999-2006. J Am Acad Dermatol. 2011;65(5, suppl 1):S26-S37.
  8. Byrd-Miles K, Toombs EL, Peck GL. Skin cancer in individuals of African, Asian, Latin-American, and American-Indian descent: differences in incidence, clinical presentation, and survival compared to Caucasians. J Drugs Dermatol. 2007;6:10-16.
  9. Hu S, Soza-Vento RM, Parker DF, et al. Comparison of stage at diagnosis of melanoma among Hispanic, black, and white patients in Miami-Dade County, Florida. Arch Dermatol. 2006;142:704-708.
  10. Hu S, Parker DF, Thomas AG, et al. Advanced presentation of melanoma in African Americans: the Miami-Dade County experience. J Am Acad Dermatol. 2004;5:1031-1032.
  11. Bellows CF, Belafsky P, Fortgang IS, et al. Melanoma in African-Americans: trends in biological behavior and clinical characteristics over two decades. J Surg Oncol. 2001;78:10-16.
  12. Pritchett EN, Doyle A, Shaver CM, et al. Nonmelanoma skin cancer in nonwhite organ transplant recipients. JAMA Dermatol. 2016;152:1348-1353.
  13. Shin S, Palis BE, Phillips JL, et al. Cutaneous melanoma in Asian-Americans. J Surg Oncol. 2009;99:114-118.
  14. Stubblefield J, Kelly B. Melanoma in non-caucasian populations. Surg Clin North Am. 2014;94:1115-1126.
  15. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  16. Pichon LC, Corral I, Landrine H, et al. Perceived skin cancer risk and sunscreen use among African American adults. J Health Psychol. 2010;15:1181-1189.
  17. Kundu RV, Kamaria M, Ortiz S, et al. Effectiveness of a knowledge-based intervention for melanoma among those with ethnic skin. J Am Acad Dermatol. 2010;62:777-784.
  18. Robinson JK, Joshi KM, Ortiz S, et al. Melanoma knowledge, perception, and awareness in ethnic minorities in Chicago: recommendations regarding education. Psychooncology. 2010;20:313-320.
  19. Hernandez C, Wang S, Abraham I, et al. Evaluation of educational videos to increase skin cancer risk awareness and sun safe behaviors among adult Hispanics. J Cancer Educ. 2014;29:563-569.
  20. Chapman LW, Ochoa A, Tenconi F, et al. Dermatologic health literacy in underserved communities: a case report of south Los Angeles middle schools. Dermatol Online J. 2015;21. pii:13030/qt8671p40n.
  21. Yanina G, Gaber R, Clayman ML, et al. Sun protection education for diverse audiences: need for skin cancer pictures. J Cancer Educ. 2015;30:187-189.
  22. Dobbinson SJ, Volkov A, Wakefield MA. Continued impact of sunsmart advertising on youth and adults’ behaviors. Am J Prev Med. 2015;49:20-28.
  23. Rodrigues MA, Ross AL, Gilmore S, et al. Australian dermatologists’ perspective on skin of colour: results of a national survey [published online December 9, 2016]. Australas J Dermatol. doi:10.1111/ajd.12556.
  24. Jacobsen A, Galvan A, Lachapelle CC, et al. Defining the need for skin cancer prevention education in uninsured, minority, and immigrant communities. JAMA Dermatol. 2016;152:1342-1347.
  25. Hernandez C, Kim H, Mauleon G, et al. A pilot program in collaboration with community centers to increase awareness and participation in skin cancer screening among Latinos in Chicago. J Cancer Educ. 2013;28:342-345.
  26. Kailas A, Solomon JA, Mostow EN, et al. Gaps in the understanding and treatment of skin cancer in people of color. J Am Acad Dermatol. 2016;74:144-149.
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  • Patients of color should be informed that they are at risk for skin cancer including melanoma.
  • Patients of color should be taught to identify suspicious skin lesions including the ABCDEs of melanoma.
  • Patients of color should be instructed to perform self-body skin examinations, especially of the palms and soles, for any evolving skin lesions. Patients should be instructed on the importance of visiting a physician for an evolving or suspicious mole or lesion.
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If you haven’t started reporting quality data for the Merit-based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Measure #112: Breast Cancer Screening

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If you haven’t started reporting quality data for the Merit-based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

Measure #112: Breast Cancer Screening

This measure is aimed at capturing the percentage of women 50-74 years old who had a mammogram to screen for breast cancer.

 

If you haven’t started reporting quality data for the Merit-based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

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A Severe Case of Paliperidone Palmitate-Induced Parkinsonism Leading to Prolonged Hospitalization: Opportunities for Improvement

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When administering long-acting injectable antipsychotics to patients with psychiatric illnesses, careful consideration of the risks vs benefits and use of care management thatincorporates interdisciplinary teams may prevent serious complications.

Many patients with psychiatric illness have difficulty with medication adherence. Patients with impaired reality testing especially are at risk.

Keck and McElroy evaluated 141 patients who were initially hospitalized for bipolar disorder prospectively over 1 year to assess adherence with medication. During the follow-up period, 71 patients (51%) were partially or totally nonadherent with medication as prescribed. The most commonly cited reason for nonadherence was denial of need.1

Clinicians and patients face additional challenges due to the deleterious effects of relapse in the setting of both schizophrenia and bipolar disorder. Almost all oral antipsychotic or mood stabilizer medications require a minimum dosing schedule to effectively treat these disorders, and some of these oral medications require regular laboratory monitoring. Moreover, some of the agents can have serious adverse effects (AEs), such as seizure or withdrawal, if stopped abruptly. Social support from family or friends may improve adherence, but many psychiatric outpatients have a smaller social support network than do patients without psychiatric illnesses.2

Long-acting injectable (LAI) antipsychotics have been available for the past 40 years. These medications have provided clinicians with an additional option for patients with schizophrenia or bipolar disorder who are nonadherent to their medication treatment plans or who desire an administration choice that is more convenient than daily oral pills.3-7 Some clinical practice guidelines recommend considering LAIs as a maintenance treatment for schizophrenia.5 Like the rest of the pharmacopoeia, these formulations have AEs, such as extrapyramidal symptoms (EPS), weight gain, and metabolic syndrome.1 The longer half-life of these drugs may make such effects difficult to reverse.

This article presents a case of the use of depot formulation paliperidone palmitate in an elderly patient with bipolar disorder who was previously on high-dose oral second generation antipsychotics. He developed severe parkinsonism during a protracted hospitalization that ended in death.

Case Presentation

Mr. W was a 68-year-old homeless white male with a history of coronary artery disease status-post coronary artery bypass surgery, obstructive sleep apnea, and bipolar 1 disorder who presented to a large rural VAMC emergency department (ED) as a transfer from an outside hospital (OSH). He originally presented at the OSH for vomiting and diarrhea, but while there, he was placed under involuntary psychiatric commitment. The involuntary commitment form noted him to be tangential and disorganized; he was found walking about the ED without clothes. During the initial psychiatry interview, the clinician noted a disorganized thought process. When asked about circumstances leading to admission, he stated he was “a scuba diver, pilot, actor, submarine commander.” He also reported he had given “seminars to 6,000 people,” he held a psychology degree, and he came from a family that owned part of the island of Kodiak, Alaska. Mr. W stated he had no mental health history and believed psychiatry was witchcraft. He reported having no hallucinations and stated he heard the voice of god. He also reported to have met god multiple times and to have been married to a supermodel.

Mr. W’s chart demonstrated a history of mental illness over 30 years and that he previously was prescribed psychiatric medications. He had multiple inpatient psychiatric admissions with grandiose ideations, disorganized behaviors, and hypersexuality. He had been prescribed quetiapine, divalproex, lithium, carbamazepine, and lorazepam. He was formally diagnosed in the past with bipolar 1 disorder. There also was a family history of psychiatric illness. His mother had received electroconvulsive therapy, and both parents had alcohol substance use disorder.

Mr. W had been homeless for 20 years and had several psychiatric admissions during this period. Mr. W also had chronic difficulty with obtaining food and taking medications as prescribed. Sometimes he would only be able to eat 1 to 2 meals per day. He often changed location and had lived in at least 7 different states. Currently, he was estranged from his family. About 19 years ago, his sister reported that the veteran had told her that he was Jesus Christ, per clinical records. His estranged sister’s statement was corroborated by past psychology consult records citing episodes of the patient hearing god 30 and 26 years before the current admission. His second ex-wife cited inappropriate sexual behavior in front of their children. He had difficulty in school, failed at least 2 grades, and joined the U.S. Navy in tenth grade. A Neurobehavioral Cognitive Status Examination given 19 years ago showed mild impairment on attention and severe impairment in memory.

The physical examination on presentation to the OSH was unremarkable. Mr. W did not cooperate with formal neurocognitive testing, and he consistently made errors during orientation testing. Complete blood count from a OSH ED laboratory test was remarkable for a mild pancytopenia with a leukocyte count of 3,100 cells/mcL, hemoglobin 13.1 g/dL, and hematocrit 38.4%. Red cell distribution width was within normal limits at 13.5%. Stool cultures showed normal fecal flora and no salmonella, shigella, or campylobacter. Thyroid-stimulating hormone (TSH) was slightly elevated at 5.32 U/mL. An electrocardiogram showed a QTc interval of 412 ms. A computerized tomography scan of his head showed no acute intracranial abnormality along with chronic ischemic changes in the brain (Table 1). Presumed cause of his nausea and diarrhea was viral gastroenteritis likely acquired at a homeless shelter.

Once stabilized, Mr. W was admitted to the VA hospital inpatient psychiatry unit under involuntary commitment for acute mania. Risperidone 0.25 mg orally twice a day was started for mood stabilization and psychosis along with trazodone 50 mg orally as needed for insomnia. Despite upward titration and change in frequency of the risperidone dose, Mr. W’s manic episode persisted. He remained on the psychiatric floor for 2 months (Figure). His TSH and free T4 were monitored during his stay, and levothyroxine was started. Risperidone was titrated to 8 mg/d. Mr. W’s Young Mania Rating Scale (YMRS) score decreased from 30 to 24. Mr. W had a mild improvement in irritability and speech rate but little change in elevated mood and delusional content.

He continued to endorse “speaking to god 16 times” even at the highest risperidone dose. The treatment team prescribed dissolvable risperidone tablets secondary to diversion concerns. In addition, the team added benztropine 0.5 mg once a day after observing a stooped posture and decreased arm swing. Mr. W noted risperidone made him “lethargic” and that his “body did not need” it. After 1 month of treatment with risperidone, the treatment team decided to cross taper the veteran from risperidone to a combination of olanzapine and divalproex secondary to inadequate treatment response.

The inpatient team started Mr. W on oral disintegrating tablets of olanzapine 5 mg once a day, and oral divalproex 1,000 mg once a day. An intramuscular backup of olanzapine was made available if oral medication was refused. Divalproex was titrated to 1,250 mg once a day to target a serum level of 61.7 µg/mL, and olanzapine was titrated to 10 mg once a day. After 9 days, the veteran showed moderate improvement in mania symptoms with a YMRS score < 20, indicating the absence of mania. However, the veteran made it very clear that he would stop taking the prescribed medication on discharge. The team elected to initiate a LAI.

The veteran received his first injection of the LAI psychiatric medication paliperidone palmitate 234 mg and a second 156-mg injection of the same medication 1 week later as per loading protocol. He was concurrently on daily oral divalproex 1,250 mg and olanzapine 10 mg. Mr. W continued to note he felt sedated during this period; his sedation worsened after the second injection. He also began to forget the location of his room and developed mumbled speech. His gait deteriorated to where he required a walker 6 days after injection and a wheelchair 3 days later. He became incontinent of urine and feces. Mr. W exhibited masked facies with severe drooling. This eventually progressed to difficulty swallowing. At the advice of speech pathology, he was downgraded to a pureed and nectar-thick liquid diet. He required assistance with meals.

Because of his sedation and parkinsonism symptoms, he was tapered off both olanzapine and divalproex. His last dose of olanzapine was on the date of his first injection and last dose of divalproex was 15 days after the second injection. The benztropine, which was originally given to counteract the effects of risperidone monotherapy, was discontinued over concern of anticholinergic load and sedation. The neurology consultant recommended carbidopa 25 mg and levodopa 100 mg 3 times per day for treatment of parkinsonism symptoms. Mr. W was only able to take 1 dose because of trouble swallowing. Twenty days after his second injection, a rapid response team (local clinical team 1 step below a code team) was called as Mr. W was unusually lethargic and unable to eat. He was then transferred to the medical floor.

While on the medical floor, dobhoff tube access was established for nutrition and to allow administration of carbidopa and levodopa. Mr. W could still speak at this time and was distraught. He stated, “I don’t know why god would do this to me.” Further workup was performed to look for other etiologies of the patient’s change in status. Creatinine kinase testing, lumbar puncture with cerebral spinal fluid (CSF) bacterial culture, CSF cryptococcal testing, and syphilis antigens were all negative. Magnetic resonance imaging of the brain demonstrated diffuse cerebral atrophy with widened cistern and sulci resulting in ex vacuo dilatation.

Neurology thought that the ventriculomegaly did not have features of normal pressure hydrocephalus and was secondary to chronic ischemic demyelination caused by chronic malnutrition. During follow-up visits, the veteran was less and less verbal. It progressed to where he answered questions only in grunts. Eight days after transfer to the medical floor, Mr. W was noted to have his neck locked in a laterally rotated position with clonus of the sternocleidomastoid. Due to concern about possibility of neck dystonia and the poor adherence of the patient with carbidopa and levodopa given orally, the psychiatric team made the recommendation to start benztropine 1 mg given twice a day, delivered via the dobhoff tube to treat both the parkinsonism and dystonia. The following day Mr. W failed a repeat swallow study and was no longer allowed to receive anything orally.

Mild icterus and jaundice were noted on physical examination along with transaminitis and elevated bilirubin. He developed a fever. Thirteen days after transfer to the medical floor, blood cultures revealed Klebsiella septicemia. Benztropine was discontinued at this time because of concern the medication was causing or exacerbating the fever. While being treated for Klebsiella sepsis, the psychiatry team addressed his continued hypophonia, inability to ambulate, masked facies, and neck dystonia with diphenhydramine 50 mg given intramuscular (IM) twice per day.

Mr. W developed several more iatrogenic complications near this time, including urinary tract infection septicemia and acute hypoxic respiratory failure with lung infiltrate on X-ray, requiring ventilator support. His clinical status led to a number of transfers in and out of the medical intensive care unit (MICU). During this time, his parkinsonism symptoms were managed through a combination of carbidopa and levodopa and amantadine. Cervical dystonia was managed with botulism toxin injections. Mr. W spent 6 weeks in the MICU until the decision was made to terminate life support, and he was taken off the ventilator. He died shortly thereafter. Autopsy findings suggested that Mr. W had severe Alzheimer disease.

 

 

Discussion

Following the IM injection of paliperidone palmitate, Mr. W had a complicated hospital stay resulting in his demise from sepsis and multiorgan failure. Severe immobilization, rigidity, and dystonia prevented Mr. W from conducting activities of daily living, which resulted in invasive interventions, such as continued foley catheterization. His sepsis was likely secondary to aspiration, catheterization, and eventual ventilation—all iatrogenic complications. Previous estimates in the U.S. have suggested a total of 225,000 deaths per year from iatrogenic causes.8

There are several areas of concern. Clearly, Mr. W had severe illness that greatly affected his life. He was estranged from family and had endured a 2-decade period of homelessness. He deserved effective treatment for his psychiatric illness to relieve his suffering. His long period of mental illness without effective treatment very likely biased the initial treatment team toward an aggressive approach.

Fragmented Care

The prolonged hospital stay and multiple complications directly led to fragmentation in Mr. W’s care. He was hospitalized for months on 3 different main services: psychiatry, medicine, and the MICU. Even when he remained on the same service, the primary members of his treatment team changed every few weeks. Many different specialties were consulted and reconsulted. Members of the specialty consult teams changed throughout the hospitalization as well. Given the nature of the local clinical administration, Mr. W likely received the most consistent team members from the attendings on the psychiatry consult-liaison service (who do not rotate) and from a local subspecialty delirium consult team (all members stay consistent except pharmacy residents).

Documentation of clinical reasoning behind treatment decisions was not ideal and occasionally lacking. This led to a tendency to “reinvent the wheel” with Mr. W’s treatment approach every few weeks. It was not until Mr. W had spent a significant amount of time on the medical service that an interdisciplinary treatment team meeting involving medicine, psychiatry, nursing, delirium, and neurology experts occurred. Although the interdisciplinary meeting helped by reviewing the hospital course, agreeing on a likely cause of the symptoms, and creating a treatment plan going forward, Mr. W was not able to recover.

Even when team members were stable, communication in a timely fashion did not always occur. At several points, expert recommendations were delayed by a day or more. Difficulties in treatment implementation were not communicated back to the specialty teams. The most significant example was a delay in recognition when Mr. W could no longer take oral pills secondary to the parkinsonism. Many days passed before an alternative liquid or dissolved medication was recommended on 2 separate occasions.

Subspecialty Consult

Addressing these documentation, communication, and transition challenges is neither easy nor unique to this large rural VA medical center. The authors have attempted to address this in the local system with the creation of a delirium team subspecialty consult service. Team members do not rotate and are able to follow patients throughout their hospital course. At the time of Mr. W’s hospitalization, the team included representatives from nursing, psychiatry, and occasionally pharmacy. Since then, it has expanded to include geriatrics and medicine. In addition to delirium being a marker for complex patients at risk for hospital complications, medical reasons for an extended length of stay could serve as a trigger for a referral to such a team of experts. In Mr. W’s case, that could have led to interdisciplinary consultation up to 2 months before it occurred. This may have led to a much better outcome.

Secondary parkinsonism is most notable with the typical antipychotics. The prevalence can vary between 50% and 75% and may be higher within the elderly population. However, all antipsychotics have a chance of demonstrating EPS. Risperidone has a low incidence at low doses; studies have shown dose-related parkinsonism at doses of 2 to 6 mg/d. Significant risk of parkinsonism is further exacerbated when drug-drug interactions are considered.9 Concurrently receiving 2 antipsychotics, olanzapine and paliperidone, initially caused the EPS. The veteran’s cerebral atrophy from significant malnutrition related to chronic homelessness, and the presence of Alzheimer disease only identified postmortem exacerbated this AE. Further complicating the management of the EPS, paliperidone palmitate has a long half-life of 25 to 49 days.9 Simply discontinuing the medication did not remove it from Mr. W’s system. Paliperidone would have continued to be present for months.

Conclusion

In this case, aggressive changes in the antipsychotic medications in a short period led to Mr. W effectively having 3 different agents in his system at the same time. This significantly elevated his risk of AEs, including parkinsonism. The clinician must be vigilant to further recognize the initial symptoms of parkinsonism on clinical presentation. Administration of clinical scales, such as the Simpson-Angus Extrapyramidal Side Effect, can help in these situations.10 Malnutrition and increased age can predispose patients to neurolepticAEs, so treatment teams should exercise caution when administering antipsychotics in such a population. Pharmacokinetic changes in all major organ systems from aging result in higher and more variable drug concentrations. This leads to an increased sensitivity to drugs and AEs.9

Given the increasing geriatric patient population in the U.S., treating mania in the elderly will become more common. Providers should carefully consider the risks vs benefit ratio for each individual because a serious adverse reaction may result in detrimental consequences. Even with severe symptoms leading to a bias toward an aggressive approach, it may be better to “start low and go slow.” Early inclusion of interdisciplinary expertise should be sought in complex cases.

References

1. Keck PE Jr, McElroy SL, Strakowski SM, Bourne ML, West SA. Compliance with maintenance treatment in bipolar disorder. Psychopharmacol Bull. 1997;33(1):87-91.

2. Henderson S, Duncan-Jones P, McAuley H, Ritchie K. The patient’s primary group. Br J Psychiatry. 1978;132:74-86.

3. Buoli M, Ciappolino V, Altamura AC. Paliperidone palmitate depot in the long-term treatment of psychotic bipolar disorder: a case series. Clin Neuropharmacol. 2015;38(5):209-211.

4. Chou YH, Chu PC, Wu SW, et al. A systematic review and experts’ consensus for long-acting injectable antipsychotics in bipolar disorder. Clin Psychopharmacol Neurosci. 2015;13(2):121-128.

5. Kishi T, Oya K, Iwata N. Long-acting injectable antipsychotics for prevention of relapse in bipolar disorder: a systematic review and meta-analysis of randomized controlled trials. Int J Neuropsychopharmacol. 2016;19(9):1-10.

6. Llorca PM, Abbar M, Courtet P, Guillaume S, Lancrenon S, Samalin L. Guidelines for the use and management of long-acting injectable antipsychotics in serious mental illness. BMC Psychiatry. 2013;13:340.

7. Spanarello S, La Ferla T. The pharmacokinetics of long-acting antipsychotic medications. Curr Clin Pharmacol. 2014;9(3):310-317.

8. Starfield B. Is US health really the best in the world? JAMA. 2000;284(4):483-485.

9. Labbate LA, Fava M, Rosenbaum JF, Arana GW. Handbook of Psychiatric Drug Therapy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.

10. Simpson GM, Angus JW. A rating scale for extrapyramidal side effects. Acta Psychiatr Scand Suppl. 1970;212:11-19.

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The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

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Dr. Welch and Dr. Turner are psychiatrists on the Consult Liaison Service at Gainesville VAMC in Florida. Dr. Brown and Dr. Downes are PGY-2 psychiatry residents, and Dr. Turner and Dr. Welch are adjunct clinical assistant professors at the University of Florida College of Medicine Department of Psychiatry in Gainesville.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

Author and Disclosure Information

Dr. Welch and Dr. Turner are psychiatrists on the Consult Liaison Service at Gainesville VAMC in Florida. Dr. Brown and Dr. Downes are PGY-2 psychiatry residents, and Dr. Turner and Dr. Welch are adjunct clinical assistant professors at the University of Florida College of Medicine Department of Psychiatry in Gainesville.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

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Related Articles
When administering long-acting injectable antipsychotics to patients with psychiatric illnesses, careful consideration of the risks vs benefits and use of care management thatincorporates interdisciplinary teams may prevent serious complications.
When administering long-acting injectable antipsychotics to patients with psychiatric illnesses, careful consideration of the risks vs benefits and use of care management thatincorporates interdisciplinary teams may prevent serious complications.

Many patients with psychiatric illness have difficulty with medication adherence. Patients with impaired reality testing especially are at risk.

Keck and McElroy evaluated 141 patients who were initially hospitalized for bipolar disorder prospectively over 1 year to assess adherence with medication. During the follow-up period, 71 patients (51%) were partially or totally nonadherent with medication as prescribed. The most commonly cited reason for nonadherence was denial of need.1

Clinicians and patients face additional challenges due to the deleterious effects of relapse in the setting of both schizophrenia and bipolar disorder. Almost all oral antipsychotic or mood stabilizer medications require a minimum dosing schedule to effectively treat these disorders, and some of these oral medications require regular laboratory monitoring. Moreover, some of the agents can have serious adverse effects (AEs), such as seizure or withdrawal, if stopped abruptly. Social support from family or friends may improve adherence, but many psychiatric outpatients have a smaller social support network than do patients without psychiatric illnesses.2

Long-acting injectable (LAI) antipsychotics have been available for the past 40 years. These medications have provided clinicians with an additional option for patients with schizophrenia or bipolar disorder who are nonadherent to their medication treatment plans or who desire an administration choice that is more convenient than daily oral pills.3-7 Some clinical practice guidelines recommend considering LAIs as a maintenance treatment for schizophrenia.5 Like the rest of the pharmacopoeia, these formulations have AEs, such as extrapyramidal symptoms (EPS), weight gain, and metabolic syndrome.1 The longer half-life of these drugs may make such effects difficult to reverse.

This article presents a case of the use of depot formulation paliperidone palmitate in an elderly patient with bipolar disorder who was previously on high-dose oral second generation antipsychotics. He developed severe parkinsonism during a protracted hospitalization that ended in death.

Case Presentation

Mr. W was a 68-year-old homeless white male with a history of coronary artery disease status-post coronary artery bypass surgery, obstructive sleep apnea, and bipolar 1 disorder who presented to a large rural VAMC emergency department (ED) as a transfer from an outside hospital (OSH). He originally presented at the OSH for vomiting and diarrhea, but while there, he was placed under involuntary psychiatric commitment. The involuntary commitment form noted him to be tangential and disorganized; he was found walking about the ED without clothes. During the initial psychiatry interview, the clinician noted a disorganized thought process. When asked about circumstances leading to admission, he stated he was “a scuba diver, pilot, actor, submarine commander.” He also reported he had given “seminars to 6,000 people,” he held a psychology degree, and he came from a family that owned part of the island of Kodiak, Alaska. Mr. W stated he had no mental health history and believed psychiatry was witchcraft. He reported having no hallucinations and stated he heard the voice of god. He also reported to have met god multiple times and to have been married to a supermodel.

Mr. W’s chart demonstrated a history of mental illness over 30 years and that he previously was prescribed psychiatric medications. He had multiple inpatient psychiatric admissions with grandiose ideations, disorganized behaviors, and hypersexuality. He had been prescribed quetiapine, divalproex, lithium, carbamazepine, and lorazepam. He was formally diagnosed in the past with bipolar 1 disorder. There also was a family history of psychiatric illness. His mother had received electroconvulsive therapy, and both parents had alcohol substance use disorder.

Mr. W had been homeless for 20 years and had several psychiatric admissions during this period. Mr. W also had chronic difficulty with obtaining food and taking medications as prescribed. Sometimes he would only be able to eat 1 to 2 meals per day. He often changed location and had lived in at least 7 different states. Currently, he was estranged from his family. About 19 years ago, his sister reported that the veteran had told her that he was Jesus Christ, per clinical records. His estranged sister’s statement was corroborated by past psychology consult records citing episodes of the patient hearing god 30 and 26 years before the current admission. His second ex-wife cited inappropriate sexual behavior in front of their children. He had difficulty in school, failed at least 2 grades, and joined the U.S. Navy in tenth grade. A Neurobehavioral Cognitive Status Examination given 19 years ago showed mild impairment on attention and severe impairment in memory.

The physical examination on presentation to the OSH was unremarkable. Mr. W did not cooperate with formal neurocognitive testing, and he consistently made errors during orientation testing. Complete blood count from a OSH ED laboratory test was remarkable for a mild pancytopenia with a leukocyte count of 3,100 cells/mcL, hemoglobin 13.1 g/dL, and hematocrit 38.4%. Red cell distribution width was within normal limits at 13.5%. Stool cultures showed normal fecal flora and no salmonella, shigella, or campylobacter. Thyroid-stimulating hormone (TSH) was slightly elevated at 5.32 U/mL. An electrocardiogram showed a QTc interval of 412 ms. A computerized tomography scan of his head showed no acute intracranial abnormality along with chronic ischemic changes in the brain (Table 1). Presumed cause of his nausea and diarrhea was viral gastroenteritis likely acquired at a homeless shelter.

Once stabilized, Mr. W was admitted to the VA hospital inpatient psychiatry unit under involuntary commitment for acute mania. Risperidone 0.25 mg orally twice a day was started for mood stabilization and psychosis along with trazodone 50 mg orally as needed for insomnia. Despite upward titration and change in frequency of the risperidone dose, Mr. W’s manic episode persisted. He remained on the psychiatric floor for 2 months (Figure). His TSH and free T4 were monitored during his stay, and levothyroxine was started. Risperidone was titrated to 8 mg/d. Mr. W’s Young Mania Rating Scale (YMRS) score decreased from 30 to 24. Mr. W had a mild improvement in irritability and speech rate but little change in elevated mood and delusional content.

He continued to endorse “speaking to god 16 times” even at the highest risperidone dose. The treatment team prescribed dissolvable risperidone tablets secondary to diversion concerns. In addition, the team added benztropine 0.5 mg once a day after observing a stooped posture and decreased arm swing. Mr. W noted risperidone made him “lethargic” and that his “body did not need” it. After 1 month of treatment with risperidone, the treatment team decided to cross taper the veteran from risperidone to a combination of olanzapine and divalproex secondary to inadequate treatment response.

The inpatient team started Mr. W on oral disintegrating tablets of olanzapine 5 mg once a day, and oral divalproex 1,000 mg once a day. An intramuscular backup of olanzapine was made available if oral medication was refused. Divalproex was titrated to 1,250 mg once a day to target a serum level of 61.7 µg/mL, and olanzapine was titrated to 10 mg once a day. After 9 days, the veteran showed moderate improvement in mania symptoms with a YMRS score < 20, indicating the absence of mania. However, the veteran made it very clear that he would stop taking the prescribed medication on discharge. The team elected to initiate a LAI.

The veteran received his first injection of the LAI psychiatric medication paliperidone palmitate 234 mg and a second 156-mg injection of the same medication 1 week later as per loading protocol. He was concurrently on daily oral divalproex 1,250 mg and olanzapine 10 mg. Mr. W continued to note he felt sedated during this period; his sedation worsened after the second injection. He also began to forget the location of his room and developed mumbled speech. His gait deteriorated to where he required a walker 6 days after injection and a wheelchair 3 days later. He became incontinent of urine and feces. Mr. W exhibited masked facies with severe drooling. This eventually progressed to difficulty swallowing. At the advice of speech pathology, he was downgraded to a pureed and nectar-thick liquid diet. He required assistance with meals.

Because of his sedation and parkinsonism symptoms, he was tapered off both olanzapine and divalproex. His last dose of olanzapine was on the date of his first injection and last dose of divalproex was 15 days after the second injection. The benztropine, which was originally given to counteract the effects of risperidone monotherapy, was discontinued over concern of anticholinergic load and sedation. The neurology consultant recommended carbidopa 25 mg and levodopa 100 mg 3 times per day for treatment of parkinsonism symptoms. Mr. W was only able to take 1 dose because of trouble swallowing. Twenty days after his second injection, a rapid response team (local clinical team 1 step below a code team) was called as Mr. W was unusually lethargic and unable to eat. He was then transferred to the medical floor.

While on the medical floor, dobhoff tube access was established for nutrition and to allow administration of carbidopa and levodopa. Mr. W could still speak at this time and was distraught. He stated, “I don’t know why god would do this to me.” Further workup was performed to look for other etiologies of the patient’s change in status. Creatinine kinase testing, lumbar puncture with cerebral spinal fluid (CSF) bacterial culture, CSF cryptococcal testing, and syphilis antigens were all negative. Magnetic resonance imaging of the brain demonstrated diffuse cerebral atrophy with widened cistern and sulci resulting in ex vacuo dilatation.

Neurology thought that the ventriculomegaly did not have features of normal pressure hydrocephalus and was secondary to chronic ischemic demyelination caused by chronic malnutrition. During follow-up visits, the veteran was less and less verbal. It progressed to where he answered questions only in grunts. Eight days after transfer to the medical floor, Mr. W was noted to have his neck locked in a laterally rotated position with clonus of the sternocleidomastoid. Due to concern about possibility of neck dystonia and the poor adherence of the patient with carbidopa and levodopa given orally, the psychiatric team made the recommendation to start benztropine 1 mg given twice a day, delivered via the dobhoff tube to treat both the parkinsonism and dystonia. The following day Mr. W failed a repeat swallow study and was no longer allowed to receive anything orally.

Mild icterus and jaundice were noted on physical examination along with transaminitis and elevated bilirubin. He developed a fever. Thirteen days after transfer to the medical floor, blood cultures revealed Klebsiella septicemia. Benztropine was discontinued at this time because of concern the medication was causing or exacerbating the fever. While being treated for Klebsiella sepsis, the psychiatry team addressed his continued hypophonia, inability to ambulate, masked facies, and neck dystonia with diphenhydramine 50 mg given intramuscular (IM) twice per day.

Mr. W developed several more iatrogenic complications near this time, including urinary tract infection septicemia and acute hypoxic respiratory failure with lung infiltrate on X-ray, requiring ventilator support. His clinical status led to a number of transfers in and out of the medical intensive care unit (MICU). During this time, his parkinsonism symptoms were managed through a combination of carbidopa and levodopa and amantadine. Cervical dystonia was managed with botulism toxin injections. Mr. W spent 6 weeks in the MICU until the decision was made to terminate life support, and he was taken off the ventilator. He died shortly thereafter. Autopsy findings suggested that Mr. W had severe Alzheimer disease.

 

 

Discussion

Following the IM injection of paliperidone palmitate, Mr. W had a complicated hospital stay resulting in his demise from sepsis and multiorgan failure. Severe immobilization, rigidity, and dystonia prevented Mr. W from conducting activities of daily living, which resulted in invasive interventions, such as continued foley catheterization. His sepsis was likely secondary to aspiration, catheterization, and eventual ventilation—all iatrogenic complications. Previous estimates in the U.S. have suggested a total of 225,000 deaths per year from iatrogenic causes.8

There are several areas of concern. Clearly, Mr. W had severe illness that greatly affected his life. He was estranged from family and had endured a 2-decade period of homelessness. He deserved effective treatment for his psychiatric illness to relieve his suffering. His long period of mental illness without effective treatment very likely biased the initial treatment team toward an aggressive approach.

Fragmented Care

The prolonged hospital stay and multiple complications directly led to fragmentation in Mr. W’s care. He was hospitalized for months on 3 different main services: psychiatry, medicine, and the MICU. Even when he remained on the same service, the primary members of his treatment team changed every few weeks. Many different specialties were consulted and reconsulted. Members of the specialty consult teams changed throughout the hospitalization as well. Given the nature of the local clinical administration, Mr. W likely received the most consistent team members from the attendings on the psychiatry consult-liaison service (who do not rotate) and from a local subspecialty delirium consult team (all members stay consistent except pharmacy residents).

Documentation of clinical reasoning behind treatment decisions was not ideal and occasionally lacking. This led to a tendency to “reinvent the wheel” with Mr. W’s treatment approach every few weeks. It was not until Mr. W had spent a significant amount of time on the medical service that an interdisciplinary treatment team meeting involving medicine, psychiatry, nursing, delirium, and neurology experts occurred. Although the interdisciplinary meeting helped by reviewing the hospital course, agreeing on a likely cause of the symptoms, and creating a treatment plan going forward, Mr. W was not able to recover.

Even when team members were stable, communication in a timely fashion did not always occur. At several points, expert recommendations were delayed by a day or more. Difficulties in treatment implementation were not communicated back to the specialty teams. The most significant example was a delay in recognition when Mr. W could no longer take oral pills secondary to the parkinsonism. Many days passed before an alternative liquid or dissolved medication was recommended on 2 separate occasions.

Subspecialty Consult

Addressing these documentation, communication, and transition challenges is neither easy nor unique to this large rural VA medical center. The authors have attempted to address this in the local system with the creation of a delirium team subspecialty consult service. Team members do not rotate and are able to follow patients throughout their hospital course. At the time of Mr. W’s hospitalization, the team included representatives from nursing, psychiatry, and occasionally pharmacy. Since then, it has expanded to include geriatrics and medicine. In addition to delirium being a marker for complex patients at risk for hospital complications, medical reasons for an extended length of stay could serve as a trigger for a referral to such a team of experts. In Mr. W’s case, that could have led to interdisciplinary consultation up to 2 months before it occurred. This may have led to a much better outcome.

Secondary parkinsonism is most notable with the typical antipychotics. The prevalence can vary between 50% and 75% and may be higher within the elderly population. However, all antipsychotics have a chance of demonstrating EPS. Risperidone has a low incidence at low doses; studies have shown dose-related parkinsonism at doses of 2 to 6 mg/d. Significant risk of parkinsonism is further exacerbated when drug-drug interactions are considered.9 Concurrently receiving 2 antipsychotics, olanzapine and paliperidone, initially caused the EPS. The veteran’s cerebral atrophy from significant malnutrition related to chronic homelessness, and the presence of Alzheimer disease only identified postmortem exacerbated this AE. Further complicating the management of the EPS, paliperidone palmitate has a long half-life of 25 to 49 days.9 Simply discontinuing the medication did not remove it from Mr. W’s system. Paliperidone would have continued to be present for months.

Conclusion

In this case, aggressive changes in the antipsychotic medications in a short period led to Mr. W effectively having 3 different agents in his system at the same time. This significantly elevated his risk of AEs, including parkinsonism. The clinician must be vigilant to further recognize the initial symptoms of parkinsonism on clinical presentation. Administration of clinical scales, such as the Simpson-Angus Extrapyramidal Side Effect, can help in these situations.10 Malnutrition and increased age can predispose patients to neurolepticAEs, so treatment teams should exercise caution when administering antipsychotics in such a population. Pharmacokinetic changes in all major organ systems from aging result in higher and more variable drug concentrations. This leads to an increased sensitivity to drugs and AEs.9

Given the increasing geriatric patient population in the U.S., treating mania in the elderly will become more common. Providers should carefully consider the risks vs benefit ratio for each individual because a serious adverse reaction may result in detrimental consequences. Even with severe symptoms leading to a bias toward an aggressive approach, it may be better to “start low and go slow.” Early inclusion of interdisciplinary expertise should be sought in complex cases.

Many patients with psychiatric illness have difficulty with medication adherence. Patients with impaired reality testing especially are at risk.

Keck and McElroy evaluated 141 patients who were initially hospitalized for bipolar disorder prospectively over 1 year to assess adherence with medication. During the follow-up period, 71 patients (51%) were partially or totally nonadherent with medication as prescribed. The most commonly cited reason for nonadherence was denial of need.1

Clinicians and patients face additional challenges due to the deleterious effects of relapse in the setting of both schizophrenia and bipolar disorder. Almost all oral antipsychotic or mood stabilizer medications require a minimum dosing schedule to effectively treat these disorders, and some of these oral medications require regular laboratory monitoring. Moreover, some of the agents can have serious adverse effects (AEs), such as seizure or withdrawal, if stopped abruptly. Social support from family or friends may improve adherence, but many psychiatric outpatients have a smaller social support network than do patients without psychiatric illnesses.2

Long-acting injectable (LAI) antipsychotics have been available for the past 40 years. These medications have provided clinicians with an additional option for patients with schizophrenia or bipolar disorder who are nonadherent to their medication treatment plans or who desire an administration choice that is more convenient than daily oral pills.3-7 Some clinical practice guidelines recommend considering LAIs as a maintenance treatment for schizophrenia.5 Like the rest of the pharmacopoeia, these formulations have AEs, such as extrapyramidal symptoms (EPS), weight gain, and metabolic syndrome.1 The longer half-life of these drugs may make such effects difficult to reverse.

This article presents a case of the use of depot formulation paliperidone palmitate in an elderly patient with bipolar disorder who was previously on high-dose oral second generation antipsychotics. He developed severe parkinsonism during a protracted hospitalization that ended in death.

Case Presentation

Mr. W was a 68-year-old homeless white male with a history of coronary artery disease status-post coronary artery bypass surgery, obstructive sleep apnea, and bipolar 1 disorder who presented to a large rural VAMC emergency department (ED) as a transfer from an outside hospital (OSH). He originally presented at the OSH for vomiting and diarrhea, but while there, he was placed under involuntary psychiatric commitment. The involuntary commitment form noted him to be tangential and disorganized; he was found walking about the ED without clothes. During the initial psychiatry interview, the clinician noted a disorganized thought process. When asked about circumstances leading to admission, he stated he was “a scuba diver, pilot, actor, submarine commander.” He also reported he had given “seminars to 6,000 people,” he held a psychology degree, and he came from a family that owned part of the island of Kodiak, Alaska. Mr. W stated he had no mental health history and believed psychiatry was witchcraft. He reported having no hallucinations and stated he heard the voice of god. He also reported to have met god multiple times and to have been married to a supermodel.

Mr. W’s chart demonstrated a history of mental illness over 30 years and that he previously was prescribed psychiatric medications. He had multiple inpatient psychiatric admissions with grandiose ideations, disorganized behaviors, and hypersexuality. He had been prescribed quetiapine, divalproex, lithium, carbamazepine, and lorazepam. He was formally diagnosed in the past with bipolar 1 disorder. There also was a family history of psychiatric illness. His mother had received electroconvulsive therapy, and both parents had alcohol substance use disorder.

Mr. W had been homeless for 20 years and had several psychiatric admissions during this period. Mr. W also had chronic difficulty with obtaining food and taking medications as prescribed. Sometimes he would only be able to eat 1 to 2 meals per day. He often changed location and had lived in at least 7 different states. Currently, he was estranged from his family. About 19 years ago, his sister reported that the veteran had told her that he was Jesus Christ, per clinical records. His estranged sister’s statement was corroborated by past psychology consult records citing episodes of the patient hearing god 30 and 26 years before the current admission. His second ex-wife cited inappropriate sexual behavior in front of their children. He had difficulty in school, failed at least 2 grades, and joined the U.S. Navy in tenth grade. A Neurobehavioral Cognitive Status Examination given 19 years ago showed mild impairment on attention and severe impairment in memory.

The physical examination on presentation to the OSH was unremarkable. Mr. W did not cooperate with formal neurocognitive testing, and he consistently made errors during orientation testing. Complete blood count from a OSH ED laboratory test was remarkable for a mild pancytopenia with a leukocyte count of 3,100 cells/mcL, hemoglobin 13.1 g/dL, and hematocrit 38.4%. Red cell distribution width was within normal limits at 13.5%. Stool cultures showed normal fecal flora and no salmonella, shigella, or campylobacter. Thyroid-stimulating hormone (TSH) was slightly elevated at 5.32 U/mL. An electrocardiogram showed a QTc interval of 412 ms. A computerized tomography scan of his head showed no acute intracranial abnormality along with chronic ischemic changes in the brain (Table 1). Presumed cause of his nausea and diarrhea was viral gastroenteritis likely acquired at a homeless shelter.

Once stabilized, Mr. W was admitted to the VA hospital inpatient psychiatry unit under involuntary commitment for acute mania. Risperidone 0.25 mg orally twice a day was started for mood stabilization and psychosis along with trazodone 50 mg orally as needed for insomnia. Despite upward titration and change in frequency of the risperidone dose, Mr. W’s manic episode persisted. He remained on the psychiatric floor for 2 months (Figure). His TSH and free T4 were monitored during his stay, and levothyroxine was started. Risperidone was titrated to 8 mg/d. Mr. W’s Young Mania Rating Scale (YMRS) score decreased from 30 to 24. Mr. W had a mild improvement in irritability and speech rate but little change in elevated mood and delusional content.

He continued to endorse “speaking to god 16 times” even at the highest risperidone dose. The treatment team prescribed dissolvable risperidone tablets secondary to diversion concerns. In addition, the team added benztropine 0.5 mg once a day after observing a stooped posture and decreased arm swing. Mr. W noted risperidone made him “lethargic” and that his “body did not need” it. After 1 month of treatment with risperidone, the treatment team decided to cross taper the veteran from risperidone to a combination of olanzapine and divalproex secondary to inadequate treatment response.

The inpatient team started Mr. W on oral disintegrating tablets of olanzapine 5 mg once a day, and oral divalproex 1,000 mg once a day. An intramuscular backup of olanzapine was made available if oral medication was refused. Divalproex was titrated to 1,250 mg once a day to target a serum level of 61.7 µg/mL, and olanzapine was titrated to 10 mg once a day. After 9 days, the veteran showed moderate improvement in mania symptoms with a YMRS score < 20, indicating the absence of mania. However, the veteran made it very clear that he would stop taking the prescribed medication on discharge. The team elected to initiate a LAI.

The veteran received his first injection of the LAI psychiatric medication paliperidone palmitate 234 mg and a second 156-mg injection of the same medication 1 week later as per loading protocol. He was concurrently on daily oral divalproex 1,250 mg and olanzapine 10 mg. Mr. W continued to note he felt sedated during this period; his sedation worsened after the second injection. He also began to forget the location of his room and developed mumbled speech. His gait deteriorated to where he required a walker 6 days after injection and a wheelchair 3 days later. He became incontinent of urine and feces. Mr. W exhibited masked facies with severe drooling. This eventually progressed to difficulty swallowing. At the advice of speech pathology, he was downgraded to a pureed and nectar-thick liquid diet. He required assistance with meals.

Because of his sedation and parkinsonism symptoms, he was tapered off both olanzapine and divalproex. His last dose of olanzapine was on the date of his first injection and last dose of divalproex was 15 days after the second injection. The benztropine, which was originally given to counteract the effects of risperidone monotherapy, was discontinued over concern of anticholinergic load and sedation. The neurology consultant recommended carbidopa 25 mg and levodopa 100 mg 3 times per day for treatment of parkinsonism symptoms. Mr. W was only able to take 1 dose because of trouble swallowing. Twenty days after his second injection, a rapid response team (local clinical team 1 step below a code team) was called as Mr. W was unusually lethargic and unable to eat. He was then transferred to the medical floor.

While on the medical floor, dobhoff tube access was established for nutrition and to allow administration of carbidopa and levodopa. Mr. W could still speak at this time and was distraught. He stated, “I don’t know why god would do this to me.” Further workup was performed to look for other etiologies of the patient’s change in status. Creatinine kinase testing, lumbar puncture with cerebral spinal fluid (CSF) bacterial culture, CSF cryptococcal testing, and syphilis antigens were all negative. Magnetic resonance imaging of the brain demonstrated diffuse cerebral atrophy with widened cistern and sulci resulting in ex vacuo dilatation.

Neurology thought that the ventriculomegaly did not have features of normal pressure hydrocephalus and was secondary to chronic ischemic demyelination caused by chronic malnutrition. During follow-up visits, the veteran was less and less verbal. It progressed to where he answered questions only in grunts. Eight days after transfer to the medical floor, Mr. W was noted to have his neck locked in a laterally rotated position with clonus of the sternocleidomastoid. Due to concern about possibility of neck dystonia and the poor adherence of the patient with carbidopa and levodopa given orally, the psychiatric team made the recommendation to start benztropine 1 mg given twice a day, delivered via the dobhoff tube to treat both the parkinsonism and dystonia. The following day Mr. W failed a repeat swallow study and was no longer allowed to receive anything orally.

Mild icterus and jaundice were noted on physical examination along with transaminitis and elevated bilirubin. He developed a fever. Thirteen days after transfer to the medical floor, blood cultures revealed Klebsiella septicemia. Benztropine was discontinued at this time because of concern the medication was causing or exacerbating the fever. While being treated for Klebsiella sepsis, the psychiatry team addressed his continued hypophonia, inability to ambulate, masked facies, and neck dystonia with diphenhydramine 50 mg given intramuscular (IM) twice per day.

Mr. W developed several more iatrogenic complications near this time, including urinary tract infection septicemia and acute hypoxic respiratory failure with lung infiltrate on X-ray, requiring ventilator support. His clinical status led to a number of transfers in and out of the medical intensive care unit (MICU). During this time, his parkinsonism symptoms were managed through a combination of carbidopa and levodopa and amantadine. Cervical dystonia was managed with botulism toxin injections. Mr. W spent 6 weeks in the MICU until the decision was made to terminate life support, and he was taken off the ventilator. He died shortly thereafter. Autopsy findings suggested that Mr. W had severe Alzheimer disease.

 

 

Discussion

Following the IM injection of paliperidone palmitate, Mr. W had a complicated hospital stay resulting in his demise from sepsis and multiorgan failure. Severe immobilization, rigidity, and dystonia prevented Mr. W from conducting activities of daily living, which resulted in invasive interventions, such as continued foley catheterization. His sepsis was likely secondary to aspiration, catheterization, and eventual ventilation—all iatrogenic complications. Previous estimates in the U.S. have suggested a total of 225,000 deaths per year from iatrogenic causes.8

There are several areas of concern. Clearly, Mr. W had severe illness that greatly affected his life. He was estranged from family and had endured a 2-decade period of homelessness. He deserved effective treatment for his psychiatric illness to relieve his suffering. His long period of mental illness without effective treatment very likely biased the initial treatment team toward an aggressive approach.

Fragmented Care

The prolonged hospital stay and multiple complications directly led to fragmentation in Mr. W’s care. He was hospitalized for months on 3 different main services: psychiatry, medicine, and the MICU. Even when he remained on the same service, the primary members of his treatment team changed every few weeks. Many different specialties were consulted and reconsulted. Members of the specialty consult teams changed throughout the hospitalization as well. Given the nature of the local clinical administration, Mr. W likely received the most consistent team members from the attendings on the psychiatry consult-liaison service (who do not rotate) and from a local subspecialty delirium consult team (all members stay consistent except pharmacy residents).

Documentation of clinical reasoning behind treatment decisions was not ideal and occasionally lacking. This led to a tendency to “reinvent the wheel” with Mr. W’s treatment approach every few weeks. It was not until Mr. W had spent a significant amount of time on the medical service that an interdisciplinary treatment team meeting involving medicine, psychiatry, nursing, delirium, and neurology experts occurred. Although the interdisciplinary meeting helped by reviewing the hospital course, agreeing on a likely cause of the symptoms, and creating a treatment plan going forward, Mr. W was not able to recover.

Even when team members were stable, communication in a timely fashion did not always occur. At several points, expert recommendations were delayed by a day or more. Difficulties in treatment implementation were not communicated back to the specialty teams. The most significant example was a delay in recognition when Mr. W could no longer take oral pills secondary to the parkinsonism. Many days passed before an alternative liquid or dissolved medication was recommended on 2 separate occasions.

Subspecialty Consult

Addressing these documentation, communication, and transition challenges is neither easy nor unique to this large rural VA medical center. The authors have attempted to address this in the local system with the creation of a delirium team subspecialty consult service. Team members do not rotate and are able to follow patients throughout their hospital course. At the time of Mr. W’s hospitalization, the team included representatives from nursing, psychiatry, and occasionally pharmacy. Since then, it has expanded to include geriatrics and medicine. In addition to delirium being a marker for complex patients at risk for hospital complications, medical reasons for an extended length of stay could serve as a trigger for a referral to such a team of experts. In Mr. W’s case, that could have led to interdisciplinary consultation up to 2 months before it occurred. This may have led to a much better outcome.

Secondary parkinsonism is most notable with the typical antipychotics. The prevalence can vary between 50% and 75% and may be higher within the elderly population. However, all antipsychotics have a chance of demonstrating EPS. Risperidone has a low incidence at low doses; studies have shown dose-related parkinsonism at doses of 2 to 6 mg/d. Significant risk of parkinsonism is further exacerbated when drug-drug interactions are considered.9 Concurrently receiving 2 antipsychotics, olanzapine and paliperidone, initially caused the EPS. The veteran’s cerebral atrophy from significant malnutrition related to chronic homelessness, and the presence of Alzheimer disease only identified postmortem exacerbated this AE. Further complicating the management of the EPS, paliperidone palmitate has a long half-life of 25 to 49 days.9 Simply discontinuing the medication did not remove it from Mr. W’s system. Paliperidone would have continued to be present for months.

Conclusion

In this case, aggressive changes in the antipsychotic medications in a short period led to Mr. W effectively having 3 different agents in his system at the same time. This significantly elevated his risk of AEs, including parkinsonism. The clinician must be vigilant to further recognize the initial symptoms of parkinsonism on clinical presentation. Administration of clinical scales, such as the Simpson-Angus Extrapyramidal Side Effect, can help in these situations.10 Malnutrition and increased age can predispose patients to neurolepticAEs, so treatment teams should exercise caution when administering antipsychotics in such a population. Pharmacokinetic changes in all major organ systems from aging result in higher and more variable drug concentrations. This leads to an increased sensitivity to drugs and AEs.9

Given the increasing geriatric patient population in the U.S., treating mania in the elderly will become more common. Providers should carefully consider the risks vs benefit ratio for each individual because a serious adverse reaction may result in detrimental consequences. Even with severe symptoms leading to a bias toward an aggressive approach, it may be better to “start low and go slow.” Early inclusion of interdisciplinary expertise should be sought in complex cases.

References

1. Keck PE Jr, McElroy SL, Strakowski SM, Bourne ML, West SA. Compliance with maintenance treatment in bipolar disorder. Psychopharmacol Bull. 1997;33(1):87-91.

2. Henderson S, Duncan-Jones P, McAuley H, Ritchie K. The patient’s primary group. Br J Psychiatry. 1978;132:74-86.

3. Buoli M, Ciappolino V, Altamura AC. Paliperidone palmitate depot in the long-term treatment of psychotic bipolar disorder: a case series. Clin Neuropharmacol. 2015;38(5):209-211.

4. Chou YH, Chu PC, Wu SW, et al. A systematic review and experts’ consensus for long-acting injectable antipsychotics in bipolar disorder. Clin Psychopharmacol Neurosci. 2015;13(2):121-128.

5. Kishi T, Oya K, Iwata N. Long-acting injectable antipsychotics for prevention of relapse in bipolar disorder: a systematic review and meta-analysis of randomized controlled trials. Int J Neuropsychopharmacol. 2016;19(9):1-10.

6. Llorca PM, Abbar M, Courtet P, Guillaume S, Lancrenon S, Samalin L. Guidelines for the use and management of long-acting injectable antipsychotics in serious mental illness. BMC Psychiatry. 2013;13:340.

7. Spanarello S, La Ferla T. The pharmacokinetics of long-acting antipsychotic medications. Curr Clin Pharmacol. 2014;9(3):310-317.

8. Starfield B. Is US health really the best in the world? JAMA. 2000;284(4):483-485.

9. Labbate LA, Fava M, Rosenbaum JF, Arana GW. Handbook of Psychiatric Drug Therapy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.

10. Simpson GM, Angus JW. A rating scale for extrapyramidal side effects. Acta Psychiatr Scand Suppl. 1970;212:11-19.

References

1. Keck PE Jr, McElroy SL, Strakowski SM, Bourne ML, West SA. Compliance with maintenance treatment in bipolar disorder. Psychopharmacol Bull. 1997;33(1):87-91.

2. Henderson S, Duncan-Jones P, McAuley H, Ritchie K. The patient’s primary group. Br J Psychiatry. 1978;132:74-86.

3. Buoli M, Ciappolino V, Altamura AC. Paliperidone palmitate depot in the long-term treatment of psychotic bipolar disorder: a case series. Clin Neuropharmacol. 2015;38(5):209-211.

4. Chou YH, Chu PC, Wu SW, et al. A systematic review and experts’ consensus for long-acting injectable antipsychotics in bipolar disorder. Clin Psychopharmacol Neurosci. 2015;13(2):121-128.

5. Kishi T, Oya K, Iwata N. Long-acting injectable antipsychotics for prevention of relapse in bipolar disorder: a systematic review and meta-analysis of randomized controlled trials. Int J Neuropsychopharmacol. 2016;19(9):1-10.

6. Llorca PM, Abbar M, Courtet P, Guillaume S, Lancrenon S, Samalin L. Guidelines for the use and management of long-acting injectable antipsychotics in serious mental illness. BMC Psychiatry. 2013;13:340.

7. Spanarello S, La Ferla T. The pharmacokinetics of long-acting antipsychotic medications. Curr Clin Pharmacol. 2014;9(3):310-317.

8. Starfield B. Is US health really the best in the world? JAMA. 2000;284(4):483-485.

9. Labbate LA, Fava M, Rosenbaum JF, Arana GW. Handbook of Psychiatric Drug Therapy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.

10. Simpson GM, Angus JW. A rating scale for extrapyramidal side effects. Acta Psychiatr Scand Suppl. 1970;212:11-19.

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Primary care may be inadequate for cancer survivors

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Primary care may be inadequate for cancer survivors

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Doctor and patient

Primary care may not meet the healthcare needs of cancer survivors in the US, according to research published in JAMA Internal Medicine.

Researchers examined 12 advanced primary care practices selected from a national registry of “workforce innovators” and found that none of these practices had a comprehensive survivorship care program in place.

In addition, there were 3 main barriers to survivorship care—not treating cancer survivors as a distinct population, limitations of electronic health records, and a lack of information and guidance for clinicians.

“This is troubling because these are highly innovative practices that have a national reputation,” said study author Benjamin Crabtree, PhD, of Rutgers Robert Wood Johnson Medical School in New Brunswick, New Jersey.

Dr Crabtree and his colleagues evaluated survivorship care* at the 12 practices, which were based in Colorado, Illinois, Maine, New York, Pennsylvania, and Washington.

Over nearly 2 years, the team spent 10 to 12 days observing each of the practices and interviewing clinicians and administrators.

In this way, the researchers identified 3 main barriers to integrating survivorship care into primary medicine.

Barrier 1

The first barrier was that clinicians did not treat cancer survivors as a distinct population or clinical category.

“There is no diagnosis code for ‘cancer survivor’ that can be entered into the medical record, which is important if you want physicians to pay attention,” Dr Crabtree said.

Some of the clinicians interviewed said their care was comprehensive enough to address the needs of all patients. Other clinicians did not understand what survivorship care entails.

Barrier 2

The second barrier was that electronic health record systems didn’t support survivorship care.

Clinicians reported an inability to identify patients with a history of cancer. Even if a patient’s cancer history was included in his or her record, it might take searching through multiple screens to find the information.

In addition, medical records were sometimes lost as patients changed clinicians over the years, which left it up to patients to report their cancer histories.

Barrier 3

The third barrier was that clinicians did not receive adequate information or guidance for follow-up care of cancer survivors.

Although some of the practices received cancer-related information about their patients, it was considered “inadequate” or “not actionable.”

Clinicians expressed concerns about their knowledge gaps in cancer care and the need to monitor changing information in oncology.

“There is nothing in the residency curriculum about cancer survivorship,” Dr Crabtree said. “There is also nothing in Continuing Medical Education courses. It’s just not there.”

Dr Crabtree and his colleagues believe these barriers must be addressed so that comprehensive cancer survivorship services can move to the forefront of primary care.

* Survivorship care includes checking for cancer recurrence, monitoring long-term effects of radiation and chemotherapy, and assessing a patient’s psychological well-being.

Publications
Topics

Photo courtesy of NIH
Doctor and patient

Primary care may not meet the healthcare needs of cancer survivors in the US, according to research published in JAMA Internal Medicine.

Researchers examined 12 advanced primary care practices selected from a national registry of “workforce innovators” and found that none of these practices had a comprehensive survivorship care program in place.

In addition, there were 3 main barriers to survivorship care—not treating cancer survivors as a distinct population, limitations of electronic health records, and a lack of information and guidance for clinicians.

“This is troubling because these are highly innovative practices that have a national reputation,” said study author Benjamin Crabtree, PhD, of Rutgers Robert Wood Johnson Medical School in New Brunswick, New Jersey.

Dr Crabtree and his colleagues evaluated survivorship care* at the 12 practices, which were based in Colorado, Illinois, Maine, New York, Pennsylvania, and Washington.

Over nearly 2 years, the team spent 10 to 12 days observing each of the practices and interviewing clinicians and administrators.

In this way, the researchers identified 3 main barriers to integrating survivorship care into primary medicine.

Barrier 1

The first barrier was that clinicians did not treat cancer survivors as a distinct population or clinical category.

“There is no diagnosis code for ‘cancer survivor’ that can be entered into the medical record, which is important if you want physicians to pay attention,” Dr Crabtree said.

Some of the clinicians interviewed said their care was comprehensive enough to address the needs of all patients. Other clinicians did not understand what survivorship care entails.

Barrier 2

The second barrier was that electronic health record systems didn’t support survivorship care.

Clinicians reported an inability to identify patients with a history of cancer. Even if a patient’s cancer history was included in his or her record, it might take searching through multiple screens to find the information.

In addition, medical records were sometimes lost as patients changed clinicians over the years, which left it up to patients to report their cancer histories.

Barrier 3

The third barrier was that clinicians did not receive adequate information or guidance for follow-up care of cancer survivors.

Although some of the practices received cancer-related information about their patients, it was considered “inadequate” or “not actionable.”

Clinicians expressed concerns about their knowledge gaps in cancer care and the need to monitor changing information in oncology.

“There is nothing in the residency curriculum about cancer survivorship,” Dr Crabtree said. “There is also nothing in Continuing Medical Education courses. It’s just not there.”

Dr Crabtree and his colleagues believe these barriers must be addressed so that comprehensive cancer survivorship services can move to the forefront of primary care.

* Survivorship care includes checking for cancer recurrence, monitoring long-term effects of radiation and chemotherapy, and assessing a patient’s psychological well-being.

Photo courtesy of NIH
Doctor and patient

Primary care may not meet the healthcare needs of cancer survivors in the US, according to research published in JAMA Internal Medicine.

Researchers examined 12 advanced primary care practices selected from a national registry of “workforce innovators” and found that none of these practices had a comprehensive survivorship care program in place.

In addition, there were 3 main barriers to survivorship care—not treating cancer survivors as a distinct population, limitations of electronic health records, and a lack of information and guidance for clinicians.

“This is troubling because these are highly innovative practices that have a national reputation,” said study author Benjamin Crabtree, PhD, of Rutgers Robert Wood Johnson Medical School in New Brunswick, New Jersey.

Dr Crabtree and his colleagues evaluated survivorship care* at the 12 practices, which were based in Colorado, Illinois, Maine, New York, Pennsylvania, and Washington.

Over nearly 2 years, the team spent 10 to 12 days observing each of the practices and interviewing clinicians and administrators.

In this way, the researchers identified 3 main barriers to integrating survivorship care into primary medicine.

Barrier 1

The first barrier was that clinicians did not treat cancer survivors as a distinct population or clinical category.

“There is no diagnosis code for ‘cancer survivor’ that can be entered into the medical record, which is important if you want physicians to pay attention,” Dr Crabtree said.

Some of the clinicians interviewed said their care was comprehensive enough to address the needs of all patients. Other clinicians did not understand what survivorship care entails.

Barrier 2

The second barrier was that electronic health record systems didn’t support survivorship care.

Clinicians reported an inability to identify patients with a history of cancer. Even if a patient’s cancer history was included in his or her record, it might take searching through multiple screens to find the information.

In addition, medical records were sometimes lost as patients changed clinicians over the years, which left it up to patients to report their cancer histories.

Barrier 3

The third barrier was that clinicians did not receive adequate information or guidance for follow-up care of cancer survivors.

Although some of the practices received cancer-related information about their patients, it was considered “inadequate” or “not actionable.”

Clinicians expressed concerns about their knowledge gaps in cancer care and the need to monitor changing information in oncology.

“There is nothing in the residency curriculum about cancer survivorship,” Dr Crabtree said. “There is also nothing in Continuing Medical Education courses. It’s just not there.”

Dr Crabtree and his colleagues believe these barriers must be addressed so that comprehensive cancer survivorship services can move to the forefront of primary care.

* Survivorship care includes checking for cancer recurrence, monitoring long-term effects of radiation and chemotherapy, and assessing a patient’s psychological well-being.

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Primary care may be inadequate for cancer survivors
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Primary care may be inadequate for cancer survivors
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