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6 Contact, Irritant, Atopic, andStasis Dermatitis oftheLower Extremity
References
1. Nedorost ST.Generalized dermatitis in clinical practice. Springer;
2012. p.1–14. ISBN 9781447128977
2. Usatine RP, Riojas M.Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82(3):249–55.
3. Adeniran V, Cherian A, Cho JO, Febrian C, Kim ET, Siwy
T, Vlahovic TC. Shoe dermatitis. Clin Podiatr Med Surg.
2021;38(4):561–8. https://doi.org/10.1016/j.cpm.2021.06.008.
4. Widman TJ, Oostman H, Storrs FJ.Allergic contact dermatitis from
medical adhesive bandages in patients who report having a reaction
to medical bandages. Dermatitis. 2008;19(1):32–7.
5. Laughter MR, Maymone MBC, Mashayekhi S, Arents BWM,
Karimkhani C, Langan SM, Dellavalle RP, Flohr C.The global burden of atopic dermatitis: lessons from the Global Burden of Disease
Study 1990–2017. Br J Dermatol. 2021;184(2):304–9. https://doi.
org/10.1111/bjd.19580.
6. David Boothe W, Tarbox JA, Tarbox MB.Atopic dermatitis: pathophysiology. Adv Exp Med Biol. 2017;1027:21–37. https://doi.
org/10.1007/978- 3- 319- 64804- 0_3.
7. Yew YW, Thyssen JP, Silverberg JI. A systematic review and
meta-analysis of the regional and age-related differences in
atopic dermatitis clinical characteristics. J Am Acad Dermatol.
2019;80(2):390–401. https://doi.org/10.1016/j.jaad.2018.09.035.
8. Huet F, Faffa MS, Poizeau F, Merhand S, Misery L, Brenaut
E.Characteristics of pruritus in relation to self-assessed severity of
atopic dermatitis. Acta Derm Venereol. 2019;99(3):279–83. https://
doi.org/10.2340/00015555- 3053.
9. Wahlgren CF.Itch and atopic dermatitis: an overview. J Dermatol.
1999;26(11):770–9. https://doi.org/10.1111/j.1346- 8138.1999.
tb02090.x.
10. Frazier W, Bhardwaj N.Atopic dermatitis: diagnosis and treatment.
Am Fam Physician. 2020;101(10):590–8.
11. Sundaresan S, Migden MR, Silapunt S. Stasis dermatitis: pathophysiology, evaluation, and management. Am J Clin Dermatol.
2017;18(3):383–90. https://doi.org/10.1007/s40257- 016- 0250- 0.
12. Patel SK, Surowiec SM. Venous insufciency. [Updated 2021
Dec 26]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls
Publishing; 2022. Available from: https://www.ncbi.nlm.nih.gov/
books/NBK430975/
13. Weng QY, Raff AB, Cohen JM, et al. Costs and consequences
associated with misdiagnosed lower extremity cellulitis.
JAMA Dermatol. 2017;153(2):141–6. https://doi.org/10.1001/
jamadermatol.2016.3816.
Concerns oftheLower Extremity inSkin
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ofColor
7
The term “skin of color” describes patients with pigmented
skin: African American, Hispanic, Asian (East, Southeast,
and South), and non-white ethnic groups such as First
Nations/American Indian/Alaskan Native/Native Hawaiian.
The U.S. Census has projected that half of the population
will be composed of people with skin of color by 2050 [1].
It is important rst to recognize the structural and biological differences between black and white skin. Skin color is
determined by the distribution of melanin, and there is no
difference in the number of melanocytes among groups. The
melanocytes, which reside in the basal layer of the epidermis, contain melanosomes lled with tyrosinase that is
involved in melanin synthesis. The amount of tyrosinase is
generally equal in black and white skin however, the distribution of melanosomes within melanocytes and keratinocytes is different. Besides the distribution of melanosomes
contributing to skin color, tyrosinase levels are ten times
higher in black skin and produce ten times more melanin
than melanocytes in white skin [2]. Injury and inammation
may stimulate melanocytes resulting in untoward pigmentation in persons of color [3].
Epidermal thickness is equivalent in black and white
skin, but there are more epidermal lipids in black skin [4].
Transepidermal water loss is lower in black skin, showing
statistical signicance on the legs in Warrier etal.’s study
[4]. Fibroblasts in the dermis of black skin are larger and
more numerous and active, factors that may explain the
prevalence of keloids and hypertrophic scars in this patient
population [5].
7.1 Pigmentation Disorders
andInammatory Conditions
7.1.1 Erythema
Recognizing erythema in darker skin types can pose a diagnostic challenge. The ery red color associated with cellulitis or the erythema accompanying psoriasis and other
inammatory disorders often appears more muted and even
violaceous in skin of color patients. A comprehensive skin
examination including comparison of a contralateral limb
may prove useful in the identication of erythema in darker
complected individuals (Figs.7.1 and 7.2).
7.1.2 Post-inammatory Hyperpigmentation
When exposed to inammation or an injury, melanocytes in
individuals with darker skin respond in an exaggerated manner. The emotional and psychological impact of the dyschromia can have a negative impact on the quality of life for the
patient [3]. Dyschromia following an inammatory condition such as acne, eczema, and psoriasis is known as postinammatory hyperpigmentation (PIH) and results from
either an increase in melanin production or uneven distribution of melanin. This excess pigment can reside in the epidermis, dermis, or both [3]. Hyperpigmentation after an
injury might result from an inuence of inammatory mediators and reactive oxygen species [3]. The resulting pigmentation may take years to resolve.
Treatment of any underlying inammatory condition is
necessary to prevent further pigmentation. Once resolved,
PIH may respond to topical hydroquinone.This compound is
not a true “bleaching” agent, but rather a tyrosinase blocker
that inhibits production of melanin. Long-term hydroquinone use may induce exogenous ochronosis characterized by
blue–black macules.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
T. C. Vlahovic, S. M. Schleicher, Atlas of Lower Extremity Skin Disease, https://doi.org/10.1007/978-3-031-07950-4_7
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7 Concerns oftheLower Extremity inSkin ofColor
Fig. 7.1 Erythema and mild edema at medial hallux nail fold of the left
foot
Other topical products used to treat PIH are topical steroids, tretinoin, licorice extract, niacinamide, and kojic acid.
Cosmetic treatments such as chemical peels, microdermabrasion, and laser produce variable results and risk worsening the condition (Figs.7.3 and 7.4).
7.1.3 Post-inammatory Hypopigmentation
Post-inflammatory hypopigmentation, or excessive
depigmentation, can result from an inflammatory condition or from a therapeutic intervention, such as long-term
topical steroid use. Loss of melanin may be either
localized or widespread [6]. The presence of a feathered
edge may assist in differentiation from vitiligo. Treatment
or removal of the underlying cause may hasten
resolution.
One form of hypopigmentation frequently encountered by
podiatric practitioners is idiopathic guttate hypomelanosis.
This condition manifests as discrete hypopigmented macules
on the anterior aspect of the legs and is most prominent in
darker skinned individuals. The cause is unknown although
some cases have been linked to sun exposure. Multiple modalities have been used to treat this disorder including cryotherapy,
topical retinoids, and lasers (Fig.7.5).
Fig. 7.2 Non-affected right foot of same patient
Fig. 7.3 Dyschromia of the lower leg
7.1.4 Vitiligo
Vitiligo is a common skin disorder that affects up to 2% of
the world population [7, 8]. The condition has an equal prevalence in males and females and almost half of the patients
develop the condition before age 20. Vitiligo manifests as
well-demarcated depigmented macules. Based on distribution, vitiligo may be classied into three subtypes: generalized, segmental, and localized [9]. The condition is most
7.1 Pigmentation Disorders andInammatory Conditions
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45
Fig. 7.4 Post-inammatory hyperpigmentation at the dorsum of the
toes
Fig. 7.5 Idiopathic guttate hypomelanosis
apparent in darker skinned individuals and may negatively
impact quality of life.
Vitiligo is an autoimmune disease believed to be caused
by cytotoxic CD8+ T-cells that suppress melanocytes [10].
Prognosis depends to some degree on age of onset and
extent of disease. Therapeutic options include ultraviolet
light as well as topical steroids and calcineurin inhibitors
although pigmentation is often difcult to achieve and
maintain. PUVA phototherapy (psoralen plus UVA light)
and narrowband UVB have also been used with some success to repigment, but have limited success in the lower
extremity. PUVA works by restimulating the melanocytes
still present in the lower portion of the hair follicle to
migrate and repigment surrounding skin [11]. Recently JAK
inhibitors have demonstrated efcacy and offer a promising
therapeutic option [12].
Fig. 7.6 Vitiligo of both anterior tibia
Sunscreen use is key to preventing further damage to the
keratinocytes in the amelanotic patches. Corrective cosmetics can be used as camouage (Fig.7.6).
7.1.5 Melanonychia
Longitudinal melanonychia describes the linear pigmented
brown to black streak seen in the toe and ngernails.
Melanonychia seen in patients with skin of color results from
activation of melanocytes in the nail matrix and extend to the
tip of the nail plate [13]. The condition may appear as a single
line or encompass the entire nail plate and is a common
occurrence in the African American population with 100% of
the nails being affected by the age of 50 [13]. In the Japanese
population nail pigmentation can be seen in 10–20% of adults
[13].
It is important to distinguish melanonychia commonly
seen in patients with skin of color from pigmentation due to
other causes including melanoma, hematoma, drugs, fungus,
and friction from shoes. Drugs such as antiretrovirals, antimalarials, metals, and psoralen (used in PUVA therapy) may
cause darkening of one or more nails. Pigmentation may fade
once the offending agent is discontinued. Trichophyton
rubrum and many molds may generate melanin-like compounds that pigment the nails. Friction from shoe gear may
cause the melanocytes in the nail matrix of the fourth and
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7 Concerns oftheLower Extremity inSkin ofColor
fth digits to become activated and result in “frictional”
brown-colored longitudinal melanonychia [13].
When determining the etiology of pigmented streaks
examine all nails. Streaks on multiple nails favor a diagnosis
of longitudinal melanonychia. Guidelines favoring diagnosis
of subungual melanoma have been proposed by Levit etal.
(Fig.7.7) [14]:
A is for age with the peak during the fth to seventh decades
of life and African-Americans, Asians, and native
Americans accounting for one-third of all melanoma
cases.
B is for breadth of 3mm or more and variegated borders at
the edge of the streak.
C is for change in the nail band or lack of change in the nail
plate with standard of care treatments.
D is for the digit most involved which is the (1) index nger,
(2) hallux, and (3) thumb.
E is for extension of the pigmentation into the proximal and/
or lateral nail fold (known as Hutchinson’s sign).
F is for family or personal history of melanoma.
7.2 Scars
Keloids, or scars that extend beyond the original area of
injury or trauma, occur more often in the African American
and Asian patients than Caucasian with a ratio range of 5:1 to
16:1 [15]. Keloids present a therapeutic challenge to the clinician due to their non-responsiveness to treatments and a
psychological challenge to the patient from a cosmetic and at
times, painful viewpoint. Hypertrophic scars, unlike keloids,
stay within the boundaries of the original trauma and may
regress in a few years. Both types of abnormal scar healing
are poorly understood as to why they occur and how to prevent them.
When choosing a treatment for a keloid or hypertrophic
scar, both the clinician and patient must have realistic expectations. The goal is to atten, depigment, and/or soften the
scar because the goal of having no visible scar is unrealistic.
Intralesional injection of triamcinolone 10mg/mL both deep
into the dermis and at the area of the dermo-epidermal junction is often a rst line treatment. It is helpful to either locally
block the area or use a topical anesthetic agent to achieve
that deep injection.
Laser therapy has been shown, in conjunction with intralesional steroid injection, to be useful in treating keloids [16].
It is important to take caution with the laser’s uence (J/cm2)
and pulse width in Fitzpatrick skin types IV–VI to not burn
the skin or cause further pigmentation changes.
In addition to the modalities described, topical treatments
for keloids include topical corticosteroids, imiquimod, and
silicone gel sheeting. If the topical methods fail, surgical excision is an option, but has a high recurrence rate (Fig.7.8) [15].
Fig. 7.7 Longitudinal melanonychia
Fig. 7.8 Keloids after hammertoe surgery
References
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47
References
1. Nijhawan RI, Alexis AF Practical approaches to medical and cosmetic dermatology in skin of color patients. Expert Rev Dermatol.
2011. http://www.medscape.org/viewarticle/739758.
2. Iozumi K, Hoganson GE, Pennella R, etal. Role of tyrosinase as
the determinant of pigmentation in cultured human melanocytes. J
Investigat Dermatol. 1993;100:806–11.
3. Grimes PE.Management of hyperpigmentation in darker racial ethnic groups. Semin Cutan Med Surg. 2009;28:77–85.
4. Warrier AG, Kligman AM, Harper RA, etal. A comparison of black
and white skin using noninvasive methods. J Soc Cosmet Chem.
1996;47:229–40.
5. Montagna W, Carlisle K.The architecture of black and white facial
skin. JAAD. 1991;24(6):929–37.
6. Ruiz-Maldonado R, de la Luz Orozco-Covarrubias
M. Postinammatory hypopigmentation and hyperpigmentation.
Semi Cutan Med Surg. 1997;16(1):36–43.
7. Bergqvist C, Ezzedine K. Vitiligo: a review. Dermatology.
2020;236(6):571–92.
8. Taïeb A, Picardo M, VETF Members. The denition and assessment of vitiligo: a consensus report of the Vitiligo European
Task Force. Pigment Cell Res. 2007;20(1):27–35. https://doi.
org/10.1111/j.1600- 0749.2006.00355.x.
9. Ahmed jan N, Masood S. Vitiligo. [Updated 2021 Aug 11]. In:
StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing;
2021. Available from: https://www.ncbi.nlm.nih.gov/books/
NBK559149/.
10. Frisoli ML, Essien K, Harris JE. Vitiligo: mechanisms of pathogenesis and treatment. Annu Rev Immunol. 2020;26(38):621–48.
https://doi.org/10.1146/annurev- immunol- 100919- 023531.
11. Falabella R. Treatment of localized vitiligo by autologous minigrafting. Arch Dermatol. 1988;124:1649–55.
12. Komnitski M, Komnitski A, Komnitski Junior A, Silva de Castro
CC.Partial repigmentation of vitiligo with tofacitinib, without exposure to ultraviolet radiation. An Bras Dermatol. 2020;95(4):473–6.
https://doi.org/10.1016/j.abd.2019.08.032.
13. Tosti A, Piraccini BM, Cadore de Farias D.Dealing with melanonychia. Semin Cutan Med Surg. 2009;28:49–54.
14. Levit EK, Kagen MH, Scher RK, etal. The ABC rule for clinical
detection of subungual melanoma. JAAD. 2000;42(2 Pt 1):269–74.
15. Kelly AP.Update on the management of keloids. Semin Cutan Med
Surg. 2009;28:71–6.
16. Connell PG, Harland CC. Treatment of keloid scars with
pulsed dye laser and intralesional steroid. J Cutan Laser Ther.
2000;2(3):147–50.
Autoimmune Diseases
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andVasculopathies oftheLower
Extremity
Autoimmune diseases affect over 24 million individuals in
the USA and the incidence is increasing [1]. More than 80
distinct disorders have been identied and research has contributed greatly to our understanding of underlying pathogenesis. Both genetic and environmental factors play a role
in the development of disease. All have in common immune
dysregulation, the specics of which help to dene each disease. Vasculopathies are a varied group of conditions marked
by inammation of blood vessels. Although many cases are
idiopathic, some are directly linked to antibody–antigen
complexes.
8
8.1 Chilblains
Chilblains, otherwise known as perniosis, is a benign vasospastic acrally located cutaneous disorder. Chilblains occur
after exposure to cold temperatures and dampness and are
subdivided into primary and secondary forms. The primary
form is idiopathic and is not associated with underlying disease. Secondary forms of pernio accompany underlying connective tissue disorder or other pathologic processes such as
cryoglobulinemia and monoclonal gammopathy [2].
Chilblains manifest as painful, red-to-purple edematous
papules and patches located on the acral surfaces of the ngers and toes. Symptoms usually begin in early winter and
often resolve by spring. Patients may develop recurrences
during subsequent winters or cold exposure. Although
benign and self-limiting, chilblains can resemble other vascular diseases such as thromboemboli and vasculitis leading to an extensive and unproductive workup [3]. Females
with a low body mass index are predominantly affected.
Transient vasospasm is believed to play a role in pathogenesis [4].
Chilblains are best prevented by avoidance of cold exposure. Calcium channel blockers such as nifedipine are used
to prevent recurrence and help promote faster healing
(Fig.8.1).
Fig. 8.1 Chilblains is a vascular reactive disorder triggered by exposure to cold and dampness
8.2 COVID Toes
COVID toes, also referred to as COVID infection-induced
chilblains, is a vascular acro-syndrome associated with the
SARS-CoV-2 novel coronavirus (COVID-19). This condition is dened as the presence of acute, self-healing, acroischemic lesions distinct from those related to acrocyanosis,
perniosis, and Schonlein-Henoch vasculitis in the absence of
meningococcal sepsis and protein C deciency [5]. Lesions
present as erythematous to violaceous discolorations, papules, or plaques of the distal foot and less frequently the ngers. Bullae and crusting are uncommon. The majority of
cases occur in younger patients and may be the only identiable symptom of viral infection. The condition is associated
with mild disease. Lesions last 10 to 14 days and resolve
spontaneously.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
T. C. Vlahovic, S. M. Schleicher, Atlas of Lower Extremity Skin Disease, https://doi.org/10.1007/978-3-031-07950-4_8
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Fig. 8.2 COVID toes is a self-limited condition associated with coronavirus infection
COVID toes are associated with an interferon response
to the virus which limits viral replication and triggers a
chilblain lupus erythematosus-like response through microangiopathic changes [6]. There is no direct link as to causality [7]. Other cutaneous manifestations associated with
COVID are urticarial and erythema multiforme-like eruptions [8] as well as nail changes including Beau’s lines
(Fig.8.2) [9].
8.3 Systemic Lupus Erythematosus
Systemic lupus erythematosus is an autoimmune disease that
may involve multiple organ systems including the skin, joints,
heart, lungs, and kidneys. There are three main subtypes of
cutaneous lupus: acute cutaneous lupus, discoid lupus, and
subacute cutaneous lupus [10]. Acute lupus is associated with
positive antinuclear antibodies (ANA) and a distinct malar or
“buttery” rash. The condition most commonly arises in
females of childbearing age. Lupus-related Raynaud’s disease occurs in up to one-third of individuals with lupus.
Discoid lupus is characterized by scarring and pigmentary
changes. The condition may involve the face, scalp, neck, and
arms and is most prevalent in African-Americans.
Subacute cutaneous lupus erythematosus is a photosensitive dermatosis that has two morphologic variants, annular,
and papulosquamous [11]. The annular form is characterized
by scaly, circular erythematous plaques which over time
coalesce in a polycyclic pattern. The papulosquamous variant resembles eczema with discrete, erythematous scaling
patches.
8 Autoimmune Diseases andVasculopathies oftheLower Extremity
Fig. 8.3 Subacute cutaneous lupus presenting with scaling, erythematous patches (Courtesy of Lawrence Schiffman, DO)
Sun avoidance and protection are of paramount importance in the management of cutaneous lupus. Therapeutic
modalities range the gamut from topical steroids to immunosuppressants (Fig.8.3).
8.4 Systemic Sclerosis
Systemic sclerosis is divided into two distinct entities:
scleroderma and morphea [12]. Scleroderma is a systemic
disease characterized by cutaneous sclerosis and internal disease involvement, whereas morphea is usually conned to
the skin. A subset of systemic sclerosis is a limited cutaneous
form that manifests calcinosis, Raynaud phenomenon,
esophageal dysmotility, sclerodactyly, and telangiectasias,
referred to as CREST syndrome.
The cause of systemic sclerosis is unknown. Vascular
anomalies, excess brosis, and autoimmune dysregulation
are factors involved in disease pathogenesis [13]. Skin lesions
are often bilateral and symmetrical and are rst noted on the
ngers and toes. Digits may take on a sausage-like appearance. Nail fold capillaroscopy shows vascular anomalies and
digital ischemia can eventuate in auto-amputation. Systemic
ndings may include interstitial lung involvement, gastroesophageal reux disease, heart failure, and renal crisis.
Morphea, or localized scleroderma, begins as erythematous and indurated inammatory lesions that progress to
atrophic, bound-down plaques. Several subsets are recognized including circumscribed, linear, generalized, and pansclerotic. All are marked by overproduction of collagen.
Early stages of morphea may respond to ultrapotent topical
steroids. Scleroderma is a systemic disease that is best managed by multi-specialties (Fig.8.4).
References
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Fig. 8.4 Fibrotic, bound-down, hyperpigmented patches and plaques
characterize morphea
8.5 Vitiligo
Vitiligo is a common skin disorder that affects up to 2% of
the world population [14, 15]. The condition has an equal
prevalence in males and females and almost half of the
patients develop the condition before age 20. Vitiligo manifests as well-demarcated depigmented macules. Based on
distribution, vitiligo may be classied into three subtypes:
generalized, segmental, and localized [16]. The condition is
most apparent in darker skinned individuals and may negatively impact quality of life.
Vitiligo is an autoimmune disease believed to be
caused by cytotoxic CD8+ T-cells that suppress melanocytes [17]. Prognosis depends to some degree on age of
onset and extent of disease. Therapeutic options include
ultraviolet light as well as topical steroids and calcineurin inhibitors although pigmentation is often difcult
to achieve and maintain. Recently JAK inhibitors have
demonstrated efcacy and offer a promising therapeutic
option (see Fig.7.6) [18].
51
References
1. National Institute of Environmental Health Sciences. Autoimmune
diseases. https://www.niehs.nih.gov/health/topics/conditions/auto-
immune/index.cfm.
2. Gordon R, Arikian A, Pakula A.Chilblains in Southern California:
two case reports and a review of the literature. J Med Case Rep.
2014;8:381.
3. Prakash S, Weisman M. Idiopathic chilblains. Am J Med.
2009;122(12):1152–5.
4. Shahi V, Wetter DA, Cappel JA, MDP D, Spittell PC.Vasospasm
is a consistent nding in pernio (chilblains) and a possible clue to
pathogenesis. Dermatology. 2015;231:274–9.
5. Mazzotta F, Troccoli T.Acute acro-ischemia in the child at the time
of COVID-19. The International Federation of Podiatrists. 2020.
https://img.beteve.cat/wp- content/uploads/2020/04/acroischemiaENG.pdf.
6. Hubiche T, Cardot-Leccia N, Le Duff F, et al. Clinical, laboratory, and interferon-alpha response characteristics of patients with
chilblain-like lesions during the COVID-19 pandemic. JAMA
Dermatol. 2021;157:202–6.
7. Pilkington S, Watson R.Should we look beyond the interferon signature in chilblain-like lesions associated with COVID-19? Br J
Dermatol. 2021; https://doi.org/10.1111/bjd.20784.
8. Daneshgaran G, Dubin DP, Gould DJ. Cutaneous manifestations
of COVID-19: an evidence-based review. Am J Clin Dermatol.
2020;21(5):627–39. https://doi.org/10.1007/s40257- 020- 00558- 4.
9. Wollina U, Kanitakis J, Baran R.Nails and COVID-19- a comprehensive review of clinical ndings and treatment. Dermatol Ther.
2021;34(5):e15100. https://doi.org/10.1111/dth.15100.
10. Maidhof W, Hilas O.Lupus: an overview of the disease and management options. P T. 2012;37(4):240–9.
11. Okon LG, Werth VP. Cutaneous lupus erythematosus: diagnosis
and treatment. Best Pract Res Clin Rheumatol. 2013;27(3):391–
404. https://doi.org/10.1016/j.berh.2013.07.008.
12. Careta MF, Romiti R.Localized scleroderma: clinical spectrum and
therapeutic update. An Bras Dermatol. 2015;90(1):62–73. https://
doi.org/10.1590/abd1806- 4841.20152890.
13. Odonwodo A, Badri T, Hariz A. Scleroderma. [Updated 2021
Aug 9]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls
Publishing; 2022. Available from: https://www.ncbi.nlm.nih.gov/
books/NBK537335/.
14. Bergqvist C, Ezzedine K. Vitiligo: a review. Dermatology.
2020;236(6):571–92.
15. Taïeb A, Picardo M, VETF Members. The denition and assessment of vitiligo: a consensus report of the Vitiligo European
Task Force. Pigment Cell Res. 2007;20(1):27–35. https://doi.
org/10.1111/j.1600- 0749.2006.00355.x.
16. Ahmed jan N, Masood S. Vitiligo. [Updated 2021 Aug 11]. In:
StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing;
2021. Available from: https://www.ncbi.nlm.nih.gov/books/
NBK559149/.
17. Frisoli ML, Essien K, Harris JE.Vitiligo: mechanisms of pathogenesis and treatment. Annu Rev Immunol. 2020;38:621–48. https://
doi.org/10.1146/annurev- immunol- 100919- 023531.
18. Komnitski M, Komnitski A, Komnitski Junior A, Silva de Castro
CC.Partial repigmentation of vitiligo with tofacitinib, without exposure to ultraviolet radiation. An Bras Dermatol. 2020;95(4):473–6.
https://doi.org/10.1016/j.abd.2019.08.032.
Benign andMalignant Lesions
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oftheLower Extremity
9
Differentiation of a benign lesion from a malignant one is
usually made clinically. Many of the former do not require
treatment unless symptomatic or cosmetically unacceptable.
For example, angiolipomas and dermatobromas may be
painful, especially with application of light pressure.
Pyogenic granulomas frequently bleed. Seborrheic and
stucco keratoses, which are often multiple and hyperpigmented, hyperkeratotic, and elevated, tend to be quite obvious and negatively impact appearance. Indeed, due to their
unsightly appearance, seborrheic keratoses have been termed
“the barnacles of life.”
Fortunately, the majority of benign lesions are amenable
to simple ofce procedures. A bleeding pyogenic granuloma
can be removed by shave excision, although recurrences are
not uncommon. Seborrheic keratoses may respond to liquid
nitrogen cryosurgery or curettage followed by electrodessication. When contemplating treatment of a benign lesion
take into account an end result that may not be ideal; postinammatory hyperpigmentation and exaggerated scar
formation.
Some cutaneous lesions have malignant potential. A
prime example is the actinic keratosis which is a precursor to
squamous cell carcinoma. As such, actinic keratoses merit
treatment. Some individuals may have dozens of lesions, and
given that healing of the lower extremity is often impaired,
prioritization of treatment to advanced lesions is often a prudent course of action.
Over two million skin cancers are diagnosed each year in
the USA. Basal cell carcinoma is the most common subtype
and fortunately this neoplasm has miniscule potential to
metastasize. However, basal cell carcinoma is locally
destructive and will gradually enlarge over time. Squamous
cell carcinoma is the second leading cause of skin cancer and
most cases are directly linked to either sun exposure or
indoor tanning. Suspect squamous cell carcinoma when confronted with a non-healing lesion in any fair-skinned middle
aged to elderly individual with a history of actinic keratoses
or chronic exposure to ultraviolet light. Squamous cell carcinomas can metastasize.
The deadliest form of skin cancer is melanoma; left
untreated this skin cancer will metastasize. Melanomas can
either arise from preexisting moles or de novo. The majority
are pigmented and clinicians should be familiar with the
ABCDEs of melanoma recognition as well as the ugly duck-
ling sign. Early recognition and treatment are of paramount
importance.
9.1 Benign Lesions
9.1.1 Acral Nevus
Acral nevus refers to a melanocytic lesion of the volar surfaces of the hands and feet. These nevi are frequently encountered in children and adolescents [1]. In adults, acral nevi are
most common in patients with darker Fitzpatrick skin types
[2]. The majority manifest as well circumscribed, pigmented
macules ranging in color from brown to black. Over time
some will involute and disappear.
Clinical differentiation of acral nevi from more serious
pathology such as acral lentiginous melanoma and atypical
Spitz nevi may be challenging. Dermoscopy is of great value
revealing a parallel furrow pattern, lattice-like pattern, or
brillar pattern [3]. The majority of acral nevi do not require
biopsy or full excision; however, periodic observation and
monitoring for change are prudent (Fig.9.1).
9.1.2 Actinic Keratoses
Actinic keratoses are localized cutaneous sites of atypical
squamous transformation. The lesions present as erythematous, hyperkeratotic papules, patches, or plaques. Several
subtypes based on histology have been identied including
acantholytic, atrophic, bowenoid, hypertrophic, lichenoid,
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
T. C. Vlahovic, S. M. Schleicher, Atlas of Lower Extremity Skin Disease, https://doi.org/10.1007/978-3-031-07950-4_9
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