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9 Benign andMalignant Lesions oftheLower Extremity
Fig. 9.3 Angiokeratomas present as wart-like papules varying in coloration from red to black
9.1.3 Angiokeratoma
Fig. 9.1 Acral nevus of the big toe. Dermoscopy revealed a parallel
furrow pattern
Fig. 9.2 Actinic keratoses are premalignant lesions that may evolve
into squamous cell carcinomas
and pigmented [4]. Lesions occur almost exclusively on sunexposed areas such as the face, hands, and arms with a
smaller percentage arising on the lower legs. Actinic keratoses are considered premalignancies with a potential to evolve
into frank squamous cell carcinomas.
Actinic keratoses most commonly arise on fair-skinned
individuals for whom photoprotection is mandatory to prevent lesion formation. Treatment modalities include liquid
nitrogen, curettage and electrodessication, photodynamic
therapy as well as topical imiquimod and uorouracil
(Fig.9.2) [5].
Angiokeratoma is a benign cutaneous lesion of blood vessels
that appears most commonly in elderly individuals [6].
Lesions present as reddened to dark blue or black papules
which over time acquire variable degrees of scale that may
resemble verrucae. Hyperkeratosis leads to a “pebbled” surface texture. Angiokeratomas are most commonly found on
the legs and do not compress with application of pressure.
Trauma often leads to bleeding. Biopsy may be necessary to
rule out melanoma. Histology reveals multiple ectatic thinwalled blood vessels within the papillary dermis underneath
a slightly hyperkeratotic epidermis (Fig.9.3).
9.1.4 Dermatobroma
Dermatobromas are commonly encountered benign neoplasms that occur most frequently on the lower extremities.
Their highest prevalence is in females with onset in middle
age [7]. Lesions may result from trauma such as an insect
bite or minor abrasion. Dermatobromas slowly increase in
size and are usually asymptomatic although tenderness may
be elicited with pressure. Lateral compression may induce a
dimple-like depression. Lesions are rm with coloration
ranging from light brown to a reddish hue. Eruptive dermatobromas may arise during pregnancy or as a consequence
of immunosuppression and HIV [8].
A number of histopathological variants have been reported
with the majority classied as brous histiocytomas. These
present as non-capsulated lesions that can extend into supercial adipose tissue. Interlacing fascicles of spindled cells
are surrounded by a collagenous stroma containing
broblasts, macrophages, and blood vessels. Excision with
narrow margins is curative (Fig.9.4).
9.1 Benign Lesions
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Fig. 9.5 Lipomas are benign tumors composed of adipose tissue. They
are compressible and moveable
Fig. 9.4 Dermatobromas present as rm nodules. They are most
common in women and have a predilection for the lower extremities
9.1.5 Lipoma
Lipoma is a tumor composed of adipose tissue that arises
within the subcutaneous layer of skin. Lesions may appear
anywhere on the body and usually manifest between the ages
of 40 and 60 [9]. Lipomas are slow growing and asymptomatic in a majority of patients. They may achieve sizes that
exceed 10 cm. Variants include pleomorphic lipoma and
angiolipoma, the latter may elicit pain when palpated.
Excision is curative.
Diagnosis is usually made based on clinical appearance.
Lipomas are benign with no potential for malignant transformation. Multiple lipomas may be associated with disorders
such as hereditary lipomatosis, Gardner Syndrome, adiposis
dolorosa, and Madelung disease (Fig.9.5) [10].
9.1.6 Neurobroma
Neurobromas are commonly encountered peripheral nerve
sheath tumors. Characteristic lesions are soft, minimally
compressible to rm, esh-colored papules or nodules that
are asymptomatic. Isolated tumors are most common on the
trunk and head but have been reported on the palms and soles
[11]. Bothersome lesions are best removed by excision.
Neurobromatosis is a group of genetic disorders characterized by an abundance of cosmetically disguring nerve
Fig. 9.6 A neurobroma is a tumor composed of nerve tissue. Multiple
lesions characterize the genetic disorder neurobromatosis
tissue tumors. The most common presentation of neurobromatosis is neurobromatosis type 1, or Von Recklinghausen’s
Disease [12]. Transmission is autosomal dominant in nature
although many cases arise by spontaneous mutation.
Accompanying ndings include café au lait spots and hamartomas within the eye (Fig.9.6).
9.1.7 Poroma
Poroma is a benign adnexal neoplasm that arises from a
sweat gland duct. First described over 50years ago, poromas
were believed to be exclusively of eccrine gland origin [13].
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Fig. 9.7 A poroma is an adnexal tumor that may arise from eccrine or
apocrine glands
9 Benign andMalignant Lesions oftheLower Extremity
A case of apocrine poroma was rst described in 1988 and
several additional cases have been documented [14].
Poromas present as slow growing, solitary, dome-shaped
papules or nodules that range in hue from esh-toned to reddish blue. The most common location is on the hands and
feet. Denitive diagnosis is made by biopsy. Full excision is
recommended as transformation into malignant porocarcinoma may transpire in a signicant percentage of lesions
(Fig.9.7) [15].
9.1.8 Pyogenic Granuloma
Pyogenic granuloma, also referred to as lobular capillary
hemangioma, is an acquired vascular tumor of the skin and
mucous membranes [16]. These benign neoplasms are fast
growing and characteristically bleed with minor trauma. They
are among the most frequently encountered growths in children and are also associated with pregnancy. Pyogenic granulomas are often precipitated by trauma and have been linked
to several classes of medications including isotretinoin [17].
Patients usually seek treatment due to episodic bleeding
episodes and ulceration. Shave excision, CO2 laser ablation,
and curettage with electrodessication are commonly used
destructive modalities although recurrence is not uncommon. Both oral and topical beta blockers are effective nonsurgical therapies (Fig.9.8) [18].
Fig. 9.8 A pyogenic granuloma is a vascular tumor found on the skin
and mucous membranes. Lesions grow rapidly and bleed
9.1.9 Seborrheic Keratosis
Seborrheic keratoses are commonly encountered benign
lesions often seen in Caucasian patients aged 50 and above
[19]. They occur with equal prevalence in males and females.
Ultraviolet light exposure is thought to be a contributing factor although lesions may occur at sites that have received
minimal or no prior sunlight. Seborrheic keratoses may be
found on any skin surface with the exception of the palms
and soles. Most lesions are hyperpigmented, have a rough
surface, and appear “stuck on.” They present as round to
ovoid, well-demarcated plaques with coloration ranging
from light tan to black. Size may exceed 3cm in diameter.
Early lesions may be esh-colored, smooth, and have a waxy
consistency. The majority of lesions are asymptomatic;
pruritus and inammation are not uncommon especially
when lesions are irritated by clothing.
Histology reveals hyperkeratosis, acanthosis, and papillomatosis. Dermatoscopic ndings include comedo-like
openings and milia-like cysts [20]. Cryosurgery and curettage are commonly utilized therapies for removal
(Fig.9.9).
9.2 Malignant Lesions
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Fig. 9.9 Seborrheic keratoses most commonly manifest as hyperkeratotic, hyperpigmented plaques
9.1.10 Stucco Keratoses
Stucco keratoses are an uncommon subtype of seborrheic
keratoses that are localized to the calves and ankles of the
lower legs [21]. Incidence is highest in elderly males. Lesions
present as gray-white to brownish papules and plaques.
Similar to seborrheic keratoses, they appear to be “stuck on,”
hence the name. Histology reveals hyperpigmentation and
often horn cysts [22].
Stucco keratoses may be cosmetically unacceptable.
Early lesions are often scratched off; liquid nitrogen cryosurgery and curettage are simple ofce procedures for removal
(Fig.9.10).
9.2 Malignant Lesions
9.2.1 Basal Cell Carcinoma
Basal cell carcinomas (BCCs) are the most common form of
skin cancer with two million cases diagnosed annually in the
USA [23]. The neoplasm is usually associated with fairskinned individuals who have a history of ample sun exposure. Over 80% of lesions are located on sun-exposed areas
and hereditary predisposition is a major contributing factor
to incidence which steadily increases with age [24]. The
majority of BCCs are classied as nodular; other variants
Fig. 9.10 Stucco keratoses are small, at to raised lesions aptly named
because of their “stuck on” appearance
include pigmented, supercial, and morpheaform [25].
BCCs of the lower extremity are uncommon. The majority
occur on the anterior lower leg and histologically are of the
supercial subtype [26].
BCCs slowly enlarge in size and rarely metastasize.
Treatment modalities include surgery, cryotherapy, photodynamic therapy, radiotherapy, and the topical therapies uorouracil and imiquimod (Fig.9.11) [27].
9.2.2 Kaposi’s Sarcoma
Kaposi’s sarcoma is a vascular neoplasm caused by the
human herpesvirus 8 (HHV-8) [28]. Dependent on stage,
Kaposi’s sarcoma may present as violaceous to erythematous
macules, plaques, or nodules. Diagnosis is conrmed by histology which reveals spindle cell proliferation, vascular
channels, and extravasated red blood cells. Mitotic gures
increase as the disease progresses.
Several clinical forms of this malignancy have been identied including a subset associated with poorly controlled
HIV and one that arises in middle-aged to elderly adults,
termed classic Kaposi’s sarcoma [29]. The decreased incidence of the former is a tribute to the effectiveness of antiretroviral therapy. The classic form occurs on the lower
extremities of individuals of Mediterranean and Eastern
European descent. Males greater than 50 years of age are
predominantly affected. Classic disease usually has a more
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9 Benign andMalignant Lesions oftheLower Extremity
a
Fig. 9.11 (a) Basal cell carcinomas are the most common form of malignancy. The majority occur on sun-exposed areas such as the head and
neck. (b) Supercial basal cell carcinomas present as well circumscribed, erythematous patches or plaques
b
Fig. 9.12 Kaposi’s sarcoma evolves from cells that line lymph or
blood vessels. The malignancy is caused by human herpesvirus 8
(Courtesy of Lawrence Schiffman, DO)
indolent course. For localized lesions full resolution has
been achieved with radiotherapy, intralesional chemotherapy, and topical imiquimod (Fig.9.12) [30].
9.2.3 Keratoacanthoma
Keratoacanthoma is a neoplasm that originates from the pilosebaceous unit. The lesion grows rapidly and presents as a
dome shape, skin colored nodule with a central debris-laden
Fig. 9.13 Keratoacanthomas are rapidly growing nodules with a central keratin plug
core. Keratoacanthomas have been linked to ultraviolet light
exposure and trauma as well as to BRAF kinase inhibitors
used to treat melanoma [31, 32].
Diagnosis of KA is conrmed by biopsy which reveals
well-differentiated squamous epithelium exhibiting a mild
degree of pleomorphism and often evidence of the keratin
plug. Differentiation from squamous cell carcinoma is often
challenging. Although tumors may spontaneously involute
within several months, metastatic spread has been reported,
and full excision is considered the treatment of choice
although this approach has been recently challenged
(Fig.9.13) [33].
9.2 Malignant Lesions
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9.2.4 Melanoma
Malignant melanoma is a potentially deadly form of skin
cancer that develops from melanocytes within the epidermis
and dermis. Subtypes include supercial spreading melanoma, lentigo maligna melanoma, acral lentiginous melanoma, and nodular melanoma. The majority of melanomas
are linked to ultraviolet light exposure. Risk factors include
fair skin, red hair, freckles, severe sunburn as a child, indoor
tanning, and a family history of this malignancy [34]. The
most common sites are the back in men and the legs in
women.
The ABCDEs of melanoma recognition are as follows:
• Asymmetry
• Borders (irregular with notching)
• Color (variegated)
• Diameter (greater than 6mm)
• Evolving or Elevated
A valuable screening tool is the “ugly duckling” sign;
nevi in the same individual tend to resemble each other,
whereas a melanoma looks different from the other pigmented lesions.
Acral lentiginous melanoma is the most common variant
found in blacks [35]. It has a worse prognosis than other
forms of melanoma. Subungual melanoma is an uncommon
form of acral melanoma that typically presents as a pigmented horizontal band under the nail plate. Spread of pigment into the surrounding skin is termed Hutchinson’s sign.
Recognition of melanoma may be facilitated by dermoscopy. Characteristic ndings include an atypical pigment
network, irregular dots and globules, and a gray-blue veil
[36]. Genetic expression proling (GEP) is a noninvasive tissue sampling technique that shows promise in early diagnosis of melanoma (Fig.9.14) [37].
9.2.5 Squamous Cell Carcinoma
Squamous cell carcinoma (SCC) is a malignant neoplasm of
keratinocytes that represents the second most common form
of skin cancer; approximately one million new SCCs are
diagnosed each year in the USA [38]. SCC may arise de
novo or from a precursor lesion such as an actinic keratosis.
Risk factors include advanced age, fair skin, chronic sun
exposure, tobacco use, and immunosuppression [39]. More
recently a link to indoor tanning has been documented [40].
Advanced tumors characteristically present as hyperkeratotic plaques and nodules. Metastases are uncommon and
overall mortality is approximately 2%. High risk tumors
59
Fig. 9.14 Keratoacanthomas are rapidly growing nodules with a central keratotic plug
include those that exceed 2 cm in diameter and have illdened margins.
Lower extremity SCCs usually present as erythematous
patches and plaques with variable degrees of crusting.
Surgical excision is the treatment of choice (Fig.9.15).
9.2.6 Mycosis Fungoides (Cutaneous T-Cell
Lymphoma)
Mycosis fungoides is the most common cutaneous T-cell
lymphoma [41]. The disorder usually progresses in severity
from patches to plaques and ultimately to tumors. The patch
stage is characterized by the appearance of nondescript macules that may possess a ne scale. Color changes are often
minimal although some cases demonstrate striking hypo- or
hyperpigmentation. Differential diagnosis includes common
conditions such as eczema, psoriasis, and tinea. Psoriasislike lesions characterize the plaque stage. Over time the disease evolves into ulcerated or fungating tumors.
Early mycosis fungoides are difcult to diagnose both
clinically and histopathologically given the similarity to less
serious skin disorders. The course is variable. Some patients
succumb within a few years of diagnosis, whereas others
may live for decades without development of cutaneous
tumors. Treatment varies by stage and early disease often
responds to potent topical steroids or nitrogen mustard
(Fig.9.16).
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9 Benign andMalignant Lesions oftheLower Extremity
a
Fig. 9.15 (a) Melanoma characterized by asymmetry, irregular bor-
ders, and variegated coloration. (b) Melanoma is the deadliest form of
skin cancer. Early recognition enhances survival. (c) Melanoma of the
Fig. 9.16 Mycosis fungoides is a T-cell lymphoma that may clinically
resemble more common skin conditions such as eczema and psoriasis
b
nail unit manifesting as longitudinal melanonychia (Courtesy of John
Turrisi, DPM)
c
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Blistering Eruptions oftheLower
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Extremity
10
Blistering eruptions range the gamut from an acute, selflimiting dermatitis such as poison ivy to the chronic, lifealtering disorder epidermolysis bullosa. Some blistering
ailments are discussed elsewhere including bullous impetigo, herpes zoster, and erythema multiforme. Blistering disorders are characterized by thin-walled, uid-lled skin
lesions. A small blister is referred to as a vesicle, whereas
larger lesions (generally greater than 5 mm) are termed
bullae.
10.1 Bullous Pemphigoid
Bullous pemphigoid is an autoimmune disease seen most
frequently in elderly populations [1]. Males and females are
affected equally with no racial predilection. Bullae present
as tense, oval, or round lesions containing serous or hemorrhagic uid arising on normal, urticarial, or erythematous
skin. Itching is variable and may be severe. Diagnosis is conrmed via histology and immunouorescence which demonstrate subepidermal blistering, an eosinophilic predominance
of inammatory inltrate, and IgG circulating autoantibodies to components of the basement membrane zone. Most
cases are idiopathic but the condition has recently been
linked to drugs including PD-1 inhibitors [2] and dipeptidyl
peptidase 4 (DPP-4) inhibitors [3].
Without treatment the disease can persist for several
months to years. High potency topical steroids and oral doxycycline may control limited disease. When this is impractical or ineffectual, oral prednisone is the mainstay of therapy.
Mycophenolate mofetil, omalizumab, and rituximab have
proven of value for control of refractory disease (Fig.10.1).
10.2 Dermatitis Herpetiformis
Dermatitis herpetiformis is an uncommon blistering disease
characterized by papulovesicles symmetrically distributed
on extensor surfaces of the extremities and buttocks. Pruritis
is near universal and ranges from moderate to severe [4]. The
condition peaks in midlife, is most prevalent in individuals of
Irish and Scandinavian decent, and is associated with
HLA-DQ2 and HLA-DQ8 haplotypes [5]. Immunological
stimulation of intestinal mucosa by ingested gluten is a key
factor in pathogenesis and deposition of IgA in the dermal
papillae is a hallmark of the disease.
The diagnosis of dermatitis herpetiformis is based on
clinical presentation along with serology, histology, and
immunouorescence. Autoantibodies against transglutaminase are frequently detected in serum. Dapsone is a cornerstone of therapy when strict dietary avoidance of gluten
cannot be achieved (Fig.10.2).
10.3 Epidermolysis Bullosa Acquisita
Epidermolysis bullosa acquisita (EBA) is a rare blistering
condition which worsens during adulthood. It is a subepithelial disorder with tense, fragile bullae accompanied by milia
and scarring. EBA can be divided into two subtypes: mechanobullous (classic EBA) and inammatory EBA [6]. The
mechanobullous non-inammatory subtype presents in
trauma prone areas such as the hands, feet, elbows, and
knees. Tense, non-inamed vesicles rupture leaving erosions. Inammatory EBA presents similar to bullous pemphigoid and other subepithelial autoimmune blistering
diseases.
EBA is caused by autoantibodies against type VII collagen which helps maintain attachment of the epidermis to the
dermis. After the autoantibodies bind, activation of complement leads to deposition of C3a and C5a which recruit leukocytes and mast cells. The result is disruption of the
© 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_10
63
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10 Blistering Eruptions oftheLower Extremity
a
Fig. 10.2 Dermatitis herpetiformis is a chronic skin condition triggered by an immune response to gluten
b
Fig. 10.1 (a) Bullous pemphigoid may present with urticarial patches
and excoriated papules. (b) Tense uid-lled bullae are a hallmark of
disease
anchoring brils in the basement membrane zones of the
skin and mucosa [7]. The condition is chronic and management entails avoidance of trauma and proper wound care
(Fig.10.3).
10.4 Acropustulosis ofInfancy
Acropustulosis of infancy is a disorder most often seen in
the rst year of life [8]. The etiology is unknown although
some cases follow infestation with scabies and a hypersen-
Fig. 10.3 Epidermolysis bullosa acquisita in an adult who has endured
years of traumatically induced bullae and skin erosions
sitivity reaction has been postulated [9]. The condition
manifests as recurrent crops of intensely pruritic vesicles
and pustules on the palms, soles, wrists, and ankles. The
initial eruption lasts for 1 to 2weeks and can subsequently
reappear several weeks later. Spontaneous remission
occurs within several months. Diagnosis is usually based
on clinical ndings. Bacterial and viral cultures are negative and histopathology reveals an intraepidermal pustule
containing polymorphonuclear neutrophils and eosinophils. When symptomatic, short-term treatment with mid
to high potency topical steroids may promote resolution
(Fig.10.4).
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