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4.6 Palmoplantar Keratoderma
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Fig. 4.5 Keratoderma climactericum of the heel
4.5 Ichthyosis
Ichthyosis is a group of cutaneous disorders characterized by
skin that is dry, thickened, and scaly. The condition may be
either hereditary or acquired. The most common form is ichthyosis vulgaris which is an autosomal dominant inherited
disorder that is estimated to affect 1in 250 individuals [6].
The disorder typically presents early in childhood and tends
to improve with age. It is often seen in association with
atopic dermatitis.
The classic sh-skin stigmata of ichthyosis vulgaris is the
result of dysregulated keratinization in the skin. This abnormal keratinization is associated with mutations in over 50
genes that encode for proteins and enzymes involved in multiple cellular functions including skin barrier homeostasis
[7]. Epidermal hyperplasia results in the formation of excess
stratum corneum and the characteristic scaly skin. Individuals
with ichthyosis have diminished or absent prolaggrin which
is synthesized in the granular layer of the epidermis and is a
major component of keratohyalin granules [8].
Diagnosis of ichthyosis vulgaris is based on the physical
ndings and family history. The disorder is chronic and often
requires continuous therapy. Topical alpha-hydroxy acids,
such as ammonium lactate, are a mainstay of treatment.
These agents work by decreasing corneocyte adhesion in the
outer stratum corneum. Acquired ichthyosis is rare, usually
appears in adulthood, and may be a marker of systemic disease including malignancy [9] (Fig.4.6).
Fig. 4.6 Ichthyosis of the leg
4.6 Palmoplantar Keratoderma
Palmoplantar keratoderma (PPK) is dened as a persistent
thickening of the epidermis of palms and soles and includes
genetic and acquired types [10]. Hereditary PPKs are rare
and may be inherited either as an autosomal dominant or
autosomal recessive manner. Inherited PPKs are caused by
mutations that result in abnormalities of keratin. Some
forms may be associated with dental abnormalities and
hearing loss.
Diagnosis of the various hereditary PPKs is based on personal and family history, histopathological ndings, and
genetic testing to identify subtypes. PPKs are subdivided
into diffuse, focal, striate (palms), and punctate forms.
Diffuse PPKs, which are the most common, involve the
entire palm or sole with or without a strict demarcation.
Focal PPKs are associated with painful calluses that often
involve the heels, whereas punctate PPKs have small punctate keratosis that can be pitted or project extra-dermally.
Acquired palmoplantar keratodermas may be focal or diffuse in nature and may be associated with internal disease,
medications, and malignancy. Findings associated with
underlying conditions merit additional workup.
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Fig. 4.7 Diffuse plantar keratoderma
Topical treatment with keratolytics such as urea, salicylic
acid, and lactic acid, along with debridement, may provide
relief. Some cases improve with oral retinoids (Fig.4.7).
4 Xerotic andHyperkeratotic Disorders oftheLower Extremity
4.7 Porokeratosis
Porokeratoses are disorders of keratinization that have a
dening histologic feature, the cornoid lamellae. This is
dened as columns of parakeratosis (retention of nuclei in
keratinocytes within the stratum corneum) “resting on a
depression where the granular layer is reduced or absent”
[10]. There are several types of porokeratoses: porokeratosis
of Mibelli, disseminated supercial porokeratosis, porokeratosis palmaris et plantaris disseminata, and the linear and
punctate types [11]. Squamous cell carcinomas may uncommonly develop within porokeratosis and lesions should be
monitored periodically for change [12].
Porokeratosis plantar discreta is a separate entity that has
similar clinical features to porokeratosis of Mibelli [13, 14]
but differs from a true porokeratosis histologically [15].
These focal and isolated lesions are more aptly referred to as
plantar keratosis or punctate keratosis. A more appropriate
term to describe a focal and isolated plantar keratotic lesion
is plantar keratosis or punctate keratosis (Fig.4.8).
4.8 Topical Therapies forXerotic
Conditions
Topical dermatologic agents are utilized to decrease scale
and transepidermal water loss enhancing the epidermal skin
barrier.
Keratolytics Urea, salicylic acid, and lactic acid creams and
lotions help remove excessive scale and soften keratin. They
Fig. 4.8 Disseminated supercial actinic porokeratosis of the leg
may enhance the penetration of topical steroids when used in
combination. Urea is used for debridement and normalization of hyperkeratotic surface lesions associated with xerosis
and ichthyosis. Urea gently dissolves the intracellular matrix,
loosens the horny layer of skin, and sheds scaly skin at regular intervals, softening hyperkeratotic areas. Salicylic acid is
an exfoliant and lactic acid is most appropriate for mild to
moderate xerosis.
Moisturizers Over-the-counter emollients can be used to
restore the function of the epidermal barrier, decrease transepidermal water loss (TEWL), and soothe the skin. Products
are best applied within a few minutes of toweling off after
bathing. Emollients, when combined with topical steroids
may prolong remission and reduce ares.
References
1. Baalham P, Birch I, Young M, Beale C. Xerosis of the feet: a
comparative study on the effectiveness of two moisturizers.
Br J Community Nurs. 2011;16(12):591–2, 594–7. https://doi.
org/10.12968/bjcn.2011.16.12.591.
2. Mukhopadhyay AK. Foot that hurts: a brief note on the history of corns and calluses. Indian J Dermatol Venereol Leprol.
2021;87:885–9.
3. Mercier MP, Blanchette V, Cantin V, Brousseau-Foley
M. Effectiveness of saline water and lidocaine injection treatment of intractable plantar keratoma: a randomised feasibility
References
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33
study. J Foot Ankle Res. 2021;14(1):30. https://doi.org/10.1186/
s13047- 021- 00467- 7.
4. Specht S, Persaud Y.Asteatotic Eczema. [2021 Jul 26]. In: StatPearls
[Internet]. Treasure Island, FL: StatPearls Publishing; 2022.
5. Deschamps P, Leroy D, Pedailles S, Mandard JC. Keratoderma
climactericum (Haxthausen’s disease): clinical signs, laboratory
ndings and etretinate treatment in 10 patients. Dermatologica.
1986;172(5):258–62. https://doi.org/10.1159/000249351.
6. Rare diseases database: ichthyosis vulgaris. National Organization
for Rare Disorders. https://rarediseases.org/rare- diseases/
ichthyosis- vulgaris.
7. Oji V, Tadini G, Akiyama M, Blanchet Bardon C, et al. Revised
nomenclature and classication of inherited ichthyoses: results of
the rst ichthyosis consensus conference in Sorèze 2009. J Am
Acad Dermatol. 2010;63(4):607–41.
8. Vahlquist A, Fischer J, Törmä H.Inherited nonsyndromic ichthyoses: an update on pathophysiology, diagnosis and treatment. Am J
Clin Dermatol. 2018;19(1):51–66.
9. Patel N, Spencer LA, English JC 3rd, Zirwas MJ.Acquired ichthyosis. J Am Acad Dermatol. 2006;55(4):647–56. https://doi.
org/10.1016/j.jaad.2006.04.047.
10. Guerra L, Castori M, Didona B, Castiglia D, Zambruno
G. Hereditary palmoplantar keratodermas. Part I. non-syndromic
palmoplantar keratodermas: classication, clinical and genetic features. J Eur Acad Dermatol Venereol. 2018;32(5):704–19.
11. Porokeratosis. Medscape. https://emedicine.medscape.com/
article/1059123- overview.
12. Kanitakis J.Porokeratoses: an update of clinical, aetiopathogenic
and therapeutic features. Eur J Dermatol. 2014;24(5):533–44.
13. Taub J, Steinberg MD. Porokeratosis plantaris discreta, a previously unrecognized dermatopathological entity. Int J Dermatol.
1970;9(2):83–90.
14. Lemont H.What’s your diagnosis? Porokeratosis plantaris discreta
(Steinberg’s lesion). J Am Podiatr Med Assoc. 2008;98(4):337–8.
15. Yanklowitz B, Harkless L.Porokeratosis plantaris discreta. A misnomer. J Am Podiatr Med Assoc. 1990;80(7):381–4.
Papulosquamous Disorders
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oftheLower Extremity
5
Papulosquamous eruptions are a heterogeneous group of disorders characterized by papules, patches, or plaques associated with varying degrees of scaling. Lesions are usually
marginated and, in acute stages, manifest erythema which at
the extreme is bright red in appearance. Scale is a manifestation of thickened stratum corneum and papules and plaques
result from acanthosis (thickening of the epidermis) or
underlying dermal inltration [1]. Papulosquamoid eruptions that are commonly encountered on the lower extremity
include psoriasis, lichen planus, and lichen striatus. Some
skin conditions, such as tinea corporis and mycosis fungoides, may be papulosquamoid in appearance.
5.1 Psoriasis
Psoriasis is a chronic immune-mediated inammatory disorder that aficts 3% of the US population [2]. Although skin
lesions are the most prominent feature of psoriasis, the condition is a complex, multisystem disease associated with
joint involvement, cardiovascular comorbidities, and
decreased quality of life [3]. Individuals with psoriasis have
an enhanced incidence of anxiety and depression.
Up to 90% of patients with psoriasis have the plaque subtype which is characterized by sharply demarcated plaques
with an adherent scale. Nails may manifest pitting, onycholysis, and oil-drop discoloration. Psoriatic arthritis is a spondyloarthropathy that often presents as an asymmetrical
oligoarthritis which over time can result in signicant joint
destruction. Associated ndings include enthesitis and
dactylitis.
Guttate, inverse, pustular, and erythrodermic psoriasis are
less frequently encountered variants. Guttate psoriasis manifests as small, scattered, erythematous, well-dened scaly
lesions predominantly on the trunk. The condition may arise
in children or adolescents following a streptococcal infection. Inverse psoriasis appears in the exural creases on areas
such as the groin, axillae, and under the breasts. This form
presents as shiny, red, well-demarcated patches without
scale. Multiple sterile pustules are the hallmark of pustular
psoriasis, which can be generalized or localized to the hands
and soles of the feet (palmoplantar psoriasis). Erythrodermic
psoriasis is characterized by widespread inammation and
exfoliation, often over a large body surface area. When
extensive, this disorder requires prompt diagnosis and treatment to prevent hospitalization.
Topical corticosteroids are rst line treatment for mild to
moderate psoriasis and are available in a variety of strengths
and formulations including creams, ointments, gels, solutions, and foams [4]. Topical corticosteroids have antiinammatory and vasoconstrictive properties. Vitamin D
analogues and vitamin A derivatives are also used topically
to treat psoriasis. Salicylic acid and coal tar formulations are
available over the counter but lack the efcacy of prescription topical agents.
Acitretin, cyclosporine, and methotrexate are oral systemic medications used to treat moderate to severe psoriasis.
All require some degree of laboratory monitoring and efcacy is variable [5]. Acitretin is teratogenic and can raise
serum triglyceride levels. Cyclosporine, especially if continued long-term, can impair renal function. Methotrexate also
is teratogenic and may induce leukopenia, pulmonary brosis, elevation of liver enzymes, and, on rare occasions, cirrhosis. Apremilast, a phosphodiesterase inhibitor, is the most
recently approved oral agent for the management of psoriasis
and psoriatic arthritis. Laboratory monitoring is not required,
but gastrointestinal side effects such as nausea and diarrhea
may be encountered. The introduction of biologic therapies
has revolutionized the treatment of psoriasis [6]. Tumor
necrosis factor-alpha (TNF-α) and interleukin (IL) inhibitors
are biologic agents that selectively inhibit cytokines involved
in the pathogenesis of this disorder. The majority are administered subcutaneously, and dosing schedules range from
weekly to quarterly depending on the agent. Tuberculosis
testing is required and all of the agents carry warnings of
increased risk for infection (Figs.5.1, 5.2, 5.3, 5.4, and 5.5).
© 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_5
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5 Papulosquamous Disorders oftheLower Extremity
Fig. 5.3 Palmoplantar pustular psoriasis is a chronic pustular dermatitis that affects the palms and soles
Fig. 5.1 Silvery, adherent scales are the hallmark of psoriasis
Fig. 5.2 Knees, elbows, and scalp are the most common locations
involved with plaque psoriasis
Fig. 5.4 Guttate psoriasis often has a sudden onset and manifests as
scaling, erythematous papules, and patches
5.2 Lichen Planus
Lichen planus is a chronic inammatory autoimmune disorder believed to be mediated by cytotoxic CD8+ T-cells [7].
The condition can affect the skin, nails, and oral mucosa.
Classic skin ndings are at-topped, polygonal, erythema-
5.3 Lichen Striatus
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Fig. 5.5 Onycholysis, discoloration, subungual debris, and pitting are
all associated with nail psoriasis
tous to violaceous papules. The wrists and ankles are the
most common sites of involvement and affected individuals
experience itching of variable intensity. Hypertrophic lichen
planus is a variant characterized by hyperpigmented plaques.
This form is most prevalent in blacks and invariably involves
the lower legs. Mucosal lichen planus often presents as a
white lacey pattern termed Wickham striae. Ulcerations are
the hallmark of erosive oral lichen planus. Disease of the
nails may manifest with thinning of the nail plate, splitting,
and pterygium formation.
Most cases of lichen planus are idiopathic although some
are induced by medications and possibly by hepatitis C viral
infection [8]. Skin lesions typically clear spontaneously
within a 2 year period. First line therapies include potent
topical steroids and, for more severe cases, oral or intramuscular steroids. Hypertrophic lichen planus may respond to
intralesional steroids although post-inammatory hyperpigmentation is a common sequela (Figs.5.6 and 5.7).
37
Fig. 5.6 Lichen planus is a papulosquamous eruption that presents
with at-topped violaceous papules affecting primarily the wrists and
ankles
5.3 Lichen Striatus
Lichen striatus is a unilateral, self-limited eruption that follows the so-called lines of Blaschko [9]. The etiology is
unknown but a signicant percentage of affected individuals
relate a family history of atopic dermatitis. The condition
most commonly occurs in preteen and adolescent females
and may involve either the trunk or extremities. The onset is
heralded by the appearance of red to esh-colored papules
with scale that rapidly extend in a band-like pattern. Nail
involvement has been reported but is rare [10].
In most individuals lichen striatus is asymptomatic and of
cosmetic concern only; however, some experience intense
pruritus. The eruption spontaneously involutes within 1 to
3years. Potent topical steroids and tacrolimus may relieve
the pruritus and hasten resolution (Fig.5.8).
Fig. 5.7 Hypertrophic lichen planus evolves into thickened plaques
and is most common on the legs
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Fig. 5.8 Lichen striatus presents as elevated papules in bands that follow the lines of Blaschko
5 Papulosquamous Disorders oftheLower Extremity
3. Takeshita J, Grewal S, Langan SM, etal. Psoriasis and comorbid
diseases: implications for management. J Am Acad Dermatol.
2017;76(3):393–403. https://doi.org/10.1016/j.jaad.2016.07.065.
4. Elmets CA, Korman NJ, Prater EF, Wong EB, Rupani RN,
Kivelevitch D, Armstrong AW, etal. Joint AAD-NPF guidelines of
care for the management and treatment of psoriasis with topical
therapy and alternative medicine modalities for psoriasis severity
measures. J Am Acad Dermatol. 2021;84(2):432–70. https://doi.
org/10.1016/j.jaad.2020.07.087.
5. Menter A, Gelfand JM, Connor C, Armstrong AW, Cordoro KM,
etal. Joint American Academy of Dermatology-National Psoriasis
Foundation guidelines of care for the management of psoriasis
with systemic nonbiologic therapies. J Am Acad Dermatol. 2020
Jun;82(6):1445–86. https://doi.org/10.1016/j.jaad.2020.02.044.
6. Kamata M, Tada Y. Efcacy and safety of biologics for psoriasis
and psoriatic arthritis and their impact on comorbidities: a literature
review. Int J Mol Sci. 2020;21(5):1690. https://doi.org/10.3390/
ijms21051690.
7. Boch K, Langan EA, Kridin K, Zillikens D, Ludwig RJ, Bieber
K.Lichen planus. Front Med (Lausanne). 2021;8:737813. https://
doi.org/10.3389/fmed.2021.737813.
8. Arnold DL, Krishnamurthy K. Lichen planus. [Updated 2021
Sep 13]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls
Publishing; 2021. Available from: https://www.ncbi.nlm.nih.gov/
books/NBK526126/.
9. Keegan BR, Kamino H, Fangman W, Shin HT, Orlow SJ, Schaffer
JV. “Pediatric blaschkitis”: expanding the spectrum of childhood acquired Blaschko-linear dermatoses. Pediatr Dermatol.
2007;24(6):621–7.
10. Iorizzo M, Rubin AI, Starace M.Nail lichen striatus: is dermoscopy
useful for the diagnosis? Pediatr Dermatol. 2019;36(6):859–63.
https://doi.org/10.1111/pde.13916.
References
1. Fox BJ, Odom RB. Papulosquamous diseases: a review. J Am
Acad Dermatol. 1985;12(4):597–624. https://doi.org/10.1016/
s0190- 9622(85)70084- 9.
2. Armstrong AW, Mehta MD, Schupp CW, Gondo GC, Bell SJ,
Grifths CEM.Psoriasis prevalence in adults in the United States.
JAMA Dermatol. 2021;157(8):940–6. https://doi.org/10.1001/
jamadermatol.2021.2007.
Contact, Irritant, Atopic, andStasis
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Dermatitis oftheLower Extremity
“Dermatitis” often serves as a catchall phrase for “a rash.”
Associated ndings usually include itching, redness, and, on
biopsy, an inammatory cell inltrate [1]. Depending on
external cause or underlying disease, dermatitis may be
either localized or diffuse in nature. History and examination
play a huge role in determining etiology and treatment plan.
Four of the most common causes of dermatitis are contact,
irritant, atopic, and stasis dermatitis.
6.1 Contact andIrritant Dermatitis
6
Contact dermatitis is a delayed hypersensitivity reaction
caused by an allergy to an external substance that contacts
the skin [2]. This allergic disorder needs to be differentiated
from an irritant dermatitis in which the inciting agent causes
physical damage to the epidermis. For example, rubbing an
abrasive cleanser against the skin will induce an irritant
dermatitis.
Common causes of contact dermatitis include poison ivy,
nickel, fragrances, and topical antibiotics. Acute reactions
manifest erythema and itch. When severe, the reaction triggers vesicles and bullae. The cause is often apparent based
on history and clinical appearance although at times patch
testing is required to pinpoint the inciting chemicals.
Skin rashes often encountered by podiatrists include shoe
dermatitis and adhesive reactions [3]. Shoe dermatitis may
result from mechanical irritation and/or a hypersensitivity
reaction. Potential allergens include rubber derivatives,
leather, dyes, and metals. Moisture aids in leaching chemicals and the combination of heat, pressure, and friction can
result in a concomitant irritant reaction. Common involved
sites are the dorsum of the great toes and sides of the feet.
Reactions induced by bandages are most likely to be irritant
in nature as opposed to allergic although both may coexist
when the dressing occludes a topical antibiotic [4].
Fig. 6.1 Irritant dermatitis secondary to chafng
Treatment of an irritant reaction entails protecting the
skin from further trauma. Management of allergic reactions
requires avoidance of the sensitizing agent. Severe allergic
dermatitis merits therapy with topical, and at times, systemic
corticosteroids (Figs.6.1, 6.2, and 6.3).
© 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_6
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Fig. 6.2 Poison ivy contains urushiol, a potent sensitizer
Fig. 6.3 Contact dermatitis to bacitracin (Courtesy of Lawrence
Schiffman, DO)
6 Contact, Irritant, Atopic, andStasis Dermatitis oftheLower Extremity
6.2 Atopic Dermatitis
Atopic dermatitis, commonly referred to as eczema, is an
inammatory condition that aficts a high percentage of
children and often persists into adulthood [5]. The disorder is
the product of immune dysregulation in conjunction with an
impaired skin barrier functionality [6]. Abnormal laggrin
proteins and defective ceramide production play a substantial role as does the release of pro-inammatory cytokines
including interleukin (IL)-4, IL-13, and IL-31. Hallmarks of
the disease include pruritus, xerosis, and erythema. More
severe cases may manifest thickened skin (lichenication),
oozing, crusting, and excoriations. In children, atopic dermatitis may be widespread with the legs frequently involved [7].
With increasing age eczema tends to be more localized com-
Fig. 6.4 Eczema is an intensely itchy inammatory disorder
monly involving the popliteal exures, lower legs, and feet.
Coin-like patches are referred to as nummular eczema.
The intensity of pruritus correlates with severity of the
disease [8]. Scratching results in mechanical damage to the
skin triggering an inammatory response that heightens itching and leads to new lesions. Eczema has been referred to as
the “itch that rashes,” this is the consequence of a selfperpetuating “itch-scratch” cycle [9]. Itch is aggravated by
extremes of temperature, wool clothing, and stress.
Management of atopic dermatitis is accomplished by
improving barrier function and reducing inammation.
Adequate moisturization helps to maintain skin integrity and
prevent are of disease. Topical corticosteroids are considered rst line treatment for atopic dermatitis [10]. Additional
prescription topical agents include calcineurin inhibitors
(tacrolimus and pimecrolimus), crisaborole, a phosphodiesterase inhibitor, and ruxolitinib, a JAK inhibitor. Some cases
improve with sunlight or ultraviolet light therapy. Refractory
disease may require systemic therapy with immunosuppressants such as glucocorticosteroids and cyclosporine. The targeted biologic dupilumab (an IL-4 and IL-13 inhibitor)
provides a revolutionary approach to the management of
moderate to severe atopic dermatitis as does the recently
approved oral JAK inhibitors abrocitinib and upadacitinib
(Figs.6.4, 6.5, and 6.6).
6.3 Stasis Dermatitis
Stasis dermatitis affects the lower legs and is a consequence
of venous hypertension and insufciency resulting from retrograde blood ow secondary to incompetent or damaged
valves [11]. Prevalence increases with advancing age and
6.3 Stasis Dermatitis
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discolorations. Chronic cases are frequently accompanied
by supercial ulcerations and at times by lipodermatosclerosis [12].
Cellulitis and allergic contact dermatitis may coexist with
stasis dermatitis or contribute to misdiagnosis [13]. Leg elevation and compression are mainstays of therapy. Topical
steroids are frequently used to manage pruritus and erythema
(Figs.6.7 and 6.8).
Fig. 6.5 A hallmark of eczema is lichenication
Fig. 6.6 Nummular eczema manifests as coin-shaped lesions
Fig. 6.7 Stasis dermatitis is bilateral and characterized by edema, ery-
thema, and scale
predisposing factors include varicosities, obesity, sedentary
lifestyle, high blood pressure, and congestive heart failure.
The medial ankle is most frequently involved with progression to the calves and feet common. Bilateral edema is
accompanied by itching, scaling, and erythematous, poorly
demarcated patches and plaques. Extravasation of blood
vessels leads to hemosiderin deposition and reddish-brown
Fig. 6.8 Stasis dermatitis may be accompanied by skin tears and
supercial ulcerations
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