Common Foot & Nail Conditions: Symptoms, Causes & Treatments
Melanocytes
Originating from the neural crest, melanocytes reside in the basal layer among keratinocytes. They possess ample clear cytoplasm, visible with Masson’s clear stain. Dendritic processes extend to the basal, spinous, and granular layers. Melanosomes produce melanin. The melano-epidermal unit consists of one melanocyte for every 36 keratinocytes, a constant ratio regardless of race or gender, though it varies across body areas. Pigmentation depends on the number, size, and distribution of melanin granules within keratinocytes, affecting skin, hair, and eyes. Two types of melanin exist: eumelanin (black-brown, large, oval melanosomes) and pheomelanin (red-yellow, small, round melanosomes). White hair lacks melanin production, while albino hair produces minimal pheomelanin.
Hypodermis (Subcutaneous Tissue)
Composed of adipose tissue and structured by adipocytes (lipocytes), the hypodermis manufactures and stores fat, giving cells a “signet ring” appearance. Lobe thickness varies by body region, being thicker in the abdomen. Its functions include protection, thermal regulation, and caloric reserve.
Dyshidrotic Eczema
Characterized by small, hard, bilateral, and symmetrical vesicular eruptions on the hands and feet. Itching is common. Located on the lateral surfaces of fingers, palms, soles, and sometimes the back of fingers. Vesicles may enlarge into blisters. Outbreaks are recurrent, hindering mobility. Etiology includes atopic dermatitis, psychological factors, medications, stress, food allergies, or eccrine sweat glands (nickel). Treatment is etiological or symptomatic (systemic antipruritics, sedatives, antihistamines, and topical corticosteroids, emollients, or keratolytics).
Juvenile Plantar Dermatitis
A localized form of atopic dermatitis affecting the feet, often accompanied by dryness. Appearing between ages 3 and 14, with no sex predominance, it typically affects the plantar surface of toes and heels, sometimes extending to the back of fingers or the entire sole. Bilateral and symmetrical, it’s facilitated by maceration, friction, athletic shoes, and fiber socks. Prevalence decreases in winter and increases in summer due to swimming pools. Clinical signs include erythema, keratosis, peeling, cracking, and itching, which can lead to scratching and staphylococcal infections.
Erosive Lichen Planus
Marked by painful erosions and ulcerations, sometimes preceded by blisters or crusts. More common on the soles but can affect palms and nails. Variable extension. Associated with onycholysis, anonychia, and bacterial superinfections. Chronic course with recurrent outbreaks. More prevalent in women and older individuals. Treatment includes oral antihistamines, oral and/or topical corticosteroids, topical immunomodulators, oral retinoids, cyclosporine A, and surgery.
Acute Simple Prurigo of Brocq
A papulovesicular dermatosis caused by type IV hypersensitivity to insects and arthropods. Extremely itchy. Affects children and adults in spring/summer. The primary lesion is a papule with a serous cap (Tommasoli’s sign) – an erythematous papule with a tiny urticarial base and a vesicle on top. Scratching can rupture vesicles, leading to crusts and superinfection. Located on exposed areas like the face and limbs, it can sometimes spread to genitals. Etiopathogenesis involves an atopic constitution, insect bites, or contact with arthropods. Treatment includes disinfecting clothes, furniture, and pets; using insect repellent; and applying local antihistamines, topical antiseptics, and topical/oral corticosteroids/antibiotics.
Erythema Nodosum
Sex and age distribution varies with etiology, being more common in middle-aged women. Located on the anterior and lateral surfaces of the legs, back of feet, thighs, and buttocks, rarely on arms. Clinically presents as hot, erythematous, prominent, painful, and ill-defined nodules that do not ulcerate. Sometimes they converge into peripheral, desquamative plaques. Color evolves from violet to yellow-brown before disappearing without scarring (contusiform dermatitis) within 4-6 weeks. Etiology includes infections (chlamydia, strep, tuberculosis, leprosy, yersinia, salmonella, and viruses like hepatitis or infectious mononucleosis), sarcoidosis, inflammatory bowel diseases (ulcerative colitis, Crohn’s disease), medications (antibiotics, sulfonamides, anxiolytics, and oral contraceptives), pregnancy, and neoplasms (lymphomas and leukemias). Treatment includes rest, addressing the underlying cause, NSAIDs, corticosteroids, oral potassium iodide, and immunosuppressants.
Palmoplantar Pustular Psoriasis (“Bib” Type)
The most common pustular form, with pustules embedded in the epidermis. Plaques are erythematous, circinate, pustular, and scaly. Itchy, painful, and cracking. Almost always bilateral and symmetrical. On hands, it appears on the thenar or hypothenar eminences; on feet, it affects the arch, heel, and inner edge. Evolution occurs through recurrent outbreaks (pustules, crusts, scales). Treatment includes general measures, topical keratolytics (salicylic acid 5-20%, urea 10-30%), retinoids (aqueous retinoic acid), corticosteroids, vitamin D derivatives (calcipotriene), and systemic treatments like phototherapy, heliotherapy, UVB phototherapy, retinoids, cytostatics, immunosuppressants, steroids, and biologic therapies.
Black Heel or Plantar Pseudochromohydrosis
Irregular, blue-black, palpable but not elevated plaques on the posterior or posterolateral heel (one or both). Painless. Appears in young individuals or adolescents. Etiopathogenesis involves sports with sudden stops and turns, causing heel strike trauma (tennis, paddle tennis, basketball). Traumatic angiopathic purpura (dermal capillary rupture with red blood cell extravasation). Self-resolving with rest. Differential diagnosis with acral lentiginous melanoma (when unilateral).
Vesicular or Dishydrosiform Tinea Pedis
Very itchy. Erythematous plaques of varying sizes with abundant tense vesicles that produce desquamation upon drying. Crusts and blisters may form. Vesicle contents may become pus (pustules). Located on the plantar arch and lateral surfaces of toes. Treatment: oral antifungals.
Interdigital Tinea Pedis (Athlete’s Foot)
A dermatophyte infection, often predisposed by foot maceration from closed shoes. Affects interdigital spaces, especially the 4th. Erythema, fissures at the bottom of the pruritic fold, and whitish areas of maceration are observed. Spreads to other interdigital spaces, back of fingers, toe pads, and sole. Often associated with onychomycosis. Treatment: oral antifungals.
Common Wart (Verruca Vulgaris)
Caused by human papillomavirus (HPV) types 1, 2, 3, 4, 7, 10, 26, and 28. Small, multiple, pink, keratotic vegetations. Infectious and autoinoculable. Viral solutions penetrate the epidermis but require an erosion for mucosal penetration. Transmission is direct or indirect, more common in children. Affects exposed areas. Spontaneous regression is possible. Does not penetrate the dermis. Frequently periungual.
Plantar Warts
Caused by HPV types 1, 2, 4, 60, 63, and 65. Indirect transmission (clothing, floor). Appears on feet, especially wet surfaces like pools. Minor trauma or maceration facilitates infection. Incubation period is weeks to months. More common in autumn and in children and young adults. Very painful (pressure and pinching sensation). Single or multiple. Brownish spots due to vessel dilation and thrombosis in dermal papillae. Endophytic growth. Rounded, well-defined, hard, embedded in skin with a dermatoscopic ring. Appears on pressure areas.
Plantar Foveolar Keratolysis (Keratolysis Sulcatum)
A non-inflammatory plantar corneal infection caused by Corynebacterium sp. Small, round, shallow, crate-like depressions (1-5 mm) that may form plaques. Appears on weight-bearing and friction areas, including interdigital spaces. Predisposition to hyperhidrosis and humid environments. Treatment: avoid maceration, topical antiseptics, and topical antibiotics.
Impetigo
Common in children during summer. Highly contagious. Subcorneal blisters. Streptococcal or staphylococcal. Vesiculobullous surface lesions with pustules, yellow discharge, and honey-colored crusts. Purulent material. Heals without scarring. Forms include bullous impetigo, giant impetigo, ecthyma, and blistering distal dactylitis.
Erysipelas
Involves epidermis, dermis, and hypodermis. Fever. Red, swollen, hot, and painful plaque. Grows peripherally. Blisters on the surface. Satellite lymphadenopathy. Affects the face in adults and legs, chest, and face in children. Recurrent outbreaks can cause lymphatic obstruction and lymphedema. Treatment includes topical antiseptics, drainage of pus, and oral, topical, or parenteral antibiotics.
Necrobiosis Lipoidica Diabeticorum
Slowly enlarging erythematous papule. Red, raised outer plaque, flattened center, and yellowish pigmentation. Atrophy and residual scarring. Bilateral and symmetrical. Appears on legs, pretibial region, and dorsum of feet. Asymptomatic, sometimes with burning or itching. Can ulcerate and become painful. May precede diabetes. Appears in both types of diabetes, more frequent in type 1 and in women over 30. Pathogenesis involves diabetic microangiopathy, vasculitis, and abnormal collagen or antibody-mediated degeneration.
Plantar Perforating Mal
Neuropathic ulceration with sensory neuropathy. Punch-like appearance. Painless. Appears on physiological or pathological blisters. Sometimes serohemorrhagic (“hemorrhagic callus”). Single or multiple (unilateral or bilateral). More frequent in adult males. Etiology includes diabetes (most common), leprosy, syringomyelia, syphilis, arteritis, and neuritis. Clinically presents as a painless, persistent, non-inflammatory, anesthetic ulcer on weight-bearing areas of the soles. Begins as a keratotic, granular, grayish element that forms a rounded, punch-like ulcer in its center. Slow onset, progressive, irregular, especially in depth. Secondary infections with cellulitis and lymphangitis may occur, sometimes leading to osteomyelitis. Treatment includes addressing the underlying cause, oral vasodilators, surgical debridement, topical antiseptics, local/systemic antibiotics, healing creams, hydrocolloid dressings, and local care to avoid pressure and friction.
Classic Kaposi’s Sarcoma
More common in males (10:1), aged 50-70, of Jewish or Mediterranean descent. Family history may be present. Slow evolution over years. 10% mortality. Asymptomatic onset on lower extremities (malleoli and sole). Bilateral. Red, purple, or brown macules and plaques that later form nodules and erode. Superficial desquamation. May ulcerate. Lower extremity edema (lymphedema). Multifocal. Caudocephalic progression (feet, legs, trunk, and upper extremities). Late systemic involvement (conjunctiva, oral mucosa, digestive tract, etc.).
Nail-Patella Syndrome
Embryopathy with absent, reduced, or misshapen nail matrix. Severity decreases from the 1st to 5th finger. Anonychia of the thumb is most common. Nails are short, narrow, and fragile (dystrophic). Lunula may be absent or triangular. Aplastic or dislocated patella.
Paronychia
Inflammation of the nail folds. Etiology includes staphylococci, Enterobacteriaceae, and herpes viruses. Infection follows trauma, punctures, onychophagia, manicure, or pedicure. May be associated with ingrown toenails. Clinically presents as erythematous, edematous, and painful nail folds. Pus collects under the fold or nail plate. Fold compression releases pus from the periungueal groove. Healing may reveal nail plate alterations due to temporary matrix damage. Treatment includes topical antiseptics, topical and oral antibiotics, and incision and drainage to prevent matrix damage. Chronic paronychia on hands is often caused by Candida albicans, with edematous, erythematous folds, proximal fibrosis, greenish or brownish nail discoloration, and surface damage due to chronic matrix inflammation.
Koilonychia
From the Greek “koilos” (spoon). Concave, soft, thin nails with non-keratinized, reverted edges. Affects hands. Pathogenesis involves a lower distal matrix than proximal or matrix angulation due to connective tissue disorders. Types include congenital (inherited ectodermal defects) and acquired/idiopathic (trauma, occupational exposure to petroleum products, acids, or alkalis; iron or vitamin deficiency; cardiovascular, renal, or thyroid diseases; and dermatological conditions like psoriasis, lichen planus, alopecia areata, or scleroderma).
Hjorth’s Pustular Parakeratosis
Affects distal finger pads, often with secondary nail changes. Frequent in children under 10. Slight female predominance. Affects fingers and toes, most commonly the first digits. Family history may be present. Clinically presents as erythema, dryness, fine scaling of the pad and periungual area. No pustules. Nails are thickened, distorted, dull, and sometimes with transverse subungual hyperkeratosis, stippling, and grooves. Persists for months or years, usually disappearing after puberty. Histologically shows acanthosis, papillomatosis, parakeratosis, dermal inflammatory infiltrate with exocytosis, and spongiosis. Resembles atypical chronic eczema or psoriasis. Considered a minimal form of atopic dermatitis or psoriasis. Treatment is unsatisfactory, consisting of topical corticosteroids, emollients, and protective measures.
Pachyonychia Congenita
Congenital nail thickening with a thickened nail bed. Also known as Jadassohn-Lewandowski syndrome (1906). Autosomal dominant inheritance. Appears at birth or childhood, rarely later (18-20 years). Associated with other keratinization disorders (palmoplantar and follicular hyperkeratosis, oral leukokeratosis, and palmoplantar hyperhidrosis). Four clinical types exist. Affects all nails. Nails are yellow-brown at birth. Progressive nail plate thickening. Subungual hyperkeratosis. Nail plates may break (painful).
Impetigo
Streptococcal skin infection. More common in children during summer. Highly contagious. Subcorneal blisters rupture easily. Vesiculobullous surface lesions with pustules, yellow discharge, and honey-colored crusts. Purulent material. Heals without scarring. Occurs when dermatoses become superinfected. Forms include bullous impetigo, giant impetigo, ecthyma, and blistering distal dactylitis (affects fingertip due to perionyx infection).
Leukonychia
White nails. Three types exist: true (matrix) – total, subtotal, or partial; punctate, transverse, or longitudinal; apparent (nail plate) – subungual tissue involvement with normal matrix and plate; caused by onycholysis or subungual tissues; and pseudoleukonychia – external origin, onychomycosis, or onychoschizia.
Distal Lateral Subungual Onychomycosis (DLSO)
The most common form. Affects toenails. Caused by dermatophytes (Trichophyton rubrum). Invasion begins at the distal nail fold and hyponychium, sometimes near the lateral sulcus. Clinically presents as distal nail thickening, proximal infection advancement (onycholysis), nail detachment, and opacity (yellowing or browning).
Proximal Subungual Onychomycosis (PSO)
Affects fingernails and toenails, typically the first finger. Invasion begins on the dorsal surface of the proximal nail fold and eponychium (nail matrix-ventral surface of the nail plate). Whitish macules appear near the lunula and move distally. Sometimes starts in waves (zebra pattern) with intense onychomadesis. In AIDS patients, rapid PSO development indicates disease progression.
White Superficial Onychomycosis (WSO)
Almost exclusively affects toenails. Caused by Trichophyton mentagrophytes. Invasion begins on the dorsal nail plate surface. Small, whitish, opaque macules with irregular contours form islets that may converge and affect the entire nail. The affected surface is rough, brittle, and crumbly.
Total Dystrophic Onychomycosis (TDO)
Complete nail plate dystrophy. Final stage of untreated onychomycosis. Slow onset. Nail plate breaks and crumbles until it disappears. Nail bed thickens with keratotic debris. Rapid onset in AIDS patients, following PSO.
Giant Melanocytic Nevus
Melanocytic nevus of the nail matrix causes linear, longitudinal, brown-black pigmentation of the nail plate. May slowly increase in size and color. More commonly acquired, though congenital forms exist. Differential diagnosis with subungual melanoma and other melanonychias. Treatment in adults is surgical removal of the nail and nevus. In children with congenital nevi, treatment is expectant with regular monitoring and/or surgery.
Diabetic Dermopathy (Pigmented Pretibial Patches)
The most frequent dermatosis associated with diabetes. No prognostic value. Small, asymptomatic, round or oval macules with distinct edges and superficial scaling. Develop central depression and mild brown pigmentation (hemosiderin). Caused by microangiopathy. More common in women over 50. Located on the external malleolus, forearm, and anterior and lateral surfaces of legs.
Lichen Planus of the Nail Unit
Affects 10% of patients. Involves one, several, or all nails. May occur alone or with skin or mucosal lesions. Presents as longitudinal grooves, fissures, thinning, pterygium, onychorrhexis, and onycholysis. Prognosis depends on matrix involvement, inflammation intensity, and residual scarring. Focal or complete matrix destruction may occur.
Yellow Nail Syndrome
Associated with respiratory disorders and lymphedema (pleural effusions, sinusitis, bronchitis, and bronchiectasis). Lymphedema causes ankle edema, also affecting hands and face. Atresia, hypoplasia, and varicose dilation of lymphatic vessels. Nails are slow-growing, thickened, hypercurved, and yellowish. Cuticles are weak, and onycholysis may occur. Affects all 20 nails. Treatment includes oral vitamin E and intralesional corticosteroids.
Glomus Tumor
Circumscribed, hemispheric, smooth, pink or violet vascular tumor. Spontaneously painful to pressure and temperature changes. Typically subungual, giving the nail a bluish hue. May break through the nail plate as it grows. MRI is recommended for diagnosis. Treatment is surgical removal, including the dense connective tissue capsule.
Sexually Transmitted Diseases: Manifestations in the Foot
Syphilis: Palmar-plantar syphilids (syphilitic nails) are erythematous papules, sometimes yellowish, surrounded by scaling. Diagnostic of syphilis. Painful upon pressure. Reiter’s syndrome: Causes sacroiliac arthritis and reactive arthritis in the lower extremities. Also causes keratoderma blennorrhagicum (crusty, scaly, circinate lesions) and nail dystrophies.
Bullosis Diabeticorum (Diabetic Blisters)
Occur in patients with long-standing diabetes and multiple complications. Usually asymptomatic, sometimes mildly painful. Located on the dorsum of feet, ankles, thighs, and legs. May recur. Higher prevalence in males (2:1). Age range: 17-84 years. Caused by microangiopathy. Types include spontaneous (clear, sterile, superficial, heal without scarring) and hemorrhagic (deeper, bleeding, dermo-epidermal separation, tend to necrosis and scarring).
Piezogenic Papules of the Foot
Small, pink or yellowish lesions on the lateral and posterior surfaces of heels. Herniations of connective tissue trabeculae. Visible when standing, disappear when lying down. May be painful. Treatment: rest.
Verrucous Carcinoma
Least aggressive squamous cell carcinoma. Caused by various HPV types. Types include oral florid papillomatosis, condylomatosis gigantea, and carcinoma cuniculatum. Carcinoma cuniculatum is a form of verrucous carcinoma of the foot. Generally good prognosis with slow growth. Well-circumscribed with a papillomatous surface. Affects males over 50. Caused by HPV types 1, 4, 6, 11, 16, and 18. Named “cuniculatum” due to its resemblance to a rabbit warren under microscopy. Exophytic masses on soles or fingers. May also exhibit endophytic growth.
Cutaneous Melanoma
Severe skin neoplasm. High invasion and metastasis potential. More common in the USA, Australia, and Europe. Incidence doubles every 10-15 years. Most common cancer in white males aged 35-44. Etiopathogenic factors include sun exposure, sunburn, UVA, fair skin, precursor lesions (atypical nevi), congenital factors, and continuous trauma. Clinically presents as a blackish-brown macule with irregular contours, irregular peripheral growth, dark and light areas (bluish or reddish), and can reach a large size. Surface may be keratotic, ulcerated, and bleeding in later stages. May be amelanotic (20% of cases).
Physical Therapy in Dermatology
Radiation therapy: Used for benign dermatoses after other treatments fail. Effective for squamous cell carcinomas and sarcomas, but not melanoma or basal cell carcinoma. Dermabrasion: Scraping and smoothing. Does not reach the hypodermis. Used for depressed scars, tattoos, and superficial benign lesions. Electrosurgery: Uses alternating current for cutting, coagulation, and desiccation. Cryosurgery: Application of intense cold (e.g., liquid nitrogen). No anesthesia required. Outpatient procedure. Fast, economical, and cosmetically satisfactory. Disadvantages: painful, no tissue for histopathology. Phototherapy: Uses UV (short, medium, or long). Laser therapy: Monochromatic light energy. Medical lasers (anti-inflammatory and healing) and surgical lasers (destroy skin by heat). Iontophoresis: Uses alternating current and contact electrodes to administer drugs. Contraindicated in patients with pacemakers, metal prostheses, pregnancy, and arrhythmias. Side effects include paresthesia, erythema, vesiculation, and minor burns.
Subungual Melanoma
Accounts for 2-3% of nail consultations. Often diagnosed late. Poor prognosis. Aggressive with high propensity for early nodal metastases. Affects hands and feet equally. More common on the first digits. Etiology includes trauma. Clinically presents as linear, blackened macules with rapid, progressive growth (longitudinal melanonychia). The entire nail may turn black. Invades the nail bed and proximal and lateral folds (Hutchinson’s sign, melanotic whitlow). Nail distortion or destruction. Pigmentation of the nail bed may occur. Vegetating lesions have a blue-green hue. Ulceration and bleeding may occur. Difficult to distinguish from subungual nevus, especially in early stages. Malignant transformation of nevi is possible. Amelanotic subungual melanoma is more difficult to diagnose and has a worse prognosis, resembling paronychia with vegetating, bleeding lesions that lift and destroy the nail plate. Treatment is surgical, with safety margins, including complete or partial amputation of the digit. Adjuvant interferon and chemotherapy are used for metastases.
Factors Affecting Nail Growth Rate
Physiological factors: Faster growth in fingernails, long fingers, dominant hand, daytime, pregnancy, youth, summer, and males. Slower growth in toenails, short fingers, non-dominant hand, nighttime, early life, old age, winter, and females. Pathological factors: Faster growth with microtrauma, onychophagia, onycholysis, psoriasis, periungual inflammation, arteriovenous shunts, and hyperthyroidism. Slower growth with immobilization, fever, systemic diseases, malnutrition, immunosuppressants, hypothyroidism, and yellow nail syndrome.
Functions of Nails
Sensory nerve endings provide tactile sensation. Nails assist in grasping objects, protect vascular and nerve structures in the nail bed, prevent pulp elevation, and serve as a defense mechanism against external aggression and itching. They also have cosmetic uses.
Embryology of the Nail Unit
Phases include plate phase, fibrilar phase, granular phase, squamous phase, and final nail phase.
The Foot in Leprosy
Caused by Mycobacterium leprae. Forms include indeterminate leprosy, tuberculoid leprosy, lepromatous leprosy, and borderline leprosy. M. leprae has an affinity for peripheral and acral areas, including the feet. Even after cure, significant sequelae may remain, including macules, nodules, infiltrations, ulcers, and deformities. Perforating plantar ulcers, neural lesions (sensory and motor disturbances), and musculoskeletal injuries (more common with late diagnosis) can occur.
Acrodermatitis Continua of Hallopeau
Affects distal finger pulps. Outbreaks of erythematous, scaly lesions progress to pustules. May extend proximally. Causes significant nail matrix damage and nail dystrophies, sometimes leading to anonychia and distal phalangeal atrophy. Chronic course. Treatment includes general measures, topical keratolytics (salicylic acid 5-20%, urea 10-30%), retinoids (aqueous retinoic acid), corticosteroids, vitamin D derivatives (calcipotriene), and systemic treatments like phototherapy, heliotherapy, UVB phototherapy, retinoids, cytostatics, immunosuppressants, steroids, and biologic therapies.
Acute Paronychia (Koenen’s Tumor)
Etiology includes staphylococci, streptococci, Enterobacteriaceae, and herpes simplex virus (herpetic whitlow). Clinically presents as erythematous, edematous, painful nail folds with purulent collection under the fold or nail plate. Fold compression releases pus. Trauma (punctures, onychophagia, manicure, pedicure) and ingrown toenails may contribute. Healing may reveal nail plate alterations due to temporary matrix damage. Treatment includes topical antiseptics, topical and oral antibiotics, and incision and drainage to prevent permanent matrix damage. Herpetic whitlow is treated with oral or topical acyclovir.
Reiter’s Syndrome
Clinical and histological lesions resemble psoriasis. Nail changes are often severe and psoriatic-like. More intense in HIV patients.
Nail Psoriasis (Squamous and Larva Migrans)
Treatment is often unsatisfactory. Options include photochemotherapy, oral cyclosporine or methotrexate, and topical corticosteroids, retinoids, vitamin D derivatives, and immunomodulators.