The terms eczema and dermatitis are used interchangeably, denoting a polymorphic inflammatory reaction pattern involving the epidermis and dermis. There are many etiologies and a wide range of clinical findings. Acute eczema/dermatitis is characterized by pruritus, erythema, and vesiculation; chronic eczema/dermatitis is characterized by pruritus, xerosis, lichenification, hyperkeratosis/scaling, and ± fissuring.
Contact Dermatitis ICD-9: 692-9 
ICD-10: L25 
Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to substances that come in contact with the skin. Irritant contact dermatitis (ICD) is caused by a chemical irritant; allergic contact dermatitis(ACD) is caused by an antigen (allergen) that elicits a type IV (cell-mediated or delayed) hypersensitivity reaction.
ICD occurs after a single exposure to the offending agent that is toxic to the skin (e.g., croton oil) and in severe cases may lead to necrosis. It is dependent on concentration of the offending agent and occurs in everyone, depending on the penetrability and thickness of the stratum corneum. There is a threshold concentration for these substances above which they cause acute dermatitis and below which they do not. This sets ICD apart from ACD, which is dependent on sensitization and thus occurs only in sensitized individuals. Depending on the degree of sensitization, minute amounts of the offending agents may elicit a reaction. Since ICD is a toxic phenomenon, it is confined to the area of exposure and is therefore always sharply marginated and never spreads. ACD is an immunologic reaction that tends to involve the surrounding skin (spreading phenomenon) and may spread beyond affected sites.
Irritant Contact Dermatitis (ICD) ICD-9: 692.9 ICD-10:L24
ICD is a localized disease confined to areas exposed to irritants.
It is caused by exposure of the skin to chemical or other physical agents that are capable of irritating the skin.
Severe irritants cause toxic reactions even after a short exposure.
Most cases are caused by chronic cumulative exposure to one or more irritants.
The hands are the most commonly affected area.
Epidemiology
ICD is the most common form of occupational skin disease, accounting for up to 80% of all occupational skin disorders. However, ICD need not be occupational and can occur in anyone being exposed to a substance irritant or toxic to the skin.
Etiology
Etiologic Agents (Table 2-1). Abrasives, cleaning agents, oxidizing agents; reducing agents, plants and animal enzymes, secretions; desiccant powders, dust, soils; excessive exposure to water.
TABLE 2-1 MOST COMMON IRRITANT/TOXIC AGENTS
Predisposing Factors. Atopy, fare skin, temperature (low), climate (low humidity), occlusion, mechanical irritation. Cement ICD tends to flare in summer in hot humid climates.
Occupational Exposure. Individuals engaged in the following occupations/activities are at risk for ICD: housekeeping; hairdressing; medical, dental, and veterinary services; cleaning; floral arranging; agriculture; horticulture; forestry; food preparation and catering; printing; painting; metal work; mechanical engineering; car maintenance; construction; fishing.
Pathogenesis
Irritants (both chemical and physical), if applied for sufficient time and in adequate concentration. The initial reaction is usually limited to the site of contact with the irritant.
Mechanisms involved in acute and chronic phases of ICD are different. Acute reactions result from direct cytotoxic damage to keratinocytes. Chronic ICD results from repeated exposures that cause damage to cell membranes, disrupting the skin barrier and leading to protein denaturation and then cellular toxicity.
ACUTE IRRITANT CONTACT DERMATITIS
Clinical Manifestation
Symptoms. Subjective symptoms (burning, stinging, smarting) can occur within seconds after exposure (immediate-type stinging), e.g., to acids, chloroform, and methanol. Delayed-type stinging occurs within 1-2 min, peaking at 5-10 min, fading by 30 min, and is caused by agents such as aluminum chloride, phenol, propylene glycol, and others. In delayed ICD, objective skin symptoms do not start until 8-24 h after exposure (e.g., anthralin, ethylene oxide, and benzalkonium chloride) and are accompanied by burning rather than itching.
Skin Findings. Minutes after exposure or delayed up to ≥24 h. Lesions range from erythema to vesiculation (Figs. 2-1 and 2-2) and caustic burn with necrosis. Sharply demarcated erythema and superficial edema, corresponding to the application site of the toxic substance (Fig. 2-1). Lesions do not spread beyond the site of contact. In more severe reactions, vesicles and blisters (Figs. 2-1 and 2-2) → erosions and/or even frank necrosis, as with acids or alkaline solutions. No papules. Configuration is often bizarre or linear (“outside job” or dripping effect) (Fig. 2-1).
Figure 2-1. Acute irritant contact dermatitis following application of a cream containing nonylvanillamid and nicotinic acid butoxyethyl ester prescribed for lower back pain The “streaky pattern” indicates an outside job. The eruption is characterized by a massive erythema with vesiculation and blister formation and is confined to the sites exposed to the toxic agent.
Figure 2-2. Acute irritant contact dermatitis on the hand due to an industrial solvent There is massive blistering on the palm.
Evolution of Lesions. Erythema with a dull, non-glistening surface (Fig. 2-1) → vesiculation (or blister formation) (Figs. 2-1 and 2-2) → erosion → crusting → shedding of crusts and scaling or (in chemical burn) erythema → necrosis → shedding of necrotic tissue → ulceration → healing.
Distribution. Isolated, localized, or generalized, depending on contact with toxic agent.
Duration. Days, weeks, depending on tissue damage.
Constitutional Symptoms
Usually none, but in widespread acute ICD “acute illness” syndrome, fever may occur.
CHRONIC IRRITANT CONTACT DERMATITIS
Cumulative ICD. Most common; develops slowly after repeated additive exposure to mild irritants (water, soap, detergents, etc.), usually on hands. Repeated exposures to toxic or sub-toxic concentrations of offending agents → disturbance of the barrier function that allows even subtoxic concentrations of offending agent to penetrate into the skin and elicit a chronic inflammatory response. Injury (e.g., repeated rubbing of the skin), prolonged soaking in water, or chronic contact after repeated, cumulative physical trauma—friction, pressure, and abrasions in individuals engaged in manual work (traumatic ICD).
Clinical Manifestation
Symptoms. Stinging, smarting, burning, and itching; pain as fissures develop.
Skin Findings. Dryness →chapping→erythema (Fig. 2-3) → hyperkeratosis and scaling → fissures and crusting (Fig. 2-4). Sharp margination gives way to ill-defined borders, lichenification.
Distribution. Usually on hands (Figs. 2-3 and 2-4). Usually starting at finger web spaces, spreading to sides and dorsal surface of hands, and then to palms. In housewives often starting on fingertips (pulpitis) (Fig. 2-3). Rarely in other locations exposed to irritants and/or trauma, e.g., in violinists on mandible or neck, or on exposed sites as in airborne ICD (see below).
Duration. Chronic, months to years.
Figure 2-3. Early chronic irritant contact dermatitis in a housewife This has resulted from repeated exposure to soaps and detergents. Note glistening fingertips (pulpitis).
Figure 2-4. (A) Chronic irritant dermatitis with acute exacerbation in a housewife The patient used turpentine to clean her hands after painting. Erythema, fissuring, and scaling. Differential diagnosis is allergic contact dermatitis and palmar psoriasis. Patch tests to turpentine were negative. (B) Irritant contact dermatitis in a construction worker who works with cement Note the hyperkeratoses, scaling, and fissuring. There is also minimal pustulation. Note that right (dominant working) hand is more severely affected than left hand.
Constitutional Symptoms
None, except when infection occurs. Chronic ICD (e.g., hand dermatitis; see below) can become a severe occupational and emotional problem.
Laboratory Examination
Histopathology. In acute ICD, epidermal cell necrosis, neutrophils, vesiculation, and necrosis. In chronic ICD, acanthosis, hyperkeratosis, and lymphocytic infiltrate.
Patch Tests. These are negative in ICD unless ACD is also present (see below).
SPECIAL FORMS OF ICD
Hand Dermatitis
Most cases of chronic ICD occur on the hands and are occupational. Often sensitization to allergens (such as nickel or chromate salts) occurs later, and then ACD is superimposed on ICD. A typical example is hand dermatitis in construction and cement workers. Cement is alkaline and corrosive, leading to chronic ICD (Fig. 2-4); chromates in cement sensitize and lead to ACD (see Fig. 2-6). In such cases, the eruption may spread beyond the hands and may even generalize.
Figure 2-6. Allergic contact dermatitis of hands: chromates Confluent papules, vesicles, erosions, and crusts on the dorsum of the left hand in a construction worker who was allergic to chromates.
Airborne ICD. Characteristically on face, neck, anterior chest, and arms. Most frequent causes are irritating dust and volatile chemicals (ammonia, solvents, formaldehyde, epoxy resins, cement, fiberglass, sawdust from toxic woods). This has to be distinguished from airborne allergic contact dermatitis (see Fig. 2-11) and photo-allergic contact dermatitis (see Section 10).
Figure 2-11. Airborne allergic contact dermatitis of the face Extremely itchy, confluent, papular, erosive, and crusted/scaly lesions with lichenification on the forehead, nose, and cheeks following exposure to pinewood dust.
Pustular and Acneiform ICD
ICD may target follicles and become pustular and papulopustular. Results from metals, mineral oils, greases, cutting fluids, and naphthalenes.
Diagnosis and Differential Diagnosis
Diagnosis is by history and clinical examination (lesions, pattern, site). Most important differential diagnosis is ACD (see Table 2-3). On palms and soles, palmoplantar psoriasis; in exposed sites, photoallergic contact dermatitis.
TABLE 2-3 DIFFERENCES BETWEEN IRRITANT AND ALLERGIC CONTACT DERMATITISa
Course and Prognosis
Healing usually occurs within 2 weeks of removal of noxious stimuli; in more chronic cases, 6 weeks or longer may be required. In the setting of occupational ICD, only one-third of individuals have complete remission and two-thirds may require allocation to another job; atopic individuals have a worse prognosis. In cases of chronic subcritical levels of irritant, some workers develop tolerance, or “hardening.”
Management
Prevention
• Avoid irritant or caustic chemical(s) by wearing protective clothing (i.e., goggles, shields, and gloves).
• If contact does occur, wash with water or weak neutralizing solution.
• Barrier creams.
• In occupational ICD that persists in spite of adherence to the above measures, change of job may be necessary.
Treatment
Acute. Identify and remove the etiologic agent. Wet dressings with Burow’s solution, changed every 2-3 h. Larger vesicles may be drained, but tops should not be removed. Topical class I—II glucocorticoid preparations. In severe cases, systemic glucocorticoids may be indicated. Prednisone: 2-week course, 60 mg initially, tapering by steps of 10 mg.
Subacute and Chronic. Remove etiologic/pathogenic agent. Potent topical glucocorticoids (betamethasone dipropionate or clobetasol propionate) and adequate lubrication. As healing occurs, continue with lubrication. The topical calcineurin inhibitors, pimecrolimus and tacrolimus, are usually not potent enough to suppress the chronic inflammation on hands sufficiently.
In chronic ICD of hands, a “hardening effect” can be achieved in most cases with topical (soak or bath) PUVA therapy (see page 60).
Systemic Treatment. Alitretinoin (approved in Europe and Canada) 0.5 mg/kg body weight po for up to 6 months. Observe contraindications to systemic retinoids.
Allergic Contact Dermatitis ICD-9: 692.9 ICD-10: L24
ACD is a systemic disease defined by hapten-specific T-cell—mediated inflammation.
One of the most frequent, vexing, and costly skin problems.
An eczematous (papules, vesicles, pruritic) dermatitis.
Due to reexposure to a substance to which the individual has been sensitized.
Epidemiology
Frequent. Accounts for 7% of occupationally related illnesses in the United States, but data suggest that the actual incidence rate is 10-50 times greater than reported in the U.S. Bureau of Labor Statistics data. Nonoccupational ACD is estimated to be three times greater than occupational ACD.
Age of Onset. All ages but uncommon in young children and in individuals older than 70 years.
Occupation. One of the most important causes of disability in industry.
Pathogenesis
ACD is a classic, delayed, cell-mediated hyper-sensitivity reaction. Exposure to a strong sensitizer results in sensitization in a week or so, while exposure to a weak allergen may take months to years for sensitization. Sensitized T cells circulate in the blood and home to the skin wherever the specific allergen is presented. Thus, all skin is hypersensitive to the contact allergen.
Allergens
Contact allergens are diverse and range from metal salts to antibiotics, dyes to plant products. Thus, allergens are found in jewelry, personal care products, topical medications, plants, house remedies, and chemicals the individual may come in contact with at work. The most common allergens in the United States are listed in Table 2-2.
TABLE 2-2 TOP-ELEVEN CONTACT ALLERGENS (NORTH AMERICAN CONTACT DERMATITIS GROUP) AND OTHER COMMON CONTACT ALLERGENSa
Clinical Manifestation
The eruption starts in a sensitized individual 48 h or days after contact with the allergen; repeated exposures lead to a crescendo reaction, i.e., the eruption worsens. Site of the eruption is confined to site of exposure.
Symptoms. Intense pruritus; in severe reactions, also stinging and pain.
Constitutional Symptoms. “Acute illness” syndrome, including fever, but only in severe ACD (e.g., poison ivy, see below).
Skin Lesions
Acute. Well-demarcated erythema and edema with superimposed closely spaced papules or nonumbilicated vesicles (Fig. 2-5); in severe reactions, bullae, confluent erosions exuding serum, and crusts. The same reaction can occur after several weeks at sites not exposed.
Figure 2-5. Acute allergic contact dermatitis on the lips due to lipstick The patient was hypersensitive to eosin. Note bright erythema, microvesiculation. At close inspection, a papular component can be discerned. At this stage, there is still sharp margination.
Subacute. Plaques of mild erythema showing small, dry scales, sometimes associated with small, red, pointed or rounded erythematous firm papules and scales (Figs. 2-6 and 2-7).
Figure 2-7. Allergic contact dermatitis due to nickel, subacute Note a mix of papular, vesicular, and crusted lesions and loss of sharp margination. The patient was a retired watchmaker who used a metal clasp on the dorsum of the left hand while repairing watches. He was known to be allergic to nickel.
Chronic. Plaques of lichenification (thickening of the epidermis with deepening of the skin lines in parallel or rhomboidal pattern), scaling with satellite, small, firm, rounded or flat-topped papules, excoriations, and pigmentation.
Arrangement. Initially, confined to area of contact with allergen [e.g., earlobe (earrings), dorsum of foot (shoes), wrist (watch or watchband), collar-like (necklace), and lips (lipstick)]. Often linear, with artificial patterns, an “outside job.” Plant contact often results in linear lesions (e.g., Rhus dermatitis, see below). Initially confined to site of contact, later spreading beyond.
Distribution. Extent. Isolated, localized to one region (e.g., shoe dermatitis), or generalized (e.g., plant dermatitis).
Course
Evolution of ACD. The duration of ACD varies, resolving in some 1-2 weeks, but gets worse as long as allergen continues to come into contact with the skin.
Acute. Erythema → papules → vesicles → erosions → crusts → scaling.
Note: In the acute forms of contact dermatitis, papules occur only in ACD, not in ICD (see Table 2-3).
Chronic. Papules → scaling → lichenification → excoriations.
Note: ACD is always confined to the site of exposure to allergen. Margination is originally sharp, but it spreads in the periphery beyond the actual site of exposure. In case of strong sensitization spreading to other parts of the body and generalization. The main differences between toxic irritant and ACD are summarized in Table 2-3.
Laboratory Examinations
Dermatopathology. Acute. Prototype of spongiotic dermatitis, with intercellular edema (spongiosis), lymphocytes and eosinophils in the epidermis, and monocyte and histiocyte infiltration in the dermis.
Chronic. Also spongiosis plus acanthosis, elongation and broadening of papillae; hyperkeratosis; and a lymphocytic infiltrate.
Patch Tests. In ACD, sensitization is present on every part of the skin; therefore, application of the allergen to any area of normal skin provokes an eczematous reaction. A positive patch test shows erythema and papules, as well as possibly vesicles confined to the test site. Patch tests should be delayed until the dermatitis has subsided for at least 2 weeks and should be performed on a previously uninvolved site (see “Clinical Tests,” Introduction).
Diagnosis and Differential Diagnosis
By history and clinical findings, including evaluation of site and distribution. Histopathology may be helpful; verification of offending agent (allergen) by patch test. Exclude ICD (Table 2-3), atopic dermatitis (AD), seborrheic dermatitis (SD) (face), psoriasis (palms and soles), epidermal dermatophytosis (KOH), fixed drug eruption, and erysipelas phytophotodermatitis.
SPECIAL FORMS OF ACD
Allergic Contact Dermatitis Due to Plants 
Termed allergic phytodermatitis (APD).
Occurs in sensitized individuals after exposure to a wide variety of plant allergens.
Characterized by an acute, very pruritic, eczematous dermatitis, often in a linear arrangement.
In the United States, poison ivy/oak are by far the most common plants implicated.
Note: Phytophotodermatitis is a different entity; it is a photosensitivity reaction occurring in any individual with a photosensitizing plant-derived chemical on the skin and subsequent sun exposure (see Section 10).
Epidemiology and Etiology
Age of Onset. All ages. Very young and very old are less likely to be sensitized. Sensitization is lifelong.
Etiology. Pentadecylcatechols, present in the Anacardiaceae plant family, are the most common sensitizers in the United States. They cross-react with other phenolic compounds such as resorcinol, hexylresorcinol, and hydroxyquinones.
Plants. Anacardiaceae Family. Poison ivy (Toxicodendron radicans), poison oak (T. quercifolium, T. diversilobum). Also poison sumac (T. vernix). Plants related to poison ivy group: Brazilian pepper, cashew nut tree, ginkgo tree, Indian marker nut tree, lacquer tree, mango tree, and rengas tree.
Geography. Poison ivy occurs throughout the United States (except extreme southwest) and southern Canada; poison oak on the west coast. Poison sumac and poison dogwood in woody, swampy areas.
Exposure. Telephone and electrical workers working outdoors. Leaves, stems, seeds, flowers, berries, and roots contain milky sap that turns to a black resin on exposure to air. Cashew oil, unroasted cashew nuts (heat destroys hapten); cashew oil in wood (Haitian voodoo dolls, swizzle sticks); resins; printer's ink. Mango rind. Marking nut tree of India: laundry marker (dhobi itch). Furniture lacquer from Japanese lacquer tree.
Season. APD usually occurs in the spring, summer, and fall; can occur year-round if exposed to stems or roots. In southwest of the United States, occurs year-round.
Pathogenesis
All Toxicodendron plants contain identical allergens. Oleoresins are present in milky sap in leaves, stems, seeds, flowers, berries, and roots and are called urushiol. The haptens are the pentadecylcatechols (1,2-dihydroxybenzenes with a 15-carbon side chain in position three). Washing with soap and water removes oleoresins.
More than 70% of people can be sensitized. Dark-skinned individuals are less susceptible to APD. After first exposure (sensitization), dermatitis occurs 7-12 days later. In a previously sensitized person (may be many decades before), dermatitis occurs in <12 h after reexposure.
Note: Blister fluid does not contain hapten and cannot spread the dermatitis.
Clinical Manifestation
Exposure. Poison Ivy/oak Dermatitis. Direct plant exposure: plant brushes against exposed skin giving rise to linear lesions (Fig. 2-8); resin usually is not able to penetrate the thick stratum corneum of palms/soles.
Figure 2-8. Allergic phytodermatitis of leg: poisonivy Linear vesicular lesions with erythema and edema on the calf at sites of direct contact of the skin 5 days after exposure with the poison ivy leaf.
Food-Containing Urushiol. Unpeeled mango or unroasted cashew nuts expose lips. Mucous membranes uncommonly experience APD, but ingestion of urushiol can produce ACD of the anus and perineum.
Skin Symptoms. Pruritus, mild to severe. Often sensed before any detectable skin changes. Pain in some cases.
Constitutional Symptoms. Sleep deprivation due to pruritus.
Skin Lesions. Initially, well-demarcated patches of erythema, characteristic linear lesions (Fig. 2-8); → papules and edematous plaques; may be severe especially on face and/or genitals, resembling cellulitis (Fig. 2-9) → microvesiculation → vesicles and/or bullae (Figs. 2-8 and 2-10) → erosions, crusts. Postinflammatory hyperpigmentation common in darker skinned individuals.
Figure 2-9. Allergic phytodermatitis of the face: poison ivy Extremely pruritic, erythema, edema, and microvesiculation in the periorbital and perioral area in a previously sensitized young man, occurring 3 days after exposure.
Figure 2-10. Acute allergic phytodermatitis, bullous This eruption occurred in a patient who had walked barefoot through a forest. It later spread as a papular eruption to the rest of the body. Similar lesions were present on the other foot and lower leg. Differential diagnosis included acute bullous contact dermatitis to caterpillars. Phytophotodermatitis was excluded because at the time of exposure, there was a heavily clouded sky and a papular eruption occurred later on. Caterpillar dermatitis was excluded because of the multiplicity of the lesions and because upon patch testing, the patient was positive to Toxicodendron haptens. Note, patch testing to urushiol is no longer done to avoid sensitization of patients.
Distribution. Most commonly on exposed extremities, where contact with the plant occurs; blotting can transfer to any exposed site; palms/soles usually spared; however, lateral fingers can be involved.
Clothing-Protected Sites. Oleoresin can penetrate damp clothing onto covered skin; wearing clothing previously contaminated with resin can reexpose the skin.
Nonexposed Sites. “Id”-like reaction or some systemic absorption can be associated with disseminated urticarial, erythema multiforme-like, or scarlatiniform lesions away from sites of exposure in some individuals with well-established APD.
Laboratory Examinations
Dermatopathology. See ACD, above.
Patch Tests with Pentadecylcatechols. Contraindicated as it can sensitize individual to hapten.
Diagnosis
By history and clinical findings only.
Differential Diagnosis
ACD to other allergens, phytophotodermatitis (see Section 10), soft-tissue infection (cellulitis, erysipelas), AD, inflammatory dermatophytosis, early herpes zoster, and fixed drug eruption.
Other Special Forms of ACD
Systemic ACD
After systemic exposure to an allergen to which the individual had prior ACD
A delayed T-cell—mediated reaction
Examples: ACD to ethylenediamine → subsequent reaction to aminophylline (which contains ethylene diamine); poison ivy dermatitis → subsequent reaction to ingestion of cashew nuts; also antibiotics, sulfonamides, propylene glycol, metal ions, sorbic acid, fragrances
Airborne ACD
Contact with airborne allergens in exposed body sites, notably the face (Fig. 2-11); also including eyelids, “V” of the neck, arms, and legs
In contrast to airborne ICD, papular from the beginning, extremely itchy
Prolnged repetitive exposure leads to dry, lichenified ACD with erosions and crusting (Fig. 2-11)
Due to plant allergens, especially from compositae, natural resins, woods, and essential oils volatizing from aroma therapy
Management of ACD
Termination of Exposure. Identify and remove the etiologic agent.
Topical Therapy. Topical glucocorticoid ointments/gels (classes I—III). Larger vesicles may be drained, but tops should not be removed. Wet dressings with cloths soaked in Burow’s solution changed every 2-3 h. Airborne ACD may require systemic treatment. Pimecrolimus and tacrolimus are effective in ACD but to a lesser degree than glucocorticoids.
Systemic Therapy. Glucocorticoids are indicated if severe and in airborne ACD. Prednisone beginning at 70 mg (adults), tapering by 5-10 mg/d over a 1- to 2-week period. In airborne ACD where complete avoidance of allergen may be impossible, immunosuppression with oral cyclosporine may become necessary.
Atopic Dermatitis ICD-9: 691.8 ICD-10: L20
An acute, subacute, or chronic relapsing skin disorder.
Very common in infancy.
Prevalence peak of 15-20% in early childhood.
Characterized principally by dry skin and pruritus; consequent rubbing leads to increased inflammation and lichenification and to further itching and scratching: itch-scratch cycle.
Diagnosis is based on clinical findings.
Often associated with a personal or family history of AD, allergic rhinitis, and asthma; 35% of infants with AD develop asthma later in life.
Associated with skin barrier dysfunction, IgE reactivity.
Genetic basis influenced by environmental factors; alterations in immunologic responses in T cells, antigen processing, inflammatory cytokine release, allergen sensitivity, infection.
Synonyms: IgE dermatitis, “eczema,” atopic eczema.
Epidemiology
Age of Onset. First 2 months of life and by the first years in 60% of patients; 30% by age 5, and only 10% between age 6 and 20 years. Rarely AD has an adult onset.
Gender. Slightly more common in males than in females.
Prevalence. Between 7% and 15% reported in population studies in Scandinavia and Germany.
Genetic Aspects. The inheritance pattern not yet ascertained. However, in one series, 60% of adults with AD had children with AD. The prevalence in children was higher (81%) when both parents had AD.
Skin Barrier Disruption. Decrease in barrier function due to impaired filagrin production, reduced ceramide levels, and increased transepidermal water loss; dehydration of skin.
Eliciting Factors. Inhalants. Specific aeroallergens, especially dust mites and pollens.
Microbial Agents. Exotoxins of Staphylococcus aureus acting as superantigens. Also group A streptococcus, rarely fungus (candida).
Autoallergens. Sera of patients with AD contain IgE antibodies directed at human proteins. Release of these autoallergens from damaged tissue could trigger IgE or T-cell responses, suggesting maintenance of allergic inflammation.
Foods. Infants and children, but not adults, have flares of AD with eggs, milk, peanuts, soybeans, fish, and wheat.
Other Exacerbating Factors
Season. In temperate climates, AD usually improves in summer, flares in winter.
Clothing. Pruritus flares after taking off clothing. Wool is an important trigger; wool clothing or blankets directly in contact with skin (also wool clothing of parents, fur of pets, carpets).
Emotional Stress. Results from the disease or is itself an exacerbating factor in flares of the disease.
Pathogenesis
Complex interaction of skin barrier, genetic, environmental, pharmacologic, and immunologic factors. Type I (IgE-mediated) hypersensitivity reaction occurring as a result of the release of vasoactive substances from both mast cells and basophils that have been sensitized by the interaction of the antigen with IgE (reaginic or skin-sensitizing antibody). Epidermal Langerhans cells possess high-affinity IgE receptors through which an eczema-like reaction can be mediated. Acute inflammation in AD is associated with a predominance of interleukin (IL) 4 and IL-13 expression, and chronic inflammation in AD with increased IL-5, granulocyte-macrophage colony-stimulating factor, IL-12, and interferon-γ. Thus, skin inflammation in AD shows a biphasic pattern of T-cell activation.
Clinical Manifestation
Skin Symptoms. Patients have dry skin. Pruritus is the sine qua non of AD—“eczema is the itch that rashes.” The constant scratching leads to a vicious cycle of itch → scratch → rash → itch → scratch.
Other Symptoms of Atopy. Allergic rhinitis, obstruction of nasal passages, conjunctival and pharyngeal itching, and lacrimation; seasonal when associated with pollen.
Skin Lesions. Acute. Poorly defined erythematous patches, papules, and plaques with or without scale. Edema with widespread involvement; skin appears “puffy” and edematous (Fig. 2-12). Erosions: moist, crusted. Linear or punctate, resulting from scratching. Secondarily infected sites: S. aureus. Oozing erosions (Figs. 2-12 and 2-13) and/or pustules (usually follicular). Skin is dry, cracked, and scaly (Fig. 2-13).
Figure 2-12. Atopic dermatitis: infantile Puffy face, confluent erythema, papules, microvesiculation, scaling, and crusting.
Figure 2-13. Atopic dermatitis: infantile type Skin of forehead is dry, cracked, and scaly. In addition, there are oozing erosions.
Chronic. Lichenification (thickening of the skin with accentuation of skin markings) (Figs. 2-14 and 2-17); follicular lichenification (especially in brown and black persons) (Fig. 2-16B). Fissures: painful, especially in flexures (Fig. 2-15A), on palms, fingers, and soles. Alopecia: lateral one-third of the eyebrows as a result of rubbing. Periorbital pigmentation, also as a result of compulsive rubbing. Characteristic infraorbital fold below eyelids (Dennie–Morgan sign).
Figure 2-14. Childhood atopic dermatitis A typical localization of atopic dermatitis in children is the region around the mouth. In this child, there is lichenification and fissuring and crusting.
Figure 2-15. (A) Childhood atopic dermatitis One of the hallmarks of atopic dermatitis is lichenification in the flexural regions as shown in this picture. Note the thickening of the skin with exaggerated skin lines and erosions. (B) Atopic dermatitis in black child. Pruritic follicular papules on posterior leg. Follicular eczema pattern is more common in African and Asian children.
Figure 2-16. Predilection sites of atopic dermatitis.
Figure 2-17. (A) Childhood atopic dermatitis This is a generalized eruption consisting of confluent, inflammatory papules that are erosive, excoriated, and crusted. (B) Generalized eruption of follicular papules that are more heavily pigmented than normal skin in a 53-year-old woman of African extraction. There is extensive lichenification.
Distribution. Predilection for the flexures, front and sides of the neck, eyelids, forehead, face, wrists, and dorsa of the feet and hands (Fig. 2-16). Generalized in severe disease (Fig. 2-17A and B).
Special Features Related to Age
Infantile AD. The lesions present as red skin, tiny vesicles on “puffy” surface. Scaling, exudation with wet crusts and cracks (fissures) (Figs. 2-12-2-14).
Childhood-Type AD. The lesions are papular, lichenified plaques, erosions, crusts, especially on the antecubital and popliteal fossae (Figs. 2-15A and B), the neck and face; may be generalized.
Adult-Type AD. There is a similar distribution, mostly flexural but also face and neck, with lichenification and excoriations being the most conspicuous symptoms (Fig. 2-17B). May be generalized.
Special Features Related to Ethnicity
In blacks and also in dark-brown skin, so-called follicular eczema is common; characterized by discrete follicular papules (Figs. 2-15B, 2-17B, and 2-18) involving hair follicles of the involved site.
Figure 2-18. Adult atopic dermatitis Lichenification does not only occur in the big flexural folds but may also affect the face as in this 53-year-old woman of Indonesian extraction.
Associated Findings
“White” Dermatographism. Stroking of involved skin will not lead to redness as in normal skin but to blanching; delayed blanch to cholinergic agents. Ichthyosis vulgaris and keratosis pilaris (see Section 4) occur in 10% of patients. Vernal conjunctivitis with papillary hypertrophy or cobblestoning of upper eyelid conjunctiva. Rare atopic keratoconjunctivitis is disabling, may result in corneal scarring. Keratoconus is rare. Cataracts occur in a small percentage.
Diagnosis
History in infancy, clinical findings.
Differential Diagnosis
SD, ICD, ACD, psoriasis, nummular eczema, dermatophytosis, early stages of mycosis fungoides. Rarely, acrodermatitis enteropathica, glucagonoma syndrome, histidinemia, phenyl-ketonuria; also, some immunologic disorders including Wiskott–Aldrich syndrome, X-linked agammaglobulinemia, hyper-IgE syndrome, and selective IgA deficiency; Langerhans cell histiocytosis, Letterer–Siwe type.
Laboratory Examinations
Bacterial Culture. Colonization with S. aureus is very common in the nares and in the involved skin; almost 90% of patients with severe AD are secondarily colonized/infected. Look out for methicillin-resistant S. aureus(MRSA).
Viral Culture. Rule out herpes simplex virus (HSV) infection in crusted lesions (eczema herpeticum; see Section 27).
Blood Studies. Increased IgE in serum, eosinophilia. HSV antigen detection for diagnosis of acute HSV infection.
Dermatopathology. Various degrees of acanthosis with rare intraepidermal intercellular edema (spongiosis). The dermal infiltrate is composed of lymphocytes, monocytes, and mast cells with few or no eosinophils.
Special Forms of AD
Hand Dermatitis. Aggravated by wetting and washing with detergents, harsh soaps, and disinfectants; leads to ICD in the atopic. Clinically indistinguishable from “normal” ICD (see page 21).
Exfoliative Dermatitis (See Section 8). Erythroderma in patients with extensive skin involvement. Generalized redness, scaling, weeping, crusting, lymphadenopathy, fever, and systemic toxicity.
Complications
Secondary infection with S. aureus and HSV (eczema herpeticum, see Section 28). Rarely keratoconus, cataracts, and keratoconjunctivitis with secondary herpetic infection and corneal ulcers.
Course and Prognosis
Untreated involved sites persist for months or years. Spontaneous, more or less complete remission during childhood occurs in >40% with occasional, more severe recurrences during adolescence. In many patients, the disease persists for 15-20 years, but is less severe. Thirty to fifty percent of patients develop asthma and/or hay fever. Adult-onset AD often runs a severe course. S. aureus infection leads to extensive erosions and crusting, and herpes simplex infection to eczema herpeticum, which may be life threatening (see Section 28).
Management
Education of the patient to avoid rubbing and scratching is most important. Use emollients.
An allergic workup is rarely helpful in uncovering an allergen; however, in patients who are hypersensitive to house dust mites, various pollens, and animal hair proteins, exposure to the appropriate allergen may cause flares. AD may exacerbate with emotional stress and sweating.
Patients should be warned of their special problems with herpes simplex and the superimposed staphylococcal infection.
Acute
1. Wet dressings and topical glucocorticoids; topical antibiotics (mupirocin ointment) when indicated.
2. Hydroxyzine, 10–100 mg four times daily for pruritus.
3. Oral antibiotics (dicloxacillin, erythromycin) to eliminate S. aureus and treat MRSA according to sensitivity as shown by culture.
Subacute and Chronic
1. Hydration (oilated baths or baths with oatmeal powder) followed by application of unscented emollients (e.g., hydrated petrolatum) is basic daily treatment to counteract xerosis; 12% ammonium lactate or 10% α-hydroxy acid lotion is very effective for xerosis. Soap showers are permissible for the body folds, but soap should seldom be used on the other parts of the skin surface.
2. Topical anti-inflammatory agents such as glucocorticoids, hydroxyquinoline preparations, and tar are the mainstays of treatment. Of these, glucocorticoids are the most effective. However, topical glucocorticoids may lead to skin atrophy if used for prolonged periods of time and if used excessively will lead to suppression of the pituitary-adrenal axis. Another problem is “glucocorticoid phobia.” Patients or their parents are increasingly aware of glucocorticoid side effects and refuse their use, no matter how beneficial they may be.
3. The calcineurin inhibitors, tacrolimus and pimecrolimus, are gradually replacing glucocorticoids in most patients. They potently suppress itching and inflammation and do not lead to skin atrophy. They are usually not effective enough to suppress acute flares but work very well in minor flares and subacute AD.
4. Oral H1-antihistamines are useful in reducing itching.
5. Systemic glucocorticoids should be avoided, except in rare instances of severe intractable disease in adults: prednisone, 60-80 mg daily for 2 days, then halving the dose each 2 days for the next 6 days. Patients with AD tend to become dependent on oral glucocorticoids. Often, small doses (5-10 mg) make the difference in control and can be reduced gradually to even 2.5 mg/d, as is often used for the control of asthma.
6. UVA-UVB phototherapy (combination of UVA plus UVB and increasing the radiation dose each treatment, with a frequency of two to three times weekly). Narrow band UV (311 nm) phototherapy and PUVA photochemotherapy are also effective.
7. In severe cases of adult AD and in normotensive healthy persons without renal disease, cyclosporine treatment (starting dose 5 mg/kg per day) is indicated when all other treatments fail, but should be monitored closely. Treatment is limited to 3-6 months because of potential side effects, including hypertension and reduced renal function. Blood pressure should be checked weekly and chemistry panels biweekly. Nifedipine can be used for moderate increases in blood pressure.
8. Patients should learn and use stress management techniques.
Suggested Algorithm of AD Management
Baseline therapy of dryness with emollients
Suppression of mild-to-moderate AD by prolonged topical pimecrolimus or tacrolimus and continued emollients
Suppression of severe flares with topical glucocorticoids followed by pimecrolimus or tacrolimus and emollients
Oral and topical antibiotics to eliminate S. aureus
Hydroxyzine to suppress pruritus
Web site: http://www.aad.org/pamphlets/eczema.html
Lichen Simplex Chronicus (LSC) ICD-9: 698.3 ICD-10: L28 
A special localized form of lichenification, occurring in circumscribed plaques.
Results from repetitive rubbing and scratching.
Lichenification is a characteristic feature of AD, whether generalized or localized.
LSC can last for decades unless the rubbing and scratching are stopped by treatment.
Occurs in individuals older than 20 years, is more frequent in women, and possibly more frequent in Asians.
Pathogenesis
Skin becomes highly sensitive to touch. The very abnormal itching hyperexcitability of lichenified skin arises in response to minimal external stimuli that would not elicit an itch response in normal skin. Many patients have AD or an atopic background.
Skin symptoms consist of pruritus, often in paroxysms. The lichenified skin is like an erogenous zone—it becomes a pleasure (orgiastic) to scratch. The rubbing becomes automatic and reflexive and an unconscious habit.
Clinical Manifestation
Skin Lesions. A solid plaque of lichenification, arising from the confluence of small papules (Fig. 2-19). Skin is palpably thickened; skin markings (barely visible in normal skin) are accentuated and can be seen readily. Excoriations. Usually dull red, later brown or black hyperpigmentation, especially in skin of color. Round, oval, linear (following path of scratching). Usually sharply defined. Isolated single lesion or several plaques. Nuchal area (female) (Fig. 2-19), scalp, ankles, lower legs, upper thighs, exterior forearms, vulva, pubis, anal area, scrotum, and groin.
Figure 2-19. Lichen simplex chronicus Confluent, papular, follicular eczema, creating a plaque of lichen simplex chronicus of the posterior neck and occipital scalp. Condition had been present for many years as a result of chronic rubbing of the area.
In black skin, lichenification may assume a special type of pattern consisting of multiple small (2-3 mm) closely set papules, a “follicular” pattern (as in Fig. 2-15B).
Differential Diagnosis
Includes a chronic pruritic plaque of psoriasis vulgaris, early stages of mycosis fungoides, ICD, ACD, and epidermal dermatophytosis.
Laboratory Examination
Dermatopathology. Hyperplasia of all components of epidermis: hyperkeratosis, acanthosis, and elongated and broad rete ridges. In the dermis, there is a chronic inflammatory infiltrate.
Management
Difficult. Explain to the patient that rubbing and scratching must be stopped. Occlusive bandages can be used at night. Topical glucocorticoid preparations or tar preparations covered by occlusive dressings are effective for legs and arms. Glucocorticoids incorporated in adhesive plastic tape are also effective, if left for 24 h. Unna boot: A gauze roll dressing impregnated with zinc oxide paste is wrapped around a large lichenified area such as the calf. It can be left on for up to 1 week.
Intralesional triamcinolone is often highly effective in smaller lesions (3 mg/mL; higher concentrations may cause atrophy). Oral hydroxyzine, 25-50 g at night, may be helpful.
Prurigo Nodularis (PN) ICD-9:698.3 ICD-10: L28.1
Is often associated with AD or occurs without AD.
PN patients with AD are younger and have reactivity to environmental allergens; nonatopic PN patients are older and lack hypersensitivities to environmental allergens.
PN usually occurs in younger or middle-aged females, who often exhibit signs of neurotic stigmatization.
PN starts with piercing pruritus that leads to picking and scratching.
Dome-shaped nodules—several millimeters to 2 cm—develop on sites in which persistent itching and scratching occur (Fig. 2-20).
Nodules are often eroded, excoriated, and sometimes even ulcerated as patients dig into them with their nails.
Usually multiple on the extremities.
Lesions persist for months after the trauma has been discontinued.
Treatment: intralesional triamcinolone, occlusive dressings with high-potency glucocorticoids. In severe cases, thalidomide 50-100 mg. Watch out for contraindications! neurotonin 300 mg po tid may be helpful.
Figure 2-20. Prurigo nodularis Multiple, firm, excoriated nodules arising at sites of chronically picked or excoriated skin. Often occurring in patients with atopy but also without it. In this 56-year-old patient, the extreme pruritus necessitated multiple hospitalizations.
Dyshidrotic Eczematous Dermatitis ICD-9:705.81 ICD-10: L30.1
Dyshidrotic eczema is a special vesicular type of hand and foot dermatitis.
An acute, chronic, or recurrent dermatosis of the fingers, palms, and soles.
Sudden onset of many deep-seated pruritic, clear “tapioca-like” vesicles (Fig. 2-21).
Large bullae can occur (pompholyx).
Later scaling fissures and lichenification.
Itching and when erosions are present pain.
Secondary bacterial infection: pustules, cellulitis, lymphangitis, and painful lymphadenopathy.
Recurrent attacks are the rule.
Treatment: topical high-potency corticosteroids, intralesional triamcinolone 3 mg/mL for small areas; in severe cases, a short course of prednisone: starting with 70 mg and tapering by 10 or 5 mg over 7 or 14 days; systemic antibiotics for secondary infection and PUVA either oral or as “soaks” (see page 60).
Synonyms: Pompholyx, vesicular palmar eczema.
Figure 2-21. Dyshidrotic eczematous dermatitis Confluent tapioca-like vesicles and crusted (excoriated) erosions on the dorsum of fingers and finger webs.
Nummular Eczema ICD-9: 692.9 ICD-10: L30.9
Nummular eczema is a chronic, pruritic, inflammatory dermatitis occurring in the form of coin-shaped plaques composed of grouped small papules and vesicles on an erythematous base (Fig. 2-22).
It is especially common on the extremities during winter months when xerosis is maximal; often seen in atopic individuals.
S. aureus is often present but pathogenic significance not proven.
Very pruritic. Course is chronic, lesions last from weeks to months.
Management: Hydrate skin with hydrated moisturizer or moisturizing cream, topical glucocorticosteroids or 2-5% crude coal tar ointment. PUVA or UVB-311 therapy very effective.
Synonyms: Discoid eczema, microbial eczema.
Figure 2-22. Nummular eczema Pruritic, round, nummular (coin-shaped) plaques with erythema, scales, and crusts on the posterior legs.
Autosensitization Dermatitis ICD-9: 692.9 ICD-10: L30.9
An often unrecognized generalized pruritic dermatitis directly related to a primary dermatitis elsewhere.
For example, a patient with venous stasis dermatitis on the lower legs may develop pruritic, symmetric, scattered, erythematous, maculopapular, or papulovesicular lesions on the trunk, forearms, thighs, or legs.
These persist and spread until the basic underlying primary dermatitis is controlled.
Similarly, autosensitization may occur as an “id” reaction in inflammatory tinea pedis and manifests as a dyshidrosiform, vesicular eruption on the feet and hands (Fig. 2-23) and papulovesicular eczematoid lesions on the trunk.
The phenomenon results from the release of cytokines in the primary dermatitis, as a result of sensitization. These cytokines circulate in the blood and heighten the sensitivity of the distant skin areas.
The diagnosis of autosensitization dermatitis is often post hoc; i.e., the distant eruption disappears when the primary dermatitis is controlled.
Oral glucocorticoids hasten the disappearance of the lesions.
Figure 2-23. Autosensitization dermatitis (“id” reaction): dermatophytid Vesicles and bullae on the finger and the lateral foot of a 21-year-old female. Bullous (inflammatory) tinea pedis was present and was associated with dermatophytid reaction. Prednisone was given for 2 weeks; pruritus and vesiculation resolved.
Seborrheic Dermatitis ICD-9: 609.1 ICD-10: L21.9 
A very common chronic dermatosis characterized by redness and scaling and occurring in regions where the sebaceous glands are most active, such as the face and scalp, the presternal area, and in the body folds. Mild scalp SD causes flaking, i.e., dandruff.
Hereditary diathesis, but Malassezia furfur may play a pathogenic role.
Increased incidence in Parkinson disease and in immunosuppressed patients (HIV/AIDS).
Synonyms: “Cradle cap” (infants), pityriasis sicca (dandruff).
Epidemiology and Etiology
Age of Onset. Infancy (within the first months), puberty, most between 20 and 50 years or older.
Sex. More common in males.
Incidence. Two to five percent of the population.
Pathogenesis, Predisposing, and Aggravating Factors
There is a hereditary diathesis, the so-called seborrheic state, with marked seborrheic and marginal blepharitis. May be associated with psoriasis as a “prepsoriasis state,” and the mix of superficial scales on scalp and eyebrows and psoriasiform plaques on the trunk suggest the use of the term seborrhiasis. M. furfur may play a role as suggested by the response to ketoconazole and selenium sulfide. There is an increase in incidence in Parkinson disease and facial paralysis and in immunosuppressed patients (HIV/AIDS and cardiac transplants). SD-like lesions occur in nutritional deficiencies (zinc deficiency, experimental niacin, and pyridoxine deficiency). Intractable SD should be a clue to the existence of HIV disease (see Section 32).
Clinical Manifestation
Duration of Lesions. Gradual onset.
Seasonal Variations. Some patients are worse in winter in a dry, indoor environment. Sunlight exposure causes SD to flare in a few patients and promotes improvement of the condition in others.
Skin Symptoms. Pruritus is variable, often increased by perspiration.
Skin Lesions. Orange-red or gray-white skin, often with “greasy” or white dry scaling macules, papules of varying size (5-20 mm), or patches, rather sharply marginated (Fig. 2-24). On the scalp, there is mostly marked scaling (“dandruff”), diffuse involvement of scalp. Scattered, discrete on the face. Nummular, polycyclic, and even annular on the trunk.
Figure 2-24. Seborrheic dermatitis of face: adult type Erythema and yellow-orange scaling the forehead, cheeks, nasolabial folds. Scalp and retroauricular areas were also involved.
Distribution and Major Types of Lesions (Based on Localization and Age). Hairy Areas of Head. Scalp, eyebrows, eyelashes (blepharitis), beard (follicular orifices); cradle cap: erythema and yellow-orange scales and crusts on the scalp in infants.
Face. The flush (“butterfly”) areas on forehead (“corona seborrhoica”), nasolabial folds, eyebrows, and glabella (Fig. 2-24). Ears: retroauricular, meatus, sticky crusts, and fissures.
Trunk. Simulating lesions of pityriasis rosea or pityriasis versicolor; yellowish-brown patches over the sternum common.
Body Folds. Axillae, groins, anogenital area, submammary areas, umbilicus, and diaper area in infants (Fig. 2-25)—presents as a diffuse, exudative, sharply marginated, brightly erythematous eruption; erosions and fissures common.
Figure 2-25. Seborrheic dermatitis: infantile type Erythema scales and crusting in the diaper region of an infant. This is difficult to distinguish in the diaper region from psoriasis and Candida has to be ruled out by KOH.
Genitalia. Often with yellow crusts and psoriasiform lesions.
Diagnosis/Differential Diagnosis
Made on clinical criteria.
Red Scaly Plaques. Common. Mild psoriasis vulgaris (sometimes may be indistinguishable), impetigo (rule out by smears for bacteria), dermatophytosis, pityriasis versicolor, intertriginous candidiasis (rule out dermatophytes and yeasts by KOH), subacute lupus erythematosus (rule out by biopsy), “seborrheic” papules in secondary syphilis (rule out Treponema pallidum by dark field); syphilis serology.
Rare. Langerhans cell histiocytosis (occurs in infants, often associated with purpura), acrodermatitis enteropathica, zinc deficiency, pemphigus foliaceus, glucagonoma syndrome.
Laboratory Studies
Dermatopathology. Focal parakeratosis, with few neutrophils, moderate acanthosis, spongiosis (intercellular edema), and nonspecific inflammation of the dermis. A characteristic feature is neutrophils at the tips of the dilated follicular openings, which appear as crusts/scales.
Course and Prognosis
The condition improves in the summer and flares in the fall. Recurrences and remissions, especially on the scalp, may be associated with alopecia in severe cases. Infantile and adolescent SD disappears with age. Seborrheic erythroderma may occur. Seborrheic erythroderma with diarrhea and failure to thrive in infants (Leiner disease) is associated with a variety of immunodeficiency disorders including defective yeast opsonization, C3 deficiency, severe combined immunodeficiency, hypogammaglobulinemia, and hyperimmunoglobulinemia.
Management
Requires initial therapy followed by chronic maintenance therapy.
Initial Topical Therapy
Scalp. Adults. Shampoos containing selenium sulfide, zinc pyrithione, and/or tar. By prescription (United States), 2% ketoconazole shampoo is very effective; lather can be used on face and chest during shower. Low-potency glucocorticoid solution, lotion, or gels following a medicated shampoo (ketoconazole or tar) for more severe cases. Pimecrolimus, 1% cream, is very beneficial.
Infants. For cradle cap, removal of crusts with warm olive oil compresses, followed by baby shampoo, 2% ketoconazole shampoo, and application of 1-2.5% hydrocortisone cream, 2% ketoconazole cream, and 1% pimecrolimus cream.
Face and Trunk. Ketoconazole shampoo, 2%. Glucocorticoid cream and lotions: initially 1% or 2.5% hydrocortisone cream; in more resistant cases, clobetasol propionate, 2% ketoconazole cream, 1% pimecrolimus cream, and 0.03% or 0.1% tacrolimus ointment.
Eyelids. Gentle removal of the crusts in the morning with a cotton ball dipped in diluted baby shampoo. Apply 10% sodium sulfacetamide in a suspension containing 0.2% prednisolone and 0.12% phenylephrine. Sodium sulfacetamide ointment alone is also effective, as is 2% ketoconazole cream, 1% pimecrolimus cream, or 0.03% tacrolimus ointment.
Intertriginous Areas. Ketoconazole, 2%. If uncontrolled with these treatments, castellani paint for dermatitis of the body folds is often very effective, but staining is a problem. Pimecrolimus cream, 1%; tacrolimus ointment, 0.03% or 0.1%.
Systemic Therapy
In severe cases, 13-cis-retinoic acid orally, 0.5 to 1 mg/kg, is highly effective. Contraception should be used in females of childbearing age. In milder cases, itraconazole 100 mg twice daily for 2 weeks is also effective.
Maintenance Therapy
Ketoconazole 2% shampoo, tar shampoos, and ketoconazole cream are effective. If these do not work, then the old “standard,” 3% sulfur precipitate and 2% salicylic acid in an oil-in-water base is effective. Also, 1-2.5% hydrocortisone cream daily will work, but patients should be monitored for signs of atrophy; 1% pimecrolimus cream and 0.03% tacrolimus ointment are safe and effective.
Asteatotic Dermatitis ICD-9: 692.89 ICD-10: L30.9
A common pruritic dermatitis that occurs especially in older persons, in the winter in temperate climates—related to the low humidity of heated houses.
The sites of predilection are the legs (Fig. 2-26), arms, and hands but also the trunk.
Dry, “cracked,” superficially fissured skin with slight scaling.
The incessant pruritus can lead to lichenification, which can even persist when the environmental conditions have been corrected.
The disorder results from too frequent bathing in hot soapy baths or showers and/or in older persons living in rooms with a high environmental temperature and low relative humidity.
Management: Avoiding over bathing with soap, especially tub baths, and increasing the ambient humidity to >50%, by using room humidifiers; also using tepid water baths containing bath oils for hydration, followed by immediate liberal application of emollient ointments, such as hydrated petrolatum. If skin is inflamed, use medium-potency glucocorticoid ointments, applied twice daily until the eczematous component has resolved.
Synonyms: Eczema craquelé (French craquelé, “marred with cracks,” such as in old china and ceramic tile).
Figure 2-26. Asteatotic dermatitis In this 65-year-old man, lesions have coalesced to involve the entire skin of the lower leg.