Eczematous Rashes

Definition

Atopic dermatitis is a chronic, relapsing, intensely pruritic, inflammatory condition of the skin that is associated with a personal or family history of atopic disease (e.g., asthma, allergic rhinitis, or atopic dermatitis). The cause of atopic dermatitis is thought to be altered skin barrier and immune function. Patients appear to have a genetic predisposition that can be exacerbated by numerous factors, including food allergy, skin infections, irritating clothes or chemicals, change in climate, and emotions. Lichenification is the clinical hallmark of chronic atopic dermatitis ( Fig. 8.1 ).

Incidence

Atopic dermatitis is predominantly a disease of childhood, with 17% of children and 6% of adults affected. It usually starts after 2 months of age, and by 5 years of age, 90% of the patients who will develop atopic dermatitis have manifested the disease. It is uncommon for adults to develop atopic dermatitis without a history of childhood eczema.

History

A history of allergic respiratory disease is found in one-third of patients with atopic dermatitis and in two-thirds of their family members. Pruritus ( Fig. 8.1D ) is the most distressing and prominent symptom.

Physical Examination

The morphology and distribution of atopic dermatitis are age-dependent ( Fig. 8.2 ). Infantile atopic dermatitis is characterized by acute-to-subacute eczema with papules, vesicles, oozing, and crusting. It is distributed over the head, diaper area, and extensor surfaces of the extremities. In children and adults, the eruption is a chronic dermatitis with lichenification and scaling. The distribution includes the neck, face, upper chest, and, characteristically, antecubital and popliteal fossae ( Fig. 8.1 ).

Individuals with atopic dermatitis have a characteristic expression. The face has mild to moderate erythema, perioral pallor, and infraorbital folds (Dennie–Morgan lines) associated with dermatitis and hyperpigmentation. The skin generally is dry and may have generalized fine, whitish scaling. The palms often have increased linear markings.

Differential Diagnosis

The differential diagnosis of atopic dermatitis includes other eczematous eruptions and scabies . The history of other family members with pruritus and a thorough skin examination that reveals burrows, particularly on the hands, are diagnostic of scabies. Infants with Langerhans cell histiocytosis and immunodeficiency syndromes such as Wiskott–Aldrich syndrome, ataxia-telangiectasia , and Swiss-type agammaglobulinemia have dermatitis that resembles atopic dermatitis, but these conditions are rare, and the infants have systemic symptoms that distinguish their conditions from atopic dermatitis.

Laboratory and Biopsy

The diagnosis of atopic dermatitis is made clinically. The skin biopsy (rarely required) reveals an eczematous change that is not specific for atopic dermatitis ( Fig. 8.1B ). Serum immunoglobulin (Ig)E concentration is frequently raised, but usually is not necessary to make the diagnosis.

Therapy

The treatment of atopic dermatitis is the same as for other eczematous eruptions and includes topical steroids, topical macrolide immunosuppressants, and systemic antihistamines. However, the use of antihistamines to reduce pruritus is largely unproven. Only sedating antihistamines may be effective for itching that interferes with sleep. Treatment should be given in appropriate strength and frequency to reduce inflammation and itching significantly. A common error is under treatment. Occasionally, a short course of systemic steroids (prednisone) is necessary to bring the disease under control. Wet dressings (plain water) and bleach baths are helpful in treating acute atopic dermatitis. Avoidance of environmental factors that enhance itching, such as woolen clothes, emotional stress, and uncomfortable climatic conditions, is important. Moisturizers reduce dry skin and itching. Ultraviolet radiation B (UVB), psoralen plus ultraviolet radiation A (PUVA), or other systemic immunosuppressants – cyclosporine (Neoral), azathioprine (Imuran), mycophenolate mofetil (CellCept), and dupilumab (Dupixent) – may be considered if satisfactory control is not achieved with initial treatment.

In some children, food allergy can cause atopic dermatitis. Skin testing or radioallergosorbent tests may help to identify foods that are responsible. Positive tests must be confirmed with controlled food challenges and elimination diets. Eggs, peanuts, milk, and wheat appear to be the most frequently offending foods. Investigators have suggested that atopic dermatitis can be prevented by avoiding cow’s milk, wheat, and eggs for the first 6 months of life. However, this approach is controversial and not generally recommended. Patients with atopic dermatitis have a higher frequency of immediate skin test reactivity in general, but hyposensitization is rarely of value in atopic dermatitis. As a last resort, severe atopic dermatitis is treated with systemic immunomodulants.

Course and Complications

Atopic dermatitis is a chronic disease punctuated by repeated acute flare-ups followed by longer periods of slow resolution. The cause of these flare-ups is frequently unknown – a feature that adds to the frustration of this disease. Most children (90%) outgrow their disease by adolescence, although as adults, some continue to have localized forms of atopic dermatitis such as chronic hand or foot dermatitis, patches of lichen simplex chronicus, or eyelid dermatitis. Longitudinal studies suggest an “atopic march” in which over half of infants and children with atopic dermatitis will progress to develop allergic rhinitis and asthma.

Atopic dermatitis is frequently complicated by skin infections. Atopic skin has a higher rate of colonization with Staphylococcus aureus . The most serious cutaneous infection is Kaposi’s varicelliform eruption . This widespread vesiculopustular eruption is caused by herpes simplex (eczema herpeticum), variola, or vaccinia virus. Patients with this infection are acutely ill and may die; for this reason, smallpox immunization was contraindicated in these patients. The hyper-IgE syndrome refers to a syndrome of atopic dermatitis characterized by recurrent pyoderma (skin infections), raised serum IgE levels, and decreased chemotaxis of mononuclear cells.

Pathogenesis

Atopic dermatitis is a multifactorial cutaneous inflammatory disease caused, in part, by gene polymorphismisms affecting the innate and adaptive immune response and the epidermal barrier function. A disrupted skin barrier (filaggrin gene mutation) and disturbed immunologic response (Th2 + Th1 cytokines, and IgE) have been implicated in the etiology of atopic dermatitis. The epidermal barrier defect results in dry skin and penetration of irritants, microbes, and antigens. The immunologic changes are most notable and frequent in patients with severe atopic dermatitis. These changes include raised serum IgE levels, defective cell-mediated immunity, decreased chemotaxis of mononuclear cells, increased T-lymphocyte activation with production of T helper Th1 and Th2 cytokines, and hyper stimulatory Langerhans cells. The increased IgE concentration is thought to reflect decreased numbers of T-suppressor cells and uninhibited production of IgE. Depressed cell-mediated immunity is manifested by an increased susceptibility to cutaneous viral and bacterial infections. In addition, responses to in vitro tests of cell-mediated immunity such as lymphocyte blastogenesis to mitogens and antigens are blunted. There are also low levels of antimicrobial peptides in lesional skin resulting in increased susceptibility to pathogens such as S. aureus , herpes simplex virus, and vaccinia virus.

Definition

Contact dermatitis ( Fig. 8.3 ) is an inflammatory reaction of the skin precipitated by an exogenous chemical. The two types of contact dermatitis are irritant and allergic. Irritant contact dermatitis is produced by a substance that has a direct toxic effect on the skin. Allergic contact dermatitis triggers an immunologic reaction that causes tissue inflammation. Examples of irritants include acids, alkalis, solvents, and detergents. Innumerable chemicals cause allergic contact dermatitis, including metals, plants, medicines, cosmetics, and rubber compounds. Clinical appearance can range from acute (vesicles) to chronic (lichenification) eczematous reactions.

Incidence

Contact dermatitis is a frequent problem that most people experience during their lifetime, whether it is irritant diaper dermatitis or allergic poison ivy or oak dermatitis. A significant cause of occupational illness (excluding injury) is caused by contact dermatitis, resulting in impairment and time lost from work. In occupational contact dermatitis, irritant is usually more common than an allergic etiology.

History

One should first determine whether the contact dermatitis is an allergic or an irritant phenomenon. Skin damage is usually evident within several hours of contact with a strong irritant. Weaker irritants, however, may require multiple applications days before the development of dermatitis. Allergic contact dermatitis usually appears 24 to 48 hours after exposure, before the development of clinical disease. Occasionally, the dermatitis may develop as soon as 8 to 12 hours after contact or may be delayed as long as 4 to 7 days. The history of a precipitating contactant may be either obvious or obscure. Detailed history of occupation, hygienic habits, and hobbies is frequently necessary to find the contactant.

Poison ivy or oak is a frequent cause of allergic contact dermatitis in the summer ( Fig. 8.4 ). The sensitizing allergens are pentadecylcatechol and heptadecylcatechol chemicals located in the sap (urushiol) of the plant. Another familiar member of this family of poisonous plants is poison sumac . Less frequently recognized family members are cashew, mango, and lacquer trees. Sensitization to poison ivy results in sensitivity to the other poisonous plants in this family. The characteristic eruption resulting from contact with poison ivy or oak is manifested by linear streaks of papules and vesicles along with cellulitic appearing plaques and patches. Contact with the smoke of burning plants can result in confluent severe dermatitis of the exposed skin.

Cosmetics (personal care products) contain fragrances and preservatives that cause allergic contact dermatitis, particularly affecting the faces of women from the use of make-up and moisturizers, for example. Paraphenylenediamine is a dye found in permanent hair coloring. Sensitization to paraphenylenediamine occurs in hairdressers and in clients who have their hair colored. When completely oxidized, as the dye on a fur coat, paraphenylenediamine is not allergenic.

Nickel sensitivity is seen most often in women as a result of wearing “cheap” pierced earrings. It is found in many metal alloys ( Fig. 8.5 ). One cannot be certain that the commonly advertised “hypoallergenic” earrings are nickel-free. Although stainless steel contains nickel, it is bound so tightly that it usually does not allow an allergic reaction to occur.

Rubber compounds are ubiquitous. Shoes and gloves are the most common sources of allergic contact dermatitis caused by these chemicals. An eczematous reaction limited to the feet or hands is typical of shoe and glove dermatitis, respectively. The most frequent rubber allergens are mercaptobenzothiazole and thiuram .

In sleuthing the causes of contact dermatitis, one must not overlook the possibility of a topical medication perpetuating or exacerbating a preexisting dermatitis. Neomycin and bacitracin , found in topical antibiotic preparations, cause allergic contact dermatitis when these agents are used to treat cuts and abrasions, chronic ulcers, and surgical wounds.

Physical Examination

Contact dermatitis may be acute or chronic. The configuration of the lesions depends on the nature of the exposure, which may result in patches or plaques with angular corners, geometric outlines, and sharp margins. Poison ivy or oak characteristically causes linear streaks of papulovesicles.

The location of the dermatitis is helpful in predicting the causative irritant or allergen. The head and neck are frequent sites of contact dermatitis from fragrances and preservatives found in cosmetics. Hair dyes, permanent wave solutions, and shampoos produce dermatitis on the scalp. Eczema of the eyelids is caused by eye cosmetics or allergens that have been transferred from the hands, such as nail polish. Photoallergic contact dermatitis from sunscreens is produced by a photoreaction between sunlight and an allergen in exposed areas of the skin, such as the head, neck, V-shaped area of the chest, and arms. The hands are the most common area of contact dermatitis from industrial chemicals, particularly an irritant reaction from detergents, petroleum products, and solvents. Dermatitis of the feet is produced by allergens in shoes, such as rubber chemicals and leather tanning agents. The groin and buttocks in infants are frequently affected by diaper dermatitis ( Fig. 8.6 ). This condition is an irritant contact dermatitis from moisture and feces. Diaper dermatitis is often complicated by secondary infection with bacteria and yeast.

Differential Diagnosis

Morphologically, contact dermatitis is identical to other eczematous eruptions and may complicate atopic or stasis dermatitis if the patient becomes sensitized to the topical preparation used to treat these dermatoses. Other causes of eczematous appearing dermatoses that may need to be ruled out include superficial fungal infections and bacterial cellulitis . In bacterial cellulitis, the skin is painful (rather than pruritic), and the patient is often febrile.

Laboratory and Biopsy

No standard testing method is available for diagnosing irritant contact dermatitis. For allergic contact dermatitis, the causative agent can be identified by patch tests, but these tests must be properly performed and interpreted (see Chapter 3 ). Patch testing is done with a screening patch test series. This series is composed of medications, fragrances, preservatives, metals, rubber compounds, and miscellaneous chemicals. Individual chemicals and special trays (e.g., allergens found in plants) supplement the screening series. The chemicals are applied to patches that are taped on the back of the test subject. After 48 hours, the patches are removed and the test site is examined for an eczematous reaction that is graded according to a standard interpretation key: a + 1 reaction indicates palpable erythema; a + 2 reaction indicates papules and vesicles; and a + 3 reaction indicates bullae. A further delayed reading 1 to 2 days after patch removal is mandatory. Although the patch-testing procedure is simple, its interpretation is often difficult. A positive patch test must be relevant to the eruption to be meaningful ( Fig 8.7 ). Unknown chemicals and potential irritants must be patch tested cautiously and are best left to trained personnel who have experience in patch testing.

Biopsy ( Fig. 8.3B ) of contact dermatitis cannot differentiate between irritant and allergic causes. Contact dermatitis also cannot be differentiated histologically from other causes of eczematous eruptions such as atopic or seborrheic dermatitis.

Therapy

Prevention of contact dermatitis is the most logical, but often most difficult, solution. Avoidance of an irritant or allergen may require a change in lifestyle or occupation. Sometimes, protective clothing is curative. Allergens that have high sensitizing potential are best used in closed systems in which workers have virtually no contact with the offending chemicals. Protective or barrier creams are of questionable benefit. Sometimes, the offending material can be substituted with another, less toxic or allergenic, chemical. Predictive testing for contact irritancy or sensitivity is standard procedure before introducing new cosmetics or chemicals.

Acute, severe, generalized contact dermatitis is treated with a short course of systemic steroids: 40 to 60 mg prednisone daily for a minimum of 5 days and then tapered over the next 5 days or 1 mL triamcinolone suspension (Kenalog-40) intramuscularly. Astringent dressings (Domeboro) or soothing baths (Aveeno) reduce weeping and itching. Milder dermatitis responds to topical steroids (see Table 4.1) or to macrolide immunosuppressants (Protopic or Elidel). Systemic antihistamines such as 10 to 25 mg hydroxyzine (Atarax) or 25 to 50 mg diphenhydramine (Benadryl) four times daily are helpful for pruritus.

Course and Complications

Acute allergic contact dermatitis subsides within 3 to 4 weeks. If the patient has repeated exposure to the contactant, chronic dermatitis will develop. With the breakdown of the epidermal barrier, secondary bacterial infection may complicate contact dermatitis. Although contact dermatitis may start locally, generalized hypersensitivity of the skin can occur, with resultant generalized dermatitis autosensitization.

Pathogenesis

Irritant contact dermatitis is a nonspecific inflammatory reaction resulting from toxic injury of the skin. Allergic contact dermatitis is a cell-mediated, delayed type IV immunologic reaction. It is divided into a sensitization phase and an elicitation phase. The sensitization phase occurs when a chemical (hapten) is applied to the skin of a nonsensitized individual. This chemical in itself is unable to induce an allergic reaction because of its small molecular size, which is usually less than 500 Daltons (Da). It must combine with an epidermal protein thought to be on the surface of the Langerhans cell (epidermal macrophage). After the formation of the hapten–protein complex, the Langerhans cell presents the allergen to T lymphocytes in the lymph node, where effector, memory, and suppressor lymphocytes are produced. The period of sensitization requires approximately 7 to 10 days. The elicitation phase occurs in sensitized individuals 1 to 2 days after reexposure to the antigen. After presentation of the antigen by Langerhans cells to memory T cells in the skin, effector T cells produce lymphokines, which recruit other inflammatory cells and produce allergic contact dermatitis. The dermatitis usually appears clinically 1 to 2 days after the elicitation exposure. The reaction is thought ultimately to be extinguished by suppressor T cells.

Definition

Essential (nonspecific) dermatitis is an epidermal eruption that may be acute ( Fig. 8.8 ) or chronic ( Fig. 8.9 ), and localized or generalized. It is a diagnosis that is made by exclusion when an underlying cause such as an allergen or irritant cannot be found, and its distribution is not typical of defined eczematous eruptions such as atopic or seborrheic dermatitis.

Incidence

Essential dermatitis is one of the eruptions most frequently seen by the clinician. Some 11% of the authors’ patients had this diagnosis.

History

Itching is the chief complaint prompting patients to seek medical attention. It is often severe enough to interfere with normal daily activities and to interrupt sleep. The itching may be episodic or constant. The patient frequently has a history of “sensitive skin” that is intolerant to topical preparations such as moisturizers, soaps, and detergents and to irritating fabrics such wool.

Physical Examination

The varied appearance of essential dermatitis occurs because of its evolution from an acute to a chronic process. Acutely, intercellular edema leads to vesiculation. Chronically, lichenification occurs. The polymorphism is manifest by vesicles, juicy papules, patches, and plaques. Secondary changes include oozing, crusting, scaling, and fissuring. Characteristic of essential dermatitis is the indistinct border between normal and abnormal skin.

Depending on the morphology and location, various types of dermatitis have been classified. Dyshidrotic eczema is characterized by deep-seated vesicles (which resemble the pearls in tapioca pudding) involving the hands (palms), feet (soles), and sides of the digits. It occurs bilaterally and symmetrically. Autosensitization or id eruption is a generalized subacute dermatitis that follows a localized acute dermatitis, usually of the feet or hands. It is thought to be a hypersensitivity reaction to a substance produced by the acute dermatitis. Xerotic eczema ( Fig. 8.10 ) is the result of low humidity and dry skin. It occurs in the winter and is manifest by dry fissured skin of the trunk and extremities. It particularly affects the elderly and the lower legs of all age groups. Nummular eczema is characterized by oval, weeping patches with crusted papulovesicles ( Fig 8.11 ). It occurs on the trunk and extremities.