Dermatitis and Eczema
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[edit] Dermatitis and Eczema
James C. Shaw
When the term eczema is used alone, it usually connotes atopic dermatitis. Dermatitis and eczema are frequently used interchangably for numerous disorders, each with qualifiers. Although these diseases have multiple etiologies, they have some clinical features in common and are therefore grouped. Symptoms of pruritus and morphologic features of erythema, papules, microvesicles, excoriation, and lichenification (in older lesions) are commonly found in all diseases within this category.
[edit] ATOPIC DERMATITIS
Atopic dermatitis is a chronic skin disease characterized by pruritus, erythema, skin inflammation, and lichenification typically distributed in flexural areas, plus a personal or family history of asthma, hay fever, or eczema. The term atopy refers to the triad of dermatitis, asthma, and hay fever.
[edit] Epidemiology
Atopy (atopic dermatitis, asthma, or hay fever) is present in 8% to 25% of populations. Atopic dermatitis is present in all races and geographic locations, but there appears to be a higher incidence in urban areas and developed countries. Although the trait runs in families, the precise genetics have not been fully elucidated. A family history of respiratory atopy can be obtained in almost 50% of patients with atopic dermatitis.[1] Mothers with respiratory atopy have atopic children more often (26%) than do fathers with respiratory atopy (13%),[2] and chromosome studies have suggested that the trait for atopy may be inherited on a maternal gene.[3]
[edit] Pathophysiology
Atopy is characterized immunologically by high concentrations of serum IgE, a high incidence of IgE-mediated response by skin test to common inhaled antigens, decreased numbers of immunoregulatory T cells, defective antibody– dependent cellular cytotoxicity, and reduced cell-mediated immunity.[1]
Criteria for making the diagnosis of atopic dermatitis have been proposed (Table 86-1). Three major criteria plus three minor criteria should be present to confirm the diagnosis.
Table 86-1 Differential Diagnosis of Dermatitis
| Diagnosis | History | Physical examination | Laboratory | Management |
|---|---|---|---|---|
| Atopic dermatitis | Onset by age 5 | Flexural distribution | Routine: none | Topical corticosteroids |
| Family history of atopy | Lichenification | Consider: | Control environment | |
| Pruritus | Papules, erythema | Culture/pustule | Antihistamines | |
| Exacerbating factors | Pustules if secondary | IgE | Emollients | |
| Coexistent hay fever, asthma | Staphylococcus aureus | |||
| Contact dermatitis | ||||
| Irritant type | Predisposing history of atopy | Hands commonly | None | Topical steroid ointments |
| Frequent water exposure | Erythema, scale, fissuring | Protect from wet exposures | ||
| Solvents | Gloves | |||
| Job description | Emollients | |||
| Allergic type | Rapid onset | Erythema, vesicles, oozing | None | Wet to dry dressings |
| Pruritus | Location corresponds to exposure | Topical or systemic corticosteroids | ||
| Exposures: | ||||
| Plants | Identify and avoid allergen | |||
| Cosmetics | ||||
| Stasis dermatitis | Gradual onset | Erythema | None | Acute: steroid ointments |
| Distal legs | Pigmentation | Long-term: compression, leg elevation, emollient ointments | ||
| Previous history of varicosities, leg trauma, etc | Edema | |||
| Fibrosis | ||||
| Xerotic dermatitis | Winter | Patchy erythema, scale on extensor areas | None | Decrease soap and water exposure |
| Low humidity | ||||
| Frequent baths | Spares folds | Liberal use of thick emollients, especially after bath | ||
| Soap use | ||||
| Pretibial common | ||||
| Steroids: short-term prn | ||||
| Dyshidrosis | Pruritic papules and vesicles on hands | Papules and small vesicles on hands | None | Systemic or topical steroids |
| Exclude fungus with KOH | ||||
| Recurrent | Antibiotics | |||
| Exclude allergen | ||||
| Nummular dermatitis | Gradual onset | Round patches | None | Steroid ointments |
| Pruritus | Erythema | KOH to exclude fungus | Tar cream, gel | |
| Frequent history of exposure to drying (see Box 86-3) | Scaling | Ultraviolet light | ||
| Oozing | ||||
| KOH, Potassium hydroxide. | ||||
[edit] Patient Evaluation
[edit] History.
A suggestive history includes onset of a dermatitis at an early age (most patients have manifestations of atopic dermatitis by age 5), pruritus, the existence of exacerbating factors (Box 86-1), and a positive family history of atopy.
| Box 86-1 - Controlling Atopic Dermatitis✢ |
Protect Skin From the Following Agents
|
[edit] Examination.
Papules, erythema, excoriations, and lichenification are the hallmarks of atopic dermatitis. In adults, flexural areas, such as the neck, antecubital fossae and popliteal fossae, are most commonly involved ( Plate 34 ). The face, wrists, and forearms are also common sites of involvement. In severe cases, any area of the body can be involved. Infants usually present with pruritic patches of erythema and papules that can be present more centrally on the face, chest, and extensor extremities. Pustules suggest secondary infection with Staphylococcus aureus. Other physical findings that support the diagnosis include xerosis, the infraorbital skin fold (Dennie-Morgan line), periorbital darkening, hyperlinear palms, keratosis pilaris, and nipple dermatitis.
[edit] Diagnosis
Diagnosis is made on the basis of personal and family history and clinical features.[4] There are no definitive laboratory tests. The differential diagnosis includes the other diseases in this chapter (see Table 86-1).
[edit] Management
The treatment of atopic dermatitis centers around the following three principles:
- Treatment of inflamed skin
- Control of itching
- Control of exacerbating factors
The first two usually require pharmacologic treatment, while control of exacerbating factors is usually nonpharmacologic.
To treat inflamed skin, topical corticosteroids are the primary modality. For mild disease, a low potency (class VI or VII) corticosteroid cream is effective. For more severe disease a medium potency (class IV or V) corticosteroid cream or ointment may be needed. Secondary infection requires oral antibiotics. Acute flares can sometimes be aborted by a short course of systemic corticosteroids (i.e., prednisone 40 to 60 mg/day for 3 to 4 days, then 20 to 30 mg/day for 3 to 4 days). The most severe cases require combinations of treatments that can include systemic corticosteroids, cyclosporin, FK-506, methotrexate, azothiaprine, and ultraviolet light therapy.
To control pruritus, antihistamines usually are helpful. Considerable trial and error may be required to identify the antihistamine best for the individual patient. Sedating H1 blockers are best. Commonly used H1 blockers include diphenhydramine, hydroxyzine, cetirizine, and doxepin. Tepid baths to hydrate and cool the skin can also relieve itching temporarily but must be followed immediately by emollients.
An important aspect of successful treatment of atopic dermatitis is the use of emollients. When used frequently and liberally, emollients can prevent drying of the skin, which is effective in the control of pruritus (see Chapter 83 ).
Controlling exacerbating factors can be helpful in the acute phase and in long-term management. There may be multiple exacerbating factors that need to be controlled (see Box 86-1).
Allergy testing by prick test in atopic dermatitis is rarely beneficial. Atopic patients frequently have allergic responses to multiple allergens, and the elimination of these is usually not feasible. In individual cases, elimination of a particular food may help control exacerbations, but in the majority of cases, searching for foods to eliminate is without benefit.
[edit] CONTACT DERMATITIS
Contact dermatitis refers to any dermatitis caused by external substances that come in contact with the skin directly. Contactants can induce either allergic or irritant contact dermatitis, either of which can be acute, subacute, or chronic.[5]
[edit] Irritant Contact Dermatitis
Irritant contact dermatitis is more common than allergic contact dermatitis. It occurs when a chemical disrupts the normal epidermal barrier and causes an inflammatory response. Most irritants are those used on a daily basis and are found in most living and work environments. These generally are low-grade irritants that require repeated exposure to produce a dermatitis (soapy water, cleansers, rubbing alcohol). Some irritants are highly caustic, producing severe dermatitis after minimal exposure (bleach, strong acids, alkalis). Although anyone can develop irritant contact dermatitis, those with compromised skin (atopic dermatitis, dry skin) are at a higher risk.
[edit] Examination.
Mild irritants produce erythema, chapped skin, dryness, and fissuring. Pruritus is usually mild to moderate. The hands are the usual site for irritant contact dermatitis (see Plate 11 ), but the face, especially the eyelids, may be affected. Severe cases can present with edema, serous oozing, and tenderness. Potent irritants cause painful bullae within hours of the exposure.
[edit] Management
The goals of treatment of irritant contact dermatitis are to restore a normal epidermal barrier and then protect it from the irritating substance. Reduced exposure to soap and water, use of emollient creams or ointments, and use of gloves in hand dermatitis may control a chronic irritant contact dermatitis. In more severe cases, corticosteroid ointments under occlusion may be necessary to treat the acute phase. Systemic corticosteroids, although potentially helpful in reducing acute inflammation, have no place in the treatment of chronic irritant contact dermatitis unless corrective measures are taken to avoid the offending contactants.
[edit] Allergic Contact Dermatitis
Allergic contact dermatitis occurs when a delayed (type IV) hypersensitivity to a substance develops. This hypersensitivity can occur after one exposure (poison ivy) or after years of repeated exposure to an antigen (fragrances, nickel).
[edit] Pathophysiology.
The antigen, usually of low molecular weight, binds to epidermal proteins and is presented by Langerhans cells to T-lymphocytes in the dermis, as well as lymph nodes, where sensitized T-lymphocytes are expanded. The allergic dermatitis occurs when the sensitized lymphocytes encounter the antigen in the skin and release inflammatory mediators. The sensitization phase takes 10 to 14 days, but dermatitis may be seen in a sensitized individual within 12 to 48 hours after reexposure.
The most common sensitizer in the United States is the oleoresin of the Rhus family of plants (poison oak, poison ivy, poison sumac). Other common sensitizers include nickel in jewelry, fragrances, preservatives in topical preparations, components in rubber, and chemicals in shoes.
[edit] History.
Intense itching in the area of exposure, followed by the development of a pruritic rash is typical of acute allergic contact dermatitis. The exposure can antedate the dermatitis by 2 weeks, if it is the result of a primary sensitization. Frequently an exact date of exposure is difficult to identify. In chronic cases, the dermatitis may have been present for months or years.
[edit] Examination.
Clinical findings include erythema, edema, papules, vesicles, and serous oozing in the involved areas. In Rhus dermatitis there are frequently linear streaks of dermatitis corresponding to areas of contact with the plant resin ( Plate 35 ). The extent of the dermatitis reflects the source of exposure, i.e., cosmetics on the face, nickel where jewelry is worn, rubber where elastic bands contact the skin, and points of shoe contact on the feet.
[edit] Management.
Wet to dry compresses with water or aluminum acetate (Burow's solution) help dry the vesicular phase when indicated (see Chapter 83 ). Topical corticosteroids are helpful after the skin is dry enough to retain the topical preparation. In severe cases, systemic corticosteroids and antihistamines may be required. Usually, elimination of the offending antigen is curative, but in persistent cases, correct identification of the antigen may require patch testing. Referral to a dermatologist for possible patch testing is especially useful when multiple potential exposures exist such as in certain work environments.
[edit] Latex Dermatitis
Latex allergy has become an increasingly prevalent medical problem frequently presenting with hand dermatitis. Serious anaphylactic reactions, including several deaths, have been caused by latex allergy during procedures involving latex exposure, such as barium enemas, vaginal examinations, and dental procedures, all of which involve mucous membranes. In addition to type I hypersensitivity reactions, latex can cause allergic contact dermatitis (type IV) and irritant contact dermatitis.[6][7]
[edit] Epidemiology and Pathophysiology.
The highest prevalence of latex sensitization (18% to 73%) occurs in individuals with spina bifida. Risk factors in this group include a history of more than five operations and atopy. Health care workers, especially those with atopy, have the second highest prevalence of latex sensitization (3% to 17%). Several foods cross react with latex; the most common of these are avocado, kiwi, banana, and chestnuts.
[edit] Clinical Manifestations and Diagnosis.
Most cases of latex allergy present with a contact hand dermatitis, either irritant or allergic. Patients may present with rhinitis or asthma from inhalation of latex or anaphylactoid reactions from mucosal contact with latex during procedures.
[edit] Patient Evaluation.
Avoidance of contact may serve as both diagnostic test and treatment in mild cases. In complicated cases, diagnostic evaluation requires patch testing with rubber additives, in vitro IgE antibody testing (radioallergosorbent test [RAST], enzyme-linked immunosorbent assay [ELISA], others), and direct skin testing with latex. Referral to an allergist or dermatologist is indicated in these instances.
[edit] Treatment.
Avoidance of latex is the best treatment. Powder-free latex gloves can eliminate airborne latex exposure. Glove liners may prevent hand dermatitis. Latex sensitive individuals are at risk for anaphylaxis during procedures and should wear a medical alert bracelet to indicate their allergy and carry an anaphylaxis kit. Patients with spina bifida should be screened before surgical operations.
[edit] Stasis Dermatitis
Stasis dermatitis occurs on the legs as a result of chronic venous insufficiency. Incompetent venous valves, inadequate tissue support, and postural hydrostatic pressure contribute to the development of venous stasis. The dermatologic changes are secondary to the effects of extravasated blood, which induces a mild inflammatory response in the dermis and subcutaneous fat, plus the low grade tissue ischemia associated with stasis at the capillary level. Superimposed allergic contact dermatitis or recurrent infections are frequently the predominant finding in patients with stasis dermatitis.
[edit] History.
Symptoms are mild in most cases of stasis dermatitis. There may be a sense of fullness or dull aching in the legs. The patient usually reports a gradual increase in pigmentation and redness.
[edit] Examination.
In early stasis dermatitis there is mottled pigmentation and slight erythema. There may be evidence of varicosities, ankle edema, and mild tenderness to deep palpation. Pulses are usually normal. In chronic cases, fibrosis may be the predominant finding, resulting in a woody, hard sclerotic lower leg.
[edit] Differential Diagnosis.
See Box 86-2.
| Box 86-2 - Differential Diagnosis of Stasis Dermatitis |
|
[edit] Management
[edit] Nonpharmacologic.
The main emphasis in the management of stasis dermatitis is to counteract the effects of gravity and posture on venous pressure. Leg elevation and compression with stockings are the most effective treatment. In mild cases, support hose alone may be sufficient. In more severe cases, daily leg elevation above the level of the head for varying amounts of time may be necessary. Exercise on a regular basis also helps to reduce venous pressure and edema.
[edit] Pharmacologic.
The inflammatory component of stasis dermatitis is treated with low or medium potency topical corticosteroids. An ointment base avoids exposure to preservatives, which can cause allergic contact dermatitis.
[edit] Xerotic Dermatitis
Xerotic (asteatotic) dermatitis is a form of mild irritant dermatitis that occurs in areas of dry skin (Box 86-3). As the skin loses hydration the stratum corneum becomes scaly and develops small cracks that gradually enlarge to form patches of erythema with scaling ( Plate 36 ). These areas are usually intensely pruritic and are worsened by low humidity and exposure to hot water, soap, or solvents. Pretibial areas are most common but the lower back, extensor arms, and thighs may be involved.
| Box 86-3 - Factors That Can Cause Xerosis |
|
[edit] Management.
Treatment of xerotic dermatitis consists of frequent use of emollients to the affected areas, especially after bathing or other water exposure. Topical medium strength corticosteroids help with the pruritus of the acute phase.
[edit] Dyshidrotic Dermatitis
Dyshidrotic dermatitis (pompholyx, dyshidrosis) is an intensely pruritic, chronic recurrent dermatitis that typically involves the palms and soles. The name is misleading, since the disorder has no relationship to eccrine sweating. The etiology of dyshidrosis is uncertain, although ingested allergens and emotional stress have been suggested Plate 37 .
[edit] History.
Intense pruritus on the palms or soles that progresses to multiple small vesicles is typical. The vesicles gradually desquamate over 1 to 2 weeks. Recurrent episodes alternating with disease-free periods are common.
[edit] Examination.
The presence of multiple small vesicles on the palmar or plantar skin, especially along the lateral aspects of the fingers, is suggestive. Desquamation, erythema, cracking, and fissuring may be seen in older lesions. The process is usually symmetric.
[edit] Differential Diagnosis.
See Box 86-4.
| Box 86-4 - Differential Diagnosis of Dyshidrotic Dermatitis |
KOH, Potassium hydroxide. |
[edit] Management.
In mild cases, medium to potent topical corticosteroids can control outbreaks. Systemic corticosteroids are occasionally required in difficult cases.
[edit] Nummular Dermatitis
Nummular dermatitis is a chronic pruritic skin eruption consisting of circular raised patches of erythematous scaly skin. The etiology is not known, although xerosis and emotional stress have been implicated. Adults tend to be affected more than children.
[edit] History.
Patients usually report patches of itchy skin that gradually enlarge in size and increase in number. Individual lesions tend to remain fixed for the duration of the disease process.
[edit] Examination.
Round patches of erythema, scaling, and occasional crust or exudation are suggestive of nummular dermatitis ( Plate 38 ). The term nummular translates literally to “coin shaped.” The distribution is usually extensor areas of extremities, the back, and buttocks. The differential diagnosis includes psoriasis and tinea corporis. A potassium hydroxide (KOH) examination of any scaly lesions is indicated.
[edit] Management.
To reduce acute inflammation, class I topical corticosteroids under occlusive dressings or intralesional corticosteroid injections (triamcinolone 5 mg/cc or betamethasone 6 mg/cc) may be necessary. Emollients throughout the day and especially after water exposure or bathing are essential. In severe cases systemic steroids, antihistamines, topical tar preparations (see Chapter 83 ) and ultraviolet light treatments can be used.
[edit] Lichen Simplex Chronicus and Prurigo Nodules
Lichen simplex chronicus is not a true dermatitis but the result of rubbing or scratching. Although lichen simplex chronicus is usually a patch or plaque of thickened skin, there is a nodular form (prurigo nodularis) that consists of raised thickened nodules with excoriations. A history of chronic persistent itching in the involved area is typical. Patients with renal or hepatic failure and late stage HIV infection commonly have this problem.
[edit] Examination.
In lichen simplex chronicus there is thickened skin with erythema and accentuation of skin lines (lichenification). Usually there is only one area of involvement. Common sites include extremities, posterior neck, buttocks, vulva, scrotum, and anal area. In prurigo nodularis there are several to multiple nodules, 0.5 cm to 1.0 cm in size, scattered over the upper back, arms, and thighs. Areas that are not convenient to reach, such as the central back and posterior thighs, tend to be spared ( Plate 39 ).
[edit] Management.
The treatment of lichen simplex chronicus consists of breaking the itch-scratch cycle. Potent corticosteroids under occlusion may be successful. Intralesional corticosteroid injections and cryotherapy with liquid nitrogen may be required in nodular cases, although the treatment of prurigo nodularis is frequently unsuccessful. Topical capsaicin, ultraviolet light therapy, antihistamines, and antidepressants can be helpful, but persistence over years is common.
[edit] REFERENCES
- ↑ 1.0 1.1 JM Hanifin: Atopic dermatitis. J Am Acad Dermatol 1982; 6:1 - 13.
- ↑ W Kuster, M Peterson, E Christophers,et al.: A family study of atopic dermatitis: clinical and genetic characteristics of 188 patients and 2,151 family members. Arch Dermatol Res 1990; 282:98 - 102.
- ↑ WOCM Cookson, RP Young, AJ Sanford,et al.: Maternal inheritance of atopic IgE responsiveness on chromosome 11q. Lancet 1992; 340:381 - 384.
- ↑ JM Hanifin, G Rajka: Diagnostic features of atopic dermatitis. Acta Derm Venerol Suppl (Stockholm) 1980; 92:44 - 47.
- ↑ AA Fisher: Contact dermatitis ed 3. Philadelphia: Lea & Febiger; 1986:
- ↑ T Michael, B Niggemann, A Moers,et al.: Risk factors for latex allergy in patients with spina bifida. Clin Exp Allergy 1996; 26:934.
- ↑ Sussman G, Gold M: Guidelines for the management of latex allergies and safe latex use in health care facilities, Am Coll Aller Asthma Immunol August, 1996.
