Harrison's Practice

Eczema and Dermatitis

Definition

  • The terms eczema and dermatitis are often used interchangeably and describe an inflammatory skin reaction to both endogenous and exogenous agents.
    • Clinical and histologic findings are variable and represent the final common expression for many disorders.
  • Commonly identified subsets within this category of skin disorders include:
    • Atopic dermatitis
      • Cutaneous expression of an atopic state, characterized by a family history of asthma, hay fever, and/or dermatitis
    • Contact dermatitis
      • Inflammatory process in skin caused by an exogenous agent that directly or indirectly injures the skin
        • Irritant contact dermatitis: caused by 1 or more inherent characteristics of a compound
        • Allergic contact dermatitis: caused by a specific immune response to the contact antigen
    • Hand eczema
      • Common, chronic form of contact dermatitis; often occupation-related
      • May be associated with atopic dermatitis or may occur alone
    • Dyshidrotic eczema
      • A blistering itchy rash of the hands and feet
    • Nummular eczema
      • Characterized by circular or oval "coin-like" lesions
    • Lichen simplex chronicus
      • May represent the end stage of various pruritic and eczematous disorders
      • Well-circumscribed plaques with lichenified or thickened skin due to chronic scratching or rubbing
    • Asteatotic eczema
      • Mildly inflammatory dermatitis that develops in areas of extremely dry skin, especially during dry winter months
      • Also known as xerotic eczema or winter itch
    • Stasis dermatitis
      • Dermatitis on the lower extremities secondary to venous insufficiency and chronic edema
    • Seborrheic dermatitis
      • Common, chronic skin disorder characterized by greasy scales overlying erythematous patches or plaques

Epidemiology

Atopic dermatitis

  • Prevalence
    • Accounts for 10–20% of visits to dermatologists
    • ~20% of infants and young children experience symptoms; 60% continue to have atopic dermatitis in adulthood.
    • > 15 million people in the U.S. are affected.
    • Increasing worldwide
  • Sex
    • Affects both men and women
  • Age
    • 50% present within first year of life.
    • 80% present by 5 years of age.

Contact dermatitis

  • Incidence
    • Occupation-related form affects > 60,000 people annually in the U.S.
    • Accounts for 4–7% of visits to dermatologists
  • Race
    • Thought to be more prevalent among white persons
  • Sex
    • Female-to-male ratio, 2:1
  • Age
    • Most common during adulthood
    • Irritative dermatitis common in infants (e.g., diaper dermatitis)

Hand eczema

  • No epidemiologic statistics available

Dyshidrotic eczema

  • Prevalence
    • ~5% to 20% of patients with hand eczema
  • Geographic distribution and seasonality
    • More common in warmer climates
    • More common in spring and summer months of temperate climates
  • Age
    • Affects all ages (mean age, 38 years)
    • Frequency decreases after middle age.

Nummular eczema

  • Sex
    • More common among men than women
  • Age
    • Most commonly seen in middle-age

Lichen simplex chronicus

  • Sex
    • Affects more women than men
  • Age
    • Usually presents from 20–50 years of age

Asteatotic eczema

  • Seasonality
    • More common in winter months
  • Age and sex
    • More common in men > 60 years of age than in women
    • Can also occur in younger patients

Stasis dermatitis

  • Age
    • Affects 6–7% of patients > 50 years of age in the U.S.
    • Incidence increases with age.
  • Sex
    • Slightly more common in women than in men

Seborrheic dermatitis

  • Prevalence
    • 3–5% worldwide
    • Dandruff occurs in 15–20% of the population.
  • Sex
    • Slightly more common in men than in women
  • Age
    • Peaks at 40 years of age; less severe in older people
    • May occur within first few weeks after birth ("cradle cap"); rare in children beyond infancy

Risk Factors

  • Atopic dermatitis
    • Genetic predisposition
      • If both parents are affected, 80% of children develop the disorder.
      • If 1 parent is affected, slightly more than 50% of children develop the disorder.
      • Personal or family history of atopy (asthma, allergic rhinitis, food allergies, or eczema)
    • Risk factors for atopic dermatitis during the first 2 years of life [1]
      • Shortening of the duration of exclusive breast-feeding
      • Male sex
      • Parental history of atopic dermatitis, asthma, or hay fever
      • Increased maternal age
      • > 37 weeks gestation
      • Increased head circumference
      • Increased birth weight
  • Contact dermatitis
    • Irritant form
      • Exposure to an irritating exogenous compound, such as a concentrated acid or base
    • Allergic form
      • Exposure to plants that contain the sensitizing antigen urushiol, an oleoresin containing the active ingredient pentadecylcatechol (especially members of the family Anacardiaceae, including the genus Toxicodendron [poison ivy, poison oak, poison sumac])
      • Exposure to skin, clothing, tools, pets, and other items that have contacted oleoresin, which may be active even after months of storage
      • Exposure to other antigens that may be more difficult to identify, especially if exposure is chronic and skin becomes thickened and scaly
  • Hand eczema or dyshidrotic eczema
    • Chronic, excessive exposure to water and detergents or other irritants
    • Exposure to rubber or latex gloves
    • Occupation that exposes hands to chronic insult
  • Nummular eczema
    • Risk factors unknown
  • Lichen simplex chronicus
    • Tendency to develop eczema or contact dermatitis
  • Asteatotic eczema
    • Dry skin
    • Drying, often cold, environmental conditions
  • Stasis dermatitis
    • Edema
    • Poor circulation, particularly associated with aging
  • Seborrheic dermatitis
    • Risk factors unknown

Etiology

  • Atopic dermatitis
    • Underlying causes are only partially defined.
    • Immunoregulatory abnormalities have been identified.
      • Increased IgE synthesis
      • Increased serum IgE specific to foods, aeroallergens, bacteria, or bacterial products
      • Increased expression of CD23 (low-affinity IgE receptor) on monocytes and B cells
      • Impaired delayed-type hypersensitivity reactions
    • Insufficient evidence to define it as a classical autoimmune disease [2]
      • Autoantigens have been identified.
      • Studies suggest that this disease is initiated, maintained, and perpetuated by the actions of cytokines, chemokines, T cells, antigen-presenting cells, and other inflammatory cells.
      • Studies suggest that this disease involves skin barrier defect and angiogenesis.
        • Mutations of the epidermal barrier protein filaggrin (encoded by FLG)
        • 70% of individuals homozygous or compound heterozygous for FLG null alleles develop atopic dermatitis.
  • Contact dermatitis
    • Irritant form
      • Irritant produces a direct local cytotoxic effect on the cells of the epidermis, with a subsequent inflammatory response in the dermis.
      • Most common irritants are wet work, soaps, and detergents.
    • Allergic form
      • Delayed-type hypersensitivity mediated by memory T lymphocytes in the skin
      • Most common cause: exposure to chemicals in certain plants
        • Poison ivy
        • Poison oak
        • Poison sumac
      • Other chemical causes
        • Nickel sulfate
        • Potassium dichromate
        • Thimerosal
        • Neomycin sulfate
        • Fragrances
        • Formaldehyde
        • Rubber-curing agents
  • Hand eczema (form of contact dermatitis)
    • Delayed-type hypersensitivity reaction, often to agents used to cross-link rubber in rubber gloves
    • Immediate-type hypersensitivity reaction, including possible anaphylactic reaction, to latex
    • Chronic, excessive exposure to water and detergents may initiate or aggravate this disorder.
  • Nummular eczema
    • Unknown
  • Lichen simplex chronicus
    • Chronic scratching or rubbing of pruritic or eczematous skin
  • Asteatotic eczema
    • Extremely dry skin being exposed in dry winter months
  • Stasis dermatitis
    • Venous insufficiency and chronic edema of the lower extremities
  • Seborrheic dermatitis
    • Unknown

Associated Conditions

Symptoms & Signs

General skin lesions

  • Primary lesions: papules, erythematous macules, and vesicles that may coalesce into patches and plaques
  • Secondary lesions: marked by weeping and crusting from infection or excoriation
  • Dry, thickened, scaling skin (lichenification) in longstanding dermatitis

Atopic dermatitis

  • Pruritus and scratching (worsened by dry skin)
  • Clinical course > 6 weeks
  • Exacerbations and remissions
  • Possible lichenification from rubbing and scratching (See Figure 1.)
  • Pattern
    • Infantile: weeping inflammatory patches and crusted plaques on face, neck, and extensor surfaces
    • Childhood and adolescent: dermatitis of flexure areas, particularly antecubital and popliteal fossae
    • Adult: usually localized as hand eczema or lichen simplex chronicus, although lesion distribution may be similar to that of childhood
  • Allergic rhinitis or asthma in 80%
  • Cutaneous stigmata of atopic dermatitis
    • Perioral pallor
    • Extra fold of skin beneath the lower eyelid (Dennie’s line)
    • Increased palmer skin markings
    • Increased incidence of cutaneous infections, particularly with Staphylococcus aureus

Contact dermatitis

  • Acute lesions: wet and edematous
  • Chronic lesions: dry, thickened, and scaly
  • Irritant form
    • Usually strictly demarcated
    • Often localized to areas of thin skin (eyelids, intertriginous areas) or areas where irritant was occluded
    • Most common on hands (hand eczema)
    • Minimal skin erythema to areas of marked edema, vesicles, and ulcers
    • Usually chronic and low-grade
  • Allergic form
    • Erythema
    • Vesiculation
    • Severe pruritus
    • Eruption, often linear, corresponding to areas where plants touched skin

Hand eczema

  • Dry, cracked skin on hands
  • Dorsal surface is preferentially involved, with sparing of the palms.
  • Variable amounts of erythema and edema
  • May begin under rings from trapped water and irritants

Dyshidrotic eczema

  • Multiple, intensely pruritic, small papules and vesicles on thenar and hypothenar eminences and sides of fingers (See Figure 2.)
  • Lesions tend to occur in crops, slowly form crusts, and then heal.

Nummular eczema

  • Circular or oval coin-like lesions
  • Initially, small edematous papules that become crusted and scaly
  • Usually on trunk or extensor surfaces of extremities, particularly pretibial areas or dorsum of hands

Lichen simplex chronicus

  • Well-circumscribed plaque(s) with lichenified or thickened skin
  • Commonly involves posterior nuchal region, dorsum of feet, or ankles
  • Chronic itching and scratching often during sleep

Asteatotic eczema

  • Pruritus
  • Fine cracks and scale, with or without erythema
  • Usually in areas of dry skin, especially on anterior surfaces of lower extremities in elderly patients

Stasis dermatitis

  • Early findings: mild erythema, scaling, and pruritus of lower extremities
  • Typical initial site: medial aspect of ankle, often over a distended vein (See Figure 3.)
  • Progressive pigmentation from chronic erythrocyte extravasation and cutaneous hemosiderin deposition
  • May become acutely inflamed, with crusting and exudate
  • If severe, may precede development of stasis ulcers

Seborrheic dermatitis

  • Greasy scales overlying erythematous patches or plaques
  • Most common on scalp
  • On the face, affects eyebrows, eyelids, glabella, and nasolabial folds (See Figure 4.)
  • Scaling of external auditory canal is common.
  • Macerated, tender postauricular areas
  • May develop on central chest, axilla, groin, submammary folds, and gluteal cleft
  • Rarely, may cause widespread generalized dermatitis
  • Within first few weeks after birth, may appear on scalp (cradle cap), face, or groin

Differential Diagnosis

  • Atopic dermatitis
    • Seborrheic dermatitis
    • Contact dermatitis
    • Impetigo
    • Psoriasis
    • Lichen simplex chronicus
    • Drug eruption
    • Pityriasis rosea
    • Zinc deficiency
    • Niacin deficiency
    • Pyridoxine deficiency
    • Scabies
    • Mycosis fungoides
    • Generalized exfoliative dermatitis
    • Stasis dermatitis
    • Wiskott-Aldrich syndrome
    • Nummular eczema
    • Hyper IgE syndrome
  • Contact dermatitis
    • Impetigo
    • Scabies
    • Atopic dermatitis
    • Dyshidrotic eczema
  • Dyshidrotic eczema

Diagnostic Approach

  • The keys to diagnosis are:
    • History of potential inciting causes and associated allergic conditions
    • Appearance of the lesion(s)
    • Location and distribution of the lesion(s)
  • Patch testing can be useful for recalcitrant cases.

Laboratory Tests

  • Radioallergosorbent testing (RAST) can identify specific causative allergens.
  • Indicated before initiating immunotherapy or desensitization
  • Useful when:
    • Skin testing is unreliable or patients refuse to submit to skin testing
    • There is a known history of severe allergic reaction to skin testing
    • Patient has generalized dermatitis
  • Used to monitor response to desensitization procedures

Imaging

  • Not indicated

Diagnostic Procedures

  • Skin scraping for mites if scabies is considered in the differential diagnosis
  • Patch testing
    • Useful in recurrent, chronic, or severe allergic contact dermatitis
    • Should be performed after initial episode has cleared
    • Not indicated in persons with widespread active dermatitis or those taking systemic glucocorticoids
  • Potassium hydroxide preparation of culture of the lesion to detect dermatophyte infection
  • Scratch testing for latex allergy
    • To identify this cause of hand eczema
    • Use extreme caution and perform only in a setting where anaphylactic reaction can be treated.

Treatment Approach

  • Goals
    • Alleviate symptoms
    • Maintain skin integrity
    • Treat secondary infections

Specific Treatments

Atopic dermatitis

General measures

  • Avoidance of cutaneous irritants
  • Adequate moisturizing
    • Warm, not hot, water for bathing
    • Limited use of soap
    • Moisturizer applied to all unaffected skin areas
      • Most effective if applied right after bathing
      • Useful emollients may contain aqueous cream, petrolatum, and/or urea.
  • Control of pruritus: antihistamines
    • Hydroxyzine, 25 mg PO 3–4 times daily as needed
    • May work to some extent through mild sedation, which also may limit their usefulness
    • Nonsedating antihistamines and selective H2-blockers are generally ineffective.

Topical anti-inflammatory agents

  • Applied to affected areas immediately after bathing, while skin is still moist
  • Cream or ointment base
  • Approximately 30 g needed to cover entire body surface of average adult
  • Low- to mid-potency glucocorticoids
    • Until recently, used in most patients
    • Second-line treatment after emollients
    • Side effects
      • Skin atrophy
      • Risk of systemic absorption, especially with more potent agents
    • Use low-potency agents for the face or intertriginous areas to minimize risk of skin atrophy.
  • Nonglucocorticoid, macrolide immunosuppressants (for patients > 2 years of age)
    • Tacrolimus, 0.03% or 0.1% ointment bid
    • Pimecrolimus, 1% cream bid
      • 2007 Cochrane database review concluded: [3]
        • Topical pimecrolimus is less effective than moderate and potent glucocorticoids and 0.1% tacrolimus.
        • Therapeutic role of topical pimecrolimus is uncertain due to the absence of key comparisons with mild glucocorticoids.
    • Replace topical glucocorticoids in some patients
    • Published reports of broader effectiveness than glucocorticoids
    • Advantages
      • No skin atrophy
      • No suppression of hypothalamic–pituitary–adrenal axis
    • Disadvantages
      • Concerns have emerged regarding potential for lymphomas and skin cancers in animals and in case reports.
      • More costly than generic topical glucocorticoids

Systemic glucocorticoids

  • Limited to severe exacerbations unresponsive to conservative topical therapy
  • Typically clear the skin only briefly
  • Skin lesion may return, possibly worsened, when therapy is discontinued.

Prompt treatment of secondary infection

  • Eczematous lesions should be cultured.
  • Systemic antibiotics active against S. aureus for crusted, weeping lesions
  • Penicillinase-resistant penicillins or cephalosporins are preferable because of frequency of macrolide-resistant organisms.
  • Dicloxacillin or cephalexin (250 mg qid for 7–10 d) is usually adequate to decrease heavy colonization.
  • More than 50% of S. aureus (SA) isolates are now methicillin resistant (MR) in some communities—community acquired MRSA (CA-MRSA).
    • Current recommendations for treatment of CA-MRSA is a 7- to 10-day course of 1 of the following:
      • Trimethoprim/sulfamethoxazole (1–2 double strength bid)
      • Minocycline (100 mg bid)
      • Doxycycline (100 mg bid)
      • Clindamycin (300–450 mg qid)
        • Inducible resistance may limit usefulness (detected by the double-disc diffusion test, which should be ordered if the isolate is erythromycin-resistant and clindamycin-sensitive).

Prophylactic measures to prevent bacterial superinfection

  • Triclosan-containing antibacterial washes
  • Intermittent nasal mupirocin

Novel/investigational therapeutic modalities for eczema/dermatitis [1]

  • Monoclonal anti-IgE therapy (omalizumab)
    • Humanized murine monoclonal antibody that binds to IgE
    • Pilot studies show mixed results.
  • Intravenous immunoglobulin
    • Results have been inconsistent.
  • Mycophenolate mofetil
    • Effective in small studies
  • Leflunomide
    • Needs further study
  • Phosphodiesterase inhibitors
    • Variable results
  • Interferon-gamma
    • Effective in small studies
  • Infliximab
    • Needs further study

Other measures

  • Role of dietary allergens in atopic dermatitis is controversial.
    • There is little evidence that dietary intervention is useful beyond infancy.
  • Immunotherapy with aeroallergens has not proved useful in atopic dermatitis.

Contact dermatitis

  • Irritant form
    • Avoidance of irritants
    • Use of protective gloves or clothing
  • Allergic form
    • Identification and removal of offending agent
    • High-potency fluorinated topical glucocorticoids to relieve symptoms while condition runs its course
    • If needed, daily oral prednisone
      • 1 mg/kg to start
      • Usually not exceeding 60 mg/d
      • Taken in the morning with food
      • Tapered over 2–3 weeks

Hand and dyshidrotic eczema

  • Avoidance of irritants
  • Identification of possible contact allergens
  • Gloves, preferably vinyl, to protect hands
  • Cool, moist compresses (dressings) to dry and debride acute inflammatory lesions and to decrease swelling, followed by application of topical glucocorticoid
  • Mid- to high-potency topical glucocorticoid in cream or ointment base
  • Treatment of coexistent dermatophyte infection, if present
  • Treatment of secondary infection by staphylococci or streptococci

Nummular eczema

  • Mid- to high-potency topical glucocorticoid in cream or ointment base

Lichen simplex chronicus

  • Treatment centers around breaking the cycle of chronic itching and scratching, which often occur during sleep.
  • High-potency topical glucocorticoids to relieve pruritus
  • Glucocorticoids applied under occlusion or injected intralesionally, if needed
  • Sedating agents to relieve pruritus
    • Oral antihistamines
    • Tricyclic antidepressants with antihistaminic activity
    • Higher doses if needed, but sedation can become bothersome or hazardous.

Asteatotic eczema

  • Topical moisturizers
    • Applied to dry skin areas twice daily
    • Applied to damp skin after bathing
  • Avoidance of cutaneous irritants, including overbathing and harsh soaps
  • Prescription emollients containing ammonium lactate or urea
    • Useful in patients with extremely dry skin, but may be associated with skin irritation
    • Emollients should be applied after leaving the bath or shower to avoid increasing the risk of falling.

Stasis dermatitis

  • Leg elevation
  • Compression stockings with gradient ≥ 30–40 mm Hg
  • Emollients
  • Mid-potency topical glucocorticoids
  • Avoidance of irritants
  • Protection of legs from injury, including scratching
  • Control of chronic edema
  • Treatment of existing ulcers
    • Exclude treatable causes (hypercoagulation, vasculitis).
    • Elevate affected limb as much as possible.
    • Use gentle debridement to keep ulcer clear of necrotic material.
    • Cover with a semi-permeable dressing under pressure.
    • Avoid applying glucocorticoids to ulcers because they may retard healing.
  • Treatment of secondary infection with appropriate antibiotics

Seborrheic dermatitis

  • Low-potency topical glucocorticoid
  • Topical antifungal agent
  • Shampoo containing coal tar and/or salicylic acid
    • Use in scalp, eyebrow, and beard areas.
    • Leave in place 3–5 minutes before rinsing.
  • High-potency topical glucocorticoid solution for severe scalp involvement
  • Do not use fluorinated topical glucocorticoids on the face because they may cause rebound worsening and steroid-induced rosacea or atrophy.
  • Alternatives to topical glucocorticoids
    • Tacrolimus and pimecrolimus
      • Especially with eyelid involvement
      • Not U.S. Food and Drug Administration-approved for these indications

Monitoring

  • Monitor for effectiveness of therapy and proper use of medications.

Complications

  • Secondary irritation or ulcers
  • Secondary infection

Prognosis

  • Atopic dermatitis
    • May resolve spontaneously
    • More than half of people affected as children will have dermatitis as adults.
  • Conditions are likely to be chronic or recurrent.
    • Goal is to control rather than eliminate outbreaks.

Prevention

  • Avoid irritants.
  • Avoid contact with known allergens.
  • Keep skin lubricated.
  • Bathe minimally in lukewarm, not hot, water.
  • Use mild, unperfumed soaps.
  • Investigational
    • Probiotics (L reuteri ATCC 55730) may reduce the incidence of IgE-associated eczema in infancy.
      • These were shown to be modestly effective when given to the mother during pregnancy and to the infant for the first year of life.[4]
    • Recent meta-analysis [5] of clinical trials of probiotics for prevention and treatment of pediatric atopic dermatitis supports efficacy of probiotics.

ICD-9-CM

  • 692.9 Contact dermatitis and other eczema, unspecified cause (includes dermatitis, not otherwise specified and eczema, not otherwise specified)

See Also

Internet Sites

  • Professionals
  • Patients
    • Homepage
      National Eczema Association for Science and Education
    • Homepage
      American College of Allergy, Asthma and Immunology
    • Homepage
      American Academy of Allergy, Asthma and Immunology
    • Homepage
      National Eczema Society

References

  1. Chang C, Keen CL, Gershwin ME: Treatment of eczema. Clin Rev Allergy Immunol 33:204, 2007  [PMID:18163227]
  2. Chan LS: Atopic dermatitis in 2008. Curr Dir Autoimmun 10:76, 2008  [PMID:18460882]
  3. Ashcroft DM et al: Topical pimecrolimus for eczema. Cochrane Database Syst Rev , 2007  [PMID:17943859]
  4. Abrahamsson TR et al: Probiotics in prevention of IgE-associated eczema: A double-blind, randomized, placebo-controlled trial. J Allergy Clin Immunol Mar 7, 2007  [PMID:17349686]
  5. Lee J, Seto D, Bielory L: Meta-analysis of clinical trials of probiotics for prevention and treatment of pediatric atopic dermatitis. J Allergy Clin Immunol 121:116, 2008  [PMID:18206506]

General Bibliography

  • Arndt KA et al (eds): Cutaneous Medicine and Surgery: An Integrated Program in Dermatology. Philadelphia, Saunders, 1996
  • Brown S, Reynolds NJ: Atopic and non-atopic eczema. BMJ 332:584, 2006  [PMID:16528081]
  • Cohen DE: Occupational dermatoses, in Handbook of Occupational Safety and Health, 2d ed, LJ DiBerardinis (ed). New York, Wiley, 1999, p 697
  • Hengge UR et al: Topical immunomodulators--progress towards treating inflammation, infection, and cancer. Lancet Infect Dis 1:189, 2001  [PMID:11871495]
  • Kay AB: Allergy and allergic diseases. Second of two parts. N Engl J Med 344:109, 2001  [PMID:11150362]
  • Nghiem P, Pearson G, Langley RG: Tacrolimus and pimecrolimus: from clever prokaryotes to inhibiting calcineurin and treating atopic dermatitis. J Am Acad Dermatol 46:228, 2002  [PMID:11807435]
  • Wolff K et al (eds): Fitzpatrick’s Dermatology in General Medicine, 7th ed. New York, McGraw-Hill, 2007
  • This topic is based on Harrison’s Principles of Internal Medicine, 17th edition, chapter 53 Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders by CO McCall and TJ Lawley.

Eczema and Dermatitis is a sample topic found in
Harrison's Practice.

To find other Harrison's Practice topics
please login or purchase a subscription.

Content Manager
Related Content
Eczema Psoriasis Cutaneous Infections Acne and Other Common Skin Disorders

more ...