Chapter 8: Dermatitis

Dermatitis (eczema) refers to a heterogeneous group of disorders that share similarities in clinical appearance and histopathologic findings, but may have very different etiologies. Eczema originates from a Greek word meaning "to boil." Acute dermatitis often appears vesicular (like water boiling on the skin), whereas chronic dermatitis may be red, scaly, and lichenified. Pruritus is a common symptom of all types of dermatitis.

The 2 major types of contact dermatitis are irritant contact dermatitis and allergic contact dermatitis. These reactions are not mutually exclusive, and may occur simultaneously in a particular patient. For example, contact allergy to a glove chemical may complicate irritant hand dermatitis due to irritating soaps used for hand washing. Furthermore, one substance may act as both an irritant and an allergen; a patient may have an allergic reaction to a preservative in a liquid soap as well as having an irritant reaction to a detergent in a soap. Common allergens include urushiol (eg, poison ivy), nickel, fragrances, preservatives, topical antibiotics (eg, neomycin, bacitracin), and paraphenylenediamine (eg, black hair dye). Common irritants include water, soap, industrial cleansers, and frictional forces.

Introduction

Irritant contact dermatitis is the most common form of contact dermatitis. It is estimated that irritant contact dermatitis represents approximately 80% of occupational contact dermatitis. Occupations at high risk include those involving repeated exposure to water and/or soap (wet work) such as health care workers, janitorial services, and food industry employees or those involving exposure to solvents such as machinists.¹

Pathophysiology

Irritant contact dermatitis is a nonimmunologic response to chemicals or physical agents such as friction that disrupt the normal epidermal barrier. Strong irritants include acids and alkalis, whereas weak irritants include soaps and cleansers. Damaged skin lacks the proper oils and moisture, thus allowing irritants to penetrate more deeply and cause further damage by triggering inflammation. Any condition that impairs skin barrier function, such as atopic dermatitis or asteatotic dermatitis/dry skin, is a risk factor for developing irritant contact dermatitis.

Clinical Presentation

History

Irritant contact dermatitis typically develops weeks after exposure to weak irritants such as hand soap or immediately after exposure to strong irritants such as bleach. It may affect any individual, given sufficient exposure to irritants, but those with a history of atopic dermatitis are at higher risk because of disruption of the normal epidermal barrier. Pruritus, pain, and burning are common symptoms.

Physical Examination

Irritant contact dermatitis is often well demarcated with a glazed appearance, but there may also be erythema, swelling, blistering, and scaling. Initially, irritant reactions are usually confined to the site of contact with the irritant. The most common locations are hands, forearms, eyelids, and face (Figures 8-1, 8-2, 8-3).

Laboratory Findings

Skin biopsies are usually not diagnostic and are only helpful to rule out noneczematous conditions such as psoriasis. Skin scrapings for fungal elements or a scabies preparation will rule out those conditions.

Diagnosis

Irritant contact dermatitis is a diagnosis of exclusion. The typical patient presents with pruritic or painful dermatitis beginning approximately 3 months after low-grade irritant exposure (eg, hand dermatitis in a nursing student) or shortly after exposure to a strong irritant or frictional exposure.

Differential Diagnosis

• ✓ Allergic contact dermatitis: This may appear identical to irritant contact dermatitis. Allergic contact dermatitis is diagnosed by patch testing.

• ✓ Atopic dermatitis: Individuals with atopic dermatitis usually have a personal or family history of atopic dermatitis (childhood eczema), allergic rhinitis, or asthma.

• ✓ Cutaneous fungal infections: Tinea infections present with annular plaques with a scaly border. Fungal hyphae causing tinea (corporis, manus, cruris, pedis) can be visualized on a potassium hydroxide (KOH) preparation from skin scrapings.

• ✓ Other eczematous skin conditions: Nummular dermatitis, dyshidrotic eczema, and lichen simplex chronicus.

• ✓ Uncommon conditions: Cutaneous T-cell lymphoma.

Management

The management of irritant contact dermatitis is 2-fold:

• Identification and removal of the irritant(s) (Table 8-1)

• Repair of the normal skin barrier

Mild soaps and moisturizers listed in Table 8-2 should be used. For irritant hand dermatitis, vinyl gloves should be worn as a barrier to unavoidable irritant exposures such as dish soap and juice from citrus fruits. Cotton gloves over a heavy emollient such as petroleum jelly overnight may also be helpful.² Each water exposure should be immediately followed by application of an emollient to prevent dehydration of the skin and restore the normal skin barrier. For cracks and fissures, application of superglue as a sealant may also be helpful. Mid-potency topical corticosteroid ointments or creams may be used twice a day as needed to treat symptoms as adjunctive therapy to aggressive moisturization (Table 8-3).

Indications for Consultation

Severe or persistent disease that does not respond to treatment.

Patient Information

National Eczema Association: www.nationaleczema.org/living-with-eczema/hand-eczema

Introduction

The most common allergen causing allergic contact dermatitis in the United States is urushiol, found in poison ivy, oak, and sumac. Of individuals patch tested by specialists in North America, the most common allergens include:

• Metals (eg, nickel 19%; cobalt 8%; chromate 5%)

• Fragrances (eg, balsam of Peru 12%; fragrance mix 12%)

• Preservatives (eg, quaternium-15 10%)

• Topical antibiotics (eg, neomycin 10%; bacitracin 9%)³

Pathophysiology

Allergic contact dermatitis is a cell-mediated, delayed, type IV hypersensitivity reaction, resulting from contact with a specific allergen to which a patient has developed a specific sensitivity. There are 2 main steps in developing allergic contact dermatitis: induction and elicitation. During the induction phase, also known as sensitization, an allergen penetrates the epidermis and is processed by antigen-presenting cells (Langerhans cells, dendritic cells, and macrophages) and presented to T lymphocytes. This initial phase generally takes between 10 and 14 days. In the elicitation phase, reexposure to the allergen causes activation of circulating effector T lymphocytes, which produce cytokines resulting in an inflammatory response.⁴ Clinical manifestations usually occur within hours to days after allergen exposure. After removal of the allergen, allergic contact dermatitis typically persists for up to 3 weeks.

Clinical Presentation

History

The patient usually complains of an intensely pruritic rash at the site of contact with the allergen.

Physical Examination

• Acute allergic contact dermatitis classically presents as papules and vesicles on an erythematous base (Figures 8-4 and 8-5).

• Chronic allergic contact dermatitis may manifest as xerosis, fissuring, and lichenified eczematous plaques.

In general, allergic contact dermatitis occurs at the site of contact with the allergen. Nickel allergy usually results in dermatitis underlying nickel-containing objects (Figure 8-6) (eg, jewelry—earlobes, neck, wrists; belt buckles—umbilicus; cell phones—cheeks). However, dermatitis in certain sites, especially the eyelids and face, may result from contact to allergens on the hands (fingernail polish) or scalp (hair products). Table 8-4 lists common allergens at selected body sites.

Laboratory Findings

Skin biopsies are usually not diagnostic and are only helpful to rule out noneczematous conditions such as psoriasis. Skin scrapings for fungal elements or a scabies preparation will rule out those conditions.

Diagnosis

The key diagnostic features of allergic contact dermatitis are pruritic vesicles or scaly, lichenified plaques that correspond to the area of contact with the allergen.

Pruritus should always be present in allergic contact dermatitis. The presence or history of vesicles is helpful in confirming the diagnosis, although this is not solely specific for allergic contact dermatitis.

Differential Diagnosis

• ✓ Irritant contact dermatitis: This may appear identical to allergic contact dermatitis.

• ✓ Atopic dermatitis: Individuals with atopic dermatitis usually have a personal or family history of atopic dermatitis (childhood eczema), allergic rhinitis, or asthma.

• ✓ Cutaneous fungal infections: Tinea infections usually present with annular plaques with a scaly border. Fungal hyphae can be visualized on a KOH preparation from skin scrapings.

• ✓ Other eczematous skin conditions: Nummular dermatitis, dyshidrotic eczema, and lichen simplex chronicus.

• ✓ Uncommon conditions: Cutaneous T-cell lymphoma and dermatitis herpetiformis.

Management

The management of allergic contact dermatitis consists of 3 steps:

• Identification of the allergen through patch testing

• Avoidance of the allergen

• Repair of the normal skin barrier

The allergen responsible for allergic contact dermatitis may be identified by patch testing with purified or specially prepared allergens. See Chapter 4 for details of patch testing. Patch testing typically occurs over 5 to 7 days. On the first day, allergens are applied to the upper back and taped in place. After about 2 days, the patches are removed and locations are marked and the patch sites are evaluated by the clinician. They are re-evaluated once again between 3 to 4 days after application. Allergic reactions manifest as palpable, pink-red, edematous and/or vesicular–bullous plaques at the patch site. After identification of the allergen by patch testing, clinical relevance is determined by evaluating potential exposures to the allergen (identifying the ingredient in the patient's products used in the location of dermatitis). If the dermatitis clears after avoidance of the allergen, this is good evidence that the allergic reaction is clinically relevant. Improvement of allergic contact dermatitis typically requires at least 3 weeks and often up to 2 months of allergen avoidance.

Patient information sheets on specific allergens, customizable lists of allergen-free products (Contact Allergen Management Plan [CAMP]), and other helpful resources are available through the American Contact Dermatitis Society Web site (www.contactderm.org). Mid- to high-potency topical corticosteroids (Table 8-3) applied twice a day are usually sufficient for treatment of allergic contact dermatitis. Restoration of the skin barrier includes mild soaps and moisturizers as listed in Table 8-2. An acute flare of widespread and extensive allergic contact dermatitis will respond to a 3-week tapering course of systemic corticosteroids. A standard adult dose consists of 40 to 60 mg of prednisone daily for 1 week, followed by a tapering dose over the next 2 weeks. Treatment with less than 3 weeks will usually result in rebound dermatitis, as this is a cell-mediated, delayed-type allergic reaction.

Indications for Consultation

Severe or persistent disease that does not respond to treatment.

Limited patch testing to about 36 allergens is performed by many general dermatologists. More extensive patch testing is typically performed by specialized dermatologists for occupational and more difficult cases.

Patient Information

American Contact Dermatitis Society: www.contactderm.org

Introduction

Atopic dermatitis is a very common skin condition that affects approximately 20% of children in developed countries. Ninety percent of patients have onset of disease before age 5 and 65% will have symptoms by 18 months of age. Rates continue to increase in developing countries, but have stabilized in developed countries. Diagnostic criteria, established by Hanifin and Rajka, and adapted by the UK Working Party in 1994, are based on clinical manifestations (Table 8-5).^5,6 More than 75% of patients will report a family history of atopy (allergic rhinitis, asthma, and dermatitis). Asthma and allergic rhinitis are seen in many patients with atopic dermatitis; however, asthma flares do not necessarily occur at the same time as skin flares. The atopic march is commonly referred to as the march from atopic dermatitis to asthma and allergic rhinitis. It is estimated that approximately 33% of all children with atopic dermatitis will go on to develop asthma. However, 50% of children with severe atopic dermatitis will go on to develop asthma and 75% will develop allergic rhinitis.⁷

The psychosocial effects of atopic dermatitis have been emphasized in recent years, and were summarized in a recent review by Kelsay et al.⁸ Chamlin et al identified 4 domains of distress⁹:

• Physical health (sleep disruption, itching, and related scratching)

• Emotional health (fussiness in children, various emotional stresses for parents)

• Physical functioning (activity restrictions, missed work)

• Social functioning (feelings of isolation, negative reactions from family members)

Pathophysiology

The etiology of atopic dermatitis is multifactorial, including a combination of genetic susceptibility and environmental triggers and/or exposures. Many gene loci have been linked to atopic dermatitis, including genes associated with increased immunoglobulin E (IgE) levels, or T lymphocyte activation. Filaggrin, a protein that is important in the barrier function of the epidermis, is also a factor in the pathogenesis of the disease.¹⁰

The association of atopic dermatitis and food allergy is a very controversial topic, as many believe that food allergies are responsible for skin flares. In rare cases, specific foods may cause worsening of atopic dermatitis. Usually elimination diets do not result is significant skin improvement.

Patients with atopic dermatitis have increased susceptibility to Staphylococcus aureus and other infections such as molluscum, herpes simplex virus (HSV), human papilloma virus (HPV), and Trichophyton rubrum and Malasezzia species. About 90% of atopic dermatitis skin lesions are colonized with microbes, usually S. aureus. This is thought to be related not only to an altered epidermal barrier but also to decreased production of antimicrobial peptides.¹¹ Recurrent infections can be problematic and drive the inflammatory cascade.

Clinical Presentation

History

The parent or patient usually complains of a rash and moderate to severe itching.

Physical Examination

The morphology of the skin lesions in atopic dermatitis is similar in all age groups. Excoriations, erythematous, scaly papules and plaques, vesicles, serous drainage, and crusts are common findings.

Three classic distributions of atopic dermatitis are recognized: infantile, childhood, and adult variants.

• Infants usually present with dermatitis involving the cheeks, trunk, and extensor extremities (Figure 8-7). The scalp may also be involved, but the diaper area is notably spared.

• Young children tend to have involvement of the posterior neck, flexor extremities (antecubital fossae and popliteal fossae), wrists, hands, ankles, and feet (Figure 8-8). Keratosis pilaris may be present on the extensor arms and thighs (Figure 8-9).

• Older children and adults have posterior neck, flexor extremities, and hand involvement. Changes of chronic atopic dermatitis, including thickened hyperkeratotic plaques with lichenification and prurigo nodularis, may also be present. Postinflammatory hypopigmentation or hyperpigmentation are common associated findings. Xerosis is a common feature.

Patients with atopic dermatitis are frequently colonized with S. aureus and they may have plaques with erosions, drainage with yellow crusting, or hemorrhagic crusting. Infections with warts and molluscum contagiosum are also more common in patients with atopic dermatitis. Susceptibility to widespread HSV infection is characteristic of atopic dermatitis. Eczema herpeticum is the result of a severe HSV infection. It presents with multiple widespread monomorphic, "punched-out" discrete erosions with hemorrhagic crusting (Figure 8-10). Usually this can be treated with oral antiviral medications. Concurrent staphylococcal infection is common in patients with eczema herpeticum. Patients may be ill-appearing or have associated fever. Parenteral antiviral medications and hospital admission may be appropriate in these cases. Rapid initiation of antiviral therapy has been shown to improve outcomes.¹²

Laboratory Findings

Skin biopsies are usually not required, but they can be helpful to rule out other disorders. Elevated serum IgE levels are common. Radioallergosorbent (RAST) testing has not been shown to be clinically relevant in the treatment of atopic dermatitis.

Diagnosis

Infants: The key diagnostic features are red, crusted, scaly, pruritic plaques on cheeks, trunk, and extensor extremities.

Older children and adults: The key diagnostic features are red, scaly pruritic plaques on the neck, antecubital and popliteal fossae, wrists, ankles, and feet. Lichenification may be present.

Differential Diagnosis

• ✓ Seborrheic dermatitis: Presents with yellow, greasy scale most commonly on head, face, and neck region. Can be widespread in infancy. Not as pruritic as atopic dermatitis.

• ✓ Psoriasis: Presents with well-demarcated, persistent plaques with overlying scale. The diaper area in infants is commonly affected.

• ✓ Contact dermatitis (irritant or allergic): Presents with well-demarcated eczematous plaques, usually localized to areas of contact.

• ✓ Dyshidrotic eczema: Presents with deep-seated noninflammatory 1 to 3 mm vesicles on the palms and soles.

• ✓ Juvenile palmar–plantar dermatosis: Presents with superficial desquamation of the feet, exacerbated by sweating.

• ✓ Tinea corporis: Presents with well-demarcated scaly, annular plaques, often with a raised border and central clearing.

• ✓ Other: Nummular dermatitis, scabies, perioral dermatitis, immune deficiency syndromes, nutritional deficiency syndromes, drug eruption, and graft-versus-host disease.

Management

• Education: Treatment begins with education of the parents, caregivers, and patients on the care of skin in atopic dermatitis.^13,14

• Hydration and restoration of the skin's barrier function: This plays a vital part in the management of atopic dermatitis. Daily 5-minute baths in lukewarm water are encouraged. Colloidal oatmeal powder (Aveeno) and bath oil (RoBathol) can be added to the tub water. Bubble bath products should be avoided. Low detergent hypoallergenic cleansers are recommended for removal of any surface crusts (Table 8-2). Allowing the water to evaporate off the skin can increase xerosis, but application of a hypoallergenic moisturizing ointment or cream (Table 8-2), within 3 minutes after exiting the tub, increases hydration and improves barrier function. Lotions and products containing alpha or beta hydroxy acids, or urea may improve xerosis, but often sting when applied to inflamed skin. Lotions containing ceramides (eg, CeraVe, Cetaphil Restoraderm) may be better tolerated. Tap water soaks or Burow's wet dressings may be helpful for crusted areas. See Table 6-5 for instructions on wet dressings. Moisturizers or topical steroids can be applied during or after the soaks.

• Topical steroids: Mild atopic dermatitis can usually be controlled with cream or ointment-based moisturizers and over-the-counter 1% hydrocortisone ointment. One percent hydrocortisone ointment can be used, once or twice a day, to any area of involvement, including the face and buttocks.

  Moderate disease, in children and adults, may require class 4 or class 5 mid-potency steroid ointments or creams (Table 8-3). Good starting regimens for the body and extremities include Derma-Smoothe FS oil twice a day after baths. The oil serves as a moisturizer, so additional moisturizers are not required with this regimen. Additional choices for older children and adults include fluocinolone 0.025% ointment and triamcinolone acetonide 0.025% or 0.1% ointments. For the face and neck, good starting choices include hydrocortisone 2.5% ointment and desonide 0.05% ointment. Creams tend to be preferred by adult patients, and may be more elegant, but also may burn or sting more than ointments when applied, and are considered less potent for a given steroid class. Systemic steroids should be used rarely as discontinuation often leads to more severe flaring.

• Topical calcineurin inhibitors: These are nonsteroidal anti-inflammatory immunosuppressant agents. They are good choices for the face and intertriginous areas, as secondary cutaneous atrophy is not a risk with their use. Pimecrolimus (Elidel) 1% cream is approved for mild to moderate atopic dermatitis in children older than 2 years, but has been studied in the 3- to 23-month age group with no severe side effects. Tacrolimus (Protopic) 0.03% ointment and 0.1% ointments are approved for moderate to severe atopic dermatitis in children older than 2 years of age. Both medications have US Food and Drug Administration (FDA) black box warnings attached for a theoretical risk of cancer (specifically lymphoma in mice who received 30-50 times higher doses than the maximum recommended human dose). Ongoing safety studies have not revealed any increased systemic immunosuppression or increased malignancy risk.¹⁵

• Antihistamines: Oral antihistamines can be helpful in breaking the "itch–scratch" cycle, but they are not considered a primary treatment for atopic dermatitis–related pruritus. Sedating agents can be especially helpful in children who have trouble falling asleep due to itching at night. Short courses can be used regularly until pruritus is improved. Diphenhydramine and hydroxyzine may be used. Additionally cetirizine (Zyrtec), loratadine (Claritin), and fexofenadine (Allegra) can be helpful in the morning due to their nonsedating effects.

• Management of active infections: Cephalexin (Keflex) is a reasonable antibiotic to start with. Standard dosing for 7 to 10 days is usually appropriate. If there is concern for methicillin-resistant S. aureus (MRSA), a culture should be sent to confirm the susceptibility. Oral trimethoprim–sulfamethoxazole (Bactrim) or clindamycin is usually acceptable in the pediatric age group. Tetracyclines should not be used in children less than 8 years old. Bleach (sodium hypochlorite) baths and mupirocin (Bactroban) ointment can be helpful in reducing bacterial load and staphylococcal carriage.¹⁶ Mupirocin ointment should be used twice daily for the first 5 days of each month in the nostrils. Bleach baths with one quarter to one half cup of bleach per full bathtub can be done once or twice a week. Bleach baths do not usually cause burning or stinging, as the chlorine concentration is low. Parents should continue with skin moisturization routine after baths.

• Avoidance of triggers: Common triggers include heat and sweat for some individuals and for others, cold, dry air. Other potential triggers include house dust mites, pet fur, wool, synthetic fabrics (eg, nylon), dyed fabrics, tobacco smoke, fragrances (which may be present in shampoos, soaps, lotions, laundry detergents, fabric softeners), saliva, or prolonged exposure to water. Fingernails should be trimmed short.

• Food allergy: Allergies to foods such as cow's milk, eggs, fish, peanuts, and wheat are more common in children with atopic dermatitis, but foods are specific triggers for flares in only a small percentage of children. There are blood (RAST) and skin prick tests that can identify specific allergens, but they are often positive in children who are not truly allergic and they are not considered to be helpful before age 2. It is important to determine which foods are relevant and cause clinical symptoms such as urticaria. Extreme food elimination diets, which have become more popular in recent years, are discouraged as they can result in nutrition and lack of essential dietary nutrients.

• Ultraviolet light therapy and systemic immunosuppressant agents: Severe widespread disease may require narrow-band ultraviolet light therapy, cyclosporine, methotrexate, azathioprine, or mycophenolate mofetil, but these should be used in consultation with specialists.

• Psychological burden of disease and quality of life issues: Controlling pruritus is an important aspect of atopic dermatitis treatment. In a quality of life study, ratings of pruritus intensity, both self-reported and parent reported, were inversely correlated with parents' quality of life (psychosomatic well-being, social life, emotional coping, and acceptance of the disease). Older children's itch has been shown to be negatively correlated with quality of life, and positively with depressed mood and catastrophic thinking.¹⁷ Nighttime itching affects both parents and children. Parents try to comfort the children at night and this can result in parental sleep deprivation and daytime exhaustion. Parental depression correlates more strongly with sleep deprivation than with severity of their child's atopic dermatitis. Sleep deprivation also has consequences for school-age children (patients and siblings), affecting cognitive function and behavior.

Prognosis

Most patients with atopic dermatitis improve with time, but a subset progresses to persistent skin disease and allergic rhinitis and/or asthma.

Indications for Consultation

• Severe or persistent disease that does not respond to treatment, especially in children, could indicate concurrent serious underlying disease.

• Patients with recurrent skin infections requiring oral or topical antibiotics.

• Patients with eczema herpeticum should be referred to dermatology and to ophthalmology emergently if there is questionable or confirmed eye involvement.

Patient Information

• Rady Children's Hospital: www.eczemacenter.org

• National Institute of Allergy and Infectious Diseases: www.niaid.nih.gov/topics/foodallergy/clinical/pages/default.aspx

• National Eczema Association: www.nationaleczema.org

Introduction

Nummular is a Greek word meaning "coin." Nummular dermatitis is a common skin disorder that presents with "coin-shaped" plaques on the extremities. It is more common in older individuals and is often associated with dry skin.

Pathophysiology

The pathophysiology of nummular dermatitis is unknown, but thought to be linked to impaired skin barrier function.

Clinical Presentation

History

The patient typically complains of an itchy rash on the extremities.

Physical Examination

The patient typically presents with round, light pink, scaly, thin, 1 to 3 cm plaques on the extremities (Figure 8-11). The plaques are typically uniform with no central clearing. The trunk may also be affected.

Laboratory Findings

Skin biopsies are usually not diagnostic and are only helpful to rule out other disorders. Examination of a KOH preparation will be negative for fungal hyphae.

Diagnosis

The key diagnostic features of nummular dermatitis are pruritic, pink, scaly plaques, with no central clearing, commonly located on the arms and legs. The trunk may also be affected.

Differential Diagnosis

• ✓ Cutaneous fungal infections: Tinea corporis may present in circular plaques but these are typically annular (ring-shaped with central clearing). Fungal hyphae can be visualized on a KOH preparation from skin scrapings.

• ✓ Allergic and irritant contact dermatitis: Allergic and irritant contact dermatitis usually do not present in coin-shaped plaques. Allergic contact dermatitis is diagnosed by patch testing.

• ✓ Atopic dermatitis: Individuals with atopic dermatitis usually have a personal or family history of atopic dermatitis (childhood eczema), allergic rhinitis, or asthma. Atopic dermatitis does not usually present with coin-shaped plaques.

• ✓ Other eczematous skin conditions including lichen simplex chronicus.

• ✓ Uncommon conditions may include cutaneous T-cell lymphoma, subacute cutaneous lupus, granuloma annulare, psoriasis, or squamous cell carcinoma in situ.

Management

The management of nummular dermatitis includes the use of mid- to high-potency topical corticosteroids (Table 8-3) twice a day, and mild soaps and moisturizers (Table 8-2).

Indications for Consultation

Severe or persistent disease that does not respond to treatment.

Patient Information

American Academy of Dermatology: http://www.aad.org/skin-conditions/dermatology-a-to-z/nummular-dermatitis

Introduction

Dyshidrotic dermatitis (sometimes called pompholyx) is a common pruritic, vesicular skin disorder of the palms and soles. Some experts consider dyshidrotic dermatitis and pompholyx to be distinct conditions, although the terms are often used interchangeably.¹⁸ Dyshidrotic dermatitis is characterized by chronic, relapsing eruptions of vesicles. Pompholyx presents as explosive eruptions of large bullae. Dyshidrotic dermatitis is common, affecting approximately 1% of the general population,¹⁸ whereas pompholyx is rare. Men and women are affected equally.

Pathophysiology

The term "dyshidrosis" (meaning "difficult sweating") is a misnomer. The condition does not involve dysfunction of sweat glands. The cause is unknown. A few studies have found a link between flares of vesicular palmoplantar dermatitis and oral ingestion of nickel in nickel-allergic patients.¹⁸ Most cases are idiopathic but often exacerbated by stress and/or sweat.

Clinical Presentation

History

The patient typically complains of pruritic or painful blisters on the palms and soles.

Physical Examination

Dyshidrotic dermatitis presents with grouped 2 to 5 mm vesicles, sometimes likened to "tapioca pudding" (Figure 8-12). The most common locations include lateral fingers, central palms, insteps, and lateral borders of the feet. Pompholyx presents as large, 1 to 5 cm bullae. Both present on a noninflammatory base, with little surrounding erythema.

Laboratory Findings

Skin biopsies are usually not diagnostic and are only helpful to rule out other disorders. Examination of a KOH preparation will be negative for fungal hyphae.

Diagnosis

The key diagnostic features of dyshidrotic dermatitis are small, grouped vesicles on the palms and/or soles.

Differential Diagnosis

• ✓ Allergic and irritant contact dermatitis of the palms and soles: Allergic and irritant contact dermatitis usually are not limited to these locations and have surrounding erythema, scale, and eczematous plaques.

• ✓ Cutaneous fungal infections: Inflammatory tinea pedis caused by Trichophyton mentagrophytes may present with vesicles, but these typically have surrounding erythema. Fungal hyphae will be visualized on a KOH preparation from skin scrapings.

• ✓ Erythema multiforme: This can present with inflammatory, "bull's-eye" bullae on the palms and soles. Skin biopsies will have specific findings.

• ✓ Scabies: This may present with vesicles and papules on the palms and soles, but usually there are burrows and more widespread lesions.

• ✓ Vesiculobullous diseases such as pemphigoid and pemphigus: Dyshidrotic eczema is typically noninflammatory and only affects the palms and soles, whereas other vesiculobullous conditions have significant surrounding erythema and commonly affect multiple body sites.

Management

Dyshidrotic dermatitis is managed with mid- to high-potency topical corticosteroids (Table 8-3) twice a day. In individuals where sweat is a significant aggravating factor, iontophoresis or onabotulinumtoxin (Botox) injections may be helpful. In patients who have a strong positive reaction to nickel, a low-nickel diet¹⁹ may be tried.

Dyshidrotic dermatitis may not completely clear with treatment and recurrences are common.

Indications for Consultation

Inflammatory bullae, severe or persistent disease that does not respond to treatment, or extension to sites other than the palms and soles.

Patient Information

American Contact Dermatitis Society—low-nickel diet: www.contactderm.org

Introduction

Lichen simplex chronicus is a term used to describe the clinical appearance of any long-standing, chronically pruritic skin condition. As a primary diagnosis, it exists without a known underlying condition or cause. As a secondary diagnosis, it results after years of scratching due to another condition, most commonly atopic dermatitis.

Pathophysiology

The exact pathophysiology is unknown. Chronic rubbing and scratching of the skin leads to thickening of the epidermis and fibrosis of the dermis. Chronic cutaneous nerve stimulation is hypothesized to result in nerve dysfunction; an "itch–scratch" cycle ensues perpetuating the need to rub and scratch affected areas.

Clinical Presentation

History

The patient typically complains of localized areas of intensely pruritic skin. Sleep is often interrupted. In some cases, the chronic rubbing and scratching becomes a subconscious or compulsive habit.

Physical Examination

Common locations for primary lichen simplex chronicus include the lateral neck, scrotum/vulva, and dorsal foot. The plaque is typically solitary, well-defined, pink to tan, thick, and lichenified (Figure 8-13). Secondary lichen simplex chronicus occurs at the sites of the underlying skin conditions such as in the antecubital and popliteal fossae in atopic dermatitis. A prurigo nodule is a term used for a lichenified papule that has been chronically picked and manipulated. Secondary prurigo nodularis may present with many widespread lichenified papules in patients with generalized pruritus due to systemic diseases such as liver or kidney disease.

Laboratory Findings

Skin biopsies are usually not diagnostic and are only helpful to rule out other disorders.

Diagnosis

The key diagnostic features of lichen simplex chronicus are chronic, intensely pruritic, lichenified plaques, mostly commonly found on the neck, genitals, or dorsum of the foot.

Differential Diagnosis

• ✓ Psoriasis: Presents with multiple, symmetric lesions most commonly on the elbows, knees and scalp.

• ✓ Psychological disorders: Usually other signs of psychological disease are present.

• ✓ Squamous cell carcinoma: This can present as a hyperkeratotic plaque, but it is typically not pruritic and rarely becomes lichenified.

Management

Primary lichen simplex chronicus is typically managed with class 1 or 2 high to superpotent topical corticosteroid ointments or creams twice a day (Table 8-3). Corticosteroid-impregnated tapes, such as Cordran Tape which can be applied directly over the plaque, are often helpful. Oral antidepressants or antihistamines, especially doxepin, may benefit individuals with nighttime itching and sleep disturbance. It is important that patients become aware of the habit or compulsion to scratch or rub, replacing these activities with pushing on the skin. Application of ice provides a better alternative. In more severe cases, behavioral therapy may be of benefit. For generalized prurigo nodularis, ultraviolet light therapy is often very helpful.

Indications for Consultation

Severe or persistent disease that does not respond to treatment.

Patient Information

PubMed Health: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001875/