The Papulosquamous Diseases or Scaly Skin Diseases
In this chapter, the discussion will be limited to those common skin diseases that show evidence of inflammation in the dermis and hyperkeratosis or desquamation of the epidermis. While infections, premalignant, or malignant dermatoses will not be specifically covered, they must always be considered in the differential diagnosis and ruled out by appropriate tests including culture and skin biopsy.
For example, the differential diagnosis of the papulosquamous reaction pattern includes psoriasis, seborrheic dermatitis, lichen planus, pityriasis rosea, drug eruption, tinea corporis, secondary syphilis, and cutaneous T-cell lymphoma.
The eczematous reaction pattern of skin includes the gamut of diseases called “eczema” or dermatitis. While eczema is inflamed skin by definition, it is more likely to manifest blisters, exudation, and crusting in the acute stages and scaling and hyperkeratosis in the later stages.
There are many subtle differences of onset, anatomic distribution, symptoms and treatment responses that help differentiate papulosquamous and eczematous reaction patterns. These will be covered in detail, as both patterns are prevalent in the geriatric population.
Psoriasis is a common inflammatory scaling dermatosis with a bilateral symmetric distribution that may be associated with a seronegative spondyloarthropathy. It affects about 2% of the world’s population with no gender preference. Up to one-third of patients develop psoriatic arthritis (PSA). The mean age of onset of psoriasis is about 30 years with a possible range from birth to senescence. We have also observed in the clinic that the extent and severity of psoriasis increases with age.
In the US, primary care physicians initially see about 60% of the estimated 150,000 new cases of psoriasis each year, but dermatologists encounter 80% of over 3 million office and hospital visits per year (1).
The pathogenesis of psoriasis is unknown, but the pathophysiology of psoriasis has been more intensively investigated than perhaps any other skin disease.
The clinical expression or lesion of psoriasis is the result of inflammation in the dermis and vascular changes leading to hyperproliferation and abnormal differentiation of the epidermis. These changes are triggered by the proper combination of genes, environmental factors (e.g, trauma and climate), and associated conditions (e.g., infections and stressful life events), and concomitant medications. Lithium, antimalarials, beta-adrenergic blockers, excessive alcohol ingestion, and cigarette smoking (2) have all been reported to induce or aggravate pre-existing psoriasis, or interfere with beneficial treatment effects.
Signs and Symptoms
There are several clinical variants of psoriasis. The most common type by far is called “plaque-type” or psoriasis vulgaris found in about 80% of patients. The typical morphology is a 1-cm or larger well-demarcated red plaque surmounted by white or silvery scales. (Fig.1) The lesions can occur anywhere, but the most commonly involved areas are the elbows, knees, scalp, sacrum, navel, intergluteal cleft, and genitalia. It is helpful to examine the latter covered areas when seeking to confirm the clinical diagnosis of psoriasis. The face is frequently spared. About 70% of patients complain of pruritus and skin pain or burning.
Active psoriasis demonstrates the Koebner phenomenon or isomorphic response whereby uninvolved skin develops psoriasis after injury, whether by accident or surgery.
In guttate or eruptive psoriasis, 0.1-1.0 cm, red, droplet-shaped lesions appear predominantly on the trunk and proximal extremities. Guttate psoriasis may be the initial presentation of psoriasis or represent an acute flare of pre-existing plaque-type psoriasis. There is frequently an antecedent history of an upper respiratory infection. In a recent study of new onset psoriasis, acute streptococcal pharyngitis was verified in 63% of cases (3).
The guttate variant is associated with younger age and accounts for about 18% of all cases of psoriasis.
Pustular psoriasis accounts for about 2% of cases and may be localized to palms and soles, (Fig. 2) glabrous skin (annular), or become generalized (von Zumbusch type). The age of onset of pustular psoriasis is about 50 years.
Clinically, it is characterized by groups of tiny sterile pustules that develop on a background of bright red skin. They may coalesce into lakes of pus followed by desquamation. The pressure-bearing areas of palms and soles are most often affected. The lesions may be observed in all stages as they evolve from clear vesicles to yellow pustules to dry reddish-brown macules. Palmoplantar pustular psoriasis is highly associated with cigarette smoking (nearly 100%) and is particulary recalcitrant to topical therapy. Patients with generalized pustular psoriasis (GPP) are acutely ill and may require admission to hospital for stabilization and specialty consultation.
GPP in patients with preceding plaque-type disease is more likely to be triggered by systemic corticosteroid treatment, whereas those with no prior history of psoriasis is more likely preceded by infection.
Psoriatic erythroderma or exfoliative dermatitis is the least common form of psoriasis accounting for about 1% of cases. The mean age of onset is 50 years with a male predominance. It usually develops during the course of chronic plaque-type psoriasis in adults. If erythroderma is the first manifestation of psoriasis, then the differential diagnosis includes drug eruption, seborrheic dermatitis, pityriasis rubra pilaris, and Sezary syndrome. Skin biopsies are essential but may still not show specific changes at this stage.
Precipitating factors include the inappropriate or excessive use of potent topical and systemic corticosteroids as well as systemic illnesses, emotional stress, and alcoholism.
The nails are involved in up to 50% of patients with psoriasis. In patients with PSA, the prevalence is more than 80%, and may be a helpful clue to diagnosis. The most common manifestation is pitting of the nail plate (Fig. 3).
Other signs of nail psoriasis are yellow-brown spots in the nail bed (oil droplet sign), subungual hyperkeratosis, and separation of the distal nail from the nail bed (onycholysis). It is important to remember that all of these nail changes resemble onychomycosis, especially in toenails, and that both conditions may coexist.
Psoriatic arthritis (PSA)
PSA is a destructive arthropathy and enthesopathy that affects up to one-third of patients with psoriasis. Arthritis occurs after the onset of skin disease in 2/3 of cases. PSA and rheumatoid arthritis (RA) have some clinical features in common. Most patients with PSA have asymmetric oligoarticular arthritis, followed in frequency by symmetric arthritis and spondyloarthritis (4).
Radiographic changes in the sacroiliac joints and cervical spine help to differentiate PSA from RA. The severity of skin involvement does not correlate with severity of PSA, however, distal interphalangeal joint involvement is likely to be associated with dystrophy of the adjacent nail. Although many of the systemic agents used to manage psoriasis are also effective for PSA, the specific treatment of PSA is beyond the scope of this chapter.
There are many effective treatments for psoriasis. These are traditionally organized into a “level” or “step ladder” approach (Table 1) according to the severity of the skin disease as judged by inflammation, thickness, scaling, estimated body surface area (BSA) involvement, symptoms, and quality of life parameters.
Excluding palmoplantar pustular psoriasis, many patients with mild to moderate disease (< 10% BSA) can be managed with a combination of topical therapy, natural sunlight, or tanning booth. Because this approach is less effective for patients with moderate to severe disease, these patients should consult a dermatologist.
Bland emollients or lubricants should be tried on mild cases first, followed by keratolytic creams or gels. Non-responders are treated with a medium to high potency corticosteroid combined with either calcipotriene or tazarotene.
The efficacy of the latter two agents is enhanced by the addition of the corticosteroid, while reducing their potential for irritation.
Natural sunlight and tanning beds are mildly therapeutic and may be combined with the topical therapies listed in Level 1. Coal tar products should not be combined with the UVA of a tanning bed or sunlight because stinging or smarting of the skin may result.
Phototherapy with narrow band UVB or PUVA is very effective and can markedly improve the majority of cases. However, maintenance is usually necessary to prevent flaring.
The disadvantages are that the treatment requires special equipment and safety training, and there are potential risks of causing sunburn and skin cancer.
Level 3-5 treatments should be used in collaboration with a specialist.
The level 5 biologic immunomodulators embrace a new paradigm of treatment of moderate to severe psoriasis for the 21st century. These “designer molecules” are monoclonal antibodies, ligand receptors, or fusion proteins that are able to antagonize antigen presenting cell-lymphocyte communication, memory-effector T-cell function, and the action of proinflammatory cytokines. They are all administered by the parenteral route. In addition, the tumor necrosis factor inhibitors are highly active in PSA as disease modifying anti-rheumatic drugs because they are all first tested and approved for RA.
- Efficacy of calcipotriene and tazarotene are enhanced by combination with medium to high potency topical corticosteroid
- Combination of coal tar products on skin with long wave ultraviolet or natural sunlight causes “smarting” reaction
- UVB or PUVA used in combination with topicals or acitretin are highly effective at clearing and maintaining psoriasis
- Level 3-5 therapies are best reserved for moderate to severe psoriasis and used in consultation with dermatologist
Seborrheic dermatitis is a common inflammatory scaling dermatosis that occurs in a distribution of skin with high concentrations of sebaceous glands, namely the scalp, face, and trunk. Dandruff, a mild manifestation of seborrheic dermatitis, is a non-inflammatory scaling condition of the scalp.
The two peak incidences are in infants and adult life. Seborrheic dermatitis has been observed with greater frequency and severity in association with AIDS, and chronic neurological conditions such as Parkinson’s disease and stroke.
Interestingly, in a series of 186 patients with seborrheic dermatitis aged 65 and older, dependency in more that one activity of daily living was a significant explanatory variable (5).
The cause of seborrheic dermatitis is multifactorial (6): sebum, climatic conditions, emotional or physical stressors, and the presence of Pityrosporum ovale, a commensal lipophilic yeast of the skin.
Signs and Symptoms
In babies, whose sebaceous glands are temporarily stimulated by maternal androgens, we recognize seborrheic dermatitis as yellow greasy adherent scales in the diaper area or on the scalp called “cradle cap”.
In adults, the lesions are red papules and patches with greasy yellow scale in the following characteristic locations: scalp, eyebrows, eyelid margins, nasolabial folds (Fig. 4), the moustache, beard and sideburn areas (if hairy), behind the ears, and the mid-chest area. The differential diagnosis includes psoriasis, and it is instructive to compare clinical morphologies: Psoriasis tends to be well demarcated with dry white or silvery scales, whereas seborrheic dermatitis is more diffuse with yellow greasy scales and sometimes exudations. At times it is impossible to separate the two entities on clinical grounds alone, and it is appropriate to use the term “sebo-psoriasis.”(Fig. 5)
Seborrheic dermatitis may also affect the groin, axillae, and submammary area causing “intertrigo” which should be differentiated from inverse psoriasis and candidiasis.
Dandruff or mild seborrheic dermatitis is usually well controlled with regular use (2-3 times weekly) of therapeutic shampoos containing selenium sulfide (1, 2.5%), zinc pyrithione, coal tar, ketoconazole (1, 2%), or ciclopirox 1%.
Inflammatory scalp conditions with pruritus may require the addition of a medium potency topical corticosteroid in an oil or hydroalcoholic vehicle, e.g. fluocinolone 0.01%, betamethasone valerate 0.1%, fluocinonide 0.05%, applied at bedtime.
Facial and intertriginous dermatitis usually responds well to twice daily applications of either anti-yeast ketoconazole cream 2% or ciclopirox gel 0.77% or mild corticosteroids such as hydrocortisone (1%, 2.5%) and desonide 0.05%. The more potent fluorinated corticosteroids are generally not recommended for these areas. Once daily applications of both the anti-yeast and the anti-inflammatory creams may be necessary for slow responders. In the past few years, many new brands of creams, gels, and cleansers containing sodium sulfacetamide 10% and sulfur 5% have been offered as adjunctive therapy for seborrheic dermatitis (7).
For the most severe or recalcitrant cases of seborrheic dermatitis, a one-week course of itraconazole 400mg daily or fluconazole 200mg daily, may be utilized to drastically reduce the population of P. ovale in the skin.
Patients should be informed that seborrheic dermatitis is a chronic relapsing condition and is therefore not curable. They should treat the skin disease intermittently for a few weeks until it clears and re-treat as necessary. Regular scalp maintenance may help to prevent facial outbreaks.
- Lather scalp with therapeutic shampoos for at least 5 min 2-3 times per week
- Combining non-fluorinated topical corticosteroid with ketoconazole cream gives optimal response for facial and intertriginous dermatitis
- Treat disease intermittently as needed and inform patient that seborrheic dermatitis is chronic and incurable
Lichen planus (LP) is a common inflammatory scaling disorder that affects about 1% of the world’s population (8). LP is a disease of middle age with an average age of onset of about 50.
The distribution of LP skin lesions is characteristic: flexor surfaces of the wrists and ankles, lumbrosacral spine, genitalia, and neck. Facial involvement is very uncommon.
Although not unique in this regard, LP is remarkable because it has a tendency to involve the entire integument producing specific clinical and histologic lesions of skin, mucous membranes, hair follicles, and the nail apparatus.
The etiology of lichen planus is unknown, but is believed to result from a cell-mediated immune response directed against the basal cell layer of epithelium (9). Histologically, a dense band-like infiltrate of lymphocytes is distributed along the basement membrane zone. Lichen planus-like rashes may occur as hypersensitivity reactions to many different drugs prescribed for hypertension, diabetes, and arthritis.
The association of LP with hepatitis C virus infection is dependent on the geographical area of the population studied, but not on the age of the subjects (10).
Signs and Symptoms
They typical skin lesion of LP is a violaceous, flat-topped, angulated papule that is usually very itchy (Fig. 6). Notwithstanding, excoriations of LP are seen uncommonly. Fine white striae may be evident on the surface of a papule or plaque.
The Koebner phenomenon occurs in LP as it does in psoriasis. The differential diagnosis includes psoriasis, pityriasis rosea, drug reaction, lupus, and secondary syphilis. A hypertrophic variant of LP on the shins clinically resembles lichen simplex chronicus, prurigo nodularis, lupus erythematosus, and keratoacanthomas. Therefore, a skin biopsy and serologic test for syphilis are often necessary to confirm the diagnosis.
Nail involvement occurs in about 10% of generalized LP cases and consists of a rough surface or longitudinal striae of the nail plate. Scarring of the nail matrix may lead to a characteristic deformity and eventually permanent loss of the nail. Similarly, hair follicle involvement of the scalp called lichen planopilaris, may lead to permanent patchy hair loss called scarring alopecia or pseudopelade.
Oral LP lesions may appear as a network of asymptomatic white lines or painful red erosions involving the buccal mucosa, tongue and gingivae. (Fig. 7).
Oral LP has been associated with candidiasis, reactions to many systemic drugs and rarely, hypersensitivity reactions to silver amalgam fillings (ref).
LP of the skin is usually self-limited and resolves on average within two years of onset, leaving dark brown post-inflammatory hyperpigmentation. Lesions of the nails, scalp, and mucous membranes tend to be chronic and much less likely to remit spontaneously.
Topical and systemic corticosteroids are the mainstay of therapy, particularly for pruritic disease. Examples of the former are fluocinonide 0.05% and halobetasol 0.05% ointments applied twice daily for 4 weeks with at least one week off to avoid cutaneous atrophy. Oral antihistamines and emollients containing anti-pruritics such as menthol, camphor, and pramoxine may be used adjunctively. For resistant or generalized LP, a burst of prednisone 60mg daily tapered over a 4- week period or an intramuscular injection of a long-acting corticosteroid such as Kenalog or triamcinolone acetonide suspension 80 mg mayinduce remission. The doses may have to be repeated, and relapses of LP are common.
Numerous other oral medications have been used empirically by dermatologists for LP with variable results: azathioprine, cyclosporine, cyclophosphamide, dapsone, griseofulvin, hydroxychloroquine, levamisole, photochemotherapy, retinoids, and thalidomide. Topical tacrolimus 0.1% ointment applied twice daily has shown modest improvement of oral but not cutaneous LP.
- LP is usually a very pruritic disease
- Besides skin, remember to examine scalp, nails, and mucous membranes for involvement
- Skin biopsy is often required for confirmation of diagnosis
- Topical or systemic corticosteroids are the mainstay of treatment
- Consult a dermatologist for recalcitrant or complicated cases.
Superficial inflammation of the skin, referred to as eczema or dermatitis, is the most common reaction pattern seen by dermatologists. The clinical morphology and histopathology are similar for all of the forms of eczema (6) described below, but the causes may differ.
The clinical changes evolve from acute to subacute to chronic. In the acute stage the skin is red, edematous, vesicular and possibly exudative. (Fig.8) Subacute lesions show less weeping and more crusting and scaling on the surface. (Fig. 9) Chronic rubbing and scratching leads to lichenification (accentuation of normal skin folds), thickening of the skin, and alterations in pigmentation. (Fig. 10) Chronic eczema may be plaque-like (lichen simplex chronicus) or nodular (prurigo nodularis). Histopathology of all forms of eczema shows edema between epidermal cells called spongiosis and collections of lymphocytes and eosinophils surrounding superficial dermal capillaries to varying degrees.
Pruritus is the sine qua non of eczema; all forms of eczema are more or less itchy.
Unlike psoriasis and lichen planus, scratching makes the itch of eczema feel better temporarily, even pleasurable, leading to fits of uncontrolled excoriations complicated by bleeding and secondary bacterial infections. In the following sections, the most common clinical forms of eczema will be covered separately: atopic, contact, nummular, stasis, dyshidrosis, photo dermatitis. Treatment, which is similar for all, will be covered in the final section.
Atopic dermatitis (AD) is familial: about 70% of patients have a family history of atopy, which includes dermatitis, rhinitis, and asthma (11). Patients have an exaggerated response to heat, cold and low humidity, and altered vascular responses to pressure and injections of histamine, cholinergic and sympathomimetic agents.
In children, AD typically presents as lichenified exudative lesions localized to the flexures of the elbows, knees, neck, wrists, and ankles. Eyelid, retroauricular, and hand dermatitis are the most common residuals in adult-life. Adult-onset AD also occurs; the localization may be typical or nonflexural with nummular, papular, or follicular patterns (12). Intermittent exacerbations of AD occur during their lifetime in 30-80% of patients when under physical or emotional stress (6). About one-third or relapses are secondary to bacterial infection.
Several immunologic abnormalities are associated with AD:
1) elevated serum IgE in 80% of patients, 2) eosinophilia during exacerbartions, and 3) reduced cell-mediated immune response which in turn leads to a higher prevalence of cutaneous viral and fungal infections.
Contact dermatitis is the result of environmental exposure of skin to a chemical or chemicals that are either irritants or allergens. It is the third most common skin ailment in the US accounting for 72 million cases generating $1.35 billion in direct costs. Irritant contact dermatitis accounts for about 80% of cases. The irritant may be simply repeated hand-washing with soap and warm water. Occupations with higher risk of irritant hand dermatitis are food service, health care, childcare, and hair styling. Other irritants besides detergents include organic solvents, oils, acids or alkaline chemicals, oxidants, fiberglass and wood dust. The hands, dorsal and palmar surfaces, are most often affected. Atopic individuals are predisposed to irritant contact dermatitis and may be obligated to avoid or change certain activities or occupations.
Allergic contact dermatitis is a delayed type hypersensitivity reaction to a chemical, usually a small molecule. Poison ivy or oak dermatitis is the most familiar paradigm of the mechanism of ACD. After the first exposure to the skin of Toxicodendron resin or oleoresin, it takes 2-3 weeks for the immune system to become sensitized. When the next exposure to the allergen occurs, it takes 12-48 hours to elicit a reaction in the skin depending on the amount of allergen exposure and the sensitivity of the individual. It is important to remember that oleoresin cross reacts with cashew nut and mango fruit.
There are many other common allergens in everyday use at home and in occupations that can cause sensitization and ACD, for example, fragrances, preservatives, hair dye, rubber, leather additives, nickel, formaldehyde in over-the-counter topical medicaments such as neomycin, bacitracin, hydrocortisone, and benzocaine.
By dint of their use in universal precautions, allergy to natural rubber latex in gloves has become an occupational hazard for doctors, dentists, and their assistants.
About 10% of health care workers are sensitized, and 1-2 % are symptomatic (13).
Patients who require frequent bladder catheterization, are also at high risk for sensitization to latex.
In ACD, the dorsal surfaces of the hands and forearms and the face are most commonly affected. Plant dermatitis is distinctly linear in distribution. (Fig. 11) The dermatitis may be localized to the anatomic site where the chemicals is repeatedly applied, for example: ears/nickel in earrings; feet/leather or rubber shoes; incisional wound/neomycin in antibiotic ointment; eyelids/preservative in cosmetic. About half of eyelid dermatitis is due to ACD, and one quarter is a symptom of AD.
Nummular dermatitis is a form of eczema of unknown cause, which begins on the legs or trunk of adults. The primary lesions are coin-shaped, 1-5 cm in diameter (14). They are red and scaly, and sometimes vesicular and crusted. They are always exquisitely pruritic and may become impetiginized from scratching. (Fig. 12)
Occasionally, there is a history of atopy or an antecedent emotional stressor. The eruption may become generalized. When there are few lesions, the differential diagnosis of tinea corporis, psoriasis, and Bowen’s disease (squamous cell carcinoma in situ) must be considered.
Nummular dermatitis has a reputation for being “treatment-resistant.” It tends to be chronic and to reoccur in the same locations.
Stasis dermatitis is a form of eczema that develops on the lower legs and ankles of adults who have a history of varicose veins, trauma or surgery to the leg, or one or more episodes of thrombophlebitis. The condition may begin as excessive dryness of the skin, followed by a pattern of superficial fissures, called eczema craquele. (Fig. 13)
Subacute dermatitis develops with dependent edema of the ankles. Post-inflammatory hyperpigmentation develops over time, and there is risk of ulcer formation after minor trauma to the malleoli. Ezcema is also commonly seen around scars where vein grafts were harvested on the legs. The dermatitis is usually itchy, but if the chief complaint is pain, then the possibility of bacterial cellulitis or deep vein thrombosis must be considered.
Dyshidrotic eczema is also known as pompholyx. It may be associated with hyperhidrosis of the palms and soles, but the eccrine sweat glands function normally. About 50% of patients have a history of atopy. The eruption is distinctive: 0.1-0.5 cm superficial tapioca-like vesicles appear on the sides of the fingers, palms (Fig. 14) and soles. The lesions are usually, but not always, pruritic. Superficial desquamation follows the resolution of the blisters. The differential diagnosis includes allergic contact dermatitis, localized pustular psoriasis, and inflammatory dermatophyte infection.
The diagnosis of eczema is usually made on clinical grounds based on morphology and distribution. However, a skin biopsy of a nummular lesion or a vesicopustule on the palm or sole may be necessary occasionally to rule out Bowen’s disease or psoriasis. Potassium hydroxide preparations in search of fungal hyphae should be examined on scaly lesions and blister fluid, particularly if they do not respond to topical corticosteroids or get worse.
Culture and sensitivity for bacteria may be performed on exudates and pus. In cases where ACD is suspected, except for plant dermatitis, allergy patch testing should be performed.
Patch test response patterns of a large group of subjects aged 65 and over was compared to young adults 20-40 years old. Results indicated an age-dependent decline of overall positive reactions and a higher rate of sensitization to allergens found in topical medicaments, e.g., neomycin, lanolin, paraben mix, and quinoline mix (15). A standard allergen screening patch test battery is commercially available (TRUE Test ). The tray consists of 23 allergen patches and one negative control, which contain 42 unique allergens and 4 complex mixtures. Collectively, the TRUE test allergens identify 28% of clinically relevant allergens in patients with documented ACD (16). A negative TRUE test, therefore, does not rule out ACD. If ACD is still suspected, the patient should be referred to a specialist for testing to an expanded panel of allergens to include unusual chemicals specifically identified from their occupations, hobbies, and medicaments.
The diagnosis of latex allergies is based on positive radioallergosorbent test (RAST) , the “wear” test or skin prick test.
There are several basic tenets of therapy that may be applied to all forms of eczema based on the stage of evolution.
Please see the Key Points below for the specific type of eczema.
Acute weeping eczema is treated with astringent and antiseptic compresses such as Burrow’s (aluminum acetate 1:40) for 20 min 2-3 times daily until exudation stops, followed by application of medium to high potency corticosteroid cream twice daily. After 2 weeks, a weaker steroid or a bland emollient such as Cetaphil , Eucerin , or Aquaphor , may be applied.
For chronically relapsing eczema, a program of 2-week cycles of topical corticosteroid followed by one week off theoretically prevents skin atrophy and tachyphylaxis.
Antihistamines of the H1-blocking sedating type may be helpful in the early stages, e.g., diphenhydramine, hydroxyzine, and doxepin.
If localized superficial infection (impetigo) is suspected, it is usually caused by Gram-positive organisms. Topical mupirocin three times daily is recommended.
Avoid neomycin in “triple-antibiotic” or Neosporin because it can sensitize inflamed skin.
If superficially infected eczema becomes generalized, or there is clinical evidence of soft tissue cellulitis, then a full course of oral antibiotics with anti-staphylococcal coverage is prescribed, e.g., dicloxacillin, cephalexin, azithromycin, ciprofloxacin, or levofloxacin. Because of the increasing prevalence of community-acquired methicillin resistant S. aureus (MRSA), it is now recommended to perform culture and sensitivity of pus or exudates before treating (17).
- Topical corticosteroids and occasional bursts of systemic steroids (e.g. Medrol dose pack, Kenalog 40mg IM injection) have historically been the mainstay of treatment
- Some cases are well-maintained on the topical immunomodulators (TIM’s) such as pimecrolimus 1% (Elidel ) cream or tacrolimus 0.1% (Protopic ) ointment twice daily.
- Recent concerns regarding TIM’s and increased risk of infections, photocarcinogenesis, and lymphoma are not relevant to the geriatric patient as long as the dermatologic diagnosis is secure
- Severe generalized, or recalcitrant cases should be referred to a dermatologist where advanced modalities such as ultraviolet light (UVB or PUVA) or immunosuppressive therapy (e.g., azathioprine, methotrexate, cyclosporine) may be initiated
- For acute ACD such as poison ivy dermatitis, administer a 4-week course of prednisone tapering from 60 mg daily or I.M. Kenalog 60 mg
- Remove or reduce direct contact with the irritating or allergenic substances
- Reduce hand washing if possible and use waterless cleanser or milder bar and liquid soaps such as Cetaphil , Purpose , and Oil of Olay brands
- Moisturize frequently and improve skin barrier function (18) with Vanicream or Theraseal
- Wear white cotton liner gloves over moisturizer or topical corticosteroid under latex or plastic gloves for food handling, dishwashing, and other wet work
- First treat for secondary infection on empiric basis, topically if localized, systemically if generalized
- Apply high potency corticosteroid ointment, e.g., clobetasol 0.05% or halobetasol 0.05%, twice daily for four weeks before switching to lower strength corticosteroids and emollients
- If response is poor, confirm clinical diagnosis with skin biopsy, then treat with systemic corticosteroids as for acute ACD (above)
- Apply medium potency corticosteroid ointment such as triamcinolone acetonide 0.1% twice daily for four weeks then switch to 1% or 2.5 % hydrocortisone ointment and liberal use of non-sensitizing emollient as listed under Contact Dermatitis
- Avoid commonly used non-prescriptive topical medicaments that contain sensitizers such as neomycin, lanolin, and benzocaine
- Recommend that support or compression stockings (10-30mmHg) be worn during the day as adjunctive therapy; they improve venous circulation, ankle swelling, and eventually, the dermatitis
- Bursts of systemic corticosteroids may be necessary to break the cycle of blistering
- Combine potent topical corticosteroid once daily with TIM once daily
- Patients who have a positive patch test to nickel may respond to a reduced nickel diet or a course of disulfiram (Antabuse, 200mg daily for eight weeks).
- For recalcitrant cases, consult a dermatologist for possible bath PUVA treatment of the hands and feet
Simply stated, photodermatitis refers to a skin eruption occurring as a reaction to a chemical or drug, either ingested or applied to skin followed by exposure to light, usually long wave ultraviolet (UVA) or visible light (19). The reaction may be either phototoxic or photoallergic. The discussion is analogous to what was stated in the previous section regarding irritant versus allergic contact dermatitis. By definition, toxic or irritant reactions are related to concentration of the chemical and can occur in everyone, whereas allergic reactions are not concentration-dependent and are much less common. Moreover, the individual must first be sensitized in order for an allergic reaction to develop upon subsequent exposures.
Clinically, phototoxic dermatitis first appears erythematous and edematous or vesicular, and develops hyperpigmentation upon resolution. Photoallergic dermatitis is eczematous.
Examples of systemic drugs that cause photosensitivity are amiodarone, furosemide, phenothiazines, sulfonamides, and thiazides.
Photoirritant contact dermatitis is most commonly caused by synthetic or naturally-occurring furocoumarins in the form of psoralens used therapeutically by dermatologists or from the juice of lime, lemon, bergamot, fig, parsnip, and celery.
Photoallergic contact dermatitis can be caused by PABA and benzophenone in sunscreens, musk ambrette in colognes, and antibacterial agents in soaps.
The only way to confirm the diagnosis of photoallergic contact dermatitis is by photo-patch testing. Referral to a dermatologist experienced with this technique is necessary.
Another conundrum to consider is whether a patient has airborne contact dermatitis or photoallergic contact dermatitis. Airborne contact dermatitis may be irritant (e.g., fiberglass, sawdust) or allergic (e.g. smoke from burning poison ivy or ragweed pollen). (Fig. 15 ) The distribution on the face, arms, and hands is similar for both, however, more submental, upper eyelid, and post-auricular sparing may be noted in photoallergic dermatitis.
- Photodermatitis may be caused by irritant or allergen and is termed phototoxic or photoallergic, respectively
- Photodermatitis may be caused by topical or systemic agents followed by exposure to longwave ultraviolet light
- The most common systemic agents are certain prescription drugs
- The most common topical agents are certain plant juices which produce bizarre patterns on the skin
- Airborne contact dermatitis may be confused with photodermatitis
- Photoallergic contact dermatitis can only be confirmed by photo-patch testing as performed by a specialist