Herpes simplex

Herpes zoster

Tinea

Tinea is a superficial dermatophyte infection of the skin and is classified by anatomical location: tinea pedis (foot), tinea cruris (groin), tinea manuum (hand), tinea corporis (body) and tinea unguium or onychomycosis (nails). Tinea cruris characteristically spares the genitalia, as opposed to candidiasis, which involves the scrotum and penis in men and the vulva in women. Tinea capitis, or fungal infection of the scalp, is rare in older adults. Heat and moisture may predispose the skin to fungal infection. Tinea manifests clinically as scaly patches or plaques with annular or serpiginous, often slightly raised, borders. Varying degrees of erythema and pruritus may be present. Tinea pedis and tinea manuum may present as diffuse scaling of the plantar or palmar surfaces. Often one hand and two feet are affected. Tinea pedis may also present with toe-web maceration. Nails are also commonly involved, showing thickening and yellow discoloration of the nail plate, onycholysis (separation of the nail plate from the nail bed) and hyperkeratotic debris under the nail plate. Greenish discoloration indicates pseudomonal superinfection of the nail. When fungal infections are mistakenly treated with topical steroids, initial improvement may be noted in scaling and inflammation. However, fungal organisms flourish and infected areas may enlarge (tinea incognito). The infection can invade the hair follicle, resulting in a deeper infection known as Majocchi’s granuloma.

Diagnosis of a fungal infection is confirmed by culture or by direct visualization under a microscope of fungal hyphae collected from scales and bathed with potassium hydroxide. Most cutaneous dermatophyte infections can be treated with a 4-week course of topical antifungal medication. Patients should be instructed to continue topical treatment for a least 1 week longer than symptoms persist to avoid discontinuing treatment prematurely. Affected areas should be kept as dry as possible, particularly the groin and toe-web spaces.

The exceptions to topical treatment are tinea unguium and tinea capitis, which may require oral antifungal agents. The drug of choice approved for the treatment of cutaneous dermatophyte infection of the scalp is griseofulvin. A dose of 10 mg/kg per day of ultramicrosized griseofulvin for 6 weeks to several months is common. Short-term terbinafine, itraconazole and fluconazole have been shown to be comparable in efficacy and safety.

Candidiasis

Candida albicans, the most frequent cause of candidiasis, thrives in warm moist areas such as the groin, the axilla and the inframammary regions. Diabetic and immunosuppressed patients, as well as those receiving systemic antibiotic therapy that reduces competing surface bacteria, are at increased risk for infection. The organism may be carried asymptomatically in the bowel, mouth and vagina.

Cutaneous candidal infection is characterized by beefy red, often moist, plaques with satellite pustules and papules. Unlike tinea cruris, candidiasis involves the skin of the genitalia. Oral candidiasis, or thrush, presents as creamy white plaques on the tongue, palate or buccal mucosa that cannot be easily scraped off.

Perleche, or angular cheilitis, is a candidal infection of the corners of the mouth, characterized by erythema, fissures and white exudate. Predisposing factors are dental malocclusion, poorly fitting dentures and deep folds at the corners of the mouth, with consequent retention of saliva and food particles in the affected area.

Candida paronychia is an infection of the skin proximal and lateral to the nails, characterized by erythema, tenderness and swelling, with separation of the nail plate from the adjacent nail folds. This condition is chronic and should be distinguished from acute paronychia, which is usually bacterial in origin. Frequent immersion of the hands in water is a predisposing factor. Confirmation of cutaneous candidiasis infection is by culture or potassium hydroxide preparation. Topical antifungal medication is usually effective, and attempts should be made to keep affected areas clean and dry.

Impetigo

Folliculitis

Erysipelas

Cellulitis

Scabies

Scabies is an intensely pruritic eruption caused by the Sarcoptes scabiei mite. The female mite burrows into the skin and deposits eggs, which hatch into larvae in a few days. Scabies is easily transmitted by skin-to-skin contact and can be readily spread between residents of the same household, nursing home, or institution. Pruritus is caused by a hypersensitivity reaction, so infestation has usually been present for weeks before it manifests clinically. Pruritus is severe and often worse at night. The clinical hallmark of a scabies infection is the burrow, which is a linear ridge, often with a tiny vesicle at one end; however, these lesions may be obscured by scratching.

Other cutaneous signs of scabies are papules, nodules and vesicles. Lesions are characteristically found in the interdigital web spaces, the flexor aspects of the wrists, the axilla, the umbilicus, around the nipples and on the genitalia. The skin is almost always excoriated and lesions are susceptible to secondary impetiginization. In elderly and physically or mentally disabled patients scabies may present less typically because of the inability to scratch and is often a long-standing infestation. The condition may mimic eczema or exfoliative dermatitis. Widespread hyperkeratotic and crusted lesions may be present.

The diagnosis is confirmed by observation of the scabies mite, eggs, or excretions in a skin scraping placed in mineral oil and examined under a microscope. A typical patient has only 10–12 adult female mites at one time, so confirmation of scabies is not always possible and diagnosis is often presumptive.

Several antiscabitic creams and lotions are effective in treating scabies. The two most commonly used are 5% permethrin cream and 1% lindane lotion or cream. Lindane, particularly if overused, can have neurotoxic side-effects. Mite resistance to lindane has developed in North America, Latin America, South America and Asia. Permethrin is the drug of choice and is thought to be a safer treatment for infants and pregnant women.

Successful treatment requires the treatment of all close personal contacts. In an inpatient or residential facility, all clinical staff, patients, selected visitors and their household contacts should be treated. The infestation can be subclinical for weeks, so infested contacts may be asymptomatic. Medication should be applied to the entire body, from the neck down (the head is also treated in infants). Particular attention should be paid to applying the cream or lotion under the fingernails and to the external genitalia. The medication should be washed off 8 hours later and, at that time, all clothing and linens should be washed in hot water, dry-cleaned or placed in a hot dryer. This process should be repeated 1 week later to kill any newly hatched larvae.

Pediculosis

Three species of Pediculosis (lice) infest humans: Pediculus humanus capitis (head lice), Pediculus humanus corporis (body lice) and Phthirus pubis (pubic lice, also known as crab lice). Transmission is by close person-to-person contact or by sharing clothing, hats or combs. Elderly individuals who have poor personal hygiene or who live in an overcrowded environment are at risk for head and body lice. Pediculosis capitis presents with scalp pruritus, which can progress to eczematous changes with impetiginization. Localized lymphadenopathy may occur. Examination reveals small, gray-white nits (ova) adherent to hair shafts. Adult lice can occasionally be found. Pediculosis corporis should be considered in a patient who presents with generalized pruritus. Secondary eczematous changes, excoriation and impetiginization can occur. Lice and nits are usually not found on the body but rather in the seams of clothing. Phthirus pubis is usually spread by sexual contact, but may also be transmitted via clothing or towels. The bases of pubic hairs should be examined for lice and nits in a patient complaining of pubic pruritus.

Pruritus

Pruritus, or itching, is a common complaint that can cause significant discomfort, and is one of the most common reasons for consultation with a dermatologist. It can occur in the presence or absence of objective cutaneous findings; associated skin eruptions may be causative (primary) or secondary. Patients who complain of pruritus should be examined for inconspicuous primary skin lesions because some pruritic skin diseases, such as bullous pemphigoid and scabies, may show little, if any, cutaneous signs initially.

Systemic disorders associated with generalized pruritus without primary skin lesions include liver and renal disease, Hodgkin lymphoma, polycythemia vera, mycosis fungoides, iron deficiency anemia, leukemias, parasitosis (usually of the gastrointestinal tract) and psychiatric disease. Some drugs (e.g. barbiturates or narcotics) can also cause itching without a skin eruption.

Disorders rarely associated with itching include diabetes mellitus, hyperthyroidism, hypothyroidism (where pruritus is usually secondary to xerosis) and solid malignancies. The most common cause of pruritus is xerosis (dry skin) and, regardless of cause, most patients complaining of pruritus benefit from treatment for xerosis (see the following section). Oral antihistamines can be helpful in some cases but should be used cautiously in the elderly.

Xerosis

Xerosis (dry skin) is quite common in the elderly and it is the most common cause of pruritus. Symptoms are often worse in the winter when central heating decreases the humidity indoors and the skin is exposed to cold and wind outdoors. Patients should be advised to avoid very hot baths or showers, as well as irritants such as harsh detergents and topically applied alcohol. Emollients should be applied liberally and frequently, especially immediately after bathing when the skin is still moist. Severely dry skin may become inflamed (see Asteatotic dermatitis).

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is a type IV cell-mediated hypersensitivity reaction. The consequence is dermatitis. The primary symptom is intense pruritus; pain is usually the result of excoriation or infection. Acute lesions tend to be vesicular, whereas chronic contact dermatitis appears scaly and lichenified. Clues to an allergic contact dermatitis are a bizarre shape or location or linear arrangement of lesions. Common contact allergens include nickel, fragrance additives, preservatives in cosmetics or medications, rubber, lanolin, chromates (used in tanning leather), topical antibiotics (especially neomycin, which is used, for example, on chronic ulcers) and topical anesthetics (e.g. benzocaine).

Treatment consists of identifying and removing the causative agent and applying mid- to high-potency topical steroids. Wet-to-dry dressings and soaks, such as Burow’s solution, soothe and dry acute vesicular lesions and promote healing. Pure petrolatum has no fragrances or preservatives and is advised when a fragrance or preservative allergy is suspected or when the allergen is unknown. If contact dermatitis is suspected and a causative agent is not apparent by history and physical examination, patch-testing, usually performed by a dermatologist, can aid in making a diagnosis. All cutaneous allergies should be documented on the patient’s chart because systemic exposure (e.g. via oral medication) to chemically related compounds may result in severe systemic allergic reactions.

Irritant contact dermatitis

Unlike allergic contact dermatitis, irritant contact dermatitis (ICD) is not immune-mediated. Given enough contact with an irritant, any patient may develop dermatitis. Common irritants are soaps and detergents. Although the elderly have a less pronounced inflammatory response to most irritants than younger patients, chronic irritant dermatitis is a common occurrence in the elderly. Clinical manifestations are identical to those of allergic contact dermatitis, and treatment is similar.

Atopic dermatitis

Atopic dermatitis, commonly referred to as eczema, is a chronic pruritic condition that is commonly associated with other concurrent conditions, such as asthma, allergic rhinitis and xerosis. Atopic dermatitis is often referred to as ‘the itch that rashes’, underscoring pruritus as the hallmark of this condition. Atopic dermatitis rarely begins in adulthood and usually improves with age. However, it can be exacerbated by environmental factors, for example the dry environment that occurs in winter as a result of central heating, woolen clothing, harsh detergents and prolonged bathing. Treatment centers on altering habits to avoid these factors and aggressively using emollients and mid-potency topical steroids.

Lichen simplex chronicus

Also known as neurodermatitis, lichen simplex chronicus is a localized pruritic eruption that results from chronic scratching and rubbing, eventuating in a scratch–itch–scratch cycle. Clinically, lesions appear erythematous or hyperpigmented, lichenified and scaly. High-potency topical steroids are often required to break the cycle. Steroid-impregnated tape, such as flurandrenolide (Cordran), applied at bedtime or after bathing and left in place for up to12 hours, also protects the lesions from being scratched. When symptoms improve, the potency of the steroid and the frequency of use can be reduced. Topical doxepin relieves pruritus and also helps break the cycle, but systemic absorption and drowsiness sometimes limit its use. If applicable, lesions can be covered with dressings, such as an Unna boot, to prevent the patient from scratching. More nodular lesions are termed prurigo nodularis, or picker’s nodules.

Asteatotic dermatitis

When skin becomes excessively dry and scaly, fissures and excoriation allow environmental irritants to penetrate and further worsen the condition, adding inflammation to dryness. This commonly occurs on the lower legs and is characterized by scaly erythematous plaques with a cracked porcelain appearance, which are caused by superficial fissures and crust. Treatment consists of the aggressive use of emollients and, initially, the additional use of a low- to mid-potency topical steroid ointment.

Stasis dermatitis

Seborrheic dermatitis

Seborrheic dermatitis is a common scaly erythematous eruption of the central part of the face (particularly eyebrows, glabella, eyelids and nasolabial folds), postauricular and beard areas, body flexures and scalp, where it is known in lay terms as dandruff. The central chest and interscapular areas can also be affected. Seborrheic dermatitis affecting the eyelids causes blepharitis and, sometimes, associated conjunctivitis.

Seborrheic dermatitis is especially prevalent among patients with neurological conditions, particularly Parkinson’s disease, facial nerve injury, poliomyelitis, syringomyelia and spinal cord injury. Neuroleptic drugs with parkinsonian side-effects can also bring about seborrheic dermatitis. Severe seborrheic dermatitis has been found with increased frequency in individuals infected with human immunodeficiency virus (HIV).

Although still a controversial theory, an inflammatory response to an overgrowth of the normally resident lipophilic yeast Pityrosporum ovale is thought to be the cause. Treatment focuses on suppressing inflammation by means of a mild-potency topical steroid such as hydrocortisone or on killing the yeast with a topical antifungal such as ketoconazole. Topical ketoconazole also exerts some anti-inflammatory effects. Seborrheic dermatitis of the scalp responds to shampoos containing selenium sulfide, zinc pyrithione, salicylic acid and tar. Ketoconazole 2% shampoo and mild topical steroid solutions can also be helpful. In some patients, ketoconazole cream or other topical imidazoles applied twice daily for 1–2 weeks induce a remission that lasts for months. For eyelid margin seborrhea, a dilution of 1-part baby shampoo to 9-parts water is applied with a cotton swab.

Intertrigo

Intertrigo is an inflammation of intertriginous skin, resulting from irritation, friction and maceration. It appears as moist, erythematous and scaly areas in the flexures. Patients may complain of pruritus or soreness. Contributing factors include obesity, poor hygiene, hot weather, irritating or occlusive products applied locally and clothing made of synthetic fabrics that do not breathe. Secondary yeast or dermatophyte infection is common and should be treated with an antifungal cream. Treatment should focus primarily on eliminating the contributing factors mentioned above. The affected areas should be kept as dry as possible. A low-potency topical steroid such as hydrocortisone is used initially to decrease inflammation and allow restoration of an intact skin barrier. Lotrisone, a commonly prescribed combination antifungal and topical steroid cream, should not be used for this condition because the steroid that it contains (betamethasone diproprionate) is too strong for use on intertriginous skin.

Burns

Chemical, thermal and ultraviolet-light injury can result in blisters in affected areas. A diagnosis can usually be made after taking a patient history. Treatment is supportive, employing cool soaks for thermal and ultraviolet burns, as well as antibiotic ointments, such as silver sulfadiazine and protective dressings. Nonsteroidal anti-inflammatory drugs, such as aspirin or indomethacin, can also be beneficial in the early treatment of sunburns.

Contact dermatitis

As discussed above, an acute contact dermatitis can result in such serious inflammation and edema that it leads to frank vesiculation. Clues to contact dermatitis are a linear arrangement of vesicles, odd-shaped lesions and sharply demarcated lesions. Treatment is outlined above (see under Dermatitis).

Bullous impetigo

This superficial staphylococcal infection presents as flaccid bullae that easily rupture, leaving yellowish crusts. Treatment is with anti-staphylococcal antibiotics, such as 250–500 mg of dicloxacillin four times a day.

Bullous pemphigoid

This is a chronic, immunologically mediated, bullous disorder characterized by tense bullae on normal or erythematous skin. Pruritus is common and mucous membrane involvement occurs in approximately 20–50% of cases. Bullous pemphigoid can have a pre-bullous phase that presents as urticaria or pruritus without distinct skin lesions. Men and women are equally affected and most patients are over 60 years of age at the onset of disease. Diagnosis is made by skin biopsy followed by routine pathology and immunofluorescence. Immunofluorescence reveals immunoglobulin G (IgG) and complement (C3) deposits at the dermal–epidermal junction of perilesional skin. Traditionally, bullous pemphigoid has been treated with systemic corticosteroids and immunosuppressive therapy. The combination of minocycline and nicotinamide has been shown to be effective in some patients. Consultation with a dermatologist is strongly advised.

Pemphigus vulgaris

Much less common than bullous pemphigoid, pemphigus vulgaris is another chronic immunologically mediated bullous disease that presents with flaccid rather than tense bullae. Often, only ruptured bullae (erosions and crusts) are present. Mucous membranes are almost always affected and may sometimes be the only manifestation of the disease. Again, the diagnosis is made by skin biopsy and immunofluorescence, which shows IgG and C3 deposited on the surface of keratinocytes. Before the advent of corticosteroids, pemphigus vulgaris was universally fatal. Today, it is treated aggressively with corticosteroids and other immunosuppressive agents, leading to long-lasting remissions.

Fragility of blood vessels

Vasculitis

Palpable purpuric papules should point to the possibility of vasculitis, although lesions of vasculitis need not always be palpable. Causes of vasculitis include: (a) drug allergy, (b) bloodborne infection (e.g. streptococcus, meningococcemia, viral hepatitis and endocarditis), (c) serum sickness, (d) collagen vascular diseases and (e) cryoglobulinemia. Wegener’s granulomatosis and polyarteritis nodosa are examples of vasculitis involving larger medium-sized vessels. When vasculitis is present in the skin, it is important to rule out systemic involvement with a urinalysis, renal and liver function tests, and a stool guaiac test. Whenever possible, treatment is directed at the underlying condition. Treatment is generally supportive, although some forms of vasculitis, particularly those with systemic involvement, may require treatment with corticosteroids, other anti-inflammatory or immunosuppressive drugs.

Pigmented purpura

In this disorder, there are several idiopathic purpuric eruptions, unrelated to any the systemic disease, that primarily affect the lower legs. Lesions may be predominantly red to purple (of recent onset) or brown to golden-brown (chronic hemosiderin deposits). No treatment is necessary or very effective.