04 Dermatology

Fungal Infection

Cutaneous fungal infections are typically characteristic for specific areas of the body and are frequently associated with:

• Warm or moist environments

• Diabetes mellitus

• Obesity

• Recent antibiotic use

Tinea versicolor, also known as pityriasis versicolor, is a cutaneous fungal infection caused by yeasts in the genus Malassezia (formerly known as Pityrosporum). It is most commonly caused by Malassezia globosa.

Malessezia, the causative genus of tinea versicolor, is a dimorphic fungus that is part of the normal skin flora and is not contagious.

Pathologic tinea versicolor is most common in the summer due to hot, humid weather.

Additional risk factors include the use of topical skin oils and hyperhidrosis (excessive sweating).

Patients with tinea versicolor classically present with hypopigmented lesions that fail to tan despite summer sun exposure.

Tinea versicolor presents with hypopigmented, hyperpigmented, or salmon-colored macules on the trunk and proximal upper extremities from the degradation of lipids that produces acids that damage melanocytes.

Diagnosis of tinea versicolor is made with a potassium hydroxide (KOH) preparation. Both hyphae and yeast cells are evident in a pattern that is described as “spaghetti and meatballs.”

First-line treatments for tinea versicolor include:

• Selenium sulfide

• Zinc pyrithione

• Topical antifungals (e.g. ketoconazole 2% cream)

Dermatophyte (non-Malassezia tinea) infections, also known as ringworm, are cutaneous fungal infections caused by:

• Epidermophyton

• Trichophyton

• Microsporum

Lesions are pruritic, erythematous, scaly plaques that have a characteristic central clearing. This gives the lesion the appearance that a ring surrounds it.

Dermatophyte infections are named based on the location of the lesion as follows:

• Head, scalp: tinea capitis

• Torso: tinea corporis

• Groin: tinea cruris

• Feet: tinea pedis

• Nail bed: tinea unguium(onychomycosis)

The diagnosis can be made with a potassium hydroxide preparation, which shows hyphae.

Treatment consists of:

• Topical antifungal medication for multiple weeks with oral antifungal in resistant cases

• Oral griseofulvin or terbinafinefor tinea capitis

• Oral terbinafine for onychomycosis

Intertrigo is as an inflammatory condition of skin folds (intertriginous areas). It is most commonly caused by Candida albicans.

Lesions are pruritic, painful, erythematous plaques most commonly found in skin creases.

The diagnosis can be made with a potassium hydroxide preparation, which shows budding yeasts with septate hyphae and pseudohyphae.

Treatment consists of topical antifungal medication and topical corticosteroids.

Hypersensitivity Skin

Hypersensitivity reactions in skin refers to allergic reactions in skin because of either cutaneous contact or ingestion of a given allergen.

Common causes of hypersensitivity skin reactions that should be remembered include:

• Plants (poison ivy, poison oak)

• Nickel

• Soaps

• Latex

Type I hypersensitivity skin reactions are caused by mast cell degranulation.

Type I reactions result in alight, diffuse rash that appears soon after exposure and lasts several hours.

Type IV hypersensitivity skin reactions are caused by lymphocyte activity. This is the mechanism of most allergic contact dermatitis.

Type IV reactions appear similarly to a measles rash(small red spots that are slightly raised and appear in clusters) and appear several days after the second exposure to an allergen.

The clinical presentation of a hypersensitivity reaction gives clues to the cause:

• Contact dermatitis causes a pruritic, erythematous rash in distinct patterns, such as lines or shapes.

• Food or drug reactions can cause a rash in a specific location or in a poorly defined area.

• Obtaining the contact and ingestion history from the patient is helpful for diagnosis.

The primary treatment is to stop the offending agent or to prevent contact with the suspected allergen.

Topical corticosteroids and antihistamines can provide relief for mild cases, but more severe cases may require oral corticosteroids.

Psoriasis

Psoriasis is a complex autoimmune inflammatory skin disease caused by adysregulation of the immune system to the skin, leading to a hyperproliferation of the epidermis.

Environmental (cold exposure, infection, medications), genetic, and immunologic (T-cell overactivity) factors seem to play a role in psoriasis.

Patients typically present with worsening erythematous scaling skin most often affecting the extensor surfaces of the elbows and knees.

Patients may also present with:

• Joint pain

• J oint swelling

• Pruritus

• Conjunctivitis

• Conjunctival dryness

• Blepharitis (inflammation of the eyelids)

The diagnosis of psoriasis is based on clinical findings of the physical exam. Skin biopsy can be used to help rule in the diagnosis when a patient presents with non-classical skin symptoms such as pustules.

On physical exam, the patient’s skin lesions are typically erythematous plaques. The classic lesion is a salmon colored patch on the extensor portions of the elbows and knees.

Uric acid levels may be elevated in some forms of psoriasis, confusing it with gout. ESR is typically normal, but can be elevated in other forms such as erythrodermic and pustular psoriasis.

Psoriasis may result in the following complications:

• Secondary bacterial infections

• Psoriatic arthritis

• Chronic conjunctivitis

• Blepharitis

Treatment of psoriasis is primarily dependent on severity of skin lesions and responsiveness to treatment. Management of mild-to-moderate psoriasis consists of either:

• Topical corticosteroids (initially)

• Topical retinoids (tazarotene)

• Topical vitamin D

• Anthralin

Phototherapy, or methotrexatein patients that have failed phototherapy, is the mainstay therapy in moderate to severe psoriasis, while cyclosporine can be used intermittently to help induce a therapeutic response.

Topical corticosteroids are used when ocular lesions are present.

Scabies

Scabies is a cutaneous infestation by the mite Sarcoptes scabiei that causes an intense pruritic lesion with characteristic distribution.

Risk factors for acquiring scabies include crowded living conditions and poor hygiene.

Scabies is transmitted person to person by direct physical contact.

Patients with a scabies infestation will present with very intense pruritus at the sites involved, which becomes worse at night and worsens after a hot bath.

The most common locations for scabies are the webs of fingers and toes, and mite burrows with nearby papules can be seen under the skin.

The diagnosis of scabies is usually clinical on the basis of history and the characteristic distribution of the skin lesions. For a more definitive diagnosis, skin scrapings can be viewed under a microscope to reveal mites and eggs.

The main complication of a scabies infestation is the spread of the infestation to close contacts, which is common.

Scabies can be treated with either topical permethrin 5% cream or oral ivermectin.

Diphenhydramine may be used to relieve the pruritus associated with scabies.

Once treatment is initiated, all clothing, bedding, towels, and linens must be washed in hot water to prevent reinfestation.

Seborrheic Dermatitis

Seborrheic dermatitis is anidiopathic form of dermatitis that commonly affects sebum-rich areas of the body (scalp, face) resulting in dry, flaky skin.

Seborrheic dermatitis most commonly occurs in healthy infants and adults, but has also been associated with other disorders such as HIV and Parkinson’s disease.

Patients with seborrheic dermatitis classically present with intermittent episodes of burning, scaling, and itching skin. Symptoms tend to worsen during the dry winter months.

"Cradle cap" is a term commonly used for infantile seborrheic dermatitis that causes scaly patches on the infants scalp.

The diagnosis of seborrheic dermatitis is based primarily on clinical presentation. Skin biopsy can be performed to help rule out other skin disorders.

One of the most common physical exam findings is a dry flaking scalp. Other common findings are pruritus, erythematous plaques, and yellowish crusting of the skin.

Seborrheic dermatitis may result in hypopigmentation, scarring and secondary bacterial infection.

Treatment of seborrheic dermatitis of the scalp consists of antifungal shampoo (e.g. ketoconazole, selenium sulfite) while other areas of the body are treated with topical corticosteroids, topical antifungals, or both.

Stevens Johnson

Stevens-Johnson syndrome (SJS)is a severe form of erythema multiforme involving mucous membranes and severe plaque formation. It is an immune-mediated hypersensitivity reaction that leads to necrosis and sloughing of the epidermis.

Stevens-Johnson syndrome represents the same process as toxic epidermal necrolysis (TEN).

• Involvement of <10% of the body surface is diagnosed as SJS

• Involvement of >30% is diagnosed as TEN

• Involvement in between is diagnosed as SJS/TEN

There are 4 etiologic categories for SJS:

• Medications (most common) (e.g. penicillin, sulfa containing drugs, NSAIDs, allopurinol, phenytoin, and carbamazepine)

• Infections (HIV, hepatitis)

• Malignancy

• Idiopathic

SJS presents with a 2-3 day prodromal period of fever and flu-like symptoms prior to the development of mucocutaneous lesions. After the prodromal period, a palpable macular rash will begin to appear, and then fluid filled blisters and ultimately sloughing of the skin.

In a patient’s first drug-exposure related case of SJS, the drug exposure typically occurs one to three weeks before the development of symptoms. The time course from prodrome until hospital discharge ranges between two to four weeks.

Blistering and swelling of the oral cavity is also seen in patients with SJS.

Conjunctival and corneal lesions are more serious complications that can lead to permanent blindess.

There are no specific diagnostic studies for SJS, but a history suggestive of drug exposure/illness, positive clinical symptoms, and a skin biopsy can help confirm clinical suspicion.

On physical examination a patient with SJS will typically have an erythematous rash which may have the appearance of a target. Other signs that raise concern of SJS include:

• Palpable rash

• Blisters

• Skin sloughing

• Tongue swelling

• Oral and lip ulcerations

• Conjunctivitis and corneal ulcerations

Lesions typically start on the face and thorax before spreading, and spare the scalp.

After a few days, vesicles and bullae form, and the skin begins to slough.Nikolsky sign (gentle lateral pressure on skin surface on an apparently uninvolved site which causes sloughing) may be positive.

Mucous membranes are almost always involved in SJS, including the oral mucosa (including tongue), conjunctiva, urethra, and pulmonary mucosa. Patients present with crusting and ulceration of the mucosal surface.

Skin biopsies are fairly specific and typically show lymphocytes within perivascular structures and full thickness epidermal detachment with a normal immunofluorescence. There will also be degeneration of the basal layer of the epidermis.

The mortality rate of SJS is about 10%. In those who survive, SJS can result in complications involving the skin, eyes, mouth, GU system, and lungs.

An early SJS complication is secondary bacterial infection.

Later dermatologic sequelae include irregular pigmentation, eruptive nevi, abnormal regrowth of nails, and alopecia.

Ophthalmologic complications include dry eye, photophobia, visual impairment, and corneal scarring that can lead to blindness. It is imperative to obtain an ophthalmology consultation in a patient with SJS to prevent ocular damage.

Genitourinary complications in women include labial and vaginal abnormalities and urinary retention.

Long-term pulmonary complications include chronic bronchitis/bronchiolitis, bronchiectasis, and obstructive disorders.

Because the most common cause of SJS is a reaction to medication, the most important first step in treatment is to stop the offending medication.

SJS is frequently treated in burn units or intensive care units with corticosteroids, analgesics, and intravenous fluids.

Ocular lesions are typically treated with moisturizing drops, topical antibiotics, and topical steroids.

TEN

Toxic Epidermal Necrolysis (TEN) is the most severe form of hypersensitivity reaction involving the mucous membranes and skin, leading to full thickness epidermal necrosis and sloughing of >30% of the body surface area.

TEN is most commonly caused by medications, but can also be caused by an infection or be idiopathic.

Medications that are known can contribute to the development of TEN include:

• NSAIDs

• Antibiotics(sulfonamides, penicillin, quinolones)

• Allopurinol

• Anticonvulsants

• Antiretrovirals(nevirapine, abacavir)

TEN typically presents with fever and flu-like symptoms 1-3 days before the development of skin lesions, which begin on the face and thorax before spreading to other areas of the body.

The skin lesions begin as an erythematous maculopapular rash which progresses to large painful blisters and ultimately sloughing.

Mucosal eruptions occur in up to 90% of patients, with oral mucosa almost always being involved. Ocular involvement can lead to conjunctival and corneal lesions that can lead to permanent scarring and blindness.

TEN is a clinical diagnosis based on findings such as:

• Skin lesions that are sensitive to touch and tend to slough off in large sheets with light touch (known as a positive Nikolsky’s sign)

• Blistering and ulcerations seen on the lips and oral mucosa

• Ocular involvement showing conjunctival redness and irritation

Laboratory findings associated with toxic epidermal necrolysis include:

• Decreased WBCs

• Decreased hemoglobin

• Decreased hematocrit

• Increased ALT and AST

Because TEN is most commonly caused by medications, the most important first step in management is to stop the offending agent.

Patients with TEN should be treated in a burn unit with intravenous hydration, corticosteroids, and intravenous immune globulin.

Ocular lesions are typically treated with moisturizing drops, topical antibiotics, and topical steroids.

Cases of TEN that are caused by HSV may benefit from the use of acyclovir.

Complications associated with TEN include:

• Severe dehydration

• Malnutrition

• Secondary bacterial infection

• Pneumonia

• Strictures and scarring

• Corneal ulceration, scarring, and even blindness.

The mortality rate of TEN is over 30%.