Integumentary System

Skin
Hair and nails
Glands
Pathophysiologic manifestations
	Inflammatory reaction of the skin
	Formation of lesions
Disorders
	Acne
	Atopic dermatitis
	Burns
	Cellulitis
	Dermatitis
	Folliculitis, furuncles, and carbuncles
	Fungal infections
	Pressure ulcer
	Psoriasis
	Scleroderma
	Warts

T he integumentary system, the largest and heaviest body system, includes the skin―the integument, or external covering of the body ― and the epidermal appendages, including the hair, nails, and sebaceous, eccrine, and apocrine glands. It protects against injury and invasion of microorganisms, harmful substances, and radiation; regulates body temperature; serves as a reservoir for food and water; and synthesizes vitamin D. Emotional well-being, including one's responses to the daily stresses of life, is reflected in the skin.

SKIN

The skin is composed of three layers: the epidermis, dermis, and subcutaneous tissues. The epidermis is the outermost layer. It's thin and contains sensory receptors for pain, temperature, touch, and vibration. The epidermal layer has no blood vessels and relies on the dermal layer for nutrition. The dermis contains connective tissue, the sebaceous glands, and some hair follicles. The subcutaneous tissue lies beneath the dermis; it contains fat and sweat glands and the rest of the hair follicles. The subcutaneous layer is able to store calories for future use in the body. (See Close-up view of the skin .)

HAIR AND NAILS

The hair and nails are considered appendages of the skin. Both have protective functions in addition to their cosmetic appeal. The cuticle of the nail, for example, functions as a seal, protecting the area between two portions of the nail from external hazards. (See Nail structure .)

GLANDS

The sebaceous glands, found on all areas of the skin except the palms and soles, produce sebum, a semifluid material composed of fat and epithelial cells. Sebum is secreted into the hair follicle and exits to the skin surface. It helps waterproof the hair and skin and promotes the absorption of fat-soluble substances into the dermis.

The eccrine glands produce sweat, an odorless, watery fluid. Glands in the palms and soles secrete sweat primarily in response to emotional stress. The other remaining eccrine glands respond mainly to thermal stress, effectively regulating temperature.

Located mainly in the axillary and anogenital areas, apocrine glands have a coiled secretory portion that lies deeper in the dermis than the eccrine glands. These glands begin to function at puberty and have no known biological function. Bacterial decomposition of the apocrine fluid produced by these glands causes body odor.

Skin color depends on four pigments: melanin, carotene, oxyhemoglobin, and deoxyhemoglobin. Each pigment is unique in its function and effect on the skin. For example, melanin, the brownish pigment of the skin, is genetically determined, though it can be altered by sunlight exposure. Excessive dietary carotene (from carrots, sweet potatoes, and leafy vegetables) causes a yellowing of the skin. Excessive oxyhemoglobin in the blood causes a reddening of the skin, and excessive deoxyhemoglobin (not bound to oxygen) causes a bluish discoloration.

CLOSE-UP VIEW OF THE SKIN The skin is composed of two major layers ― the epidermis and dermis. The epidermis consists of five strata, shown below. Subcutaneous tissue lying beneath the dermis consists of loose connective tissue that attaches the skin to underlying structures. <center></center>

PATHOPHYSIOLOGIC MANIFESTATIONS

Clinical manifestations of skin dysfunction include the inflammatory reaction of the skin and the formation of lesions.

Inflammatory reaction of the skin

An inflammatory reaction occurs with injury to the skin. The reaction can only occur in living organisms. Although a beneficial response, it's usually accompanied by some degree of discomfort at the site. Irritation changes the epidermal structure, and consequent increase of immunoglobulin E (IgG) activity. Other classic signs of inflammatory skin responses are redness, edema, and warmth, due to bioamines released from the granules of tissue mast cells and basophils.

Formation of lesions

Primary skin lesions appear on previously healthy skin in response to disease or external irritation. They're classified by their appearance as macules, papules, plaques, patches, nodules, tumors, wheals, cysts, vesicles, bullae, or pustules. (See Recognizing primary skin lesions .)

NAIL STRUCTURE The following illustration shows the anatomic components of a fingernail. <center></center>

Modified lesions are described as secondary skin lesions. These lesions occur as a result of rupture, mechanical irritation, extension, invasion, or normal or abnormal healing of primary lesions. These include atrophy, erosions, ulcers, fissures, crusts, scales, lichenification, excoriation, and scars. (See Recognizing secondary skin lesions .)

DISORDERS

Trauma, abnormal cellular function, infection, and systemic disease may cause disruptions in skin integrity.

Acne

Acne is a chronic inflammatory disease of the sebaceous glands. It's usually associated with a high rate of sebum secretion and occurs on areas of the body that have sebaceous glands, such as the face, neck, chest, back, and shoulders. There are two types of acne: inflammatory , in which the hair follicle is blocked by sebum, causing bacteria to grow and eventual rupture of the follicle; and noninflammatory , in which the follicle doesn't rupture but remains dilated.

AGE ALERT Acne occurs in both males and females. Acne vulgaris develops in 80% to 90% of adolescents or young adults, primarily between ages 15 and 18. Although the lesions can appear as early as age 8, acne primarily affects adolescents.

Although the severity and overall incidence of acne is usually greater in males, it tends to start at an earlier age lasts longer in females.

The prognosis varies and depends on the severity and underlying cause(s); with treatment, the prognosis is usually good.

Causes

The cause of acne is multifactorial. Diet isn't believed to be a precipitating factor. Possible causes of acne include increased activity of sebaceous glands and blockage of the pilosebaceous ducts (hair follicles).

Factors that may predispose to acne include:

• heredity
• androgen stimulation
• certain drugs, including corticosteroids, corticotropin (ACTH), androgens, iodides, bromides, trimethadione, phenytoin (Dilantin), isoniazid (Laniozid), lithium (Eskalith), and halothane
• cobalt irradiation
• hyperalimentation
• exposure to heavy oils, greases, or tars
• trauma or rubbing from tight clothing
• cosmetics
• emotional stress
• unfavorable climate
• oral contraceptive use. (Many females experience acne flare-up during their first few menses after starting or discontinuing oral contraceptives.)

RECOGNIZING PRIMARY SKIN LESIONS The most common primary lesions are illustrated below. BULLA Fluid-filled lesion more than ?" (2 cm) in diameter (also called a blister) (e.g., severe poison oak or ivy dermatitis, bullous pemphigoid, second-degree burn) COMEDO Plugged pilosebaceous duct, exfoliative, formed from sebum and keratin (e.g., blackhead [open comedo], whitehead [closed comedo]) CYST Semisolid or fluid-filled encapsulated mass extending deep into the dermis (e.g., acne) MACULE Flat, pigmented, circumscribed area less than 3 / 8 " (1 cm) in diameter (e.g., freckle, rubella) NODULE Firm, raised lesion; deeper than a papule, extending into dermal layer; ?" to ?" (0.5 to 2 cm) in diameter (e.g., intradermal nevus) PAPULE Firm, inflammatory, raised lesion up to ?" (0.5 cm) in diameter, may be same color as skin or pigmented (e.g., acne papule, lichen planus) PATCH Flat, pigmented, circumscribed area more than ” (1 cm) in diameter (e.g., herald patch [pityriasis rosea]) PLAQUE Circumscribed, solid, elevated lesion more than 3 / 8 " (1 cm) in diameter; elevation above skin surface occupies larger surface area compared with height (e.g., psoriasis) PUSTULE Raised, circumscribed lesion usually less than 3 / 8 " (1 cm) in diameter; containing purulent material, making it a yellow-white color (e.g., acne pustule, impetigo, furuncle) TUMOR Elevated solid lesion more than ?" (2 cm) in diameter, extending into dermal and subcutaneous layers (e.g., dermatofibroma) VESICLE Raised, circumscribed, fluid-filled lesion less than ?" (0.5 cm) in diameter (e.g., chicken pox, herpes simplex) WHEAL Raised, firm lesion with intense localized skin edema, varying in size and shape; color ranging from pale pink to red, disappears in hours (e.g., hive [urticaria], insect bite)

RECOGNIZING SECONDARY SKIN LESIONS The most common secondary lesions are illustrated below. ATROPHY Thinning of skin surface at site of disorder (e.g., striae, aging skin) CRUST Dried sebum, serous, sanguineous, or purulent exudate overlying an erosion or weeping vesicle, bulla, or pustule (e.g., impetigo) EROSION Circumscribed lesion involving loss of superficial epidermis (e.g., rug burn, abrasion) EXCORIATION Linear scratched or abraded areas, often self-induced (e.g., abraded acne, eczema) FISSURE Linear cracking of the skin extending into the dermal layer (e.g., hand dermatitis [chapped skin]) LICHENIFICATION Thickened, prominent skin markings by constant rubbing (e.g., chronic atopic dermatitis) SCALE Thin, dry flakes of shedding skin (e.g., psoriasis, dry skin, newborn desquamation) SCAR Fibrous tissue caused by trauma, deep inflammation, or surgical incision; red and raised (recent), pink and flat (6 weeks), and depressed (old) (e.g., on a healed surgical incision) ULCER Epidermal and dermal destruction may extend into subcutaneous tissue; usually heals with scarring (e.g., pressure sore or ulcer)

Pathophysiology

Androgens stimulate sebaceous gland growth and the production of sebum, which is secreted into dilated hair follicles that contain bacteria. The bacteria, usually Propionibacterium acne and Staphylococcus epidermis , are normal skin flora that secrete lipase. This enzyme interacts with sebum to produce free fatty acids, which provoke inflammation. Hair follicles also produce more keratin, which joins with the sebum to form a plug in the dilated follicle.

Signs and symptoms

The acne plug may appear as:

• a closed comedo, or whitehead (not protruding from the follicle and covered by the epidermis)
• an open comedo, or blackhead (protruding from the follicle and not covered by the epidermis; melanin or pigment of the follicle causes the black color).

Rupture or leakage of an enlarged plug into the epidermis produces inflammation, characteristic acne pustules, papules, or, in severe forms, acne cysts or abscesses (chronic, recurring lesions producing acne scars).

In women, signs and symptoms may include increased severity just before or during menstruation when estrogen levels are at the lowest.

Complications

Complications of acne may include:

• acne conglobata
• scarring (when acne is severe)
• impaired self-esteem (mostly adolescents afflicted).

Diagnosis

Diagnosis of acne vulgaris is confirmed by characteristic acne lesions, especially in adolescents.

Treatment

Topical treatments of acne include the application of antibacterial agents, such as benzyl peroxide (Benzac 5 or 10), clindamycin (Cleocin), or benzyl peroxide plus erythromycin (Benzamycin) antibacterial agents. These may be applied alone or with tretinoin (Retin-A; retinoic acid), which is a keratolytic. Keratolytic agents, such as benzyl peroxide and tretinoin, dry and peel the skin in order to help open blocked follicles, moving the sebum up to the skin level.

Systemic therapy consists primarily of:

• antibiotics, usually tetracycline, to decrease bacterial growth (reduced dosage for long-term maintenance when the patient is in remission)
• culture to identify a possible secondary bacterial infection (for exacerbation of pustules or abscesses while on tetracycline or erythromycin drug therapy)
• oral isotretinoin (Accutane) to inhibit sebaceous gland function and abnormal keratinization (16- to 20-week course of isotretinoin limited to patients with severe papulopustular or cystic acne not responding to conventional therapy due to its severe adverse effects)
• for females only, antiandrogens: birth control pills, such as norgestimate/ethinyl estradiol (Ortho TriCyclen) or spironolactone
• cleansing with an abrasive sponge in order to dislodge superficial comedones
• surgery to remove comedones and to open and drain pustules (usually on an outpatient basis)
• dermabrasion (for severe acne scarring) with a high-speed metal brush to smooth the skin (performed only by a well-trained dermatologist or plastic surgeon)
• bovine collagen injections into the dermis beneath the scarred area to fill in affected areas and even out the skin surface (not recommended by all dermatologists).

Atopic dermatitis

Atopic (allergic) dermatitis (also called atopic or infantile eczema) is a chronic or recurrent inflammatory response often associated with other atopic diseases, such as bronchial asthma and allergic rhinitis. It usually develops in infants and toddlers between ages 1 month and 1 year, usually in those with a strong family history of atopic disease. These children often develop other atopic disorders as they grow older.

Typically, this form of dermatitis flares and subsides repeatedly before finally resolving during adolescence, but it can persist into adulthood. Atopic dermatitis affects about 9 of every 1,000 persons.

Causes

Possible causes of atopic dermatitis include food allergy, infection, irritating chemicals, extremes of temperature and humidity, psychological stress or strong emotions (flare ups). These causes may be exacerbated by genetic predisposition.

AGE ALERT About 10% of childhood cases of atopic dermatitis are caused by allergy to certain foods, especially eggs, peanuts, milk, and wheat.

Pathophysiology

The allergic mechanism of hypersensitivity results in a release of inflammatory mediators through sensitized antibodies of the immunoglobulin E (IgE) class. Histamine and other cytokines induce an inflammatory response that results in edema and skin breakdown, along with pruritus.

Signs and symptoms

Possible signs and symptoms of atopic dermatitis are:

• erythematous areas on excessively dry skin; in children, typically on the forehead, cheeks, and extensor surfaces of the arms and legs; in adults, at flexion points (antecubital fossa, popliteal area, and neck)
• edema, crusting, and scaling due to pruritus and scratching
• multiple areas of dry, scaly skin, with white dermatographia, blanching, and lichenification with chronic atrophic lesions
• pink pigmentation and swelling of upper eyelid with a double fold under the lower lid (Morgan's, Dennie's, or mongolian fold) due to severe pruritus
• viral, fungal, or bacterial infections and ocular disorders (common secondary conditions).

Complications

Possible complications include:

• cataracts developing between ages 20 and 40
• Kaposi's varicelliform eruption (eczema herpeticum), a potentially serious widespread cutaneous viral infection (may develop if the patient comes in contact with a person infected with herpes simplex)
• subclinical (not requiring treatment) skin infection that may progress to cellulitis.

Diagnosis

Diagnosis of atopic dermatitis may involve:

• family history of atopic disorders (helpful in diagnosis)
• typical distribution of skin lesions
• ruling out other inflammatory skin lesions, such as diaper rash (lesions confined to the diapered area), seborrheic dermatitis (moist or greasy scaling with yellow-crusted patches), and chronic contact dermatitis (lesions affect hands and forearms, not antecubital and popliteal areas)
• serum IgE levels (often elevated but not diagnostic).

Treatment

Treatments include:

• eliminating allergens and avoiding irritants (strong soaps, cleansers, and other chemicals), extreme temperature changes, and other precipitating factors
• preventing excessive dryness of the skin (critical to successful therapy)
• topical application of a corticosteroid ointment, especially after bathing, to alleviate inflammation (moisturizing cream between steroid doses to help retain moisture); systemic antihistamines, such as Benadryl (diphenhydramine)

AGE ALERT Chronic use of potent fluorinated corticosteroids may cause striae or atrophy in children.

• administering systemic corticosteroid therapy (during extreme exacerbations)
• applying weak tar preparations and ultraviolet B light therapy to increase thickness of stratum corneum
• administering antibiotics (for positive culture for bacterial agent).

Burns

Burns are classified as first degree, second-degree superficial, second-degree deep partial thickness, third-degree full thickness, and fourth degree. A first-degree burn is limited to the epidermis. The most common example of a first-degree burn is sunburn, which results from exposure to the sun. In a second-degree burn, the epidermis and part of the dermis are damaged. A third-degree burn damages the epidermis and dermis, and vessels and tissue are visible. In fourth-degree burns, the damage extends through deeply charred subcutaneous tissue to muscle and bone. A major burn is a horrifying injury needing painful treatment and a long period of rehabilitation.

Each year in the United States, about 2 million persons receive burn injuries. Of these, 300,000 are burned seriously, and more than 6,000 die, making burns this nation's third leading cause of accidental death. About 60,000 people are hospitalized each year for burns. Most significant burns occur in the home; home fires account for the highest burn fatality rate.

In victims younger than 4 years and older than 60 years, there's a higher incidence of complications and thus a higher mortality rate. Immediate, aggressive burn treatment increases the patient's chance for survival. Later, supportive measures and strict aseptic technique can minimize infection. Meticulous, comprehensive burn care can make the difference between life and death. Survival and recovery from a major burn are more likely once the burn wound is reduced to less than 20% of the total body surface area (BSA).

Causes

Thermal burns, the most common type, frequently result from:

• residential fires
• automobile accidents
• playing with matches
• improper handling of firecrackers
• scalding accidents and kitchen accidents (such as a child climbing on top of a stove or grabbing a hot iron)
• parental abuse of (in children or elders)
• clothes that have caught on fire.

Chemical burns result from contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants.

Electrical burns usually result from contact with faulty electrical wiring or high-voltage power lines. Sometimes young children chew electrical cords.

Friction or abrasion burns occur when the skin rubs harshly against a coarse surface.

Sunburn results from excessive exposure to sunlight.

Pathophysiology

The injuring agent denatures cellular proteins. Some cells die because of traumatic or ischemic necrosis. Loss of collagen cross-linking also occurs with denaturation, creating abnormal osmotic and hydrostatic pressure gradients that cause the movement of intravascular fluid into interstitial spaces. Cellular injury triggers the release of mediators of inflammation, contributing to local and, in the case of major burns, systemic increases in capillary permeability. Specific pathophysiologic events depend on the cause and classification of the burn. (See Classifications of burns .)

First-degree burns. A first-degree burn causes localized injury or destruction to the skin (epidermis only) by direct (such as chemical spill) or indirect (such as sunlight) contact. The barrier function of the skin remains intact, and these burns aren't life threatening.

Second-degree superficial partial-thickness burns. These burns involve destruction to the epidermis and some dermis. Thin-walled, fluid-filled blisters develop within a few minutes of the injury. As these blisters break, the nerve endings become exposed to the air. Because pain and tactile responses remain intact, subsequent treatments are very painful. The barrier function of the skin is lost.

Second-degree deep partial-thickness burns. These burns involve destruction of the epidermis and dermis, producing blisters and mild to moderate edema and pain. The hair follicles are still intact, so hair will grow again. Compared with second-degree superficial partial-thickness burns, there's less pain sensation with this burn because the sensory neurons have undergone extensive destruction. The areas around the burn injury remain very sensitive to pain. The barrier function of the skin is lost.

Third- and fourth-degree burns. A major burn affects every body system and organ. A third-degree burn extends through the epidermis and dermis and into the subcutaneous tissue layer. A fourth-degree burn involves muscle, bone, and interstitial tissues. Within only hours, fluids and protein shift from capillary to interstitial spaces, causing edema. There's an immediate immunologic response to a burn injury, making burn wound sepsis a potential threat. Finally, an increase in calorie demand after a burn injury increases the metabolic rate.

CLASSIFICATIONS OF BURNS The depth of skin and tissue damage determines burn classification. The following illustration shows the four degrees of burn classifications. <center></center>

Signs and symptoms

Signs and symptoms depend on the type of burn and may include:

• localized pain and erythema, usually without blisters in the first 24 hours (first-degree burn)
• chills, headache, localized edema, and nausea and vomiting (more severe first-degree burn)
• thin-walled, fluid-filled blisters appearing within minutes of the injury, with mild to moderate edema and pain (second-degree superficial partial-thickness burn)
• white, waxy appearance to damaged area (second-degree deep partial-thickness burn)
• white, brown, or black leathery tissue and visible thrombosed vessels due to destruction of skin elasticity (dorsum of hand most common site of thrombosed veins), without blisters (third-degree burn)
• silver-colored, raised area, usually at the site of electrical contact (electrical burn)
• singed nasal hairs, mucosal burns, voice changes, coughing, wheezing, soot in mouth or nose, and darkened sputum (with smoke inhalation and pulmonary damage).

Complications

Possible complications of burns include:

• loss of function (burns to face, hands, feet, and genitalia)
• total occlusion of circulation in extremity (due to edema from circumferential burns)
• airway obstruction (neck burns) or restricted respiratory expansion (chest burns)
• pulmonary injury (from smoke inhalation or pulmonary embolism)
• adult respiratory distress syndrome (due to left-sided heart failure or myocardial infarction)
• greater damage than indicated by the surface burn (electrical and chemical burns) or internal tissue damage along the conduction pathway (electrical burns)
• cardiac arrhythmias (due to electrical shock)
• infected burn wound
• stroke, heart attack, or pulmonary embolism (due to formation of blood clots resulting from slower blood flow)
• burn shock (due to fluid shifts out of the vascular compartments, possibly leading to kidney damage and renal failure)
• peptic ulcer disease (due to decreased blood supply in the abdominal area)
• disseminated intravascular coagulation (more severe burn states)
• added pain, depression, and financial burden (due to psychological component of disfigurement).

Diagnosis

Diagnosis involves determining the size and classifying the wound. The following methods are used to determine size:

• percentage of BSA covered by the burn using the Rule of Nines chart
• Lund-Browder chart (more accurate because it allows BSA changes with age); correlation of the burn's depth and size to estimate its severity. (See Using the Rule of Nines and the Lund and Browder chart .)

Major burns are classified as:

• third-degree burns on more than 10% of BSA
• second-degree burns on more than 25% of adult BSA (over 20% in children)
• burns of hands, face, feet, or genitalia
• burns complicated by fractures or respiratory damage
• electrical burns
• all burns in poor-risk patients.

Moderate burns are classified as:

• third-degree burns on 2% to 10% of BSA
• second-degree burns on 15% to 25% of adult BSA (10% to 20% in children).

Minor burns are classified as:

• third-degree burns on less than 2% of BSA
• second-degree burns on less than 15% of adult BSA (10% in children).

Treatment

Initial burn treatments are based on the type of burn and may include:

• immersing the burned area in cool water (55°F [12.8°C]) or applying cool compresses (minor burns)
• pain medication as needed or anti-inflammatory medications
• covering the area with an antimicrobial agent and a nonstick bulky dressing (after debridement); prophylactic tetanus injection as needed
• maintaining an open airway; assessing airway, breathing, and circulation; checking for smoke inhalation immediately on receipt of the patient; assisting with endotracheal intubation; and giving 100% oxygen (first immediate treatment for moderate and major burns)
• controlling active bleeding
• covering partial-thickness burns over 30% of BSA or full-thickness burns over 5% of BSA with a clean, dry, sterile bed sheet (because of drastic reduction in body temperature, do not cover large burns with saline-soaked dressings)
• removing smoldering clothing (first soaking in saline solution if clothing is stuck to the patient's skin), rings, and other constricting items
• immediate I.V. therapy to prevent hypovolemic shock and maintain cardiac output (lactated Ringer's solution or a fluid replacement formula; additional I.V. lines may be needed)
• antimicrobial therapy (all patients with major burns)
• complete blood count, electrolyte, glucose, blood urea nitrogen, and serum creatinine levels; arterial blood gas analysis; typing and cross-matching; urinalysis for myoglobinuria and hemoglobinuria
• closely monitoring intake and output, frequently checking vital signs (every 15 minutes), possibly inserting indwelling urinary catheter
• nasogastric tube to decompress the stomach and avoid aspiration of stomach contents
• irrigating the wound with copious amounts of normal saline solution (chemical burns)
• surgical intervention, including skin grafts and more thorough surgical cleansing (major burns)
• not treating the burn wound itself for a patient being transferred to a specialty hospital within 4 hours, but wrapping the patient in a sterile sheet and blanket for warmth, elevating the burned extremity, and preparing the patient for transport.

USING THE RULE OF NINES AND THE LUND AND BROWDER CHART You can quickly estimate the extent of an adult patient's burn by using the Rule of Nines. This method divides an adult's body surface area into percentages. To use this method, mentally transfer your patient's burns to the body chart shown below, then add up the corresponding percentages for each burned body section. The total, an estimate of the extent of your patient's burn, enters into the formula to determine his initial fluid replacement needs. You can't use the Rule of Nines for infants and children because their body section percentages differ from those of adults. For example, an infant's head accounts for about 17% at the total body surface area compared with 7% for an adult. Instead, use the Lund and Browder chart. <center> <br /> <br /> </center>

Upon discharge or during prolonged care:

• increased caloric intake due to increased metabolic rate to promote healing and recovery
• teaching the patient and giving complete discharge instructions for home care; stressing importance of keeping the dressing clean and dry, elevating the burned extremity for the first 24 hours, and having the wound rechecked in 1 to 2 days.

Cellulitis

Cellulitis is an infection of the dermis or subcutaneous layer of the skin. It may follow damage to the skin, such as a bite or wound. As the cellulitis spreads, fever, erythema, and lymphangitis may occur.

A cellulitis infection may occur after a person sustains surface skin damage, such as from a bite or wound injury.

If treated in a timely manner, the prognosis is usually good. Persons with other contributing health factors, such as diabetes, immunodeficiency, and impaired circulation, have an increased risk for developing or spreading cellulitis.

Causes

Possible causes of cellulitis are bacterial and fungal infections, commonly group A streptococcus and Staphylococcus aureus .

Pathophysiology

As the offending organism invades the compromised area, it overwhelms the defensive cells (neutrophils, eosinophils, basophils, and mast cells) that break down the cellular components that normally contain and localize the inflammation. As cellulitis progresses, the organism invades tissue around the initial wound site.

Signs and symptoms

Signs and symptoms of cellulitis are:

• erythema and edema due to inflammatory responses to the injury (classic signs)
• pain at the site and possibly surrounding area
• fever and warmth due to temperature increase caused by infection.

Complications

Possible complications of cellulitis include:

• sepsis (untreated cellulitis)
• progression of cellulitis to involve more tissue area
• local abscesses
• thrombophlebitis
• lymphangitis in recurrent cellulitis.

Diagnosis

Diagnosis is based on:

• visual examination and inspection of the affected area
• white blood cell count showing mild leukocytosis with a left shift
• mildly elevated erythrocyte sedimentation rate
• culture and gram stain results of fluid from abscesses and bulla positive for the offending organism.

Treatment

Treatment of cellulitis may include:

• oral or I.V. penicillin (drug of choice for initial treatment) unless patient has known penicillin allergy
• warm soaks to the site to help relieve pain and decrease edema by increasing vasodilation
• pain medication as needed to promote comfort
• elevation of infected extremity to promote comfort and decrease edema.

AGE ALERT Cellulitis of the lower extremity is more likely to develop into thrombophlebitis in an elderly patient.

Dermatitis

Dermatitis is an inflammation of the skin that occurs in several forms: atopic (see “ Atopic dermatitis ”), seborrheic, nummular, contact, chronic, localized neurodermatitis (lichen simplex chronicus), exfoliative, and stasis. (See Types of dermatitis .)

Folliculitis, furuncles, and carbuncles

Folliculitis is a bacterial infection of a hair follicle that causes a pustule to form. The infection can be superficial (follicular impetigo or Bockhart's impetigo) or deep (sycosis barbae).

Furuncles, also known as boils, are another form of deep folliculitis. Carbuncles are a group of interconnected furuncles. (See Forms of bacterial skin infection .)

The incidence of folliculitis in the general population is difficult to determine because many affected people never seek treatment.

With appropriate treatment, the prognosis for patients with folliculitis is good. The disorder usually resolves within 2 to 3 weeks. The prognosis for patients with carbuncles depends on the severity of the infection and the patient's physical condition and ability to resist infection.

Causes

The most common cause of folliculitis, furuncles, and carbuncles is coagulase-positive Staphylococcus aureus .

Other causes may include:

• Klebsiella, Enterobacter , or Proteus organisms (causing gram-negative folliculitis in patients on long-term antibiotic therapy, such as for acne)
• Pseudomonas aeruginosa (thriving in a warm environment with a high pH and low chlorine content ― “hot tub folliculitis”).

Predisposing risk factors include:

• infected wound
• poor hygiene
• debilitation
• tight clothes
• friction
• immunosuppressive therapy
• exposure to certain solvents.

Pathophysiology

The affecting organism enters the body, usually at a break in the skin barrier (such as a wound site). The organism then causes an inflammatory reaction within the hair follicle.

Signs and symptoms

Folliculitis, furuncles, and carbuncles have different signs and symptoms.

• Folliculitis shows as pustules on the scalp, arms, and legs in children and the trunk, buttocks, and legs in adults.
• Furuncles show as hard, painful nodules, commonly on the neck, face, axillae, and buttocks. The nodules enlarge for several days, then rupture, discharging pus and necrotic material; after the nodules rupture, subsiding pain but erythema and edema persisting for days or weeks.
• Carbuncles show as extremely painful, deep abscesses draining through multiple openings onto the skin surface, usually around several hair follicles; with accompanying fever and malaise. Carbuncles are now rare.

Complications

Possible complications are:

• scarring
• bacteremia
• metastatic seeding of a cardiac valve defect or arthritic joint.

Diagnosis

Diagnosis is based on:

• patient history showing preexistent furuncles (carbuncles)
• physical examination showing the presence of the skin lesion to diagnose either folliculitis or carbuncle
• wound cultures of the infected site (usually showing S. aureus )
• possibly elevated white blood cell count (leukocytosis).

TYPES OF DERMATITIS TYPE CAUSES SIGNS AND SYMPTOMS TREATMENT AND INTERVENTIONS Seborrheic dermatitis   A subacute skin disease affecting the scalp, face, and occasionally other areas that's characterized by lesions covered with yellow or brownish-gray scales. Unknown; stress, immunodeficiency, and neurologic conditions may be predisposing factors; related to the yeast Pityrosporum ovale (normal flora) Eruptions in areas with many sebaceous glands (usually scalp, face, chest, axillae, and groin) and in skin folds Itching, redness, and inflammation of affected areas; lesions may appear greasy; fissures may occur Indistinct, occasionally yellowish scaly patches from excess stratum corneum (dandruff may be a mild seborrheic dermatitis) Removal of scales with frequent washing and shampooing with selenium sulfide suspension (most effective), zinc pyrithione, or tar and salicylic acid shampoo Application of topical corticosteroids and antifungals to involved area Nummular dermatitis   A subacute form of dermatitis characterized by inflammation in coin-shaped, scaling, or vesicular patches, usually pruritic. Possibly precipitated by stress, dry skin, irritants, or scratching Round, nummular (coin-shaped), red lesions, usually on arms and legs, with distinct borders of crusts and scales Possible oozing and severe itching Summertime remissions common, with wintertime recurrence Elimination of known irritants Measures to relieve dry skin: increased humidification, limited frequency of baths, use of bland soap and bath oils, and application of emollients Application of wet dressings in acute phase Topical corticosteroids (occlusive dressings or intralesional injections) for persistent lesions Tar preparations and antihistamines to control itching Antibiotics for secondary infection Same as for atopic dermatitis Contact dermatitis   Often sharply demarcated inflammation of the skin resulting from contact with an irritating chemical or atopic allergen (a substance producing an allergic reaction in the skin) and irritation of the skin resulting from contact with concentrated substances to which the skin is sensitive, such as perfumes, soaps, or chemicals. Mild irritants: chronic exposure to detergents or solvents Strong irritants: damage on contact with acids or alkalis Allergens: sensitization after repeated exposure Mild irritants and allergens: erythema and small vesicles that ooze, scale, and itch Strong irritants: blisters and ulcerations Classic allergic response: clearly defined lesions, with straight lines following points of contact Severe allergic reaction: marked erythema, blistering, and edema of affected areas Elimination of known allergens and decreased exposure to irritants, wearing protective clothing such as gloves, and washing immediately after contact with irritants or allergens Topical anti-inflammatory agents (including corticosteroids), systemic corticosteroids for edema and bullae, antihistamines, and local applications of Burow's solution (for blisters) Same as for atopic dermatitis Hand or foot dermatitis   A skin disease characterized by inflammatory eruptions of the hands or feet. In many cases unknown, but may result from irritant or allergic contact Excessively dry skin often a contributing factor 50% of patients are atopic Redness and scaling of the palms or soles May produce painful fissures Some cases present with blisters (dyshidrotic eczema) Same as for nummular dermatitis Severe cases may require systemic steroids TYPE CAUSES SIGNS AND SYMPTOMS TREATMENT AND INTERVENTIONS Localized neurodermatitis (lichen simplex chronicus, essential pruritus)   Superficial inflammation of the skin characterized by itching and papular eruptions that appear on thickened, hyperpigmented skin. Chronic scratching or rubbing of a primary lesion or insect bite or other skin irritation May be psychogenic Intense, sometimes continual scratching Thick, sharp-bordered, possibly dry, scaly lesions with raised papules and accentuated skin lines (lichenification) Usually affects easily reached areas, such as ankles, lower legs, anogenital area, back of neck, and ears One or several lesions may be present; asymmetric distribution Scratching must stop; then lesions disappear in about 2 weeks Fixed dressings or Unna's boot to cover affected areas Topical corticosteroids under occlusion or by intralesional injection Antihistamines and open wet dressings Emollients Patient informed about underlying cause Exfoliative dermatitis   Severe skin inflammation characterized by redness and widespread erythema and scaling, covering virtually the entire skin surface. Preexisting skin lesions progressing to exfoliative stage, such as in contact dermatitis, drug reaction, lymphoma, leukemia, or atopic dermatitis May be idiopathic Generalized dermatitis, with acute loss of stratum corneum, erythema, and scaling Sensation of tight skin Hair loss Possible fever, sensitivity to cold, shivering, gynecomastia, and lymphadenopathy Hospitalization, with protective isolation and hygienic measures to prevent secondary bacterial infection Open wet dressings, with colloidal baths Bland lotions over topical corticosteroids Maintenance of constant environmental temperature to prevent chilling or overheating Careful monitoring of renal and cardiac status Systemic antibiotics and steroids Same as for atopic dermatitis Stasis dermatitis   A condition usually caused by impaired circulation and characterized by eczema of the legs with edema, hyperpigmentation, and persistent inflammation. Secondary to peripheral vascular diseases affecting the legs, such as recurrent thrombophlebitis and resultant chronic venous insufficiency Varicosities and edema common, but obvious vascular insufficiency not always present Usually affects the lower leg just above internal malleolus or sites of trauma or irritation Early signs: dusky-red deposits of hemosiderin in skin, with itching and dimpling of subcutaneous tissue Later signs: edema, redness, and scaling of large areas of legs Possible fissures, crusts, and ulcers Measures to prevent venous stasis: avoidance of prolonged sitting or standing, use of support stockings, weight reduction in obesity, and leg elevation Corrective surgery for underlying cause After ulcer develops, encourage rest periods with legs elevated, open wet dressings, Unna's boot (zinc gelatin dressing provides continuous pressure to affected areas), and antibiotics for secondary infection after wound culture

Treatment

Appropriate treatments include:

• cleaning the infected area thoroughly with antibacterial soap and water
• applying warm, wet compresses to promote vasodilation and drainage from the lesions
• applying topical antibiotics, such as mupirocin ointment or clindamycin or erythromycin solution.

Specific treatments include:

• folliculitis (extensive infection) ― giving systemic antibiotics, such as a cephalosporin (Ancef) or dicloxacillin (Diclocil)
• furuncles ― incision and drainage of ripe lesions after applying warm, wet compresses, then giving systemic antibiotics
• carbuncles ― systemic antibiotic therapy and incision and drainage.

Fungal infections

Fungal infections of the skin are often regarded as superficial infections affecting the hair, nails, and dermatophytes (the dead top layer of the skin). They are unique in that they infect and survive on the keratin within these structures. The most common fungal infections are tinea and candidiasis.

FORMS OF BACTERIAL SKIN INFECTION The degree of hair follicle involvement in bacterial skin infection ranges from superficial erythema and pustule of a single follicle to deep abscesses (carbuncles) involving several follicles. <center></center>

Tinea infections are classified by the body location in which they occur. (See Common sites of tinea infections .) Tinea commonly infects children and adolescents. Obese patients are also at greater risk for these infections. Some forms, such as tinea cruris (a fungal infection of the groin), infect one gender more than the other. Tinea crusis occurs more commonly in males.

Candidiasis can infect the skin or mucous membranes. These infections are also classified according to the infected site or area. Candida organisms are the normal flora found in some people (on the skin, in the mouth, GI tract, and genitalia).

Candidiasis usually occurs in children and immunosuppressed individuals. There are also higher rates of candidiasis in pregnant women and in patients with diabetes mellitus, as well as those with indwelling catheters and I.V. lines.

The prognosis for tinea and candidiasis is very good. It usually responds well to appropriate drug therapy and resolves completely. It's also important to reduce risk factors to obtain a good outcome from the infection. Antifungal therapy usually resolves candidiasis, but if risk factors aren't avoided, a chronic condition can develop.

Causes

Tinea infections are caused by:

• Microsporum, Trichophyton , or Epidermophyton organisms
• contact with contaminated objects or surfaces.

Risk factors for tinea include:

• obesity
• exposure to the causative organisms
• antibiotic therapy with suppression of normal flora
• softened skin from prolonged water contact, such as with water sports or diaphoresis.

Causes of candidiasis include:

• overgrowth of Candida organisms and infection due to depletion of the normal flora (such as with antibiotic therapy)
• neutropenia and bone marrow suppression in immunocompromised patients (at greater risk for the disseminating form)
• Candida albicans , normal GI flora (cause candidiasis in susceptible patients)
• Candida overgrowth in the mouth (thrush).

COMMON SITES OF TINEA INFECTIONS TYPE SITE Tinea capitis Scalp Tinea corporis Skin areas excluding scalp, face, hands, feet, and groin Tinea cruris Groin Tinea pedis Foot Tinea manus Hand Tinea unguium or onychomycosis Nails

Pathophysiology

In tinea infections, the tinea fungi attack the outer, dead skin layers. These fungi prefer a dark, warm, moist environment. Tinea infections can be spread from human to human, animal to human, or soil to human. Tinea corpis, for example, can be contracted from animals infected with Microsporium canis or Trichophyton mentagrophytes , and also from humans infected with Trichophyton rubrum .

In candidiasis, the Candida organism penetrates the epidermis after it binds to integrin receptors and adhesion molecules. The secretion of proteolytic enzymes facilitates tissue invasion. An inflammatory response results from the attraction of neutrophils to the area and from activation of the complement cascade.

Signs and symptoms

Signs and symptoms of tinea include:

• erythema and pustules in a ring-like formation
• itching, often severe.

Signs and symptoms of candidiasis are:

• superficial papules and pustules
• erythematous and edematous areas of the infected epidermis or mucous membrane (with progression of inflammation, a white-yellow, curd-like crust covering the infected area)
• severe pruritus and pain at the lesion sites (common)
• white coating of the tongue and possibly lesions in the mouth (thrush).

Complications

Possible complications include:

• secondary bacterial infections of wounds opened by scratching
• ulcers with chronic forms (candidiasis lesions)
• candidal meningitis, endocarditis, or septicemia due to systemic disseminating candidiasis.

Diagnosis

Diagnosis is based on:

• fungal culture to determine the causative organism and suggest the mode of infection transmission (tinea infection)
• microscopic examination of a potassium hydroxide-treated skin scraping and culture (candida infection).

Treatment

Treatment includes:

• topical antifungal agents such as ketoconazole (Nizoral), believed to inhibit yeast growth by altering cell membrane permeability (tinea pedis, tinea cruis, and tinea corpuris)
• oral therapy with griseofulvin (Fulvicin) (drug of choice) if no response to topical treatment, to arrest fungal cell activity by disrupting its miotic spindle structure (tinea)
• oral ketoconazole (Nizoral; second choice) for infections resistant to griseofulvin therapy, to make the fungus more susceptible to osmotic pressure
• eliminating risk factors (tinea and candidiasis)
• oral nystatin (Mycostatin) and topical antifungals such as miconazole (Monistat) (candidiasis)
• I.V. amphotericin B (Fungizone) or oral ketonazole (Nizoral) (systemic infections).

STAGING PRESSURE ULCERS The staging system described below is based on the recommendations of the National Pressure Ulcer Advisory Panel (NPUAP) (Consensus Conference, 1991) and the Agency for Health Care Policy and Research (Clinical Practice Guidelines for Treatment of Pressure Ulcers, 1992). The stage 1 definition was updated by the NPUAP in 1997. STAGE 1 A stage 1 pressure ulcer is an observable pressure-related alteration of intact skin. The indicators, compared with the adjacent or opposite area on the body, may include changes in one or more of the following factors: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), or sensation (pain or itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin; in darker skin, the ulcer may appear with persistent red, blue, or purple hues. STAGE 2 A stage 2 pressure ulcer is characterized by partial-thickness skin loss involving the epidermis or dermis. The ulcer is superficial and appears as an abrasion, blister, or shallow crater. STAGE 3 A stage 3 pressure ulcer is characterized by full-thickness skin loss involving damage or necrosis of subcutaneous tissue, which may extend down to, but not through, the underlying fascia. The ulcer appears as a deep crater with or without undermining of adjacent tissue. STAGE 4 Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or support structures (for example, tendon or joint capsule) characterize a stage 4 pressure ulcer. Tunneling and sinus tracts also may be associated with stage 4 pressure ulcers.

Pressure ulcer

Pressure ulcers, commonly called pressure sores or bedsores, are localized areas of cellular necrosis that occur most often in the skin and subcutaneous tissue over bony prominences. These ulcers may be superficial, caused by local skin irritation with subsequent surface maceration, or deep, originating in underlying tissue. Deep lesions often go undetected until they penetrate the skin, but by then, they've usually caused subcutaneous damage. (See Staging pressure ulcers .)

Most pressure ulcers develop over five body locations: sacral area, greater trochanter, ischial tuberosity, heel, and lateral malleolus. Collectively, these areas account for 95% of all pressure ulcer sites. Patients who have contractures are at an increased risk for developing pressure ulcers due to the added pressure on the tissue and the alignment of the bones.

AGE ALERT Age also has a role in the incidence of pressure ulcers. Muscle is lost with aging, and skin elasticity decreases. Both these factors increase the risk for developing pressure ulcers.

Partial-thickness ulcers usually involve the dermis and epidermis; these wounds heal within a few weeks. Full-thickness ulcers also involve the dermis and epidermis, but in these wounds, the damage is more severe and complete. There may also be damage to the deeper tissue layers. Ulcers of the subcutaneous tissue and muscle may require several months to heal. If the damage has affected the bone in addition to the skin layers, osteomyelitis may occur, which will prolong healing times.

Causes

Possible causes of pressure ulcers include:

• immobility and decreased level of activity
• friction causing damage to the epidermal and upper dermal skin layers
• constant moisture on the skin causing tissue maceration
• impaired hygiene status, such as with fecal incontinence, leading to skin breakdown
• malnutrition (associated with pressure ulcer development)
• medical conditions such as diabetes and orthopedic injuries (predispose to pressure ulcer development)
• psychological factors, such as depression and chronic emotional stresses (may have a role in pressure ulcer development).

Pathophysiology

A pressure ulcer is caused by an injury to the skin and its underlying tissues. The pressure exerted on the area causes ischemia and hypoxemia to the affected tissues because of decreased blood flow to the site. As the capillaries collapse, thrombosis occurs, which subsequently leads to tissue edema and progression to tissue necrosis. Ischemia also adds to an accumulation of waste products at the site, which in turn leads to the production of toxins. The toxins further break down the tissue and eventually lead to the death of the cells.

Signs and symptoms

Signs and symptoms of pressure ulcers may include:

• blanching erythema, varying from pink to bright red depending on the patient's skin color; in dark-skinned people, purple discoloration or a darkening of normal skin color (first clinical sign); when the examiner presses a finger on the reddened area, the “pressed on” area whitens and color returns within 1 to 3 seconds if capillary refill is good
• pain at the site and surrounding area
• localized edema due to the inflammatory response
• increased body temperature due to initial inflammatory response (in more severe cases, cool skin due to more severe damage or necrosis)
• nonblanching erythema (more severe cases) ranging from dark red to purple or cyanotic; indicates deeper dermal involvement
• blisters, crusts, or scaling as the skin deteriorates and the ulcer progresses
• usually dusky-red appearance, doesn't bleed easily, warm to the touch, and possibly mottled (deep ulcer originating at the bony prominence below the skin surface).

Complications

Possible complications of pressure ulcers include:

• progression of the pressure ulcer to a more severe state (greatest risk)
• secondary infections such as sepsis
• loss of limb from bone involvement.

Diagnosis

Diagnosis is based on:

• physical examination showing presence of the ulcer
• wound culture with exudate or evidence of infection
• elevated white blood cell count with infection
• possibly elevated erythrocyte sedimentation rate
• total serum protein and serum albumin levels showing severe hypoproteinemia.

Treatment

Treatment for pressure ulcers includes:

• repositioning by the caregiver every 2 hours or more often if indicated, with support of pillows for immobile patients; a pillow and encouragement to change position for those able to move
• foam, gel, or air mattress to aid in healing by reducing pressure on the ulcer site and reducing the risk for more ulcers
• foam, gel, or air mattress on chairs and wheelchairs as indicated
• nutritional assessment and dietary consult as indicated; nutritional supplements, such as vitamin C and zinc, for the malnourished patient; monitoring serum albumin and protein markers and body weight
• adequate fluid intake (I.V. if indicated) and increased fluids for a dehydrated patient
• good skin care and hygiene practices (for example, meticulous hygiene and skin care for the incontinent patient to prevent breakdown of the affected tissue and skin)
• stage II, cover ulcer with transparent film, polyurethane foam, or hydrocolloid dressing
• stage II or IV, loosely fill wound with saline- or gel-moistened gauze, manage exudate with absorbent dressing (moist gauze or foam) and cover with secondary dressing
• clean, bulky dressing for certain types of ulcers, such as decubiti
• surgical debridement for deeper wounds stage III or IV as indicated.

Psoriasis

Psoriasis is a chronic, recurrent disease marked by epidermal proliferation and characterized by recurring partial remissions and exacerbations. Flare-ups are often related to specific systemic and environmental factors, but may be unpredictable. Widespread involvement is called exfoliative or erythrodermic psoriasis.

Psoriasis affects about 21% of the population in the United States. Although this disorder often affects young adults, it may strike at any age, including infancy. Genetic factors predetermine the incidence of psoriasis; researchers have discovered a significantly greater incidence of certain human leukocyte antigens (HLA) in families with psoriasis.

Flare-ups can usually be controlled with therapy. Appropriate treatment depends on the type of psoriasis, extent of the disease, the patient's response, and the effect of the disease on the patient's lifestyle. No permanent cure exists, and all methods of treatment are palliative.

Causes

Causes of psoriasis include:

• genetically determined tendency to develop psoriasis
• possible immune disorder, as shown by in the HLA type in families
• environmental factors
• isomorphic effect or Koebner's phenomenon, in which lesions develop at sites of injury due to trauma
• flare-up of guttate (drop-shaped) lesions due to infections, especially beta-hemolytic streptococci.

Other contributing factors include:

• pregnancy
• endocrine changes
• climate (cold weather tends to exacerbate psoriasis)
• emotional stress.

Pathophysiology

A skin cell normally takes 14 days to move from the basal layer to the stratum corneum, where it's sloughed off after 14 days of normal wear and tear. Thus, the life-cycle of a normal skin cell is 28 days compared with only 4 days for a psoriatic skin cell. This markedly shortened cycle doesn't allow time for the cell to mature. Consequently, the stratum corneum becomes thick and flaky, producing the cardinal manifestations of psoriasis.

Signs and symptoms

Possible signs and symptoms include:

• itching and occasional pain from dry, cracked, encrusted lesions (most common)
• erythematous and usually well-defined plaques, sometimes covering large areas of the body (psoriatic lesions)
• lesions most commonly on the scalp, chest, elbows, knees, back, and buttocks
• plaques with characteristic silver scales that either flake off easily or thicken, covering the lesion; scale removal can produce fine bleeding
• occasional small guttate lesions (usually thin and erythematous, with few scales), either alone or with plaques.

Complications

Possible complications of psoriasis include:

• spread to fingernails, producing small indentations or pits and yellow or brown discoloration (about 60% of patients)
• accumulation of thick, crumbly debris under the nail, causing it to separate from the nailbed (onycholysis).

Rarely, psoriasis becomes pustular, taking one of two forms:

• localized pustular psoriasis, with pustules on the palms and soles that remain sterile until opened
• generalized pustular (Von Zumbusch) psoriasis, often occurring with fever, leukocytosis, and malaise, with groups of pustules coalescing to form lakes of pus on red skin (also remain sterile until opened), commonly involving the tongue and oral mucosa
• arthritic symptoms, usually in one or more joints of the fingers or toes, the larger joints, or sometimes the sacroiliac joints, which may progress to spondylitis, and morning stiffness (some patients).

Diagnosis

Diagnosis is based on the following factors:

• patient history, appearance of the lesions, and, if needed, the results of skin biopsy
• serum uric acid level (usually elevated in severe cases due to accelerated nucleic acid degradation), but without indications of gout
• HLA-Cw6, -B13, and -Bw57 (may be present in early-onset familial psoriasis).

Treatment

Treatment may include:

• ultraviolet B (UVB) or natural sunlight exposure to retard rapid cell production to the point of minimal erythema
• tar preparations or crude coal tar applications to the affected areas about 15 minutes before exposure to ultraviolet B, or left on overnight and wiped off the next morning
• gradually increasing exposure to UVB (outpatient treatment or day treatment with UVB avoids long hospitalizations and prolongs remission)
• steroid creams and ointments applied twice daily, preferably after bathing to facilitate absorption, and overnight use of occlusive dressings to control symptoms of psoriasis
• intralesional steroid injection for small, stubborn plaques
• anthralin ointment (Anthra-Derm) or paste mixture for well-defined plaques (not applied to unaffected areas due to injury and staining of normal skin); petroleum jelly around affected skin before applying anthralin
• anthralin (Anthra-Derm) and steroids (anthralin application at night and steroid use during the day)
• calcipotriene ointment (Dovonex), a vitamin D analogue (best when alternated with a topical steroid)
• Goeckerman regimen (combines tar baths and UVB treatments) to help achieve remission and clear the skin in 3 to 5 weeks (severe chronic psoriasis)
• Ingram technique (variation of the Goeckerman regimen) using anthralin (Anthra-Derm) instead of tar
• administration of psoralens (plant extracts that accelearte exfoliation) with exposure to high intensity UVA (PUVA therapy)
• cytotoxin, usually methotrexate (Folex) (last-resort treatment for refractory psoriasis)
• acitretin (Soriatant), a retinoid compound (extensive psoriasis)
• cyclosporine (Neoral), an immunosuppressant (in resistive cases)
• low-dose antihistamines, oatmeal baths, emollients, and open wet dressings to help relieve pruritus
• aspirin and local heat to help alleviate the pain of psoriatic arthritis; nonsteroidal anti-inflammatory drugs in severe cases
• tar shampoo followed by a steroid lotion (psoriasis of the scalp)
• no effective topical treatment for psoriasis of the nails.

Scleroderma

Scleroderma (also known as systemic sclerosis) is an uncommon disease of diffuse connective tissue disease characterized by inflammatory and then degenerative and fibrotic changes in the skin, blood vessels, synovial membranes, skeletal muscles, and internal organs (especially the esophagus, intestinal tract, thyroid, heart, lungs, and kidneys). There are several forms of scleroderma, including diffuse systemic sclerosis, localized, linear, chemically induced localized, eosinophilia myalgia syndrome, toxic oil syndrome, and graft-versus-host disease.

AGE ALERT Scleroderma is an uncommon disease. It affects women three to four times more often than men, especially between ages 30 and 50 years. The peak incidence of occurrence is in 50- to 60-year-olds.

Scleroderma is usually a slowly progressing disorder. When the condition is limited to the skin, the prognosis is usually favorable. However, approximately 30% of patients with scleroderma die within 5 years of onset. Death is usually caused by infection or renal or cardiac failure.

Causes

The cause of scleroderma is unknown, but some possible causes include:

• systemic exposure to silica dust or polyvinyl chloride
• anticancer agents such as bleomycin (Blenoxane) or nonnarcotic analgesics such as pentazocine hydrochloride (Talwin)
• fibrosis due to an abnormal immune system response
• underlying vascular cause with tissue changes initiated by a persistent perfusion.

Pathophysiology

Scleroderma usually begins in the fingers and extends proximally to the upper arms, shoulders, neck, and face. The skin atrophies, edema and infiltrates containing CD4+ T cells surround the blood vessels, and inflamed collagen fibers become edematous, losing strength and elasticity, and degenerative. The dermis becomes tightly bound to the underlying structures, resulting in atrophy of the affected dermal appendages and destruction of the distal phalanges by osteoporosis. As the disease progresses, this atrophy can affect other areas. For example, in some patients, muscles and joints become fibrotic.

Signs and symptoms

Possible signs and symptoms of scleroderma are:

• skin thickening, commonly limited to the distal extremities and face, but which can also involve internal organs (limited systemic sclerosis)
• CREST syndrome (a benign subtype of limited systemic sclerosis): Calcinosis, Raynaud's phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasia
• generalized skin thickening and involvement of internal organs (diffuse systemic sclerosis)
• patchy skin changes with a teardrop-like appearance known as morphea (localized scleroderma)
• band of thickened skin on the face or extremities that severely damages underlying tissues, causing atrophy and deformity (linear scleroderma)

AGE ALERT Atrophy and deformity with scleroderma are most common in childhood.

• Raynaud's phenomenon (blanching, cyanosis, and erythema of the fingers and toes); progressive phalangeal resorption may shorten the fingers (early symptoms)
• pain, stiffness, and swelling of fingers and joints (later symptoms)
• taut, shiny skin over the entire hand and forearm due to skin thickening
• tight and inelastic facial skin, causing a mask-like appearance and “pinching” of the mouth; contractures with progressive tightening
• thickened skin over proximal limbs and trunk (diffuse systemic sclerosis)
• frequent reflux, heartburn, dysphagia, and bloating after meals due to GI dysfunction
• abdominal distention, diarrhea, constipation, and malodorous floating stool.

Complications

Complications of scleroderma include:

• compromised circulation due to abnormal thickening of the arterial intima, possibly causing slowly healing ulcerations on fingertips or toes leading to gangrene
• decreased food intake and weight loss due to GI symptoms
• arrhythmias and dyspnea due to cardiac and pulmonary fibrosis; malignant hypertension due to renal involvement, called renal crisis (may be fatal if untreated; advanced disease).

Diagnosis

Diagnosis of scleroderma may include:

• typical cutaneous changes (the first clue to diagnosis)
• slightly elevated erythrocyte sedimentation rate, positive rheumatoid factor in 25% to 35% of patients, and positive antinuclear antibody test results
• urinalysis showing proteinuria, microscopic hematuria, and casts (with renal involvement)
• hand X-rays showing terminal phalangeal tuft resorption, subcutaneous calcification, and joint space narrowing and erosion
• chest X-rays showing bilateral basilar pulmonary fibrosis
• GI X-rays showing distal esophageal hypomotility and stricture, duodenal loop dilation, small-bowel malabsorption pattern, and large diverticula
• pulmonary function studies showing decreased diffusion and vital capacity
• electrocardiogram showing nonspecific abnormalities related to myocardial fibrosis
• skin biopsy showing changes consistent with disease progression, such as marked thickening of the dermis and occlusive vessel changes.

Treatment

There's no cure for scleroderma. Treatment aims to preserve normal body functions and minimize complications and may include:

• immunosuppressants, such as cyclosporine (Neoral) or chlorambucil (Leukeran) (common palliative medications)
• vasodilators and antihypertensives; such as nifedipine (Adalat), prazosin (Minipress), or topical nitroglycerin (Nitrol); digital sympathectomy; or, rarely, cervical sympathetic blockade to treat Raynaud's phenomenon
• digital plaster cast to immobilize the area, minimize trauma, and maintain cleanliness; possible surgical debridement for chronic digital ulceration
• antacids (to reduce total acid level in GI tract), omeprazole (Prilosec; antiulcer drug to block the formation of gastric acid), periodic dilation, and a soft, bland diet for esophagitis with stricture
• broad-spectrum antibiotics to treat small-bowel involvement with erythromycin or tetracycline (preferred drugs) to counteract the bacterial overgrowth in the duodenum and jejunum related to hypomotility
• short-term benefit from vasodilators, such as nifedipine (Adalat) or hydralazine (Apresoline), to decrease contractility and oxygen demand, and cause vasodilation (for pulmonary hypertension)
• angiotensin-converting enzyme inhibitor to preserve renal function (early intervention in renal crisis)
• physical therapy to maintain function and promote muscle strength, heat therapy to relieve joint stiffness, and patient teaching to make performance of daily activities easier (for hand debilitation).

Warts

Warts, also known as verrucae, are common, benign, viral infections of the skin and adjacent mucous membranes. Although their incidence is greatest in children and young adults, warts occur at any age. The prognosis varies; many types of warts resolve spontaneously, whereas others need more vigorous and prolonged treatment. Most persons eventually develop an immune response to the papillomavirus that causes the warts to disappear spontaneously. An immune response may develop to some types of warts, but this immune response can be delayed for many years.

Causes

Warts are caused by:

• human papillomavirus (HPV)
• transmission by touch and skin-to-skin contact
• spread on the affected person by autoinoculation.

Pathophysiology

HPV replicates in the epidermal cells, causing irregular thickening of the stratum corneum in the infected areas. People who lack the virus-specific immunity are susceptible to the virus.

Signs and symptoms

Signs and symptoms depend on the type of wart and its location and may include:

• rough, elevated, rounded surface, most frequently occurring on extremities, particularly hands and fingers; most prevalent in children and young adults (common warts [verruca vulgaris])
• single, thin, threadlike projection; commonly occurring around the face and neck (filiform)
• rough, irregularly shaped, elevated surface, occurring around edges of fingernails and toenails (when severe, extending under the nail and lifting it off the nailbed, causing pain [periungual])
• multiple groupings of up to several hundred slightly raised lesions with smooth, flat, or slightly rounded tops, common on the face, neck, chest, knees, dorsa of hands, wrists, and flexor surfaces of the forearms (usually occur in children but can affect adults); often linear distribution due to spread by scratching or shaving (flat or juvenile)
• slightly elevated or flat; occurring singly or in large clusters (mosaic warts), primarily at pressure points of the feet (plantar)
• fingerlike, horny projection arising from a pea-shaped base, occurring on scalp or near hairline (digitale)
• usually small, pink to red, moist, and soft, occurring singly or in large cauliflower-like clusters on the penis, scrotum, vulva, and anus; although transmitted through sexual contact, it's not always venereal in origin (condyloma acuminatum [moist wart]).

Complications

Possible complications are:

• autoinoculation
• scar formation
• chronic pain after plantar wart removal and scar formation
• nail deformity after injury to nail matrix
• cervical cancer, with increased risk if a woman smokes (certain strains of HPV)
• esophageal warts (in newborn exposed to genital warts).

AGE ALERT The presence of perianal warts in children may be a sign of sexual abuse.

Diagnosis

Diagnosis is based on:

• physical examination of the patient
• sigmoidoscopy with recurrent anal warts to rule out internal involvement necessitating surgery.

Treatment

If immunity develops, warts resolve by themselves. Treatments may include:

• skin irritants, such as salicylic acid or formaldehyde, applied to the wart to try to stimulate an immune response
• curettage or cryosurgery
• carbon dioxide laser treatment for recalcitrant warts of on the feet, groin, or nail bed
• abstinence or condom use until warts are eradicated; partners should also be examined and treated as needed (genital warts).