The 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 ones 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. Its 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. (SeeClose-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. (SeeNail 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.

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, its 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. Theyre classified by their appearance as macules, papules, plaques, patches, nodules, tumors, wheals, cysts, vesicles, bullae, or pustules. (SeeRecognizing primary skin lesions.)

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. (SeeRecognizing 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. Its 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; andnoninflammatory, in which the follicle doesnt rupture but remains dilated.

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 isnt 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.)

Pathophysiology

Androgens stimulate sebaceous gland growth and the production of sebum, which is secreted into dilated hair follicles that contain bacteria. The bacteria, usuallyPropionibacterium acneandStaphylococcus 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 beforeor 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.

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 edemaand 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 (Morgans, Dennies, 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
• Kaposis 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)

• 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, andmore than 6,000 die, making burns this nations 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, theres a higher incidence of complications and thus a higher mortality rate. Immediate, aggressive burn treatment increases the patients 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. (SeeClassifications 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 arent 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, theres 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-degreeburn involves muscle, bone, and interstitial tissues. Within only hours, fluids and protein shift from capillary to interstitial spaces, causing edema. Theres 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.

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 burns depth and size to estimate its severity. (SeeUsing 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 notcover large burns with saline-soaked dressings)
• removing smoldering clothing (first soaking in saline solution if clothing is stuck to the patients skin), rings, and other constricting items
• immediate I.V. therapy to prevent hypovolemic shock and maintain cardiac output (lactated Ringers 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.

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 andStaphylococcus 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.

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. (SeeTypes 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 Bockharts impetigo) or deep (sycosis barbae).

Furuncles, also known as boils, are another form of deep folliculitis. Carbuncles are a group of interconnected furuncles. (SeeForms 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 patients physical condition and ability to resist infection.

Causes

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

Other causes may include:

• Klebsiella, Enterobacter, orProteusorganisms (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 showingS. aureus)
• possibly elevated white blood cell count (leukocytosis).

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 a