Chapter 54: Nursing Care of Patients with Skin Disorders

Pressure Ulcers: Therapeutic Measures

Treatment varies according to the size, depth, and stage of the pressure ulcer; the special needs of the patient; and health care provider preference. All pressure must be removed from the affected area for healing to occur. Cleanliness must be maintained. Basic treatment includes débridement, cleansing, and dressing of the wound to provide a moist and healing environment. - Débridement Débridement is the removal of dead or nonviable tissue from a wound to help clean the wound and facilitate formation of granulation tissue. It may be done with or without surgery. Nonsurgical débridement includes mechanical, enzymatic, and autolytic methods. Surgical débridement is used only if the patient has sepsis or cellulitis or to remove extensive echar. Eschar is a black or brown hard scab or dry crust, or thick, black, leather-like tissue that forms from necrotic tissue. It may hide the true depth of the wound and must be removed for the wound to heal. MECHANICAL DÉBRIDEMENT. Scissors and forceps can be used for mechanical débridement to selectively remove nonviable tissue. Whirlpool baths and wet-to-dry saline gauze dressings may also be used for mechanical débridement. ENZYMATIC DÉBRIDEMENT. Enzymatic débridement involves application of a topical enzyme débriding agent.These agents vary as to application methods, so careful reading of instructions is necessary. Most débriding agents are proteolytic enzymes that selectively digest necrotic tissue. AUTOLYTIC DÉBRIDEMENT. Autolytic débridement is the use of a synthetic dressing or moisture-retentive dressing over the ulcer. The eschar then self-digests via the action of the enzymes that are present in the fluid environment of the wound. This method is not used for infected wounds, because the infection would worsen. SURGICAL DÉBRIDEMENT. Surgical débridement involves the removal of devitalized tissue, slough, or thick, adherent es- char with a scalpel, scissors, or other sharp instrument. - Wound Cleaning The ulcer should be thoroughly cleansed using a whirlpool, a handheld showerhead, or an irrigating system with a pressure between 4 and 15 pounds per square inch (psi).A 30-mL syringe with an 18-gauge needle works well for this purpose. Pressure less than 4 psi does not adequately cleanse the wound, and pressure greater than 15 psi may damage tissue. Wounds heal more rapidly in a moist environment, with minimal bacterial colonization and a healing temperature. This takes 12 hours to occur after the wound is covered with an occlusive dressing. - Wound Dressings Dressings vary according to size, location, depth, stage of ulcer, and preference of the ordering practitioner . Commonly used dressing materials include hydrogel dressings, polyurethane films, hydrocolloid wafers, biological dressings, alginates, and cotton gauze. - Negative Pressure Wound Therapy In NPWT, a wound is packed loosely with a sterile sponge and then covered with an occlusive dressing. A vacuum source is placed in the wound, and gentle negative pressure is applied. The negative pressure allows excess drainage and infectious material to be removed. NPWT also maintains a moist environment for optimal healing.

Parasitic Skin Disorders: Scabies

- Pathophysiology and Etiology Scabies is a contagious skin disease caused by the mite Sarcoptes scabiei. It results from intimate or prolonged skin contact or prolonged contact with infected clothing, bedding, or animals. - Signs and Symptoms The major complaints are itching and rash. Itching can be intense, especially at night. Itching be gins about 1 month after infestation and may persist for days to weeks after treatment. - Therapeutic Measures Topical scabicides (permethrin/Elimite, crotamiton/Crotan) are used for chemical disinfection.

Skin Lesions: Malignant Skin Lesions

- Pathophysiology and Etiology The most common skin malignancies include basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. The major cause of skin malignancies is overexposure to ultraviolet rays, most commonly sunlight. Other factors include being fair skinned and blue eyed, genetic tendencies, history of x-ray therapy, exposure to certain chemical agents (e.g., arsenic, paraffin, coal tar), burn scars, chronic osteomyelitis, and immunosuppressive therapy. - Prevention Risk of most types of skin cancer can be reduced by limiting or avoiding direct exposure to UV rays.

Pressure Ulcers: Signs and Symptoms

A developing pressure ulcer begins with a reddened area, usually over a bony prominence, that does not blanch with pressure. A pressure ulcer stays red and does not blanch. The most common sites for pressure ulcers are the sacrum, heels, elbows, lateral malleoli, greater trochanters, ischial tuberosities, base of the skull, scapulae, and ears.

Pressure Ulcers: Prevention

USE A VALIDATED ASSESSMENT TOOL. Use an assessment tool such as the Braden or Norton scale to assess patients for physical condition, mental status, activity, mobility, and in- continence to determine the risk for pressure ulcers. Advanced age, lo w diastolic blood pressure, elevated body temperature, and inadequate current intake of protein are all risk factors associated with the development of pressure ulcers. CLEANSE THE SKIN. Gently cleanse the skin daily with tepid water and mild soap to prevent drying. To reduce friction, pat the skin dry rather than rubbing it dry. PREVENT DAMAGE FROM INCONTINENCE. If incontinence is a problem, clean the skin promptly with tepid water and mild soap, pat dry, and apply a moisture barrier to prevent breakdown. AVOID MASSAGING BONY PROMINENCES. Avoid massaging bony prominences or reddened skin areas; blood vessels are damaged by massage when ischemia is present or when they lie over a bone. MAINTAIN MOBILITY. Maintain the highest possible level of mobility, as follows: • Teach patients to shift their weight every 15 minutes if possible when lying or sitting. • Provide frequent active or passive range-of-motion exercises, as well as turning according to a written repositioning schedule. If patients are on bedrest, turn and reposition them at least every 2 hours, but preferably more often because ischemia development begins after 20 to 40 minutes of pressure. • When positioning patients on their side, place them at a 30-degree angle or less and not directly on the trochanter because this area is especially sensitive to pressure and can quickly break down. If patients are placed on the trochanter, they usually become restless and squirm around to get off the trochanter. • If the patient is seated in a chair, repositioning every hour is important. A mobility program specific to the patient must be developed. REDUCE PRESSURE, FRICTION, AND SHEAR DAMAGE. Avoid elevating the head of the bed more than 30 degrees to reduce pressure on the coccyx and friction and shear damage from sliding down in the bed. ELEVATE HEELS AND AVOID PRESSURE ON CALVES. Elevate heels off the bed with pillows placed lengthwise under the calf or with heel elevators. PREVENT ISCHEMIA. Avoid the use of donut-shaped cushions. They create a circle of pressure that cuts of f the circulation to the surrounding tissue, promoting ischemia rather than preventing it. PROTECT SKIN CONTACT SURFACES. Pad skin contact surfaces, especially bony prominences, so the y do not press against each other. USE PRESSURE-REDUCING MATTRESSES AND CUSHIONS. Provide an appropriate pressure-relieving or pressure-reducing mattress and chair cushion for immobile patients. PREVENT MALNUTRITION AND DEHYDRATION. Prevent malnutrition and dehydration by ensuring an adequate intake of protein, calories, and fluid; pro vide 2500 mL of fluid each day if not contraindicated by other medical problems.

Pressure Ulcers: Pathophysiology and Etiology

Essentially, a pressure ulcer is a lesion caused by prolonged pressure against the skin. This may result from spending a prolonged period in one position, causing the weight of the body to compress the capillaries against a bed or chair , especially over bony prominences. Those at risk are immobile patients, those with decreased circulation, and those with impaired sensory perception or neurologic function. Friction is the rubbing of the skin surface with an external mechanical force. Also referred to as "sheet burns," this can happen when the patient is dragged or pulled across bed linens instead of being lifted. Shearing occurs when the patient slides down in bed when the head of the bed is raised, or when being pulled or repositioned without being lifted off the sheets.

Cultural Considerations

• Darker skinned people have a tendency toward an overgrowth of connective tissue components concerned with the protection against infection and repair after injury. Keloid formation is one example of this tendency toward overgrowth of connective tissue. Lymphoma and systemic lupus erythematosus may occur due to this overgrowth of connective tissue. • Some African American men have facial hair that is kinky, curls back on itself, and penetrates the skin, which can result in pustules and small keloids. Many use depilatories or electric razors to prevent nicking the skin, which can also cause keloids. • Darker skinned people have an increased incidence of birthmarks and Mongolian spots compared with lighter skinned people. Mongolian spots disappear over time. The nurse must be cautious not to mistake these spots for bruising, which can indicate injury or abuse. • For people with light skin, such as those of German, Polish, and Irish descent, prolonged exposure to the sun may in- crease the incidence of skin cancer. Teach patients to protect themselves from sun exposure to reduce their risk of skin cancer. Nevi (freckles and skin discolorations) occur more often in lighter skinned individuals. They are most common in European Americans, followed by Asians, and then darker skinned African Americans.

Pressure Ulcers: Diagnostic Tests

Sw ab cultures and culture and sensitivity tests may be done to identify the causative organism in suspected infection sites. Results need to be interpreted to distinguish between true wound infection and bacterial colonization.

Inflammatory Skin Disorders: Dermatitis

- Pathophysiology and Etiology Dermatitis is inflammation of the skin and is characterized by itching, redness, and skin lesions, with varying borders and distribution patterns. There are three common types of dermatitis: contact dermatitis, atopic dermatitis, and seborrheic dermatitis. Contact dermatitis is caused by exposure to an allergen or irritant such as soap, perfume, or poison ivy. Atopic dermatitis tends to be hereditary and is associated with allergies, asthma, and hay fever. Seborrheic dermatitis occurs most often on the scalp, usually in individuals with oily skin. - Prevention The patient should prevent irritation to the skin by avoiding irritants, allergens, and excessive heat and dryness and by controlling perspiration. - Signs and Symptoms Itching and rashes or lesions are the main clinical manifestations of dermatitis. - Complications The lesion or rash worsens with continued irritation, exposure to offending agents, or scratching. Infections of the skin are common and may be due to the many open areas and breaks in the skin, as well as the patient' s reluctance to properly wash the affected area because of pain from the lesions. Some infections can also become systemic. - Diagnostic Tests Diagnosis is usually based on history, symptoms, and clinical findings. If infection is suspected, cultures of the lesions may be ordered to identify the infecting agent. - Therapeutic Measures Treatment varies according to symptoms. Basic treatment objectives are to control itching, alleviate discomfort and pain, decrease inflammation, control or prevent crust formation and oozing, prevent infection, prevent further damage to the skin, and heal the lesions as much as possible. Itching (pruritus) and discomfort can be some what relieved by antihistamines, analgesics, and antipruritic medications as ordered. Colloidal oatmeal preparations added to baths may also help. Steroids such as hydrocortisone or methylprednisolone may be used to suppress inflammation. Tub baths and wet dressings help control oozing and prevent further crust formation.

Herpes Zoster (Shingles)

- Pathophysiology and Etiology Herpes zoster, or shingles, is an acute inflammatory and infectious disorder that produces a painful vesicular eruption on bright red edematous plaques along the distribution of nerves from one or more posterior ganglia. Herpes zoster is caused by the varicella zoster virus—the same virus that causes chickenpox. The incubation period of herpes zoster is 7 to 21 days. Vesicles appear in 3 to 4 days. The total duration of the outbreak can vary from 10 days to 5 weeks. This disease occurs most commonly in older adults or in those who have a diminished resistance, such as the patient with acquired immunodeficiency syndrome (AIDS), the patient on immunosuppressant agents, or the patient with a malignancy or injury to the spine or a cranial nerve. - Prevention Avoidance of persons with herpes zoster during the contagious phase (a few days before eruption until vesicles dry or scab) is the best prevention. Varicella vaccine (Varivax) in children and adults who have not had chickenpox can reduce the risk of becoming infected with varicella. Another newer vaccine, Zostavax, is recommended for all patients over age 60 who have had chickenpox. It reduces the risk of shingles outbreak, and reduces the severity if it does occur. - Signs and Symptoms In addition to the vesicles and plaques, there may be irritation, itching, fever, malaise, and, depending on the location of lesions, visceral involvement. Lesions may be very painful; the incidence of pain increases with age. Complications Postherpetic neuralgia, persistent dermatomal pain, and hyperesthesia are common in older adults and can last for weeks to months after the lesions have healed. The incidence and severity of these complications increase with age. Ophthalmic herpes zoster affects the fifth cranial nerve and can be a serious complication. - Diagnostic Tests Diagnosis is usually confirmed by history and physical examination of the patient and associated signs and symptoms. Cultures may be ordered if secondary bacterial infections are suspected. - Therapeutic Measures Treatment is aimed at controlling the outbreak, reducing pain and discomfort, and pre venting complications. Mild cases may heal without medication. Antiviral agents such as acyclovir are used for more severe cases and are most effective if started within 72 hours of the onset of the rash. Analgesics may be prescribed for pain and discomfort.Anticonvulsants (gabapentin/Neurontin) or antidepressants (amitriptyline/Elavil) may also be effective for neuropathic pain. Use of corticosteroids is controversial, but they may help reduce discomfort and improve quality of life when used with antiviral agents. Topical steroids should not be applied if a secondary infection is present because they suppress the immune system.

Nursing Processes for the Patient with a Pressure Ulcer

- Data Collection • Stage I: The skin is still intact, but the area is red and does not blanch when pressed. There may also be warmth, hardness, and discoloration of the skin. A stage I ulcer may be difficult to detect on a dark-skinned person. • Stage II: There is a break in the skin, with partial-thickness skin loss of epidermis, dermis, or both. The ulcer may appear as an abrasion, a shallow crater, or a blister. Stage II ulcers do not contain slough (yellow fibrous tissue). • Stage III: There is full-thickness skin loss, which extends to the subcutaneous fat but not to the fascia. The ulcer looks like a deep crater and may have undermining of adjacent tissue. Bone, tendon, and muscle are not visible. • Stage IV: There is full-thickness skin loss with exposed muscle, bone, or support structures such as tendons. Slough or eschar may be present. There may be undermining and sinus tracts (tunneling). • Unstageable: The base of the ulcer is covered by slough or eschar so that the depth cannot be evaluated. The wound bed must be debrided before staging and treatment can take place. One exception, according to NPUAP (2007), is stable, dry, intact eschar on the heels. It serves as the body's natural (biological) cover and should not be removed. Observe wound exudate. Two common types of wound exudate are serosanguineous and purulent. Serosanguineous exudate is fluid consisting of serum and blood. It is blood-tinged, amber-colored fluid. Purulent fluid is a fluid that contains pus. It can vary in color and have different odors, depending on which bacteria are present. Creamy yellow pus may indicate Staphylococcus. Beige pus that has a fishy odor may suggest Proteus. Green-blue pus with a fruity odor may indicate Pseudomonas. Brown pus with a fecal odor may suggest Bacteroides. The wound must be cultured to accurately identify bacteria.

Inflammatory Skin Disorders: Psoriasis

- Pathophysiology and Etiology Psoriasis is a chronic inflammatory skin disorder in which the epidermal cells proliferate abnormally fast. Usually, epidermal cells take about 27 days to shed. With psoriasis, the cells shed every 4 to 5 days. The abnormal keratin forms loosely adherent scales with dermal inflammation. The exact cause is not known; however, it is autoimmune in nature, with T cells attacking healthy skin cells, causing an increase in skin cell, T-cell, and white cell production. Aggravating factors include streptococcal pharyngitis, emotional upset, stress, hormonal changes, cold weather, skin trauma, smoking, alcohol, and certain drugs. - Prevention Because the exact etiology is not known, measures to prevent exacerbation of symptoms are specific to the patient's circumstances. - Signs and Symptoms Signs and symptoms vary according to the patient and the particular type of psoriasis. Lesions are red papules that join to form plaques with distinct borders. Silvery scales develop on untreated lesions. Areas most often affected are the elbows and knees, scalp, umbilicus, and genitals. Other signs and symptoms include nail involvement, involvement in the gluteal fold (called intergluteal pinking), itching, and dry or brittle hair. - Complications Psoriatic arthritis can develop after the psoriasis has developed. If the psoriasis becomes severe and widespread, fever, chills, increased cardiac output, and benign lymphadenopathy can result. - Diagnostic Tests Usually, diagnosis is based on physical assessment alone. Skin biopsy or other diagnostic tests may be performed to rule out concurrent disease or secondary infection. - Therapeutic Measures Psoriasis is a chronic dis- ease with remissions and exacerbations. Basic treatment objectives are to decrease the rapid epidermal proliferation, inflammation, and itching and scaling.

Acne Vulgaris

- Pathophysiology and Etiology Acne vulgaris is a common skin disorder of the sebaceous glands and their hair follicles that usually occurs on the face, chest, upper back, and shoulders. The etiology is multifocal. The most common cause is hormonal changes during puberty. Acne occurs when the ducts through which this sebum flows become plugged. - Signs and Symptoms The initial lesions are called comedones (singular:comedo). Closed comedones, or whiteheads, are small white papules with tiny follicular openings. - Therapeutic Measures Medical treatment helps prevent new lesions and helps control current lesions. Effective topical agents include benzoyl peroxide (Desquam-X, Benzagel), which is an antibacterial agent that may help prevent pore plugging; antibiotics (erythromycin, tetracycline) to kill bacteria in follicles; and vitamin A acid (Retin-A, tretinoin) to loosen pore plugs and pre vent occurrence of new comedones. Systemic antibiotics (long term, low dose) and isotretinoin (Accutane) are usually reserved for severe cases of acne.

Cellulitis

- Pathophysiology and Etiology Cellulitis is inflammation of the skin and subcutaneous tissue resulting from infection, usually with Staphylococcus or Streptococcus bacteria. Methicillin-resistant Staphylococcus aureus (MRSA) is becoming a common cause and is resistant to many antibiotics. Cellulitis can occur as a result of skin trauma; as a secondary bacterial infection of an open wound, such as a pressure ulcer; or it may be unrelated to skin trauma. It most often occurs in the extremities, especially the lower legs. - Prevention Good hygiene and prevention of cross-contamination are important. If an open wound is present, preventing infection and promoting healing are critical. - Signs and Symptoms The initial sign of cellulitis is a localized area of inflammation that may become more generalized if not treated promptly . Common clinical manifestations include warmth, redness, localized edema, pain, tenderness, fever, and lymphadenopathy. The infection can worsen rapidly and become systemic if not treated properly. - Diagnostic Tests Culture and sensitivity testing of any pustules or drainage is necessary to identify the infecting organism. Blood cultures may also be indicated to rule out bacteremia. - Therapeutic Measures Topical and systemic antibiotics are prescribed according to culture and sensitivity test results. Débridement of nonviable tissue is necessary if an open wound is present. Systemic antibiotics are indicated if fe ver and lymphadenopathy are present. Elevation of the extremity can reduce pain and swelling. Monitor vital signs and report hypotension and tachycardia, because such changes can indicate systemic infection.

Fungal Infections

- Pathophysiology and Etiology Dermatomycosis, or a fungal infection of the skin, occurs when there is an impairment of the skin integrity in a warm, moist environment. This infection occurs through direct contact with infected humans, animals, or objects. Tinea is the term used to describe fungal skin infections.

Parasitic Skin Disorders: Pediculosis

- Pathophysiology and Etiology Pediculosis is an infestation by lice. There are three basic types: pediculosis capitis (head lice), pediculosis corporis (body lice), and pediculosis pubis (pubic, or crab, lice). - Signs and Symptoms Pediculosis capitis can result in no itching or intense itching and scratching, especially at the back of the head. - Therapeutic Measures Medical treatment is aimed at killing the parasites and mechanically removing nits. Over-the-counter (OTC) pediculicides containing pyrethrins or permethrin are the most commonly recommended compounds.

Pemphigus

- Pathophysiology and Etiology Pemphigus is an acute or chronic, serious skin disease characterized by the appearance of bullae (large fluid-filled blisters) of various sizes on otherwise normal skin and mucous membranes. The autoimmune response that occurs in pemphigus causes a patient's own antibodies to attack the skin and mucous membranes and destroy the protein "glue" that holds the cells together. - Signs and Symptoms Successive crops of bullae suddenly appear on skin or mucous membranes. The bullae are fragile and flaccid. They enlarge, rupture, and form painful, raw, eroded, partial-thickness wounds that bleed, ooze, and form crusts. Pemphigus usually originates in the oral mucosa and then spreads to the trunk. Large areas of the body become involved. - Diagnostic Tests A positive Nikolsky's sign is a characteristic finding. This occurs when there is sloughing or blistering of normal skin when minimal pressure is applied. A biopsy of a blister reveals acantholysis, or separation of epidermal cells from one another. - Therapeutic Measures Treatment is aimed at controlling the disease, healing the skin, and preventing complications. Corticosteroids in large doses and immunosuppressants are prescribed to control the disease and bring about remission. Biological therapy (rituximab/Rituxan) targets the offending white blood cells. Medicated mouthwashes may be prescribed for mouth lesions.Antibiotic and antifungal agents are prescribed as needed for secondary infections. - Nursing Care Monitor fluid balance with regular intake and output, body weight, and blood pressure measurement. Encourage the patient to maintain adequate fluid intake. Offer cool drinks often to lessen discomfort.

Herpes Simplex: Pathophysiology and Etiology

There are two types of herpes simplex: that caused by type 1 virus (HSV -1), which occurs above the waist and causes a fe ver blister or cold sore (Fig. 54.4), and that caused by type 2 virus (HSV-2), which occurs below the waist and causes genital herpes. The primary infection occurs through direct contact, respiratory droplet, or fluid exposure from another infected person. Following the initial infection, the virus lies dormant in nerve ganglia near the spinal column, where the immune system cannot destroy it. Crusts eventually form, and the lesions heal in about 1 week. The lesions are contagious for 2 to 4 days before dry crusts form. - Prevention Avoidance of contact with a known infected lesion during the blistering phase can pre vent the primary lesions. - Signs and Symptoms Some patients may have a prodromal phase of burning or tingling at the site for a few hours before eruption. The area becomes erythematous and swollen. Vesicles and pustules erupt in 1 to 2 days. There may also be redness with no blistering. Lesions can burn, itch, and be painful. The attacks vary in frequency but diminish with age. The patient is contagious with each outbreak until scabs are formed. - Complications If herpes simplex is present in the vagina at childbirth, the newborn may be infected (meningoencephalitis or a panvisceral infection may occur). If the person touches the afected area and then rubs the eyes, the eyes can become severely infected. Secondary bacterial infection of lesions can occur . Rarely, herpes encephalitis can occur. This is deadly if not treated promptly. - Diagnostic Tests Cultures of the lesions provide a definitive diagnosis. Most lesions are diagnosed on the basis of history, signs, and symptoms. - Therapeutic Measures There is no complete cure for herpes simple x. Recurrences will happen. Topical acyclovir (Zovirax) ointment is the drug of choice for primary lesions, to suppress the multiplication of vesicles. Docosanol (Abreva) is an over-the-counter topical antiviral agent that may be effective. Oral antivirals (acyclovir, famciclovir, or valacyclovir) may be recommended for severe or frequent attacks (six or more attacks per year) or for patients who are immunosuppressed.