UNIT 2

HIV Symptomatic (CDC Category B: 200 to 499 CD4+ T Lymphocytes/mm3)

= Over time, the number of CD4+ T cells gradually falls. Category B consists of symptomatic conditions in HIV-infected patients that are not included in the conditions listed in category C. These conditions also must meet one of the following criteria: (1) the condition is due to HIV infection or a defect in cellular immunity, or (2) the condition is considered to have a clinical course or to require management that is complicated by HIV infection.

Stem cells

(undifferentiated cells) in the bone marrow generate lymphocytes (a type of WBC) (Fig. 36-2). There are two types of lymphocytes: B lymphocytes (B cells), which mature in the bone marrow and enter the circulation as precursors to antibody-secreting cells or memory cells, and T lymphocytes (T cells), which move from the bone marrow to the thymus, where they mature into several kinds of cells with different helper functions (Fig. 36-3).

Hydration

Adds moisture to a wound Gauze (saturated with saline solution), hydrogels, wound care systems

Enzyme immunoassay (EIA)

Antibodies are detected, resulting in positive results. May have false-negative results within the window period. formerly referred to as the enzyme-linked immunosorbent assay (ELISA) test, identifies antibodies directed specifically against HIV.

Pressure

Any boney prominence Erythremic or purplish in discoloration due to pressure Minimal to large amounts exudate Poorly to well defined

Tissue Engineered Skin

Apligraf and Dermagraft are dressings made up of a bioabsorbable matrix of collagen or suture material that contains living cytokines and fibroblasts. When applied to wounds, these agents stimulate platelet activity and potentially decrease wound-healing time (Bryant & Nix, 2016). Bioengineered skin works by maintaining wound moisture, providing a structure for regeneration of cells, and supplying beneficial cytokines.

Vesicle, bulla

Circumscribed, elevated, palpable mass containing serous fluid Vesicle: less than 0.5 cm Bulla: greater than 0.5 cm Vesicles: Herpes simplex/zoster, chickenpox, poison ivy, second-degree burn (blister) Bulla: Pemphigus, contact dermatitis, large burn blisters, poison ivy, bullous impetigo

HIV

Clinical Manifestations During the first stage of infection, the patient may be asymptomatic or may exhibit various signs and symptoms. The patient's health history should alert the health care provider about the need for HIV screening based on the patient's sexual practices, IV/injection drug use, and receipt of blood transfusions. Patients who are in later stages of HIV infection may have a variety of symptoms related to their immunosuppressed state. HIV often causes opportunistic infections (OIs). With widespread availability and improved effectiveness of ARVs, clinical occurrence of OIs has plummeted. OIs and other common manifestations are discussed below. Respiratory Manifestations Dyspnea (labored breathing), cough, chest pain, and fever are associated with various OIs, such as those caused by Pneumocystis jiroveci, Mycobacterium avium-intracellulare, CMV, and Legionella species. Neurologic Manifestations An estimated 80% of all patients with AIDS experience some form of neurologic involvement during the course of HIV infection. Many neuropathologic disorders are underreported because patients may have neurologic involvement without overt signs or symptoms. Neurologic complications involve central, peripheral, and autonomic functions. HIV-associated neurocognitive disorders (HAND) can affect memory, attention, language, and executive functioning. Neurologic dysfunction results from direct effects of HIV on nervous system tissue, OIs, primary or metastatic neoplasms, cerebrovascular changes, metabolic encephalopathies, or complications secondary to therapy. Immune system response to HIV infection in the CNS includes inflammation, atrophy, demyelination, degeneration, and necrosis. Integumentary Manifestations Cutaneous manifestations are associated with HIV infection and the accompanying OIs and malignancies. KS (described earlier) and OIs, such as herpes zoster and herpes simplex, are associated with painful vesicles that disrupt skin integrity. Molluscum contagiosum is a viral infection characterized by multiple grouped lesions. Seborrheic dermatitis is associated with an indurated, diffuse, scaly rash involving the scalp and face (see Chapter 52). Patients with AIDS also may exhibit a generalized eosinophilic folliculitis associated with dry, flaking skin or atopic dermatitis, such as eczema or psoriasis Gynecologic Manifestations Persistent, recurrent vaginal candidiasis or bacterial vaginosis may be the first sign of HIV infection in women. Past or present genital ulcer disease is a risk factor for the transmission of HIV infection. Women with HIV infection are more susceptible to and have increased rates of incidence and recurrence of genital ulcer disease and venereal warts. Ulcerative STIs, such as chancroid, syphilis, and herpes, are more severe in women with HIV infection. Human papillomavirus (HPV) causes venereal warts and is a risk factor for cervical intraepithelial neoplasia, a cellular change that is frequently a precursor to cervical cancer. Women with HIV are 10 times more likely to develop cervical intraepithelial neoplasia than are those not infected with HIV. Immunologic Manifestations Immune reconstitution inflammatory syndromes (IRIS) have been described for mycobacterial infections, including disease caused by MAC and M. tuberculosis, PCP, toxoplasmosis, hepatitis B and hepatitis C, CMV infection, varicella-zoster virus infection, cryptococcal infection, and progressive multifocal leukoencephalopathy. Immune reconstitution syndromes are characterized by fever and worsening of the clinical manifestations of the OI, or the appearance of new manifestations developing weeks after the initiation of ART. It is important to determine the absence or reappearance of the underlying OI, new drug toxicity, or a new OI. If the syndrome represents an immune restoration response, adding nonsteroidal anti-inflammatory agents (NSAIDs) or corticosteroids to alleviate the inflammatory reaction is appropriate. The inflammation might take weeks to months to subside (Sax et al., 2014). The nurse should be alert to signs of immune reconstitution syndrome and advise the patient to seek health care if he or she is feeling sicker with no clear explanation. Medical and Nursing Management Treatment Regimen . In general, ARV medications should be offered to all individuals, regardless of CD4 cell count to reduce the morbidity and mortality of HIV infection (DHHS, 2016). In addition, ARV therapy (ART) is recommended to prevent HIV transmission. Even with these overriding recommendations from DHHS, treatment decisions are individualized based on a number of factors, including CD4+ T-cell count, HIV RNA (viral load), severe symptoms of HIV disease or AIDS, and willingness of the patient to adhere to a lifelong treatment regimen. Medications More than 28 approved ARV agents, belonging to 6 classes, are available for the design of combination regimens. Effective regimens contain at least three virologically active medications from at least two classes. The six classes currently approved by the FDA are the nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), PIs, integrase strand transfer inhibitors (INSTIs), CCR5 antagonist, and fusion inhibitor (see Table 39-2, [DHHS, 2015]). Side Effects Many of the ARV agents that prolong life may simultaneously cause lipodystrophy syndrome and place the person at risk for early-onset hypercholesterolemia, heart disease, and diabetes. Fat redistribution syndrome, which consists of lipoatrophy (Fig. 37-4), lipohypertrophy, or both in localized areas, is also known as lipodystrophy syndrome. This syndrome is one of the most frequent systemic side effects associated with the use of ARV medications, especially PIs, and affects up to 58% of patients (Sax et al., 2014). Many people who have lipodystrophy experience an increase in fat loss in the legs, arms, face, or a buildup of fat around the abdomen and at the base of the neck, or both. Patients also may experience an increase in breast size. All of these adverse effects can have a profound impact on a patient's psychological well-being due to the increased stress of stigmatization.Facial wasting, characterized as a sinking of the cheeks, eyes, and temples caused by the loss of fat tissue under the skin, may be treated by injectable fillers such as poly-L-lactic acid (Sculptra).

Foods Peanuts, tree nuts (e.g., walnuts, pecans, cashews, almonds), shellfish (e.g., shrimp, lobster, crab), fish, milk, eggs, soy, wheat Medications Antibiotics (especially penicillin and sulfa antibiotics), allopurinol, radiocontrast agents, anesthetic agents (lidocaine, procaine), vaccines, hormones (insulin, vasopressin, adrenocorticotropic hormone [ACTH], aspirin, nonsteroidal anti- inflammatory drugs [NSAIDs]). Other Pharmaceutical/Biologic Agents Animal serums (tetanus antitoxin, snake venom antitoxin, rabies antitoxin), antigens used in skin testing Insect Stings Bees, wasps, hornets, yellow jackets, ants (including fire ants) Latex Medical and nonmedical products containing latex

Common Causes of Anaphylaxis

Venous

Commonly located in the lower leg just above the ankle (gaiter region) Dark red, "ruddy" Moderate to large amounts exudate Poorly defined; irregular

Secondary

Deficiency results from some interference with an already developed immune system; usually acquired later in life

Crust

Dried residue of serum, blood, or pus on skin surface Large, adherent crust is a scab Residue left after vesicle rupture: impetigo, herpes, eczema

Wheal

Elevated mass with transient borders; often irregular; size and color vary Caused by movement of serous fluid into the dermis; does not contain free fluid in a cavity (as, for example, a vesicle does) Urticaria (hives), insect bites

Scales

Flakes secondary to desquamated, dead epithelium that may adhere to skin surface; color varies (silvery, white); texture varies (thick, fine) Dandruff, psoriasis, dry skin, pityriasis rosea

Negative Pressure Wound Therapy

In this therapy, an open-cell, reticulated foam, gauze, or specially designed dressing is placed into the wound, sealed with semi-occlusive drape, and exposed to subatmospheric pressure via an evacuation tube connected to a computerized pump. It is used for acute and chronic open wounds. It also can be used on partial to full-thickness wounds, as well as partial-thickness burns.

Fissure

Linear crack in the skin that may extend to dermis Chapped lips or hands, athlete foot

Autoimmunity

Normal protective immune response paradoxically turns against or attacks the body, leading to tissue damage

FOOD ALLERGY

Pathophysiology IgE-mediated food allergy, a type I hypersensitivity reaction, occurs in about 2% of the adult population; it is thought to occur in people who have a genetic predisposition combined with exposure to allergens early in life through the GI or respiratory tract or nasal mucosa. Researchers also have identified a second type of food allergy, a non-IgE-mediated food allergy syndrome in which T cells play a major role (Ferri, 2016). Almost any food can cause allergic symptoms, some even resulting in anaphylaxis. The most common offenders are seafood (lobster, shrimp, crab, clams, fish), legumes (peanuts, peas, beans, licorice), seeds (sesame, cottonseed, caraway, mustard, flaxseed, sunflower seeds), tree nuts, berries, egg white, buckwheat, milk, and chocolate. Peanut and tree nut (e.g., cashew, walnut) allergies are responsible for severe food allergy reactions in children and may result in anaphylactic death. The most common cause of anaphylactic death reported in adults is due to stings from insects, whereas in children, anaphylaxis to food may be more common (Chang, 2010; Schwartz, 2016). Clinical Manifestations and Assessment The clinical symptoms are classic allergic symptoms (urticaria, dermatitis, wheezing, cough, laryngeal edema, angioedema) and GI symptoms (itching; swelling of lips, tongue, and palate; abdominal pain; nausea; cramps; vomiting; and diarrhea). Medical Management Therapy for food hypersensitivity includes elimination of the food responsible for the hypersensitivity. Pharmacologic therapy is necessary for patients who cannot avoid exposure to offending foods and for patients with multiple food sensitivities not responsive to avoidance measures. Medication therapy involves the use of H1-blockers, antihistamines, adrenergic agents, corticosteroids, and cromolyn sodium. An essential aspect of management is teaching patients and family members to recognize symptoms associated with an anaphylactic reaction, when and how to administer life-saving medication (epinephrine), and when to call for emergency help.

Neuropathic

Plantar surface over metatarsal heads Typically red (unless coexisting ischemia) Moderate to large amounts exudate Well defined

Enzymatic Débridement

Several commercially available products contain the same enzymes that the body produces naturally. These are called enzymatic débriding agents; an example is a collagenase (Santyl). Application of these products speeds the rate at which necrotic tissue is removed. This method is slower and no more effective than surgical débridement.

Ulcer

Skin loss or damage at or extending past the epidermis. May include necrotic tissue development, bleeding or scarring Stasis ulcer of venous insufficiency, pressure ulcer

Scar (cicatrix)

Skin mark left after healing of a wound or lesion; represents replacement by connective tissue of the injured tissue Young scars: red or purple Mature scars: white or glistening Healed wound or surgical incision

ULCERATION

Superficial loss of surface tissue as a result of death of cells is called an ulceration. A simple ulcer, such as the kind found in a small, superficial, partial-thickness burn, tends to heal by granulation if kept clean and protected from injury. If exposed to the air, the serum that escapes will dry and form a scab, under which the epithelial cells grow and cover the surface completely. The four most common ulcers noted are arterial, venous, neuropathic/diabetic, and pressure ulcers

Proliferation Stage.

The circulating lymphocyte containing the antigenic message returns to the nearest lymph node. Once in the node, the sensitized lymphocyte stimulates some of the resident dormant T and B lymphocytes to enlarge, divide, and proliferate. T lymphocytes differentiate into cytotoxic (or killer) T cells, whereas B lymphocytes produce and release antibodies. Enlargement of the lymph nodes in the neck in conjunction with a sore throat is one example of the inflammatory response during immune activation.

basement membrane zone

The epidermis and the dermis are separated by a structure called the. This zone contains proteins that can target various autoantibodies that can be found in patients with autoimmune blistering diseases (Anderson, 2012).

Inflammatory Response.

The inflammatory response is a major function of the natural immune system that is elicited in response to tissue injury or pathogens. Chemical mediators assist this response by minimizing blood loss, walling off the pathogen, activating phagocytes, and promoting formation of fibrous scar tissue and regeneration of injured tissue. The inflammatory response is facilitated by physical and chemical barriers inherent in the body.

rete ridges.

The junction of the epidermis (basement membrane zone, BMZ) and dermis is an area of many undulations and furrows called This junction anchors the epidermis to the dermis and permits the free exchange of essential nutrients between the two layers. If the BMZ is interrupted, it must re-form to successfully achieve healing of the tissue

BASAL CELL AND SQUAMOUS CELL CARCINOMA

The most common types of skin cancer are basal cell carcinoma (BCC) and squamous cell (epidermoid) carcinoma (SCC). The third most common type, malignant melanoma, is discussed separately. Skin cancer is diagnosed by biopsy and histologic evaluation. BOX 52-7 Risk Factors for Skin Cancer Fair-skinned, fair-haired, blue-eyed people, particularly those of Celtic origin, with insufficient skin pigmentation to protect underlying tissues People who sustain sunburn and who do not tan Chronic sun exposure (certain occupations, such as farming, construction work) Exposure to chemical pollutants (industrial workers in arsenic, nitrates, coal, tar and pitch, oils and paraffins) Sun-damaged skin (elderly people) History of x-ray therapy for acne or benign lesions Scars from severe burns Chronic skin irritations Immunosuppression Genetic factors Clinical Manifestations and Assessment BCC is the most common type of skin cancer. It generally appears on sun-exposed areas of the body and is more prevalent in regions where the population is subjected to intense and extensive exposure to the sun. The incidence is proportional to the age of the patient (average, 60 years of age) and the total amount of sun exposure, and it is inversely proportional to the amount of melanin in the skin. BCC usually begins as a small, waxy nodule with rolled, translucent, pearly borders; telangiectatic vessels may be present. As it grows, it undergoes central ulceration and, sometimes, crusting (Fig. 52-6). The tumors appear most frequently on the face. BCC is characterized by invasion and erosion of contiguous (adjoining) tissues. It rarely metastasizes, but recurrence is common. However, a neglected lesion can result in the loss of a nose, an ear, or a lip. Other variants of BCC may appear as shiny, flat, gray or yellowish plaques. SCC is a malignant proliferation arising from the epidermis. Although it usually appears on sun-damaged skin, it may arise from normal skin or from pre-existing skin lesions. It is of greater concern than BCC because it is a truly invasive carcinoma, metastasizing by the blood or lymphatic system. Metastases account for 75% of deaths from SCC. The lesions may be primary, arising on the skin and mucous membranes, or they may develop from a precancerous condition, such as actinic keratosis (lesions occurring in sun-exposed areas), leukoplakia (premalignant lesion of the mucous membrane), or scarred or ulcerated lesions. SCC appears as a rough, thickened, scaly tumor that may be asymptomatic or may involve bleeding (see Fig. 52-6). The border of an SCC lesion may be wider, more infiltrated, and more inflammatory than that of a BCC lesion. Secondary infection can occur. Exposed areas, especially of the upper extremities and of the face, lower lip, ears, nose, and forehead, are common sites. The incidence of BCC and SCC is increased in all people who are immunocompromised, including those infected with HIV. Clinically, the tumors have the same appearance as in people who are not HIV-infected; however, in patients with HIV, the tumors may grow more rapidly and recur more frequently. These tumors are managed the same as those for the general population. Frequent follow-up (every 4 to 6 months) is recommended to monitor for recurrence. Surgical Management The primary goal is to remove the tumor entirely. The best way to maintain cosmetic appearance is to place the incision properly along natural skin tension lines and natural anatomic body lines.

Verrucae: Warts

Warts are common, benign skin tumors caused by infection with the human papillomavirus, which belongs to the DNA virus group. People of all ages may be affected, but the warts occur most frequently in patients between 12 and 16 years of age. They may be treated with locally applied laser therapy, liquid nitrogen, salicylic acid plasters, or electrodesiccation. Genitalia and perianal warts are known as condylomata acuminata. They may be transmitted sexually. Condylomata that affect the uterine cervix predispose the patient to cervical cancer. They are treated with liquid nitrogen, cryosurgery, electrosurgery, topically applied trichloroacetic acid, and curettage.

HIV Asymptomatic (CDC Category A: More Than 500 CD4+ T Lymphocytes/mm3)

When a viral set point is reached, a chronic, clinically asymptomatic state begins. Despite its best efforts, the immune system rarely, if ever, fully eliminates the virus. By about 6 months, the rate of viral replication reaches a lower but relatively steady state that is reflected in the maintenance of viral levels at a set point. This set point varies greatly from patient to patient and dictates the subsequent rate of disease progression; on average, 8 to 10 years pass before a major HIV-related complication develops. In this prolonged, chronic stage, patients feel well and have few if any symptoms. Apparent good health continues because CD4+ T-cell levels remain high enough to preserve defensive responses to other pathogens.

Role of Interferons IFNs

are cytokines. They have antiviral and antitumor properties. In addition to responding to viral infection, IFNs are produced by T lymphocytes, B lymphocytes, and macrophages in response to antigens. They modify the immune response by suppressing antibody production and cellular immunity. They also facilitate the cytolytic (cell destruction) role of lymphocytes, macrophages, and NK cells. Research continues on the pathways that IFNs use to transmit signals from cell membranes to the nucleus. IFNs are undergoing extensive testing to evaluate their effectiveness in treating tumors and AIDS (Andzinski et al., 2016).

The eccrine sweat glands

are found in all areas of the skin. Their ducts open directly onto the skin surface. The thin, watery secretion called sweat is produced in the basal, coiled portion of the eccrine gland and is released into its narrow duct.

The apocrine sweat glands

are larger than eccrine sweat glands and are located in the axillae, anal region, scrotum, and labia majora. Their ducts generally open onto hair follicles. The apocrine glands become active at puberty. In women, they enlarge and recede with each menstrual cycle. Apocrine glands produce a milky sweat that is sometimes broken down by bacteria to produce the characteristic underarm odor.

Pastes

are mixtures of powders and ointments and are used in inflammatory blistering conditions. They adhere to the skin and may be difficult to remove without using oil (e.g., olive oil or mineral oil). Pastes are applied with a wooden tongue depressor or gloved hand.

Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS)

are potentially fatal skin disorders and the most severe forms of erythema multiforme. These diseases are mucocutaneous reactions that constitute a spectrum of reactions, with TEN being the most severe. The mortality rate from TEN is 30% to 35%. TEN and SJS are triggered by a reaction to medications. Antibiotics, especially sulfonamides, antiseizure agents, nonsteroidal anti-inflammatory drugs (NSAIDs), are the medications implicated most frequently (Bryant, 2016). Risk Factors These conditions occur in patients of all ages and both genders. The incidence is increased in older people because of their use of many medications. People who are immunosuppressed, including those with HIV infection and AIDS, have a high risk of SJS and TEN. Although the incidence of TEN and SJS in the general population is about 2 to 3 cases per 1 million people in the United States, the risk associated with sulfonamides in HIV-positive individuals may approach 1 case per 1,000 (Bryant, 2016). Most patients with TEN have an abnormal metabolism of the medication; the mechanism leading to TEN seems to be a cell-mediated cytotoxic reaction. Clinical Manifestations and Assessment TEN and SJS are characterized initially by conjunctival burning or itching, cutaneous tenderness, fever, cough, sore throat, headache, extreme malaise, and myalgias (i.e., aches and pains). These signs are followed by a rapid onset of erythema involving much of the skin surface and mucous membranes, including the oral mucosa, conjunctiva, and genitalia. In severe cases of mucosal involvement, there may be danger of damage to the larynx, bronchi, and esophagus from ulcerations. Large, flaccid bullae develop in some areas; in other areas, large sheets of epidermis are shed, exposing the underlying dermis. Fingernails, toenails, eyebrows, and eyelashes may be shed along with the surrounding epidermis. The skin is excruciatingly tender, and the loss of skin leaves a weeping surface similar to that of a total-body, partial-thickness burn; hence the condition is also referred to as "scalded skin syndrome." Histologic studies of frozen skin cells from a fresh lesion and cytodiagnosis of collections of cellular material from a freshly denuded area are conducted. A history of use of medications known to precipitate TEN or SJS may confirm medication reaction as the underlying cause. Immunofluorescent studies may be performed to detect atypical epidermal autoantibodies. A genetic predisposition to erythema multiforme has been suggested but has not been confirmed in all cases. Medical and Nursing Management The goals of treatment include control of fluid and electrolyte balance, prevention of sepsis, and prevention of ophthalmic complications. Supportive care is the mainstay of treatment. All nonessential medications are discontinued immediately. If possible, the patient is treated in a regional burn center because aggressive treatment similar to that for severe burns is required. Skin loss may approach 100% of the total body surface area. Surgical débridement or hydrotherapy in a Hubbard tank (large steel tub) may be performed to remove involved skin. Tissue samples from the nasopharynx, eyes, ears, blood, urine, skin, and unruptured blisters are obtained for culture to identify pathogenic organisms. IV fluids are prescribed to maintain fluid and electrolyte balance, especially in the patient who has severe mucosal involvement and who cannot easily take oral nourishment. Because an indwelling IV catheter may be a site of infection, fluid replacement is carried out by nasogastric tube and then orally as soon as possible. Initial treatment with systemic corticosteroids is controversial. Some experts argue for early high-dose corticosteroid treatment. However, in most cases, the risk of infection, the complication of fluid and electrolyte imbalance, the delay in the healing process, and the difficulty in initiating oral corticosteroids early in the course of the disease outweigh the perceived benefits. In patients with TEN thought to result from a medication reaction, corticosteroids may be administered; however, the patient should be monitored closely for adverse effects. Systemic antibiotic therapy is used with extreme caution. Temporary biologic dressings (e.g., pigskin, amniotic membrane) or plastic semi-permeable dressings (e.g., Vigilon) may be used to reduce pain, decrease evaporation, and prevent secondary infection until the epithelium regenerates. Meticulous oropharyngeal and eye care is essential when there is severe involvement of the mucous membranes and the eyes.

Mast cell stabilizers

are used prophylactically (before exposure to allergens) to prevent the onset of symptoms and to treat symptoms once they occur. They are also used therapeutically in chronic allergic rhinitis. Intranasal cromolyn sodium (NasalCrom) is a spray that acts by stabilizing the mast cell membrane, thus reducing the release of histamine and other mediators of the allergic response (Ferri, 2016). This spray is as effective as antihistamines but less effective than intranasal corticosteroids in the treatment of seasonal allergic rhinitis. The patient must be informed that the beneficial effects of the medication may take a week or so to manifest.

The acute or intermediate phase of burn care

follows the emergent/resuscitative phase and begins 48 to 72 hours after the burn injury. During this phase, attention is directed toward continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance (Table 53-5), and GI function. Infection prevention, burn wound care, pain management, and nutritional support are priorities at this stage.

Primary dressings

have only a protective function and maintain a moist environment for natural healing. They include those that just cover the area (e.g., DuoDERM, Tegaderm) and may remain in place for several days.

T cells

include effector T cells, suppressor T cells, and memory T cells. Two major categories of effector T cells exist: helper T cells and cytotoxic T cells. These effector T cells participate in the destruction of foreign organisms. T cells interact closely with B cells, indicating that humoral and cellular immune responses are not separate, unrelated processes but, rather, branches of the immune response that interact.

Provocative testing

involves the direct administration of the suspected allergen to the sensitive tissue, such as the conjunctiva, nasal or bronchial mucosa, or GI tract (by ingestion of the allergen), with observation of target organ response. This type of testing is helpful in identifying clinically significant allergens in patients who have a large number of positive tests. Major disadvantages of this type of testing are the limitation of one antigen per session and the risk of producing severe symptoms, particularly bronchospasm, in patients with asthma.

The rule of nines (Fig. 53-2)

is a simple and common way to estimate the extent of burns. The system assigns percentages in multiples of nine to major body surfaces with the perineum forming the remaining 1%. This method must be modified in the pediatric population because of the proportionally larger heads and smaller limbs in children.

Atopic dermatitis

is a type I immediate hypersensitivity disorder characterized by inflammation and hyperreactivity of the skin, often causing pruritus. Although most commonly seen in children, the prevalence among adults has increased in the past 5 years. Recent studies confirm atopic dermatitis will persist through adulthood in up to 50% of individuals (Mortz et al., 2015). Other terms used to describe this skin disorder include atopic eczema, atopic dermatitis/eczema, and atopic dermatitis/eczema syndrome (AEDS). Clinical Manifestations and Assessment Most patients with atopic dermatitis have significant elevations of serum IgE and peripheral eosinophilia. Pruritus and hyperirritability of the skin (most commonly seen in flexural folds) are the most consistent features of atopic dermatitis and are related to large amounts of histamine in the skin (Fig. 38-3). Excessive dryness of the skin with resultant itching is related to changes in lipid content, sebaceous gland activity, and sweating. In response to stroking of the skin, immediate redness appears on the skin and is followed in 15 to 30 seconds by pallor, which persists for 1 to 3 minutes. Years of chronically irritated skin resulting in excessive itching can cause lichenification, or a leathery hardened appearance to the affected area. Lesions develop secondary to the trauma of scratching and appear in areas of increased sweating and hypervascularity. Atopic dermatitis is chronic, with remissions and exacerbations, reoccurrences often occurring with allergy flare-ups (Mortz, Andersen, Dellgren, Barington, & Bindslev-Jensen, 2015). It is important to note that atopic dermatitis is often the first step in a process that leads to asthma and allergic rhinitis, otherwise known as the "allergic/atopic triad. Medical Management Treatment of patients with atopic dermatitis must be individualized. Guidelines for treatment include decreasing itching and scratching by wearing cotton fabrics; washing with a mild detergent; humidifying dry heat in winter; maintaining room temperature at 20°C to 22.2°C (68°F to 72°F); using antihistamines, such as diphenhydramine (Benadryl); and avoiding animals, dust, sprays, and perfumes. Keeping the skin moisturized with daily baths to hydrate the skin and the use of topical skin emollients is encouraged and remains the main treatment for atopic dermatitis (Ferri, 2016). Topical corticosteroids are used to prevent inflammation, and any infection is treated with antibiotics to eliminate Staphylococcus aureus when indicated. Use of immunosuppressive agents, such as cyclosporine (Neoral, Sandimmune), tacrolimus (Prograf, Protopic), and pimecrolimus (Elidel), may be effective in inhibiting T cells and mast cells involved in atopic dermatitis (Moskowitz, 2014).

Spray and aerosol

preparations may be used on any widespread dermatologic condition (e.g., 3M Cavilon Skin Protectant; Convatec Aloe Vesta Skin Protectant). They evaporate on contact and are used infrequently.

Powders

usually have a talc, zinc oxide, bentonite, or cornstarch base and are dusted on the skin with a shaker or applied with cotton sponges. Although their therapeutic action is brief, powders act as hygroscopic agents that absorb and retain moisture from the air and reduce friction between skin surfaces and clothing or bedding.

antigenic determinant.

The portion of the antigen involved in binding with the antibody.The most efficient immunologic responses occur when the antibody and antigen fit like a lock and key (Fig. 36-6). Poor fit can occur with an antibody that was produced in response to a different antigen. This phenomenon is known as cross-reactivity. For example, in acute rheumatic fever, the antibody produced against Streptococcus pyogenes in the upper respiratory tract may cross-react with the patient's heart tissue, leading to mitral valve abnormalities.

Hydrogels

are polymers with a water content of 90% to 95%. They are available in impregnated sheets or as gel in a tube. Their high moisture content makes them ideal for autolytic débridement of wounds. They are semitransparent, allowing for wound inspection without dressing removal. They are comfortable and soothing for the painful wound. They require a secondary dressing to keep them in place. Hydrogels are appropriate for superficial wounds with high serous output, such as abrasions, skin graft sites, and draining venous ulcers.

Intralesional therapy

consists of injecting a sterile suspension of medication (usually a corticosteroid) into or just below a lesion. Although this treatment may have an anti-inflammatory effect, local atrophy may result if the medication is injected into subcutaneous fat. Skin lesions treated with intralesional therapy include psoriasis, keloids, and cystic acne.

Anaphylaxis

is defined as a severe allergic reaction that is rapid in onset and can cause various systemic reactions, including death (Ferri, 2016). Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunologic reaction between a specific antigen and an antibody. The reaction results from a rapid release of IgE-mediated chemicals, which can induce a severe, life-threatening allergic reaction. Pathophysiology Anaphylaxis occurs when the body's immune system produces specific IgE antibodies toward a substance that is normally nontoxic (e.g., food such as a peanut) (Box 38-1). When the person first ingests the peanut, for example, there are no physical reactions manifested. Instead, antibodies are produced for that specific substance, and then those antibodies are stored in the immune system for future re-exposure. If the substance is ingested again, the body releases excess amounts of the protein histamine. Large amounts of histamine released into the body may cause flushing, urticaria, angioedema, hypotension, and bronchoconstriction (Fig. 38-1). These systemic changes (most commonly in the dermatologic, respiratory, cardiovascular, and gastrointestinal [GI] tracts) characteristically produce clinical manifestations within seconds or minutes after antigen exposure. In severe cases, these symptoms may cause shock. If no medical intervention is sought, death may ensue The diagnosis of anaphylaxis is predominantly based on objective findings during clinical examination, despite potential negative laboratory testing (i.e., serum IgE levels or tryptase levels [a protease of human mast cells that has been implicated as a pathologic mediator of numerous allergic and inflammatory conditions]). Some providers continue to utilize prick and intradermal skin testing to assist in diagnosis; however, a positive test result cannot confirm a diagnosis due to asymptomatic sensitization (when the body's cells detect the allergen but re-exposure does not cause physical or immunologic effects). Clinical Manifestations and Assessment The severity depends on the degree of allergy and the dose of allergen (Porth, 2015; Simons, 2010). Anaphylactic reactions consist of three basic patterns: uniphasic, biphasic, and protracted reactions. Uniphasic reactions occur as an exclusive incident where the patient develops symptoms within 30 minutes of allergen exposure that resolve spontaneously within 1 to 2 hours, either with or without medical treatment. In biphasic responses, the patient will have an initial reaction, followed by subsequent symptoms up to 8 hours after the first reaction. These patients should be managed in the emergency room. Finally, a protracted reaction is just that: a reaction that may last for a prolonged period of time, up to 32 hours, and may include cardiogenic or septic shock and respiratory distress despite medical treatment (Lieberman, 2014). Mild systemic reactions consist of peripheral tingling and a sensation of warmth, possibly accompanied by a sensation of fullness in the mouth and throat. Nasal congestion, periorbital swelling, pruritus, sneezing, and tearing of the eyes also can be expected. Moderate systemic reactions may include flushing, warmth, anxiety, and itching in addition to any of the milder symptoms. More serious reactions include bronchospasm and edema of the airways or larynx with dyspnea, cough, and wheezing. Both mild and moderate reactions begin within 2 hours of exposure. Severe systemic reactions, however, have an abrupt onset with the same signs and symptoms described previously. These symptoms progress rapidly to bronchospasm, laryngeal edema, severe dyspnea, cyanosis, and hypotension. Dysphagia (difficulty swallowing), abdominal cramping, vomiting, diarrhea, and seizures also can occur. Cardiac arrest and coma may follow. Medical Management . Initially, respiratory and cardiovascular functions are evaluated. If the patient is in cardiac arrest, cardiopulmonary resuscitation is instituted. Oxygen is provided in high concentrations during cardiopulmonary resuscitation or if the patient is cyanotic, dyspneic, or wheezing. At first response, epinephrine, in a 1:1,000 dilution, is administered subcutaneously in the upper extremity or thigh and may be followed by a continuous IV infusion. Epinephrine is the first-line treatment of anaphylaxis as it is the only medication that may halt cardiac or respiratory arrest, which typically occurs 5 to 30 minutes after exposure to an allergen (Lieberman, 2014). Most adverse events associated with administration of epinephrine (e.g., adrenaline) occur when the dose is excessive or given intravenously. Patients at risk for adverse effects include elderly patients and those with hypertension, arteriopathies (diseases of the arteries), or known ischemic heart disease Antihistamines and corticosteroids also may be administered to prevent recurrences of the reaction and to treat urticaria and angioedema, although they are not the first-line treatment. . IV fluids (e.g., normal saline solution), volume expanders, and vasopressor agents are administered to maintain blood pressure and normal hemodynamic status. Glucagon stimulates the enzyme adenylate cyclase, and its activation results in the intracellular accumulation of the second messenger cyclic adenosine monophosphate (cAMP). Increased levels of cAMP improve the suppressive actions that epinephrine exerts on the biochemical events responsible for the anaphylactic response. Patients who have experienced anaphylactic reactions and received epinephrine should be transported to the local emergency department for observation and monitoring because of the risk for a "rebound" reaction usually within 4 to 10 hours after the initial allergic reaction. Patients with severe reactions are monitored closely for 12 to 14 hours in a facility that can provide emergency care, if needed.

Ointments

retard water loss and lubricate and protect the skin. Ointments are better moisturizers or hydrators of the skin due to better adherence to the skin and pharmacologic formulations (Kanfer, Tettley-Amialo, Au, & Hughes-Formella, 2016). They are the preferred vehicle for delivering medication to patients with chronic or localized dry skin conditions, such as eczema or psoriasis (e.g., triamcinolone). Other ointments are used to aid in healing and treatment of pressure ulcers, varicose ulcers, and dehiscent wounds (e.g., Xenaderm). Ointments are applied with a wooden tongue depressor or gloved hand and applied up to twice a day.

Latex allergy,

the allergic reaction to natural rubber proteins, has been implicated in rhinitis, conjunctivitis, contact dermatitis, urticaria, asthma, and anaphylaxis. Over the past 80 years, the numbers of individuals affected with this allergy has dropped drastically due to the processing of nonlatex materials and nonpowdered latex gloves used in health care settings. Despite numbers and studies confirming this, the severity of illness associated with a latex allergy remains a nursing priority. Pathophysiology Routes of exposure to latex products can be cutaneous, percutaneous, mucosal, parenteral, or aerosol. Allergic reactions are more likely with exposure via the mucous membrane or from the parenteral route but also can occur with cutaneous contact or inhalation. The most frequent source of exposure is cutaneous, which usually involves the wearing of natural latex gloves. The powder used to facilitate putting on latex gloves can become a carrier of latex proteins from the gloves; when the gloves are put on or removed, the particles become airborne and can be inhaled or settle on the skin, mucous membranes, or clothing. Mucosal exposure can occur from the use of latex condoms, catheters, airways, and nipples. Parenteral exposure can occur from IV lines or hemodialysis equipment. In addition to latex-derived medical devices, many household items also contain latex. Examples of medical and household items containing latex and a list of alternative products are found in Table 38-4. Clinical Manifestations and Assessment Several different types of reactions to latex are possible: irritant contact dermatitis, allergic dermatitis, and latex allergy. Table 38-5 lists the causes, symptoms, and management of each. The diagnosis of latex allergy is based on the history and diagnostic test results. Sensitization is detected by skin testing, RAST, or enzyme-linked immunosorbent assay (ELISA). Skin tests should be performed only by clinicians who have expertise in their administration and interpretation and who have the necessary equipment available to treat local or systemic allergic reactions to the reagent.

effector stage,

either the antibody of the humoral response or the cytotoxic (killer) T cell of the cellular response reaches and connects with the antigen on the surface of the foreign pathogen. The connection initiates a series of events that, in most instances, results in the total destruction of the invading microbes or the complete neutralization of the toxin. The events involve interplay of antibodies (humoral immunity), complement, and action by the cytotoxic T cells (cellular immunity). Figure 36-5 summarizes the stages of the immune response.

suppressor T cell,

has the ability to decrease B cell production, thereby keeping the immune response at a level that is compatible with health (e.g., sufficient to fight infection adequately without attacking the body's healthy tissues). Memory cells are responsible for recognizing antigens from previous exposure and mounting an immune response.

Active dressings

improve the healing process and decrease healing time. They include skin grafts and biologic skin substitutes. Both interactive and active dressings create a moist environment at the interface of the wound with the dressing.

Fibromyalgia (FM)

is a chronic syndrome characterized by widespread nonarticular musculoskeletal pain or multiple tender points lasting more than 3 months and other general physical symptoms, such as fatigue (NIAMS, 2014b). The pain in FM is not due to tissue damage or inflammation, thus making it fundamentally different from other rheumatic disorders and many other pain conditions. According to the 1990 ACR criteria, which specify 11 or more tender points, FM affects women more frequently than men (10:1 ratio). . A hallmark of FM is that individuals display diffuse hyperalgesia (increased pain to normally painful stimuli) and/or allodynia (pain to normally nonpainful stimuli). This suggests that these individuals have a fundamental problem with central dysfunction (pain processing mechanisms) that results in central pain sensitization. These findings of centralization of pain have been corroborated by advanced neuroimaging techniques and appear to be due, in part, to imbalances in levels of neurotransmitters that affect pain and sensory transmission Clinical Manifestations and Assessment The core features of CWP and tenderness are almost invariably accompanied by a wide range of symptoms, the most common of which are sleep disturbances, fatigue, morning stiffness, muscle weakness, paresthesias, cognitive dysfunction ("fibro fog"), chronic headaches, mood disturbances, and irritable bowel syndrome (CDC, 2015c; Clauw, 2015; Wolfe & Rasker, 2013). CWP is pain that is typically both above and below the waist on both sides of the body and involves the axial skeleton (neck, back, or chest). The patient complains of a widespread burning pain and often is unable to discriminate if pain occurs in the muscles, joints, or soft tissues. Physical examination typically reveals point tenderness at 11 or more of 18 identified sites characteristically described in ACR 1990 criteria Medical Management The pharmacotherapy of FM is mechanism-based; many have been tested to a greater or lesser extent. NSAIDs may be used to treat the diffuse muscle aching and stiffness. Tramadol is the only opiate shown to provide some relief. Many drugs have been used off-label to treat FM. Pregabalin (Lyrica), an analgesic, anxiolytic, and anticonvulsant (α2-δ receptor ligand agent) is the first to receive FDA approval for FM use. Psychotropic agents have been used to reduce pain centrally, even in the absence of depression: serotonin noradrenaline reuptake inhibitors or SNRIs (duloxetine, milnacipran), least selective serotonin reuptake inhibitors or SSRIs (fluoxetine, paroxetine), dopaminergic agents (pramipexole), and antidepressants, particularly tricyclics Individualized programs of exercise are used to decrease muscle weakness and discomfort and to improve the general deconditioning that occurs in affected patients.

Scleroderma

("hard skin") is a relatively rare disease that is poorly understood; the cause is unknown. Potential triggers include exposure to certain environmental and occupational agents (e.g., silica dust, heavy metals, polyvinyl chloride) and drugs (e.g., bleomycin, cocaine, fenfluramine appetite suppressants), infection, and human cytomegalovirus (CMV) and other viruses (Varga & Lafyatis, 2015). Scleroderma is classified into localized and systemic (systemic sclerosis), with subclassifications within each one. Pathophysiology Like other diffuse connective tissue diseases, scleroderma has a variable course, featuring remissions and exacerbations. Systemic scleroderma (SSc) is a progressive, chronic, devastating, and debilitating disease with a prognosis not as optimistic as that of SLE. Pathogenesis integrates three cardinal features: vascular injury and damage, activation of innate and adaptive arms of the immune system autoimmunity, and generalized interstitial and vascular fibrosis. Scleroderma commonly begins with skin involvement. Mononuclear cells cluster on the skin and stimulate lymphokines to stimulate procollagen. Insoluble collagen is formed and accumulates excessively in the tissues. Initially, the inflammatory response causes edema formation, with a resulting skin appearance that is taut, smooth, and shiny. The skin then undergoes fibrotic changes, leading to loss of elasticity and movement. Eventually, the tissue degenerates and becomes nonfunctional. This chain of events, from inflammation to degeneration, also occurs in blood vessels, synovium, skeletal muscles, and internal organ(s) of the heart, lungs, GI tract, and kidneys (Varga, 2013; Varga, 2015). Clinical Manifestations and Assessment Scleroderma starts insidiously with Raynaud phenomenon and swelling in the hands. The hallmark of scleroderma is when the skin and the subcutaneous tissues become increasingly hard and rigid and cannot be pinched up from the underlying structures (fibrosis). Wrinkles and lines are obliterated. The skin is dry because sweat secretion over the involved region is suppressed. The extremities stiffen and lose mobility. The condition spreads slowly; for years, these changes may remain localized in the hands and the feet. The face appears masklike, immobile, and expressionless, and the mouth becomes rigid. The changes within the body, although not visible directly, are vastly more important than the visible changes. The left ventricle of the heart is involved, resulting in heart failure. The esophagus hardens, interfering with swallowing. The lungs become scarred, impeding respiration. Digestive disturbances occur because of hardening (sclerosing) of the intestinal mucosa. Progressive kidney failure may occur. The patient may manifest a subset of limited cutaneous SSc symptoms referred to as the CREST syndrome Cutaneous Symptoms of Scleroderma Be alert for the CREST symptoms: Calcinosis (calcium deposits in the tissues) Raynaud phenomenon (spasm of blood vessels in response to cold or stress) Esophageal dysfunction (acid reflux and decrease in mobility of esophagus) Sclerodactyly (thickening and tightening of skin on fingers and hands) Telangiectasia (capillary dilation that forms vascular red marks on surface of skin) Assessment focuses on the hallmark sclerotic changes (thickening) in the skin, contractures in the fingers, and color changes or ulcerations in the fingertips due to poor circulation (Boin & Wigley, 2013; Hoogen et al., 2013). Assessment of systemic involvement requires a systems review with special attention to GI, pulmonary, renal, and cardiac symptoms. Limitations in mobility and self-care activities should be assessed along with the impact the disease has had (or will have) on body image. A skin biopsy is performed to identify cellular changes specific to scleroderma. Pulmonary studies show ventilation-perfusion abnormalities. Echocardiography evaluates left ventricular function and pulmonary arterial pressure and identifies pericardial effusion (often present with cardiac involvement). Esophageal studies demonstrate reflux esophagitis (early discriminator) and dysmotility in most patients with scleroderma. Autoantibody testing, particularly ANA, is the most useful laboratory test, with a positive result common in more than 95% of patients with scleroderma and antisclerodermal antibody (anti-scl) 70 Medical and Nursing Management No specific medication regimen has proved effective in modifying the disease process in scleroderma, but, along with antiarthritic drugs, various medications are used to treat organ system involvement. Calcium-channel blockers may provide improvement in symptoms of Raynaud phenomenon. ACE inhibitors appear to have improved survival of renal scleroderma crisis, and now there are many therapeutic agents approved for use in pulmonary hypertension

Allergen desensitization

(allergen immunotherapy, hyposensitization) is primarily used to treat IgE-mediated diseases by injections of allergen extracts. Immunotherapy involves the administration of gradually increasing quantities of specific allergens to the patient until a dose is reached that is effective in reducing disease severity from natural exposure (Schwartz, 2016). Immunotherapy is treatment in the form of vaccine therapy (better known as "allergy shots") and, if available, sublingual medication. This type of therapy provides an adjunct to symptomatic pharmacologic therapy and can be used when avoidance of allergens is not possible. Goals of immunotherapy include reducing the level of circulating IgE, increasing the level of blocking antibody IgG, and reducing the sensitivity of mediator cells. Immunotherapy has been most effective for ragweed pollen; however, treatment also has been effective for grass, tree pollen, cat dander, and house dust mite allergens.

A full-thickness burn

(formerly called a third- or fourth-degree burn) involves total destruction of the dermis and extends into the subcutaneous fat. It can also involve muscle and bone. It heals by contraction or epithelial migration. Wound color ranges widely from mottled white to red, brown, or black. Skin can appear charred and leathery, and hair follicles and sweat glands are destroyed. These burns are so severe that the patient no longer experiences a pain sensation. Healing does not happen spontaneously; this injury will require surgery, and significant scarring is expected

Allergic rhinitis

(hay fever, seasonal allergic rhinitis), a type I hypersensitivity reaction and the most common form of chronic respiratory allergic disease, remains the fifth most common chronic disease in the United States. It is one of the most common reasons for visits to primary care practitioners. Symptoms are similar to those of viral rhinitis but usually are more persistent and demonstrate seasonal variation; rhinitis is considered to be the allergic form if the symptoms are caused by an allergen-specific IgE-mediated immunologic response. However, a sizable proportion of patients with rhinitis have mixed rhinitis, or coexisting allergic and nonallergic rhinitis Because allergic rhinitis is induced by airborne pollens or molds, it is activated by the following seasonal occurrences: Early spring: Tree pollen (oak, elm, poplar), mold spores Early summer: Rose pollen (rose fever), grass pollen (timothy, red-top) Early fall: Weed pollen (ragweed), mold spores Clinical Manifestations and Assessment Typical signs and symptoms of allergic rhinitis include sneezing and nasal congestion; clear, watery nasal discharge; itchy eyes and nose; and lacrimation (Ferri, 2016). Drainage of nasal mucus into the pharynx, otherwise known as postnasal drip, results in multiple attempts to clear the throat and results in a dry cough, hoarseness, or scratchy throat. Headache, pain over the paranasal sinuses, and epistaxis can accompany allergic rhinitis. The symptoms of this chronic condition depend on environmental exposure and intrinsic host responsiveness. Allergic rhinitis can affect quality of life by also producing fatigue, loss of sleep, poor concentration, and interference with physical activities. Of great concern is the risk of developing persistent asthma and other comorbid conditions (chronic otitis media and sinusitis, obstructive sleep apnea, airway inflammation, etc.) from uncontrolled allergic rhinitis Diagnosis of seasonal allergic rhinitis is based on history, physical examination, and diagnostic test results. On objective examination, a patient suffering with allergic rhinitis may appear fatigued (the patient may complain of not feeling well-rested after a full night's sleep); the patient may present with any of the following conditions: Allergic "shiners" (gray-black discoloration below lower eye lids that some refer to as "raccoon eyes"); Puffy eyes; Clear or cloudy fluid surrounding the tympanic membranes; Nasal congestion or rhinorrhea; Marked erythema of palpebral conjunctivae associated with increased tearing; Enlarged nasal turbinates that are a pale-bluish color and boggy in texture; Enlarged anterior cervical lymph nodes; Cobblestoned appearance on the posterior pharynx (due to chronic postnasal drip and nasal congestion); and Sinus tenderness on palpation (Seidman et al., 2015). Diagnostic tests include nasal smears, peripheral blood counts, total serum IgE, epicutaneous and intradermal testing, radioallergosorbent test (RAST), food elimination and challenge, and nasal provocation tests. Results indicative of allergy as the cause of rhinitis include increased levels of IgE and eosinophil and positive reactions on allergen testing. Medical Management The goal of therapy is to provide relief from symptoms and encourage adherence to therapeutic regimens. Therapy may include one or all of the following interventions: avoidance therapy, pharmacotherapy, immunotherapy, and homeopathic modalities.

Cytotoxic T cells

(killer T cells) attack the antigen directly by altering the cell membrane and causing cell lysis (disintegration) and by releasing cytolytic enzymes and cytokines. Lymphokines can recruit, activate, and regulate other lymphocytes and WBCs. These cells then assist in destroying the pathogen. Delayed-type hypersensitivity is an example of an immune reaction that protects the body from antigens through the production and release of lymphokines (see later discussion).

superficial partial-thickness burn

(one of two types of second-degree burns), the epidermis is destroyed and a small portion of the underlying dermis (deep, vascular inner portion of skin) is injured. The skin is blistered, the exposed dermis is red and moist, and hair follicles are intact. These burns will heal in 14 to 21 days usually without scarring.

humoral immune response

(sometimes called the antibody response), begins with the B lymphocytes, which can transform themselves into plasma cells that manufacture antibodies. These antibodies are highly specific proteins that are transported in the bloodstream and attempt to disable pathogens.

A deep partial-thickness burn

(the second of the two types of second-degree burns), extends into the reticular layer of the dermis (dense connective tissue that gives the skin strength and elasticity and houses sweat glands, lymph vessels, and hair follicles) and is hard to distinguish from a full-thickness burn. It is red or white, mottled, and can be moist or fairly dry. The patient is in severe pain. Deep partial burns usually take longer than 3 weeks to heal (3 to 8 weeks) and can heal with permanent scarring (some of these burns tend to have a better appearance when grafted).

response stage

, the differentiated lymphocytes function in either a humoral or a cellular capacity. The production of antibodies by the B lymphocytes in response to a specific antigen begins the humoral response. Humoral refers to the fact that the antibodies are released into the bloodstream and, therefore, reside in the plasma (fluid fraction of the blood). With the initial cellular response, the returning sensitized lymphocytes migrate to areas of the lymph node other than those areas containing lymphocytes programmed to become plasma cells. Here, they stimulate the residing lymphocytes to become cells that will attack microbes directly, rather than through the action of antibodies. These transformed lymphocytes are known as cytotoxic (killer) T cells. The T stands for thymus, signifying that, during embryologic development of the immune system, these T lymphocytes spent time in the thymus of the developing fetus. Viral rather than bacterial antigens induce a cellular response. This response is manifested by the increasing number of T lymphocytes (lymphocytosis) seen on the complete blood counts (CBC) of people with viral illnesses, such as infectious mononucleosis (cellular immunity is discussed in further detail later in this chapter).

Hypersensitivity

A hypersensitivity reaction is an abnormal, heightened reaction to any type of stimulus. Usually it does not occur with the first exposure to an allergen, but it is a reflection of excessive or atypical immune responses. To promote understanding of the immunopathogenesis of disease, hypersensitivity reactions have been classified into four specific types of reactions: Anaphylactic (type 1) Hypersensitivity, Cytotoxic (type II) Hypersensitivity, Immune Complex (type III) Hypersensitivity, and Delayed-Type (type IV) Hypersensitivity. Most allergies are identified as either type I or type IV hypersensitivity reactions.

Lund and Browder Method

A more precise, age-specific method of estimating the extent of a burn is the Lund and Browder method, which recognizes the percentage of surface area of various anatomic parts, especially the head and legs, in relation to growth. Because of changes in body proportion with growth, the calculated TBSA changes with age as well (Bittner, 2015). By dividing the body into very small areas and providing an estimate of the proportion of TBSA accounted for by each body part, one can obtain a reliable estimate of TBSA burned.

Absorption

Absorbs exudate Alginates, composite dressings, foams, gauze, hydrocolloids, hydrogels

Physical and Chemical Barriers.

Activation of the natural immunity response is enhanced by processes inherent in physical and chemical barriers. The processes prevent or delay the entry into the body of various pathogens before infection can develop. Physical surface barriers include intact skin, mucous membranes, and cilia of the respiratory tract, which prevent pathogens from gaining access to the body. The cilia of the respiratory tract, along with coughing and sneezing responses, filter and clear pathogens from the upper respiratory tract before they can invade the body further. Chemical barriers, such as mucus, acidic gastric secretions, enzymes in tears and saliva, and substances in sebaceous and sweat secretions, act in a nonspecific way to destroy invading bacteria and fungi. For example, in addition to dissolving food, hydrochloric acid in the stomach destroys pathogens present in food or swallowed mucus (Porth, 2015). Viruses are countered by other means, such as interferon (IFN). Interferon, one type of biologic response modifier, is a nonspecific viricidal protein that is naturally produced by the body and is capable of activating other components of the immune system.

Hair follicles

An outgrowth of the skin, hair is present over the entire body except for the palms and soles. The hair consists of a root formed in the dermis and a hair shaft that projects beyond the skin. It grows in a cavity called a hair follicle (see Fig. 51-1). Proliferation of cells in the bulb of the hair causes the hair to form. undergo cycles of growth and rest. The rate of growth varies; beard growth is the most rapid, followed by hair on the scalp, axillae, thighs, and eyebrows. The growth or anagen phase may last up to 6 years for scalp hair, whereas the telogen or resting phase lasts approximately 4 months. During telogen, hair is shed from the body. The hair follicle recycles into the growing phase spontaneously, or it can be induced by plucking out hairs. Growing and resting hairs can be found side by side on all parts of the body. About 90% of the 100,000 hair follicles on a normal scalp are in the growing phase at any one time, and 50 to 100 scalp hairs are shed each day. In conditions in which inflammation causes damage to the root of the hair, regrowth is possible. However, if inflammation causes damage to the hair follicle, stem cells are destroyed and the hair does not grow. Hair in different parts of the body serves different functions. The hairs of the eyes (i.e., eyebrows and lashes), nose, and ears filter out dust, microbes, and airborne debris. Hair color is supplied by various amounts of melanin within the hair shaft. Gray or white hair reflects the loss of pigment. Hair quantity and distribution can be affected by endocrine conditions. For example, Cushing syndrome causes hirsutism, especially in women; hypothyroidism (i.e., underactive thyroid) causes coarse hair; while hyperthyroidism (i.e., overactive thyroid) is associated with fine hair. In many cases, chemotherapy and radiation therapy cause hair thinning or weakening of the hair shaft, resulting in partial or complete alopecia from the scalp and other parts of the body.

Unstageable

An unstageable lesion shows full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth and, therefore, stage cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as the body's natural (biologic) cover and should not be removed. Suspected Deep Tissue Injury (DTI) Suspected deep tissue injury (DTI) appears as a purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. DTI may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment.

Angiomas

Angiomas are benign vascular tumors that involve the skin and the subcutaneous tissues. They are present at birth and may occur as flat, violet-red patches (port-wine angiomas) or as raised, bright-red, nodular lesions (strawberry angiomas). The latter tend to involute spontaneously within the first few years of life, but port-wine angiomas usually persist indefinitely. Most patients use masking cosmetics (i.e., Covermark or Dermablend) to camouflage the lesions. The argon laser is being used on various angiomas with some success. Treatment of strawberry angiomas is more successful if undertaken as soon after birth as possible.

Collagen Dressings

These dressings stimulate the wound and accelerate wound healing. Some forms can be left on for up to 7 days. They are used for minimal to moderate exudating wounds that are partial to full thickness. Examples are Promogran and ColActive.

Débridement

Autolytic; covers a wound and allows enzymes to self-digest sloughed skin Chemical or enzymatic; applied topically to break down devitalized tissue Mechanical; removes devitalized tissue with mechanical force Absorption beads, pastes, powders; alginates; composite dressings; foams; hydrate gauze; hydrogels; hydrocolloids; transparent films; wound care systems Enzymatic débridement agents Wound cleansers, gauze (wet to dry), whirlpool

PSORIASIS

Considered one of the most common skin diseases, psoriasis affects approximately 2% of the population, appearing more often in people of European ancestry. It is thought that this chronic, noninfectious, inflammatory disease stems from a hereditary defect that causes overproduction of keratin. Onset may occur at any age, but psoriasis is most common in people between 15 and 35 years of age. Psoriasis has a tendency to improve and then recur periodically throughout life (Augustin & Radtke, 2016). Pathophysiology Although the primary cause of psoriasis is unknown, a combination of specific genetic makeup and environmental stimuli may trigger the onset of disease. Current evidence supports an immunologic basis for the disease (Mrowietz & Reich, 2009). Periods of emotional stress and anxiety aggravate the condition, and trauma, infections, and seasonal and hormonal changes also are trigger factors. Epidermal cells are produced at a rate that is about six to nine times faster than normal. The cells in the basal layer of the skin divide too quickly, and the newly formed cells move so rapidly to the skin surface that they become evident as profuse scales or plaques of epidermal tissue. The psoriatic epidermal cell may travel from the basal cell layer of the epidermis to the stratum corneum and be cast off in 3 to 4 days, which is in sharp contrast to the normal 26 to 28 days. As a result of the increased number of basal cells and rapid cell passage, the normal events of cell maturation and growth cannot take place. This abnormal process does not allow the normal protective layers of the skin to form. Clinical Manifestations and Assessment Lesions appear as red, raised patches of skin covered with silvery scales. The scaly patches are formed by the buildup of living and dead skin resulting from the vast increase in the rate of skin cell growth and turnover (Fig. 52-4). If the scales are scraped away, the dark-red base of the lesion is exposed, producing multiple bleeding points. These patches are not moist and may be pruritic. One variation of this condition is called guttate (in the shape of a drop) psoriasis because the lesions remain about 1 cm wide and are scattered like raindrops over the body. This variation is believed to be associated with a recent streptococcal throat infection. Psoriasis may range in severity from a cosmetic source of annoyance to a physically disabling and disfiguring disorder. Particular sites of the body tend to be affected most by this condition; they include the scalp, the extensor surface of the elbows and knees, the lower part of the back, and the genitalia. Bilateral symmetry is a feature of psoriasis. In approximately one fourth to one half of patients, the nails are involved, with pitting, discoloration, crumbling beneath the free edges, and separation of the nail plate. When psoriasis occurs on the palms and soles, it can cause pustular lesions called palmar pustular psoriasis. The presence of the classic plaque-type lesions generally confirms the diagnosis of psoriasis. Because the lesions tend to change histologically as they progress from early to chronic plaques, biopsy of the skin is of little diagnostic value. There are no specific blood tests for diagnosing the condition. When in doubt, the health care provider should assess for signs of nail and scalp involvement and for a positive family history. Complications Asymmetric rheumatoid factor-negative arthritis of multiple joints occurs in about 5% of people with psoriasis. The arthritic development can occur before or after the skin lesions appear. The relationship between arthritis and psoriasis is not understood, although recent studies suggest there is interplay among genetics, environmental factors, and the immune system (Augustin & Radtke, 2016). Erythrodermic psoriasis, an exfoliative psoriatic state, involves disease progression that affects the total body surface. The patient is acutely ill, with impaired temperature regulation and fluid and protein loss. Erythrodermic psoriasis often appears in people with chronic psoriasis after infections, after exposure to certain medications, or following withdrawal of systemic corticosteroids. Medical and Nursing Management The goals of management are to slow the rapid turnover of epidermis, to promote resolution of the psoriatic lesions, and to control the natural cycles of the disease. There is no known cure. The therapeutic approach should be one that the patient understands; it should be cosmetically acceptable and minimally disruptive to the patient's lifestyle. Treatment involves the commitment of time and effort by the patient and possibly the family. First, any precipitating or aggravating factors are addressed. An assessment is made of lifestyle because psoriasis is significantly affected by stress. The patient is informed that treatment of severe psoriasis can be time-consuming, expensive, and aesthetically unappealing at times. Removal of Scales The most important principle of psoriasis treatment is gentle removal of scales. This can be accomplished with baths. Oils (e.g., olive oil, mineral oil, Aveeno Oilated Oatmeal Bath) or coal tar preparations (e.g., Balnetar) can be added to the bath water and a soft brush used to scrub the psoriatic plaques gently. After bathing, the application of emollient creams containing alpha-hydroxy acids (e.g., Lac-Hydrin, Penederm) or salicylic acid continues to soften thick scales. The patient and family should be encouraged to establish a regular skin care routine that can be maintained even when the psoriasis is not in an acute stage. Pharmacologic Therapy With the recent addition of biologic medications, four types of therapy are now commonly used: topical, intralesional, oral, and injectable (Table 52-5). Topical Agents Topically applied agents are used to slow the overactive epidermis without affecting other tissues. These agents include lotions, ointments, pastes, creams, and shampoos. Topical corticosteroids may be applied for their anti-inflammatory effect. Intralesional Agents Intralesional injections of the corticosteroid triamcinolone acetonide (Aristocort, Kenalog-10, Trymex) can be administered directly into highly visible or isolated patches of psoriasis that are resistant to other forms of therapy. Care must be taken to ensure that the medication is not injected into unaffected skin. Photochemotherapy One treatment for severely debilitating psoriasis is a psoralen (phototoxic) medication (e.g., methoxsalen) combined with ultraviolet-A (PUVA) light therapy. Ultraviolet light is the portion of the electromagnetic spectrum containing wavelengths ranging from 180 to 400 nm. In this treatment, the patient takes a photosensitizing medication (usually 8-methoxypsoralen) in a standard dose and is subsequently exposed to long-wave ultraviolet light as the medication plasma levels peak. Although the mechanism of action is not completely understood, it is thought that when psoralen-treated skin is exposed to ultraviolet-A light, the psoralen binds with DNA and decreases cellular proliferation. PUVA is not without its hazards; it has been associated with long-term risks of skin cancer, cataracts, and premature aging of the skin

Coating antigens' surfaces Neutralizing the antigens if they are toxins Precipitating the antigens out of solution if they are dissolved

Antibodies react with antigens by:

NK cells,

another subpopulation of lymphocytes, defend against microorganisms and some types of malignant cells (Grossman et al., 2014). NK cells are capable of directly killing pathogens and producing cytokines. The helper T cells contribute to the differentiation of null and NK cells.

balneotherapy,

Baths or soaks, as are useful when large areas of skin are affected. The baths remove crusts, scales, and old medications and relieve the inflammation and pruritus (itching) that accompany acute dermatoses. Additional information about therapeutic baths is given in Box 52-1.

Cherry angiomas (bright red "moles") Diminished hair, especially on scalp and pubic area Dyschromias (color variations): Solar lentigo (liver spots) Melasma (dark discoloration of the skin) Lentigines (freckles) Neurodermatitis (itchy spots) Seborrheic keratoses (crusty brown "stuck-on" patches) Spider angiomas (network of dilated capillaries radiating from a central arteriole) Telangiectasias (red marks on skin caused by stretching of the superficial blood vessels) Wrinkles (a small fold, ridge, or crease in the skin) Xerosis (dryness) Xanthelasma (yellowish waxy deposits on upper and lower eyelids) Ichthyosis (fish scale appearance of the skin)

Benign Changes in Elderly Skin

Hypersensitivity

Body produces inappropriate or exaggerated responses to specific antigens

thermal (including electrical burns), radiation, electrical, chemical.

Burns are categorized as

Alginates

Calcium alginates (e.g., AlgiSite M, Kaltostat, Sorbsan, Algicell) are derived from brown seaweed and consist of very absorbent calcium alginate fibers that can absorb 20 times their weight (Bryant & Nix, 2016). They are useful in areas where the tissue is highly irritated or macerated. The alginate dressing forms a moist pocket over the wound while the surrounding skin stays dry. The dressing also reacts with wound fluid and forms a foul-smelling coating. Alginates work well when packed into a deep cavity, wound, or sinus tract with heavy drainage. They are nonadherent and require a secondary dressing.

Moisture-Retentive Dressings

Commercially produced moisture-retentive dressing can perform the same functions as wet dressings but are more efficient at removing exudate because of their higher moisture-vapor transmission rate; some have reservoirs that can hold excessive exudate. A number of moisture-retentive dressings are already impregnated with saline solution, petrolatum, zinc-saline solution, hydrogel, or antimicrobial agents, thereby eliminating the need to coat the skin to avoid maceration. Depending on the product used and the type of dermatologic problem encountered, most moisture-retentive dressings may remain in place from 12 to 24 hours; some can remain in place as long as a week.

Complement System

Circulating plasma proteins, known as complement, are made in the liver and other sites and activated when an antibody connects with its antigen. There are more than 35 of these plasma or membrane proteins, and they are an important additional component of the immune system (Paul, 2012). Destruction of an invading or attacking organism or toxin is not achieved merely by the binding of the antibody and antigens; destruction also requires activation of complement, the arrival of killer T cells, or the attraction of macrophages. Complement has three major physiologic functions: defending the body against bacterial infection, bridging natural and acquired immunity, and disposing of immune complexes and the by-products associated with inflammation.

They are effective against gram-negative organisms and even fungi. They are clinically effective. They penetrate the eschar but are not systemically toxic. They do not lose their effectiveness, allowing another infection to develop. They are cost-effective, available, and acceptable to the patient. They are easy to apply and remove, minimizing nursing care time.

Criteria for choice of topical agents include the following:

Cysts

Cysts of the skin are epithelium-lined cavities that contain fluid or solid material. Epidermal cysts (epidermoid cysts) occur frequently and are slow-growing, firm, elevated tumors frequently noted on the face, neck, upper chest, and back. Removal of the cysts provides a cure. Pilar cysts (trichilemmal cysts), formerly called sebaceous cysts, frequently are found on the scalp. They originate from the middle portion of the hair follicle and from the cells of the outer hair root sheath. Treatment is surgical removal.

Irritant contact dermatitis

Damage to skin because of irritation and loss of epidermoid skin layer; not an allergic reaction. Can be caused by excessive use of soaps and cleansers, multiple hand-washings, inadequate hand drying, mechanical irritation (e.g., sweating, rubbing inside powdered gloves), exposure to chemicals added during the manufacturing of gloves, and alkaline pH of powdered gloves. Reaction may occur with first exposure, is usually benign, and is not life-threatening. Acute: redness, edema, burning, discomfort, itching Chronic: dry, thickened, cracked skin Referral for diagnostic testing Avoidance of exposure to irritant Thorough washing and drying of hands Use of powder-free gloves with more frequent changes of gloves Changing glove types Use of water- or silicone-based moisturizing creams, lotions, or topical barrier agents Avoidance of oil- or petroleum-based skin agents with latex products because they cause breakdown of the latex product

Antigen/antibody

Detects HIV antibodies and p24 antigen; detects early acute infection.

Primary

Deficiency results from improper development of immune cells or tissues; usually congenital or inherited

Allergic contact dermatitis

Delayed hypersensitivity (type IV) reaction. Usually affects only area in contact with latex; reaction is usually to chemical additives used in the manufacturing process rather than to latex itself. Cause of reaction is T cell-mediated sensitization to additives of latex. Reaction is not life-threatening and is far more common than a type I reaction. Slow onset; occurs 18-24 hours after exposure. Resolves within 3-4 days after exposure. More severe reactions may occur with subsequent exposures. Pruritus, erythema, swelling, crusty thickened skin, blisters, other skin lesions Referral for diagnosis (patch tests) and treatment Thorough washing and drying of hands Use of water- or silicone-based moisturizing creams, lotions, or topical barrier agents Avoidance of oil- or petroleum-based products unless they are latex-compatible Avoidance of identified causative agent because continued exposure to latex products in the presence of breaks in skin may contribute to latex protein sensitization

Stage IV

Description There is full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. These ulcers often include undermining and tunneling. The depth of a Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule), making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable. Treatment See Stage III treatment. In addition, surgical intervention may be necessary when the ulcer is extensive, when complications (e.g., fistula) exist, and when the ulcer does not respond to treatment. Surgical procedures include débridement, incision and drainage, bone resection, and skin grafting. Osteomyelitis is a common complication of wounds of Stage IV depth. See Chapter 41 for more information on osteomyelitis.

Stage III

Description There is full-thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. The ulcer may include undermining and tunneling. The depth of a Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue, and Stage III ulcers here can be shallow. In contrast, areas of significant adiposity can develop Stage III pressure ulcers that are extremely deep. Bone/tendon is not visible or directly palpable. Treatment Stage III and IV pressure ulcers are characterized by extensive tissue damage. In addition to the measures listed for Stage I, these advanced, draining, necrotic pressure ulcers must be cleaned (débrided) to create an area that will heal. Necrotic, devitalized tissue favors bacterial growth, delays granulation, and inhibits healing. Wound cleaning and dressing are uncomfortable; therefore, the nurse must prepare the patient for the procedure by explaining what will occur and administering prescribed analgesia. Débridement may be accomplished by wet-to-damp dressing changes, mechanical flushing of necrotic and infective exudate, application of prescribed enzyme preparations that dissolve necrotic tissue, or surgical dissection. If an eschar covers the ulcer, it is removed surgically to ensure a clean, vitalized wound. Exudate may be absorbed by dressings or special hydrophilic powders, beads, or gels. Cultures of infected pressure ulcers are obtained to guide the selection of antibiotic therapy. After the pressure ulcer is clean, a topical treatment is prescribed to promote granulation. New granulation tissue must be protected from reinfection, drying, and damage, and care should be taken to prevent pressure and further trauma to the area. Dressings, solutions, and ointments applied to the ulcer should not disrupt the healing process. Multiple agents and protocols are used to treat pressure ulcers, but consistency is an important key to success. Objective evaluation of the pressure ulcer (e.g., measurement of the size and depth of the pressure ulcer, inspection for granulation tissue) for response to the treatment protocol must be made every 4-6 days. Taking photographs at weekly intervals is a reliable strategy for monitoring the healing process, which may take weeks to months.

Stage I

Description Ulcer appears as intact skin with nonblanchable erythema of a localized area, usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, and warmer or cooler in temperature as compared to adjacent tissue. Stage I may indicate patients who are "at risk" (a heralding sign of risk). Treatment To permit healing of Stage I pressure ulcers, the pressure is removed to allow increased tissue perfusion; nutritional status and fluid and electrolyte balance are maintained; friction and shear are reduced; and moisture to the skin is avoided.

Stage II

Description Ulcer appears as partial-thickness loss of dermis, presenting as a shallow open ulcer with a red or pink wound bed, without slough. It may also present as an intact or open/ruptured serum-filled blister. It may be a shiny or dry shallow ulcer without slough or bruising (bruising indicates suspected deep tissue injury). This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. Treatment In addition to measures listed for Stage I pressure ulcers, a moist environment, in which migration of epidermal cells over the ulcer surface occurs more rapidly, should be provided to aid wound healing. The ulcer is gently cleansed with sterile saline solution. Use of a heat lamp to dry the open wound is avoided as is the use of antiseptic solutions that damage healthy tissues and delay wound healing. Semipermeable occlusive dressings, hydrocolloid wafers, or wet saline dressings are helpful in providing a moist environment for healing and in minimizing the loss of fluids and proteins from the body.

NEUROPATHIC ULCERS

Diabetic foot ulcers are also known as neuropathic ulcers or lower extremity neuropathic disease (LEND). These ulcers occur due to reduced blood supply to the nerves, also known as microvascular damage, which can lead to neuropathy. Neuropathy is classified as loss of sensation. Risk factors include history of amputations or ulcers, long duration of diabetes and/or poor glucose control, limited joint mobility, long history of smoking, obesity, poor vision, poor footwear, vascular insufficiency, structural deformities and callus formation, absence of protective sensation, and autonomic neuropathy, causing decreased sweating and dry feet (Driver, Brentton, Allen, & Park, 2016). Early prevention can be achieved through comprehensive annual foot examinations, glycemic control, limiting other health complications, and offloading (pressure relief). Wound management may include débridement, treatment of infection if needed, and topical, specialty wound care dressing and/or adjunctive therapies (Driver et al., 2016). For further information related to diabetic neuropathy, refer to Chapter 30.

Nodule, tumor

Elevated, palpable, solid mass that extends deeper into the dermis than a papule Nodule: 0.5-2 cm; circumscribed Tumor: greater than 1-2 cm; tumors do not always have sharp borders Nodules: Lipoma, squamous cell carcinoma, poorly absorbed injection, dermatofibroma Tumors: Larger lipoma, carcinoma

Papule, plaque

Elevated, palpable, solid mass with a circumscribed border Plaque may be coalesced papules with flat top Papule: less than 0.5 cm Plaque: greater than 0.5 cm Papules: Elevated nevi, warts, lichen planus Plaques: Psoriasis, actinic keratosis

Cyst

Encapsulated fluid-filled or semisolid mass in the subcutaneous tissue or dermis Sebaceous cyst, epidermoid cysts

stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum . Each layer becomes more differentiated (i.e., mature and with more specific functions) as it rises from the basal stratum germinativum layer to the outermost stratum corneum layer.

Five distinct layers compose the epidermis; from innermost to outermost they are the

Full-thickness (similar to third-degree)

Flame Prolonged exposure to hot liquids Electric current Chemical Contact Epidermis, entire dermis, and sometimes subcutaneous tissue; may involve connective tissue, muscle, and bone Pain free Shock Hematuria (blood in the urine) and possibly hemolysis (blood cell destruction) Possible entrance and exit wounds (electrical burn) Dry; pale white, leathery, or charred Broken skin with fat exposed Edema Eschar sloughs Grafting necessary Scarring and loss of contour and function; contractures Loss of digits or extremity possible

Macule, patch

Flat, nonpalpable skin color change (color may be brown, white, tan, purple, red) Macule: less than 1 cm, circumscribed border Patch: greater than 1 cm, may have irregular border Freckles, flat moles, petechia, rubella, vitiligo, port wine stains, ecchymosis

Prompt fluid resuscitation maintains the BP in the low-normal range and improves CO. In general, the greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn. As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment. As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases. If kidney and cardiac function is adequate, urinary output increases. Lactated Ringer's (LR) solution is the preferred IV fluid for burn resuscitation because the sodium (130 mEq/L) and potassium (K+; 4 mEq/L) concentrations are similar to normal intravascular levels (sodium of 135 to 145 mEq/L and K+ of 3.5 to 5 mEq/L). LR also contains lactate (28 mEq/L), which can be converted by the liver to bicarbonate (the blood buffer) to aid in correcting the metabolic acidosis frequently seen in burn shock. Patients with large burn wounds are at risk for abdominal compartment syndrome, especially if fluid resuscitation is delayed. Fluid shifts into the abdominal cavity, causing increased abdominal distention that interferes with pulmonary ventilation. The volume loss into the peritoneal space results in a decreasing CO, hypotension, and a decreasing urine output. The increased intra-abdominal pressure compresses the inferior vena cava and restricts blood flow and perfusion to abdominal organs, further compromising renal, hepatic, and visceral organ function. The adult patient who is critically ill will have an intra-abdominal pressure that varies with respiration of approximately 5 to 7 mm Hg but may be higher in patients with obesity (Kirkpatrick et al., 2013). Bladder pressures of greater than 25 mm Hg are an indicator of increasing abdominal pressure, resulting in inadequate organ perfusion, and indicate the need for abdominal decompression. Clinical presentation may include a tense, distended abdomen, progressive oliguria (urine output below 400 mL), and increased ventilatory requirements (Sheridan, 2016). Patients with a major burn develop massive systemic edema. As fluid resuscitation proceeds, the edema worsens. As the taut, burned tissue becomes unyielding to the edema underneath its surface, it begins to act like a tourniquet, especially if the burn is circumferential. This complication is similar to a compartment syndrome. The provider may need to perform an escharotomy, a surgical incision into the eschar (also referred to as "black wound" because of the wounds appearance of thick, dry, black necrotic tissue) to relieve the constricting effect of the burned tissue. Refer to Chapter 42 for details on compartment syndrome. Burn shock is a physiologic insult combining hypovolemic and distributive shock. Circulating blood volume decreases dramatically during burn shock due to severe capillary leak with variation of serum sodium levels in response to fluid resuscitation. Usually, hyponatremia (sodium depletion) is present. Immediately after burn injury, hyperkalemia (excessive potassium) results from massive cell destruction. The outcome is a dramatic outpouring of fluids, electrolytes, and proteins into the interstitium with rapid equilibrium of intravascular and interstitial compartments. These changes are reflected in loss of circulating plasma volume, hemoconcentration, massive edema formation, decreased urine output, and depressed cardiovascular function (Latenser, 2015). Lactic acidosis is frequently seen in burn shock due to hypovolemia and hypoperfusion; thus, while the lactate in LR IV solution can be converted to base bicarbonate to correct the acidemia, the goal of treatment is aimed at reversing the hypoperfusion. Hypokalemia (potassium depletion) may occur later, with fluid shifts and inadequate potassium replacement. However, plasma lactate levels are significant markers of shock and resuscitation, and appear to be correlated to predict morbidity and outcome. A normal serum lactic acid level in venous blood is 0.5 to 2.2 mEq/L. See discussion of fluid and electrolyte changes in the Emergent/Resuscitative Phase later in the chapter.

Fluid and Electrolyte Alterations burns

Acute/intermediate

From beginning of diuresis to near completion of wound closure Wound care and closure Prevention or treatment of complications, including infection Nutritional support

Rehabilitation

From major wound closure to return to patient's optimal level of physical and psychosocial adjustment Prevention of scars and contractures Physical, occupational, and vocational rehabilitation Functional and cosmetic reconstruction Psychosocial counseling

Emergent/resuscitative

From onset of injury to completion of fluid resuscitation First aid Prevention of shock Prevention of respiratory distress Detection and treatment of concomitant injuries Wound assessment and initial care

TINEA

Fungi—tiny members of a subdivision of the plant kingdom that feed on organic matter—are responsible for various common skin infections. In some cases, they affect only the skin and its appendages (hair and nails). In other cases, internal organs are involved, and the diseases may be life-threatening. However, superficial infections rarely cause even temporary disability and usually respond readily to treatment. Secondary infection with bacteria, Candida, or both organisms may occur. The most common fungal skin infection is tinea (Fig. 52-3), which is also called ringworm because of its characteristic appearance of a ring or rounded tunnel under the skin. Tinea infections affect the head, body, groin, feet, and nails. Table 52-4 summarizes the tinea infections. To obtain a specimen for diagnosis, the lesion is cleaned and a scalpel or glass slide is used to remove scales from the margin of the lesion. The scales are dropped onto a slide to which potassium hydroxide has been added. The diagnosis is made by examination of the infected scales microscopically for spores and hyphae or by isolating the organism in culture. Under Wood's light, a specimen of infected hair appears fluorescent; this may be helpful in diagnosing some cases of tinea capitis.

Two potential gastrointestinal (GI) complications may occur: paralytic ileus (absence of intestinal peristalsis) and Curling ulcer. Decreased peristalsis and bowel sounds are manifestations of paralytic ileus resulting from burn trauma. Gastric distention and nausea may lead to vomiting unless gastric decompression is initiated. Gastric bleeding secondary to massive physiologic stress may be signaled by occult blood in the stool, regurgitation of "coffee ground" material from the stomach, or bloody vomitus. These signs suggest gastric or duodenal erosion (Curling ulcer).

Gastrointestinal Alterations burns

Keloid

Hypertrophied scar tissue secondary to excessive collagen formation during healing; elevated, irregular, red Greater incidence among African Americans Keloid of ear piercing or surgical incision

Skin Tests

If a skin test is indicated, there is a reasonable suspicion that a specific allergen is producing symptoms in an allergic patient. However, several precautionary steps must be observed before skin testing with allergens is performed: Testing is not performed during periods of bronchospasm. Epicutaneous tests (scratch or prick tests) are performed before other testing methods in an effort to minimize the risk of systemic reaction. Emergency equipment must be readily available to treat anaphylaxis. skin testing include prick skin tests, scratch tests, and intradermal skin testing. After negative prick or scratch tests, intradermal skin testing is performed with allergens that are suggested by the patient's history to be problematic. The back is the most suitable area of the body for skin testing because it permits the performance of many tests. The multitest applicator is a commercially available device with multiple test heads that allows simultaneous administration of antigens by multiple punctures at different sites. A negative response on a skin test cannot be interpreted as an absence of sensitivity to an allergen. Such a response may occur with insufficient sensitivity of the test or with use of an inappropriate allergen in testing. Therefore, it is essential to observe the patient undergoing skin testing for an allergic reaction, even if the previous response was negative. A positive reaction, evidenced by the appearance of an urticarial wheal (round, reddened skin elevation) (Fig. 36-9), localized erythema (diffuse redness) in the area of inoculation or contact, or pseudopodia (irregular projection at the end of a wheal) with associated erythema is considered indicative of sensitivity to the corresponding antigen. False-negative results may occur because of improper technique, outdated allergen solutions, or prior use of medications that suppress skin reactivity. Corticosteroids and antihistamines, including over-the-counter allergy medications, suppress skin test reactivity and usually are withheld for 48 to 96 hours before testing, depending on the duration of their activity. False-positive results may occur because of improper preparation or administration of allergen solutions. Interpretation of positive or negative skin tests must be based on the history, physical examination, and other laboratory test results. The following guidelines are used for the interpretation of skin test results: Skin tests are more reliable for diagnosing atopic sensitivity in patients with allergic rhinoconjunctivitis (nasal congestion, runny nose, postnasal drip, sneezing, red eyes [conjunctivitis], and itching of the nose or eyes) than in patients with asthma. Positive skin tests correlate highly with food allergy. The use of skin tests to diagnose immediate hypersensitivity to medications is limited because usually metabolites of medications, not the medications themselves, are responsible for causing hypersensitivity.

Wound bed: Inspect for necrotic, slough, granulation or epithelial tissue, exudate, color, and odor. Wound edges and margins: Observe for undermining (i.e., extension of the wound under the surface skin) or epibole (rolled edges), and evaluate for condition. Wound size: Measure in centimeters (cm), as appropriate, to determine diameter and depth of the wound and surrounding erythema. Surrounding skin: Assess for color, suppleness and moisture, irritation, induration (abnormal firmness of tissue), and scaling.

If acute open wounds or lesions are found on inspection of the skin, a comprehensive assessment should be made and documented. This assessment should address the following issues:

Respiratory System Changes in respiratory rate Cough (dry or productive) Abnormal lung sounds (wheezing, crackles, rhonchi, stridor) Rhinitis Hyperventilation Bronchospasm Hypoxemia Cardiovascular System Hypotension Tachycardia Arrhythmia Vasculitis Anemia Gastrointestinal System Hepatosplenomegaly Colitis Vomiting Diarrhea Genitourinary System Frequency and burning on urination Hematuria Discharge Musculoskeletal System Joint mobility, edema, and pain Skin Rashes Pruritus Lesions Dermatitis Hematomas or purpura Edema, angioedema, or urticaria Inflammation Flushing Discharge Neurosensory System Cognitive dysfunction Hearing loss Visual changes Headaches and migraines Ataxia Tetany

Immune Dysfunction Be alert for the following signs and symptoms:

Gammopathies

Immunoglobulins are overproduced

The immunologic defenses of the body are greatly altered by a serious burn injury as it diminishes resistance to infection. The loss of skin integrity is compounded by the release of abnormal inflammatory factors. There is a significant impairment of the production and release of granulocytes and macrophages from bone marrow; the resulting immunosuppression places the patient with burn injury at high risk for sepsis (see Chapter 54 for details on septicemia).

Immunologic Alterations burns

Indications Allergic rhinitis, conjunctivitis, or allergic asthma History of a systemic reaction to Hymenoptera and specific IgE antibodies to Hymenoptera venom Desire to avoid the long-term use, potential adverse effects, or costs of medications Lack of control of symptoms by avoidance measures or use of medications Contraindications Use of beta blocker or angiotensin-converting inhibitor therapy, which may mask early signs of anaphylaxis Presence of significant pulmonary or cardiac disease or organ failure Inability of the patient to recognize or report signs and symptoms of a systemic reaction Nonadherence of the patient to other therapeutic regimens and low probability that patient will adhere to immunization schedule (often weekly for an indefinite period) Inability to monitor the patient for at least 30 minutes after administration of immunotherapy Absence of equipment or adequate personnel to respond to allergic reaction if one occurs

Immunotherapy: Indications and Contraindications

Keloids

Keloids are benign overgrowths of fibrous tissue at the site of a scar or trauma. They appear to be more common among dark-skinned people. Keloids are asymptomatic but may cause disfigurement and cosmetic concern. The treatment, which is not always satisfactory, consists of surgical excision, intralesional corticosteroid therapy, and radiation.

Erosion

Loss of superficial epidermis that does not extend to dermis; depressed, moist area Ruptured vesicles, scratch marks

Manage high-output wounds

Manages excessive quantities of exudate Pouching systems

Maintain moist environment

Manages moisture levels in a wound and maintains a moist environment Composites, contact layers, foams, gauze (impregnated or saturated), hydrogels, hydrocolloids, transparent films, wound care systems

Pigmented nevi: Moles

Moles are common skin tumors of various sizes and shades, ranging from yellowish brown to black. They may be flat, macular lesions or elevated papules or nodules that occasionally contain hair. Most pigmented nevi are harmless lesions. However, in rare cases, malignant changes occur, and a melanoma develops at the site of the nevus. Nevi that show a change in color or size, become symptomatic (e.g., itch), or develop irregular borders should be removed to determine if malignant changes have occurred. Moles that occur in unusual places (palms of the hands and soles of the feet) should be examined carefully for any irregularity and for notching of the border and variation in color. Nevi larger than 1 cm should be examined carefully. Excised nevi should be examined histologically.

the major priorities for any trauma patient. Vital signs and respiratory status are monitored closely. Circulation, sensation, and mobility (CSM) of burn area is assessed hourly. Refer to Chapter 40 for details on musculoskeletal assessment. Hourly, the nurse will assess warmth, capillary refill, pulses, sensation, and movement of the affected extremity using the unaffected extremity for comparison. A Doppler (ultrasound device) is useful to assess perfusion of the affected extremity. Elevation of burned extremities is crucial to decrease edema. Loss of pulse or sensation must be reported to the provider immediately. Assessment includes monitoring of fluid intake and output. Urine output is measured hourly. Burgundy-colored/pigmented urine suggests muscle damage. Administering and monitoring IV therapy is a major nursing responsibility. Body temperature, body weight, current illnesses, and use of medications are assessed. A head-to-toe assessment is performed, focusing on signs and symptoms of concomitant illness, injury, or developing complications. Assessing the extent of the burn wound continues and is facilitated with anatomic diagrams (described previously).

Nursing assessment in the emergent phase of burn injury focuses on

Nails

On the dorsal surface of the fingers and toes, a hard, transparent plate of keratin, called the nail, overlies the skin. The nail grows from its root, which lies under a thin fold of skin called the cuticle. The nail protects the fingers and toes by preserving their highly developed sensory functions, such as for picking up small objects. Nail growth is continuous throughout life, with an average growth of 0.1 mm daily. Growth is faster in fingernails than toenails and tends to slow with aging. Complete renewal of a fingernail takes about 170 days, whereas toenail renewal takes 12 to 18 months.

PERINEAL AND PERIANAL PRURITUS

Pathophysiology Pruritus of the genital and anal regions may be caused by small particles of fecal material lodged in the perianal crevices or attached to anal hairs. Alternatively, it may result from perianal skin damage caused by scratching, moisture, and decreased skin resistance as a result of corticosteroid or antibiotic therapy. Other possible causes of perianal itching include local irritants such as scabies and lice, local lesions such as hemorrhoids, fungal or yeast infections, and pinworm infestation. Foods associated with anal pruritus include coffee, tea, cola, beer, chocolate, and tomatoes. Occasionally, no cause for genital and anal pruritus can be identified. Medical and Nursing Management The nurse instructs the patient to follow proper hygiene measures and to discontinue home and over-the-counter remedies. The perineal or anal area should be rinsed with lukewarm water and blotted dry with cotton balls. Premoistened tissues may be used after defecation. Cornstarch can be applied in the skinfold areas to absorb perspiration. As part of health teaching, the nurse instructs the patient to avoid bathing in water that is too hot and to avoid using bubble baths, sodium bicarbonate, and detergent soaps, all of which aggravate dryness. To keep the perineal or perianal skin as dry as possible, patients should avoid wearing underwear made of synthetic fabrics. Local anesthetic agents should not be used because of possible allergic effects. The patient should also avoid vasodilating agents or stimulants (e.g., alcohol, caffeine) and mechanical irritants, such as rough or woolen clothing. A diet that includes adequate fiber may help maintain soft stools and prevent minor trauma to the anal mucosa.

This initiative comprises four strategies: making HIV testing a routine part of medical care, implementing new models for diagnosing HIV infections outside medical settings, preventing new infections by working with HIV-infected people and their partners, and further decreasing perinatal transmission of HIV (CDC, 2007). BOX 37-1 Risk Behaviors Associated with HIV Infection and AIDS Sharing injection drug use equipment (aka "works") Having sexual relations with infected individuals (both male and female) People who received HIV-infected blood or blood products (especially before blood screening was instituted in 1985) Infants born to mothers with HIV infection not taking ART medication Health Promotion Safer Sexual Behaviors Encourage patients to be tested for HIV. Advise patients to abstain from sharing sexual fluids. Advise patients to reduce the number of sexual partners to one. Encourage patients to use latex condoms always. If the patient is allergic to latex, polyurethane condoms should be used. Advise patients to avoid using cervical caps or diaphragms without using a condom as well. Recommend patients always use dental dams for oral-genital or anal stimulation. Advise patients to use water-based lubricants to decrease condom breakage. Advise patients to avoid anal intercourse because this practice may injure tissues. Advise patients to avoid manual-anal intercourse. Encourage patients not to ingest urine or semen. Educate patients about nonpenetrative sexual activities, such as body massage, social kissing (dry), mutual masturbation, fantasy, and sex films. Advise patients to avoid sharing needles, razors, toothbrushes, sex toys, or blood-contaminated articles. Encourage patients who are HIV-positive to inform previous, present, and prospective sexual and drug-using partners of their HIV-positive status. If the patient is concerned for his or her safety, advise the patient that many states have anonymous partner notification programs through the public health department to notify people who have been exposed to HIV. Advise HIV-positive patients to avoid donating blood, plasma, body organs, or sperm

Prevention and Education HIV

Protect periwound skin

Prevents moisture and mechanical trauma from damaging delicate tissue around the wound Composites, foams, hydrocolloids, pouching systems, skin sealants, transparent film dressings

Pack or fill dead space

Prevents premature wound closure or fills shallow areas and provides absorption Absorbent beads, powders, pastes; alginates, composites, foams, gauze (impregnated and nonimpregnated)

Diathermy

Produces electrical current to promote warmth and new tissue growth Ultrasound and microwave (diathermy)

Provide therapeutic compression

Provides appropriate levels of support to the lower extremities in venous stasis disease Compression bandages, wraps, support stockings

Protect and cover wound

Provides protection from the external environment Composites, compression bandages/wraps, foams, gauze dressings, hydrogels, hydrocolloids, transparent film dressings

Inhalation injury necessitates prolonged hospitalization and remains a major cause of morbidity and mortality. An inhalation injury can occur when a person is trapped inside a burning structure or involved in an explosion that leads to the inhalation of superheated air, steam, and noxious gas. Inhalation injury has a significant impact on a patient's ability to survive (DeKoning, 2016). Clinical consequences can include upper airway edema, bronchospasm, small airway occlusion, loss of ciliary clearance, increased dead space, intrapulmonary shunting, decreased lung compliance, chest wall compliance, tracheobronchitis, and pneumonia (Sheridan, 2016). Pulmonary injuries fall into two categories: upper airway injury, and inhalation injury below the glottis, including carbon monoxide poisoning. Upper airway injury results from direct heat and edema. It is manifested by mechanical obstruction of the upper airway as small particles may reach the terminal bronchioles, causing bronchospasms and edema. Direct injury to the upper airway causes airway swelling that typically leads to maximal edema in the first 24 to 48 hours after injury and often requires a short course of endotracheal intubation for airway protection (Friedstat, Endorf, & Gibran, 2014). Inhalation injury below the glottis results from inhaling noxious gases or steam. The injury results directly from chemical irritation of the pulmonary tissues at the alveolar level. These injuries cause loss of ciliary action, hypersecretion, severe mucosal edema, and possibly bronchospasm. The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli). Expectoration of carbon particles in the sputum is the cardinal sign of this injury. Carbon monoxide is probably the most common cause of inhalation injury because it is a by-product of the combustion of organic materials and, therefore, is present in smoke. The pathophysiologic effects are caused by tissue hypoxia, a result of carbon monoxide combining with hemoglobin to form carboxyhemoglobin (COHb or HbCO), which competes with oxygen for available hemoglobin-binding sites. The affinity of hemoglobin for carbon monoxide is 250 times greater than that for oxygen. Administering 100% oxygen is essential to accelerate the removal of carbon monoxide from the hemoglobin molecule. Monitor oxygen saturation by pulse oximetry, but be aware that pulse oximetry readings will be falsely elevated in patients with elevated carboxyhemoglobin levels. Simply subtract the measured COHb level from the pulse oximetry value to determine the true oxygen saturation Pulmonary abnormalities are not always immediately apparent. More than half of all patients with burn injuries with pulmonary involvement do not initially demonstrate pulmonary signs and symptoms. Any patient with possible inhalation injury must be observed for at least 24 hours for respiratory complications. Indicators of possible pulmonary damage include the following: History indicating that the burn occurred in an enclosed area Burns of the face or neck Singed nasal hair Hoarseness, voice change, dry cough, stridor Sooty or bloody sputum Labored breathing or tachypnea (rapid breathing) and other signs of reduced oxygen levels (hypoxemia) Erythema and blistering of the oral or pharyngeal mucosa

Pulmonary Alterations burns

Pustule

Pus-filled vesicle or bulla Acne, impetigo, furuncles, carbuncles

Viral load

Quantifies HIV RNA in the plasma. Monitors efficacy of ART through virologic suppression. Goal is undetectable.

Depletion of protein reserves results in atrophy of lymphoid tissues, depression of antibody response, reduction in the number of circulating T cells, and impaired phagocytic function. As a result, susceptibility to infection is greatly increased. During periods of infection or serious illness, nutritional requirements may be altered further, potentially contributing to depletion of stores of protein, fatty acid, vitamin, and trace elements and causing even greater risk of impaired immune response and sepsis. Patients whose nutritional status is compromised have a delayed postoperative recovery and often experience more severe infections and delayed wound healing. The nurse must assess the patient's nutritional status and caloric intake. The nurse is responsible for assuming a proactive role in ensuring the best possible nutritional intake for all patients as a vital step in preventing untoward treatment outcomes.

ROLE OF NUTRITION OF IMMUNE SYSTEM

Immune Response Function

Recent research has confirmed a definite action of Langerhans cells (specialized cells in the skin) in facilitating the uptake of IgE-associated allergens. This action plays a pivotal role in the pathogenesis of atopic dermatitis and other allergic diseases, such as asthma and allergic rhinitis (Amin, 2012; James, Berger, & Elston, 2016b). These findings support the concept of a systemic regulatory mechanism as a trigger for allergic diseases and suggest that this trigger can be aggravated by local inflammation

Recognition Stage.

Recognition of antigens as foreign, or nonself, by the immune system is the initiating event in any immune response. The body accomplishes recognition using lymph nodes and lymphocytes for surveillance. Lymph nodes continuously discharge lymphocytes into the bloodstream. These lymphocytes patrol the tissues and vessels that drain the areas served by that node. T cells present in primary lymphoid tissue that have not been presented with an antigen are called naïve and are capable of responding to a vast array of antigens (Paul, 2012). Macrophages play an important role in helping the circulating lymphocytes process the antigens. Both macrophages and neutrophils have receptors for antibodies and complement (a system of proteins found in normal blood plasma that combines with antibodies to destroy pathogens, to be discussed later in this chapter); as a result, they coat microorganisms with antibodies, complement, or both, enhancing phagocytosis. Then the engulfed microorganisms are subjected to a wide range of toxic intracellular molecules. When foreign materials enter the body, circulating lymphocytes come into physical contact with the surfaces of these materials. Upon contact with the foreign material, naïve lymphocytes, with the help of macrophages, either remove the antigen from the surface or obtain an imprint of its structure, initiating the process of acquired immunity and antigen recognition in preparation for subsequent re-exposure to the antigen (Abbas et al., 2016; Paul, 2012).

Rehabilitation Phase

Rehabilitation begins immediately after the burn has occurred and often extends for years after injury. In the aftermath of the acute stages of burn injury, the patient increasingly focuses on the alterations in self-image and lifestyle that may occur. Wound healing, psychosocial support, and restoration of maximal functional activity remain priorities so that the patient can have the best quality of life both personally and socially. The body goes through many changes as it heals. As the burn wound becomes a burn scar, the burn survivor may be faced with new complications. Often reconstructive surgery to improve body appearance and function is needed.

Cleansing

Removes purulent drainage, foreign debris, and devitalized tissue Wound cleansers

Kidney function may be altered as a result of decreased blood volume. If muscle damage occurs, myoglobin and hemoglobin are released from the muscle cells and excreted by the kidney; this is common in high-voltage injuries or deep thermal burns. The urine will have a pigmented appearance. Adequate fluid volume replacement restores renal blood flow, increasing the glomerular filtration rate and urine volume. Fluids should be titrated to achieve a urine output of 2 mL/kg/hr (Sheridan, 2016). If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resulting in acute tubular necrosis and kidney failure. Blood urea nitrogen (BUN), serum creatinine levels, and urinary output are monitored to evaluate kidney function. Diuretics have no role in this phase of patient management unless fluid overload has occurred (Nemer & Clark, 2016).

Renal Alterations birns

photoallergic contact dermatitis

Resembles allergic dermatitis but requires light exposure in addition to allergen contact to produce immunologic reactivity. Similar to allergic dermatitis Photopatch test Same as for allergic and irritant dermatitis

phototoxic Contact Dermatitis

Resembles the irritant type but requires sun and a chemical in combination to damage the epidermis. Similar to irritant dermatitis Photopatch test Same as for allergic and irritant dermatitis

Allergic contact dermatitis

Results from contact of skin and allergenic substance. Has a sensitization period of 10-14 days. Vasodilation and perivascular infiltrates on the dermis Intracellular edema Usually seen on dorsal aspects of hand Patch testing (contraindicated in acute, widespread dermatitis) Avoidance of offending material Burow solution (aluminum acetate in water) is a drying agent for weeping skin lesions or cool water compress Systemic corticosteroids (prednisone) for 7-10 days Topical corticosteroids for mild cases Oral antihistamines to relieve pruritus

Irritant contact dermatitis

Results from contact with a substance that chemically or physically damages the skin on a nonimmunologic basis. Occurs after first exposure to irritant or repeated exposures to milder irritants over an extended time. Dryness lasting days to months Vesiculation, fissures, cracks Most common on hands and lower arms Clinical picture Appropriate negative patch tests Identification and removal of source of irritation Application of hydrophilic cream or petrolatum to soothe and protect Topical corticosteroids and compresses for weeping lesions Antibiotics for infection, and oral antihistamines for pruritus

Cytomegalovirus

Retinitis is the most common clinical manifestation of CMV. Before the use of ARVs, 30% of patients experienced CMV retinitis with a high incidence of blindness. The incidence of CMV retinitis has been reduced by 80% with these medications. Peripheral retinitis might be asymptomatic or present with floaters, scotomata (a loss of vision within the visual field), or reduced visual acuity. CMV retinitis has characteristic fluffy yellow-white retinal lesions with or without intraretinal hemorrhage visualized on funduscopic examination. Blood vessels near the lesions might appear to be sheathed. Patients with CD4+ counts of less than 50 should be examined by an ophthalmologist on a yearly basis (Sax et al., 2014).

. As a rule, if the skin is acutely inflamed (i.e., hot), erythematous (red), and edematous (swollen) and draining, it is best to apply wet or specialty dressings and/or soothing lotions. For chronic conditions in which the skin surface is dry and scaly, water-soluble emulsions, creams, ointments, and pastes are used. The therapy is modified as the responses of the skin indicate.

Reversing skin Inflammation

connective tissue diseases.

Rheumatic disorders with diffuse inflammation and degeneration in the connective tissuesThese disorders share similar clinical features and may affect some of the same organs. The characteristic clinical course is one of exacerbations and remissions. Although the diffuse connective tissue diseases have unknown causes, they are thought to be the result of immunologic abnormalities in which the immune system loses its ability to tell the difference between foreign invaders and the body's normal cells. The common connective tissue diseases, RA, systemic lupus erythematosus (SLE), and scleroderma, are presented in detail.

SCABIES

Scabies is an infestation of the skin by the itch mite Sarcoptes scabiei. The disease may be found in people living in substandard hygienic conditions, but it can occur in anyone. Infestations may or may not be associated with sexual activity. The mites frequently involve the fingers, and hand contact may produce infection. In children, overnight stays with friends or the exchange of clothes may be a source of infection. Clinical Manifestations and Assessment It takes approximately 4 weeks from the time of contact for the patient's symptoms to appear. The patient complains of severe itching caused by a delayed type of immunologic reaction to the mite or its fecal pellets. During examination, the nurse asks the patient where the pruritus is most severe. A magnifying glass and a penlight are held at an oblique angle to the skin while a search is made for the small, raised burrows created by the mites. The burrows may be multiple, straight or wavy, brown or black, thread-like lesions, most commonly observed between the fingers and on the wrists. Other sites are the extensor surfaces of the elbows, the knees, the edges of the feet, the points of the elbows, around the nipples, in the axillary folds, under pendulous breasts, and in or near the groin or gluteal fold, penis, or scrotum. Red, pruritic eruptions usually appear between adjacent skin areas. However, the burrow is not always visible. Any patient with a rash may have scabies. One classic sign of scabies is the increased itching that occurs during the overnight hours, perhaps because the increased warmth of the skin has a stimulating effect on the parasite. Hypersensitivity to the organism and its products of excretion also may contribute to the pruritus. If the infection has spread, other members of the family and close friends also complain of pruritus about a month later. Secondary lesions are quite common and include vesicles, papules, excoriations, and crusts. Bacterial superinfection may result from constant excoriation of the burrows and papules. The diagnosis is confirmed by recovering S. scabiei or the mites' by-products from the skin. A sample of superficial epidermis is scraped from the top of the burrows or papules with a small scalpel blade. The scrapings are placed on a microscope slide and examined through a microscope at low power to demonstrate evidence of the mite Medical and Nursing Management The patient is instructed to take a warm, soapy bath or shower to remove the scaling debris from the crusts and then to dry thoroughly and allow the skin to cool. A prescription scabicide, such as lindane (Kwell), crotamiton (Eurax), or 5% permethrin (Elimite), is applied thinly to the entire skin from the neck down, sparing only the face and scalp (which are not affected in scabies). The medication is left on for 12 to 24 hours, after which the patient is instructed to wash thoroughly. One application may be curative, but it is advisable to repeat the treatment in 1 week.

Deep partial-thickness (similar to second-degree)

Scalds Flash flame Contact Epidermis, upper dermis, portion of deeper dermis Pain Hyperesthesia Sensitive to cold air Blistered, mottled red base; broken epidermis; weeping surface Edema Recovery in 3-8 weeks Some scarring and depigmentation contractures Infection may convert it to full thickness

SEBORRHEIC DERMATITIS

Seborrhea is excessive production of sebum (secretion of sebaceous glands) in areas where sebaceous glands are normally found in large numbers, such as on the face, scalp, eyebrows, eyelids, sides of the nose and upper lip, malar regions (cheeks), ears, axillae, under the breasts, in the groin, and in the gluteal crease of the buttocks. Seborrheic dermatitis is a chronic inflammatory disease of the skin with a predilection for areas that are well supplied with sebaceous glands or lie between skin folds, where the bacteria count is high. Clinical Manifestations and Assessment Two forms of seborrheic dermatitis can occur, an oily form and a dry form. Either form may start in childhood and continue throughout life. The oily form appears moist or "greasy." There may be patches of yellowish-red or gray-white, greasy skin, with white dry scaling macules and/or papules, with slight erythema, predominantly on the forehead, nasolabial fold, beard area, scalp, and between adjacent skin surfaces in the regions of the axillae, groin, and breasts (Clark, Pope, & Jaboori, 2015). Small pustules or papulopustules resembling acne may appear on the trunk. The dry form, consisting of flaky desquamation of the scalp with a profuse amount of fine, powdery scales, is commonly called dandruff. The mild forms of the disease are asymptomatic. When scaling occurs, it is often accompanied by pruritus, which may lead to scratching and secondary infections and excoriation. Seborrheic dermatitis has a genetic predisposition. Hormones, nutritional status, infection, and emotional stress influence its course. The remissions and exacerbations of this condition should be explained to the patient. If a person has not previously been diagnosed with this condition and suddenly appears with a severe outbreak, a complete history and physical examination should be considered. Medical and Nursing Management Because there is no known cure for seborrhea, the objective of therapy is to control the disorder and allow the skin to repair itself. Seborrheic dermatitis of the body and face may respond to a topically applied glucocorticoid cream or low-potency topical steroids (e.g., desonide), which allays the secondary inflammatory response (Clark et al., 2015). However, glucocorticoids should be used with caution near the eyelids, because they can induce glaucoma and cataracts in predisposed patients. Patients with seborrheic dermatitis may develop a secondary candidal (yeast) infection in body creases or folds and may have to use a topical antifungal (e.g., ciclopirox or ketoconazole) (Clark et al., 2015). To avoid this, patients should be advised to ensure maximum aeration of the skin and to clean areas where there are creases or folds in the skin carefully. Patients with persistent candidiasis should be evaluated for diabetes. Ultraviolet radiation therapy can be beneficial as a form of treatment as well. The mainstay of dandruff treatment is proper, frequent shampooing (at least three times weekly) with medicated shampoos. Two or three different types of shampoo should be used in rotation to prevent the seborrhea from becoming resistant to a particular shampoo. The shampoo is left on at least 5 to 10 minutes. As the condition of the scalp improves, the treatment can be less frequent. Antiseborrheic shampoos include those containing selenium sulfide suspension, zinc pyrithione, salicylic acid or sulfur compounds, and tar shampoo that contains sulfur or salicylic acid. Instructions for using medicated shampoos are reinforced for people with dandruff who require treatment. Frequent shampooing is contrary to some cultural practices; the nurse should be sensitive to these differences when teaching the patient about home care. A person with seborrheic dermatitis is advised to avoid external irritants, excessive heat, and perspiration; rubbing and scratching prolong the disorder. To avoid secondary infection, the patient should air the skin and keep skin folds clean and dry. The patient is cautioned that seborrheic dermatitis is a chronic problem that tends to reappear. The goal is to keep it under control. Patients need to be encouraged to adhere to the treatment program. Those who become discouraged and disheartened by the effect on body image should be treated with sensitivity and encouraged to express their feelings.

Minor Burn Injury

Second-degree burn of less than 15% total body surface area (TBSA) in adults or less than 10% TBSA in children Third-degree burn of less than 2% TBSA not involving special care areas (eyes, ears, face, hands, feet, perineum, joints) Excludes all patients with electrical injury, inhalation injury, or concurrent trauma and all at-risk patients (i.e., extremes of age, intercurrent disease)

Moderate, Uncomplicated Burn Injury

Second-degree burns of 15-25% TBSA in adults or 10-20% in children Third-degree burns of less than 10% TBSA not involving special care areas Excludes all patients with electrical injury, inhalation injury, or concurrent trauma; all at-risk patients (i.e., extremes of age, intercurrent disease)

Major Burn Injury

Second-degree burns of at least 25% TBSA in adults or at least 20% in children All third-degree burns 10% or more TBSA All burns involving eyes, ears, face, hands, feet, perineum, joints All patients with inhalation injury, electrical injury, or concurrent trauma; all at-risk patients

Change Signs and Symptoms Activation of IgE and subsequent release of chemical mediators Feeling of impending doom or fright Histamine release Sweating; sneezing; shortness of breath; nasal pruritus, urticaria, and angioedema (swelling of the deep dermis or subcutaneous or submucosal tissues); nasal mucosal edema; profuse watery rhinorrhea; itching; nasal congestion Increased vascular permeability, subsequent decrease in peripheral resistance and leakage of plasma fluids Hypotension, shock, and possible cardiac arrhythmias Increased capillary permeability and mast cell degranulation Edema of upper respiratory tract, resulting in hypopharyngeal and laryngeal obstruction Bronchiole smooth muscle contraction and increased mucus production Hoarseness, stridor, wheezing, and use of accessory muscles Smooth muscle contraction of intestines and bladder Severe stomach cramps, nausea, diarrhea; urinary urgency and incontinence

Signs and Symptoms ANAPHYLAXIS

Vitamin Synthesis

Skin exposed to ultraviolet light can convert substances necessary for synthesizing vitamin D (cholecalciferol). Vitamin D is essential for preventing osteoporosis and rickets, a condition that causes bone deformities and results from a deficiency of vitamin D, calcium, and phosphorus (Box 51-1).

Superficial

Thermal injury (heat/cold), electromagnetic energy, solar radiation or topical caustic chemicals Involves only the epidermis Erythema and edema of skin Redness, swelling, does not blister, pain Three days or less

Superficial partial-thickness (similar to first-degree)

Sunburn Low-intensity flash Epidermis; possibly a portion of dermis Tingling Hyperesthesia (supersensitivity) Pain that is soothed by cooling Reddened; blanches with pressure; dry Minimal or no edema Possible blisters Complete recovery within 5-10 days; usually no scarring Peeling

Cellular Immune Response

T lymphocytes are responsible primarily for cellular immunity. Several types of T cells exist, each with designated roles in the defense against bacteria, viruses, fungi, parasites, and malignant cells. T cells attack foreign pathogens directly rather than by producing antibodies. T cells are either naïve—capable of reacting to new antigens—or activated—having the memory of previous antigen exposure (Paul, 2012). Cellular reactions are initiated by the binding of an antigen to an antigen receptor located on the surface of a naïve T cell. This may occur with or without the assistance of macrophages. The activated T cells then carry the antigenic message, or blueprint, to the lymph nodes, where the production of other T cells is stimulated. Some T cells remain in the lymph nodes and retain a memory for the antigen. Other T cells migrate from the lymph nodes into the general circulatory system and ultimately to the tissues, where they remain until they either come in contact with their respective antigens or die.

Loss of skin also results in an inability to regulate body temperature. Therefore patients with burn injuries may exhibit low body temperatures in the early hours after injury. Then, as hypermetabolism resets core temperatures, the patient becomes hyperthermic for much of the post-burn period, even in the absence of infection.

Thermoregulatory Alterations burns

Antigen Recognition

The B lymphocytes appear to respond to some antigens by triggering antibody formation directly; however, in response to other antigens, they need the assistance of T cells to trigger antibody formation. The T lymphocytes are part of a surveillance system that is dispersed throughout the body and recycles through the general circulation, tissues, and lymphatic system. With the assistance of macrophages, the T lymphocytes are believed to recognize the antigen of a foreign pathogen. The T lymphocyte picks up the antigenic message, or "blueprint," of the antigen and returns to the nearest lymph node with that message. B lymphocytes stored in the lymph nodes are subdivided into thousands of clones, each responsive to a single group of antigens having almost identical characteristics. When the antigenic message is carried back to the lymph node, specific clones of the B lymphocyte are stimulated to enlarge, divide, proliferate, and differentiate into plasma cells capable of producing specific antibodies to the antigen. Other B lymphocytes differentiate into B-lymphocyte clones with a memory for the antigen. These memory cells are responsible for the more exaggerated and rapid immune response in a person who is exposed to the same antigen repeatedly.

Thermoregulation

The body continuously produces heat as a result of the metabolism of food, which produces energy. This heat is dissipated primarily through the skin. Evaporation from the skin aids heat loss by conduction. Heat is conducted through the skin into water molecules on its surface, causing the water to evaporate. The water on the skin surface may be from insensible perspiration, sweat, or the environment. Under normal conditions, metabolic heat production is balanced by heat loss, and the internal temperature of the body is maintained constant at approximately 37°C (98.6°F). The rate of heat loss depends primarily on the surface temperature of the skin, which is a function of the blood flow to the skin. Increased blood flow to the skin results in more heat delivered to the skin and a greater rate of heat loss from the body. In contrast, decreased skin blood flow decreases the skin temperature and helps conserve heat for the body. When the temperature of the body begins to fall, as occurs on a cold day, the blood vessels of the skin constrict, thereby reducing heat loss from the body. Sweating is another process by which the body can regulate the rate of heat loss. Sweating does not occur until the core body temperature exceeds 37°C (98.6°F), regardless of skin temperature. In extremely hot environments, the rate of sweat production may be as high as 1 L per hour. Under some circumstances (e.g., emotional stress), sweating may occur as a reflex and may be unrelated to the need to lose heat from the body.

CD4/CD8 ratio

These are markers found on lymphocytes. HIV kills CD4+ cells, which results in a significantly impaired immune system. Used in decision to initiate ART and use of prophylactic medications.

Specialty Absorptive Dressings

These are used for heavily exudating wounds. The dressings absorb copious amounts of drainage. Examples of these are Exudry and ABD pads.

Anaphylactic (Type I) Hypersensitivity

The most severe form of hypersensitivity reaction or immune-mediated reaction is anaphylaxis. An unanticipated severe allergic reaction that is often explosive in onset, anaphylaxis is characterized by edema in many tissues, including the larynx, and often is accompanied by hypotension, bronchospasm, and cardiovascular collapse in severe cases. Mast cells in any organ system may be involved; however, the primary foci are the cardiovascular, skin, respiratory, and gastrointestinal systems (sites where mast cells are abundant) (Schwartz, 2016). Type I or anaphylactic hypersensitivity is an immediate reaction beginning within minutes of exposure to an antigen. This reaction is mediated by IgE antibodies and typically occurs on re-exposure to a specific antigen. If chemical mediators continue to be released, a delayed reaction may occur up to 24 hours after allergen exposure. Refer to Chapter 38 for more details on anaphylaxis.

primary infection.

The period from infection with HIV to the development of antibodies to HIV is known as This period is characterized by intense viral replication and widespread dissemination of HIV throughout the body. During primary infection, a window period occurs, during which a person with HIV infection tests negative on the HIV antibody blood test. Although antibodies to the HIV envelope glycoproteins typically can be detected in the sera of HIV-infected individuals by 2 to 3 weeks after infection, most of these antibodies lack the ability to inhibit virus infection. By the time neutralizing antibodies can be detected, HIV-1 is firmly established in the host. During this period, there are high levels of viral replication and destruction of CD4+ T cells, resulting in high levels of HIV in the blood and a dramatic drop in CD4+ T-cell counts from the normal range of 500 to 1,500 cells/mm3 of blood. Detectable levels of virus can occur as early as 72 hours after exposure; this provides the rationale for immediate initiation of prophylaxis. About 3 weeks into this acute phase, the person may display symptoms similar to mononucleosis, such as fever, enlarged lymph nodes, rash, muscle aches, and headaches. These symptoms resolve within another 1 to 3 weeks as the immune system begins to recuperate. That is, the CD4+ T-cell population responds in ways that cause other immune cells, such as CD8+ lymphocytes, to increase their killing of infected, virus-producing cells. The body produces antibody molecules in an effort to contain the virus; they bind to free HIV particles (outside cells) and assist in their removal. This balance between the amount of HIV in the body and the immune response is referred to as the viral set point; it results in a steady state of infection that can last for years. Primary HIV infection, the time during which the viral burden set point is achieved, includes the acute symptomatic and early infection phases. During this initial stage, viral replication is associated with dissemination in lymphoid tissue (lymph nodes, spleen, tonsils and adenoids, and the thymus) and a distinct immunologic response. The final level of the viral set point is inversely correlated with disease prognosis; that is, the higher the viral set point, the poorer the prognosis. The primary infection stage is part of CDC category A.

Protection

The stratum corneum, the outer layer of the epidermis, provides the most effective barrier to epidermal water loss to maintain a homeostatic environment and penetration of environmental factors, such as chemicals, microbes, and insect bites. Various lipids are synthesized in the stratum corneum and are the basis for the barrier function of this layer. These are long-chain lipids that are better suited than phospholipids for water resistance. The presence of these lipids in the stratum corneum creates a relatively impermeable barrier for water egress and for the entry of toxins, microbes, and other substances that come in contact with the surface of the skin. Some substances do penetrate the skin but meet resistance in trying to move through the channels between the cell layers of the stratum corneum. Microbes and fungi, which are part of the body's normal flora, cannot penetrate unless there is a break in the skin barrier.

Fluid Balance

The stratum corneum, the outermost layer of the epidermis, has the capacity to absorb water, thereby preventing an excessive loss of water and electrolytes from the internal body and retaining moisture in the subcutaneous tissues. When skin is damaged, as occurs with a severe burn, large quantities of fluids and electrolytes may be lost rapidly, possibly leading to circulatory collapse, shock, and death. The skin is not completely impermeable to water. Small amounts of water continuously evaporate from the skin's surface. This evaporation, called insensible perspiration, amounts to approximately 600 mL daily in a normal adult. Insensible water loss varies with the body and ambient temperature. In a person with a fever, the fluid loss increases. If the fever is between 38.3°C (101°F) and 39.4°C (103°F), a loss of 500 mL per 24 hours is anticipated; whereas if the temperature if over 39.4°C (over 103°F), a loss of 1,000 mL at a minimum is expected (Porat & Dinarello, 2015).

Hypodermis

The subcutaneous tissue, or hypodermis, is the innermost layer of the skin. It is primarily adipose tissue, which provides a cushion between the skin layers, muscles, and bones. It promotes skin mobility, molds body contours, and insulates the body. Fat is deposited and distributed according to the person's gender and in part accounts for the difference in body shape between men and women. Overeating results in increased deposition of fat beneath the skin. The subcutaneous tissues and the amount of fat deposited are important factors in body temperature regulation.

Hypertrophic Scarring

The wound is in a dynamic state for 1.5 to 2 years after the burn occurs. If appropriate measures are instituted during this active period, the scar tissue can lose its redness and soften. Healed areas that are prone to hypertrophic scarring require the patient to wear a pressure garment. Pressure needs to be continuous. Gentle superficial massage aids in softening the connective tissue. Patients must be instructed about the need for lubrication and protection of the healing skin and the need to use pressure garments for at least 1 year after the injury. Treatment during rehabilitation is expected to include elastic pressure garments, splints, and exercise under the supervision of an experienced physical and occupational therapy team.

Lichenification

Thickening and roughening of the skin or accentuated skin markings that may be secondary to repeated rubbing, irritation, scratching Contact dermatitis

Atrophy

Thin, dry, transparent appearance of epidermis; loss of surface markings; secondary to loss of collagen and elastin; underlying vessels may be visible Aged skin, arterial insufficiency

Arterial

Tips of toes, pressure points, areas of trauma Pale or necrotic Minimal amount exudate Well defined

Latex allergy

Type I IgE-mediated immediate hypersensitivity to plant proteins in natural rubber latex. In sensitized people, anti-latex IgE antibody stimulates mast cell proliferation and basophil histamine release. Exposure can be through contact with the skin, mucous membranes, or internal tissues, or through inhalation of traces of powder from latex gloves. Severe reactions usually occur shortly after parenteral or mucous membrane exposure. People with any type I reaction to latex are at high risk of anaphylaxis. Local: swelling, redness, edema, itching Mild systemic: rhinitis, flushing, conjunctivitis Severe systemic: urticaria, laryngeal edema, bronchospasm, asthma, severe vasodilation angioedema, including anaphylaxis, cardiovascular collapse, and death All above reactions can occur within minutes after exposure. Immediate treatment of reaction with epinephrine, fluids, vasopressors, and corticosteroids, and airway and ventilator support, with close monitoring for recurrence for next 12-14 hours Prompt referral for diagnostic evaluation Treatment and diagnostic evaluation in latex-free environment Strict avoidance of allergy testing and management Assessment of all patients for symptoms of latex allergy Teaching of patients and family members about the disorder and about the importance of preventing future reactions by avoiding latex Encouraging wearing of a medical alert bracelet that identifies latex allergy for emergency situations Warning labels can be attached to car windows to alert police and paramedics about the driver's or passenger's latex allergy in case of a motor vehicle crash. Carrying an EpiPen at all times and being prepared and able to use it

Cytotoxic (Type II) Hypersensitivity

Type II, or cytotoxic, hypersensitivity occurs when the system mistakenly identifies a normal constituent of the body as foreign. This reaction may be the result of a cross-reacting antibody, possibly leading to damage to cells and tissues. Several disorders are associated with type II hypersensitivity reactions, including myasthenia gravis, in which the body mistakenly generates antibodies against normal nerve ending receptors; or Goodpasture syndrome, in which antibodies are generated against lung and renal tissue, producing lung damage and kidney failure; or they may be associated with drug-induced immune hemolytic anemia, Rh-hemolytic disease of the newborn, and incompatibility reactions in blood transfusions.

Immune Complex (Type III) Hypersensitivity

Type III, or immune complex, hypersensitivity involves immune complexes that are formed when antigens bind to antibodies. These complexes are cleared from the circulation by phagocytic action. If these type III complexes are deposited in tissues or vascular endothelium, two factors contribute to injury: the increased amount of circulating complexes and the presence of vasoactive amines. As a result, there is an increase in vascular permeability and tissue injury. The joints and kidneys are particularly susceptible to this type of injury. Type III hypersensitivity is associated with systemic lupus erythematosus, rheumatoid arthritis, certain types of nephritis, and some types of bacterial endocarditis.

Delayed-Type (Type IV) Hypersensitivity

Type IV, or delayed-type hypersensitivity, also known as cellular hypersensitivity, occurs 24-72 hours after exposure to an allergen. It is mediated by sensitized T cells and macrophages. An example of this reaction is the effect of an intradermal injection of tuberculin antigen or purified protein derivative (PPD). Sensitized T cells react with the antigen at or near the injection site. Lymphokines are released and attract, activate, and retain macrophages at the site. These macrophages then release lysozymes, causing tissue damage. Edema and fibrin are responsible for the positive tuberculin reaction. Another example of a type IV hypersensitivity reaction is contact dermatitis resulting from exposure to allergens, such as cosmetics, adhesive tape, topical agents (e.g., povidone-iodine), medication additives, and plant toxins. The most common immune-mediated reaction to local anesthetics is a type IV hypersensitivity reaction. The primary exposure results in sensitization. Re-exposure causes a hypersensitivity reaction with resultant symptoms, such as pruritus, erythema, and raised lesions.

ARTERIAL ULCERS

Ulcers related to problems with arterial circulation are seen in patients with hypertension, diabetes, cigarette smoking, hypercholesterolemia, obesity, and sedentary lifestyle. Arterial ulcers are caused by lower extremity arterial disease (LEAD), which is inadequate blood flow to the tissue, resulting in severe tissue ischemia, and which can create ulcers that are extremely painful (Doughty & Sparks-Defriese, 2016). This condition is also referred to as peripheral arterial disease (PAD), peripheral vascular disease (PVD), or peripheral arterial occlusive disease (PAOD). In patients with LEAD and ulcers, treatment of the ulcers is concurrent with treatment of the arterial disease. Management includes the use of the dressings and/or tissue perfusion improvement. Perfusion and tissue oxygenation can improve outcomes via surgical options (bypass graft, angioplasty), medications (antiplatelets, vasodilators, hemorheologics [decrease the viscosity of the blood], antilipemics [decrease lipid levels], analgesics), lifestyle changes, and adjunctive therapies (hyperbaric oxygen therapy) (Doughty & Sparks-Defriese, 2016). If these interventions are instituted early in the progression of an ulcer, the condition can often be effectively improved. Surgical amputation of an affected limb is a last resort.

Mechanical Débridement

Wet-to-dry dressings are still used, but not very much. It is considered a nonselective method of débridement, which removes necrotic tissue and absorbs small to large amounts of exudates. This method exposes healthy tissue in the wound and can damage it as well. Wet dressings (wet compresses applied to the skin) were traditionally used for acute, weeping, inflammatory lesions. They have become almost obsolete because of the many newer products available for wound care (Ramundo, 2016).

AIDS (CDC Category C: Fewer Than 200 CD4+ T Lymphocytes/mm3)

When the CD4+ T-cell level drops below 200 cells/mm3 of blood, the person has AIDS. As levels decrease to fewer than 100 cells/mm3, the immune system is significantly impaired. Once a patient has had a category C condition, he or she maintains a permanent diagnosis of AIDS even if the immune system recuperates. This classification has implications for entitlements (i.e., disability benefits, housing, and food stamps) because these programs are often linked to an AIDS diagnosis. Although the revised classification system of the CDC emphasizes CD4+ T-cell counts, it allows for the count of CD4+ T-cells to be expressed as a percentage (percentage of CD4+ T cells compared with total lymphocytes). The CD4+ percentage is less subject to variation on repeated measurements than is the absolute CD4+ T-cell count. A CD4+ percentage of less than 14% of the total lymphocytes is consistent with an AIDS diagnosis. The percentage, as compared with the absolute number of CD4+ T cells, becomes particularly important when the patient has a heightened immune response to infections in addition to HIV.

The phagocytic immune response The humoral or antibody immune response The cellular immune response

When the body is invaded or attacked by bacteria, viruses, or other pathogens, it has three means of defense:

secondary immunodeficiencies

affect the normal immune system of the patient, resulting in increased susceptibility to infection and certain types of cancer. Extrinsic and intrinsic factors, such as nonimmune systemic disorders like HIV infection, immunosuppressive therapy, prolonged illness or hospitalization, and aging, trigger secondary immunodeficiency. These factors cause impaired immune response through loss or destruction of lymphocytes, such as CD4 cell depletion, or decreased production of lymphocytes, as in the effects of irradiation on bone marrow lymphocyte production (Stiehm, 2014). Patients with immunosuppression from secondary immunodeficiencies are referred to as immunocompromised hosts. The most common secondary immunodeficiency is AIDS.

HERPES ZOSTER

also called shingles, is an infection caused by the varicella-zoster virus, a member of a group of DNA viruses. The viruses causing chickenpox and herpes zoster are indistinguishable, hence the name varicella-zoster virus. The disease is characterized by a painful vesicular eruption along the area of distribution of the sensory nerves from one or more posterior ganglia. Pathophysiology After a case of chickenpox runs its course, the varicella-zoster viruses responsible for the outbreak lie dormant inside nerve cells near the brain and spinal cord. Later, when these latent viruses are reactivated because of declining cellular immunity, they travel by way of the peripheral nerves to the skin, where the viruses multiply and create a red rash of small, fluid-filled vesicles. About 10% of adults get shingles during their lifetimes, usually after 50 years of age. There is an increased frequency of herpes zoster infections among patients with weakened immune systems and cancers (especially leukemias and lymphomas), those on chemotherapy, and in individuals who are HIV infected. Clinical Manifestations and Assessment The eruption is usually accompanied or preceded by pain, which may radiate over the entire region supplied by the affected nerves. The pain may be burning, lancinating (tearing or sharply cutting), stabbing, or aching. Some patients have no pain, but itching and tenderness may occur over the area. Sometimes, malaise and gastrointestinal (GI) disturbances precede the eruption. The patches of grouped vesicles appear on the red and swollen skin. The early vesicles, which contain serum, later may become purulent, rupture, and form crusts. The inflammation is usually unilateral, involving the thoracic, cervical, or cranial nerves in a band-like configuration. Usually the blisters are confined to a narrow region of the face or trunk (Fig. 52-2). The clinical course varies from 1 to 3 weeks. If an ophthalmic nerve is involved, the patient may have eye pain. Inflammation and a rash on the trunk may cause pain with the slightest touch. The healing time varies from 7 to 26 days. Herpes zoster in healthy adults is usually localized and benign. However, in patients who are immunosuppressed, the disease may be severe and disabling. Medical and Nursing Management There is evidence that infection is arrested if oral antiviral agents, such as acyclovir (Zovirax), valacyclovir (Valtrex), or famciclovir (Famvir), are administered within 24 hours of the initial eruption. IV acyclovir, if started early, is effective in significantly reducing the pain and halting the progression of the disease. In older patients, the pain from herpes zoster may persist as postherpetic neuralgia (persistent pain of the affected nerve after healing) for months after the skin lesions disappear. The goals of herpes zoster management are to relieve the pain and to reduce or avoid complications, which include infection, scarring, and postherpetic neuralgia and eye complications. Pain is controlled with analgesics because adequate pain control during the acute phase helps prevent persistent pain patterns. Systemic corticosteroids may be prescribed for patients older than 50 years of age to reduce the incidence and duration of postherpetic neuralgia. Healing usually occurs more quickly in those who have been treated with corticosteroids. Triamcinolone (Aristocort, Kenacort, Kenalog) injected subcutaneously under painful areas is effective as an anti-inflammatory agent. Ophthalmic herpes zoster occurs when an eye is involved. This is considered an ophthalmic emergency, and the patient should be referred to an ophthalmologist immediately to prevent the possible sequelae of keratitis, uveitis, ulceration, and blindness. People who have been exposed to varicella by primary infection or by vaccination are not at risk for infection after exposure to patients with herpes zoster.

Pruritus

While not a disorder but a manifestation, pruritus (itching) is one of the most common symptoms of patients with dermatologic disorders. GENERAL PRURITUS Pathophysiology Itch receptors are unmyelinated, penicillate (brush-like) nerve endings that are found exclusively in the skin, mucous membranes, and cornea. Although pruritus is usually caused by a primary skin disease with resultant rash or lesions, it may occur without a rash or lesion. This is referred to as essential pruritus, which generally has a rapid onset, may be severe, and interferes with normal daily activities. Pruritus may be the first indication of a systemic internal disease, such as diabetes mellitus, blood disorders, or cancer (occult malignancy of the breast or colon; Hodgkin disease, other lymphomas). It may also accompany kidney, liver, and thyroid diseases (Box 52-2). Some common oral medications, such as aspirin, antibiotics, hormones (i.e., estrogens, testosterone, or oral contraceptives), and opioids (i.e., morphine or cocaine) may cause pruritus directly or by increasing sensitivity to ultraviolet light. Certain soaps and chemicals, radiation therapy, prickly heat (miliaria), and contact with woolen garments are also associated with pruritus. Pruritus may also be caused by psychological factors, such as excessive stress in family or work situations. Scratching the pruritic area causes the inflamed cells and nerve endings to release histamine, which produces more pruritus, generating a vicious itch-scratch cycle. If the patient responds to an itch by scratching, the integrity of the skin may be altered, and excoriation, erythema, raised areas (i.e., wheals), infection, or changes in pigmentation may result. Pruritus usually is more severe at night and is less frequently reported during waking hours, most likely because the person is distracted by daily activities. At night, when there are few distractions, even the slightest pruritus cannot be ignored easily. Severe itching can be debilitating. Medical and Nursing Management In general, washing with soap and hot water is avoided. Bath oils containing a surfactant that makes the oil mix with bath water (e.g., Alpha-Keri) may be sufficient for cleaning. A warm bath with a mild soap followed by application of a bland emollient to moist skin can control xerosis (dry skin). Applying a cold compress, or cool agents that contain menthol and camphor (which constrict blood vessels) may also help relieve pruritus. If baths have been prescribed, the nurse reminds the patient to use tepid (not hot) water and to shake off the excess water and blot between intertriginous areas (body folds) with a towel. Rubbing vigorously with the towel is avoided because this overstimulates the skin and causes more itching. It also removes water from the stratum corneum (horny layer or outermost layer of the epidermis). Immediately after bathing, the patient should lubricate the skin with an emollient to trap moisture. The nurse instructs patient to avoid situations that cause vasodilation, such as exposure to an overly warm environment and ingestion of alcohol or hot foods and liquids. Activities that result in perspiration should be limited because perspiration may irritate and promote pruritus. If the patient is troubled at night with itching that interferes with sleep, the nurse can advise wearing cotton clothing next to the skin rather than synthetic materials. The room should be kept cool and humidified. Vigorous scratching should be avoided and nails kept trimmed to prevent skin damage and infection. When the underlying cause of pruritus is unknown and further testing is required, the nurse explains each test and the expected outcome. Topical corticosteroids may be beneficial as anti-inflammatory agents to decrease itching. Oral antihistamines are even more effective because they can overcome the effects of histamine released from damaged mast cells. An antihistamine, such as diphenhydramine (Benadryl) or hydroxyzine (Atarax), prescribed in a sedative dose at bedtime, may be beneficial in producing a restful and comfortable sleep. Nonsedating antihistamine medications, such as fexofenadine (Allegra), are more appropriate to relieve daytime pruritus. Tricyclic antidepressants may be prescribed for pruritus of neuropsychogenic origin. If pruritus continues, further investigation of a systemic problem is advised.

Osteoarthritis,

also known as degenerative joint disease, is a chronic, noninflammatory (even though inflammation may be present), progressive disorder that causes cartilage deterioration in synovial joints and vertebrae. It particularly affects the weight-bearing joints, knees and hips, and joints of the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the fingers (Shelton, 2013). OA is the most common and most frequently disabling of the joint disorders; it is overdiagnosed and trivialized and frequently over- or undertreated. The functional impact of OA on quality of life, especially for elderly patients, is often ignored. OA has been classified as both primary (idiopathic), with no prior event or disease related to the OA, and secondary, resulting from previous joint injury or inflammatory disease. The distinction between primary and secondary OA is not always clear, but often the clinical presentation and symptoms are similar. Risk Factors for Osteoarthritis (OA) Aging Obesity (mechanical loading from a higher body mass index is associated with an increased risk of knee OA; the link between OA and adipose-derived leptin is now recognized as a metabolically active contributor to inflammatory cascades) Genetic predisposition Joint location (joint-specific, age-related articular cartilage changes, varying joint responsiveness to cytokines) Malalignment of joints (can lead to rapid development of OA; congenital and developmental disorders, e.g., poorly reduced intra-articular fractures, developmental dysplasia of the hip) Trauma (also can lead to rapid development of OA; overuse or abuse of joints, as occurs in high-impact sports; previous joint damage; excessive loading or forces, such as that seen in pneumatic drill operators, or frequent squatting position, such as catchers in baseball, where up to 10 times body weight may be transmitted to the knee.) Gender (differences in incidence after 50 years of age may be the result of postmenopausal estrogen deficiency; articular chondrocytes possess functional estrogen receptors) Pathophysiology . In OA, changes in articular cartilage occur first; eventually, changes to secondary soft tissue may occur. OA is characterized by erosion of the articular cartilage combined with hypertrophy of bone at the joint margins, resulting in formation of new bone known as osteophytes or bone spurs (Fig. 39-1) and subchondral (the bony plate that supports the articular cartilage) sclerosis. In addition, OA is characterized by a range of biochemical and morphologic alterations of the synovial membrane and joint capsule. In general, a combination of cartilage degradation, bone stiffening, and reactive inflammation of the synovium occurs (Aigner, Schmitz, & Salter, 2015). Understanding of OA has been expanded greatly beyond what previously was thought of as simply "wear and tear" related to aging. Clinical Manifestations and Assessment The general clinical manifestations of OA are pain, stiffness, and functional disability (Altman, 2015; Harris & Crawford, 2015). Pain in one or more joints typically is worsened by activities and is alleviated by rest. Although osteoarthritic pain is unusual during the night or at rest, there are exceptions, including in patients with mild OA using joints for several hours, in patients with advanced OA with destructive arthropathy, and in patients with an acute inflammatory flare-up of OA. Stiffness may be defined as a sensation of a gelling or tightening of the involved joint that usually occurs after inactivity, such as in the morning or when rising after sitting for a prolonged period. Morning stiffness usually resolves after less than 10 minutes (no more than 30 minutes' duration), in contrast to prolonged stiffness seen in inflammatory disorders. Functional impairment is reflected in limited range of motion (ROM) and patient report of limited ability to perform day-to-day activities. Typically OA is diagnosed by an overall clinical impression based on the patient's age and history, location of joint abnormalities, and radiographic findings. Limited passive movement can be the first and only physical sign of symptomatic OA. During joint examination, crepitus, a continuous grating sensation, may be felt or heard as the joint goes through ROM. Physical assessment of the musculoskeletal system reveals joint enlargement, resulting from joint effusion or bony swelling or both. This is most easily detected in the patient's knees by the evidence of patellar tap or by the elicitation of a fluid thrill (wave test). Joint deformities reflect advanced disease with joint destruction, which then contributes to misalignment, joint instability (causing a sensation in the knees of "giving way" or "locking"), and limb shortening. Fingers also can be misaligned in the presence of Heberden (enlargements of DIP joints) or Bouchard nodes (enlargements of PIP joints) Radiographic assessment has long been considered the gold standard to diagnose OA and to establish severity of joint damage; to monitor disease activity, progression, and response to therapy; and to search for complications of the disorder or the treatment. Standard x-rays of affected joints show osteophytes, the most characteristic feature of OA, and, in more advanced disease, joint space narrowing and sclerosis Arthroscopy is a more appropriate gold standard in the evaluation of OA, allowing direct visualization of cartilage surface integrity. Medical and Nursing Management Nonpharmacologic treatment measures mentioned earlier in the chapter are the core for OA management and should be maintained throughout the patient's course of the disease. Interventions mainly center around rest and joint protection, heat application with some use of cold, and weight reduction and exercise. The ACR recommends that the use of TENS and traditional Chinese acupuncture be reserved for patients who are candidates for total joint reconstructive surgery but are either unwilling to undergo the surgery or have medical contraindications to these procedures. CAM therapies for symptom management have become an increasingly popular avenue of treatment, particularly movement therapies such as T'ai chi and yoga (Yan et al., 2013). Regarding nutritional supplements (e.g., glucosamine often in combination with chondroitin), more research is needed because study findings on glucosamine are inconsistent as to the effectiveness of pain management in OA. For persistent, moderate to severe OA and erosive RA, reconstructive surgery and corticosteroids are used often. Reconstructive surgery is indicated when pain cannot be relieved by conservative measures and the threat of loss of independence is eminent. Surgical procedures include synovectomy (excision of the synovial membrane), arthrodesis (surgical fusion of the joint), tenorrhaphy (suturing of a tendon), and osteotomy (to alter the distribution of weight within the joint). The procedure used most commonly is arthroplasty, a surgical repair and replacement of the joint. Surgery is not performed during disease flare ups.

Null lymphocytes,

a subpopulation of lymphocytes, destroy antigens already coated with antibody. These cells have special Fc receptor sites on their surface that allow them to connect with the Fc end of antibodies; this is known as antibody-dependent, cell-mediated cytotoxicity.

first-degree burn,

a superficial burn damages only the epidermis (outer layer of the skin). The area is red and dry, with slight swelling but no blister, and painful, like a sunburn. These burns heal in about 7 days with usually no scarring.

Dermatitis medicamentosa,

a type I hypersensitivity disorder, is the term applied to skin rashes associated with certain medications. Although people react differently to each medication, certain medications tend to induce eruptions of similar types. Rashes are among the most common adverse reactions to medications and occur in approximately 2% to 3% of hospitalized patients. Clinical Manifestations and Assessment In general, drug reactions appear suddenly, have a particularly vivid color, manifest with characteristics that are more intense than the somewhat similar eruptions of infectious origin, and, with the exception of bromide and the iodide rashes, disappear rapidly after the medication is withdrawn. Rashes may be accompanied by systemic or generalized symptoms, such as bronchospasm, urticaria, and significant angioedema. Medical and Nursing Management Upon discovery of a medication allergy, the causative agent must be discontinued immediately and treatment initiated for any symptoms the patient is experiencing. Once stable, the patient is warned that he or she has a hypersensitivity to a particular medication and is advised not to take it again. Patients should carry information identifying the hypersensitivity, and subsequent reaction experienced, with them at all times.

Contact dermatitis,

a type IV delayed hypersensitivity reaction, is an acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens. Types There are four basic types: allergic, irritant, phototoxic, and photoallergic (Table 38-3). Eighty percent of cases are caused by excessive exposure to or additive effects of irritants (e.g., soaps, detergents, plants, organic solvents). Skin sensitivity may develop after brief or prolonged periods of exposure, and the clinical picture may appear hours or weeks after the sensitized skin has been exposed. Clinical Manifestations and Assessment Symptoms include itching, burning, erythema, skin lesions (vesicles), and edema, followed by weeping, crusting, and, finally, drying and peeling of the skin. In severe responses, hemorrhagic bullae may develop. Repeated reactions may be accompanied by thickening of the skin and pigment changes. Secondary invasion by bacteria may develop in skin that is abraded by rubbing or scratching. Usually, there are no systemic symptoms unless the eruption is widespread.

Rheumatic disorders

affect the joints, bones, muscles, and connective tissues. These conditions can be minor illnesses, or they can be life-threatening. Systemic effects caused by rheumatic disorders or diseases result in obvious limitations in mobility and activities of daily living (ADL) as well as more subtle manifestations, such as pain, fatigue, insomnia, and disturbed body image. Organ failure and death may be an end result for some rheumatic disorders. The rheumatic condition may be the patient's primary health problem or a secondary diagnosis. OVERVIEW . The symptom that most commonly causes a person to seek medical attention is pain. Other common symptoms include joint swelling, limited movement, stiffness, weakness, and fatigue. The onset of these conditions may be acute or insidious, with a course possibly marked by periods of remission (a period when disease symptoms are reduced or absent) and exacerbation (a period when symptoms occur or increase). Antiarthritic drugs fall into three major groups: nonsteroidal anti-inflammatory drugs (NSAIDs) including salicylates (e.g., aspirin), disease-modifying antirheumatic drugs (DMARDs), and glucocorticoids (adrenal corticosteroids) Nonpharmacologic treatment measures include the use of heat or cold, weight reduction, joint rest and avoidance of joint overuse, orthotic devices (e.g., splints, braces) to support inflamed joints, and an exercise regimen. Occupational and physical therapy can help the patient adopt self-management strategies. Other nonpharmacologic modalities, such as massage, yoga, pulsed electromagnetic fields, transcutaneous electrical nerve stimulation (TENS), and music therapy, have been used in the treatment of arthritis Common choices of complementary and alternative medicine (CAM) used by patients with rheumatologic disorders include dietary supplements, herbal therapies, mind/body and spiritual practices, manual/manipulative therapies, biostimulation, vagus nerve stimulation, and topical ointments Goals and Strategies for Rheumatic Diseases Major Goals Management Strategy Suppress inflammation and the autoimmune response Optimize pharmacologic therapy (anti-inflammatory and disease-modifying agents) Control pain Protect joints; ease pain with splints/orthoses, thermal modalities, relaxation techniques Maintain or improve joint mobility Implement exercise programs for joint motion and muscle strengthening and overall health Maintain or improve functional status Make use of adaptive devices and techniques Increase patient's knowledge of disease process Provide and reinforce patient teaching Promote self-management by patient compliance with the therapeutic regimen Promote social support and encouragement of change-based interventions compatible with therapeutic regimen and lifestyle Rheumatic Disorders Each synovial joint has a given range of motion, and the synovial fluid within a joint has three primary functions: lubrication, nutrient distribution, and shock absorption. Inflammation is manifested in the joints as synovitis. Rheumatic disorders always involve damage to the articular cartilages. Because articular cartilages involve some degree of inflammation and degeneration, the rheumatic disorders can be classified as either inflammatory (e.g., RA) or degenerative, noninflammatory (e.g., OA). In the inflammatory rheumatic disorder classification, the primary process starts with inflammation due to an altered immune function. The inflammatory reaction includes swelling, pain, and loss of function (see Chapter 36 for the inflammatory and immunologic processes). Degeneration then occurs as a secondary process, spreading to the articular surfaces. The cause of degeneration of the articular cartilage is poorly understood but believed to be metabolically active and, therefore, is more accurately called degradation. On the other hand, in the degenerative (noninflammatory) rheumatic disorder classification, inflammation occurs as a secondary process. The resultant secondary synovitis is usually milder, is more likely to be seen in advanced disease, and represents a reactive process. The synovitis is thought to result mainly from degeneration due to mechanical irritation of two bone surfaces. As the articular cartilage becomes damaged, the matrix (noncellular component of tissue) begins to break down; the exposed cartilage changes from a slick, smooth gliding surface to a rough fibrous network of collagen fibers. Later this network may be converted to bone, locking the articulating elements into position. Fixation of a joint, called ankylosis, eliminates the friction but at the drastic cost of immobility.

Burns

are a dynamic injury set that result in a cascade of local tissue and systemic inflammatory effects depending on the percentage of TBSA involved. Local effects of burns include the denaturation of protein (which results in the disruption and potential destruction of cells), liberation of vasoactive substances, and the formation of edema. As a result of the cellular injury, the osmotic and hydrostatic pressure gradients are disrupted and intravascular fluid leaks into interstitial spaces. This damage is distributed throughout the injury as some cells die instantly, some are irreversibly damaged, and some—if appropriate interventions occur—will survive. There are three distinct zones that appear in a bull's eye pattern. The zone of coagulation (in the center) is where the tissue is completely destroyed; the zone of stasis surrounds the nonviable tissue and is potentially viable; the zone of hyperemia has increased blood flow secondary to the natural inflammatory response (Fig. 53-3). Burns that exceed 20% TBSA may produce a local and a systemic response and are considered major burn injuries. The incidence and significance of pathophysiologic changes are proportional to the extent of burn injury, with a maximal response seen in burns covering 60% or more TBSA (Sheridan, 2016). Additionally, burns of 60% TBSA cause depressed myocardial contractility; this, in combination with the loss of circulating plasma volume, hemoconcentration, and massive edema formation (Latenser, 2015), results in both distributive and hypovolemic shock (see Chapter 54). Fluid volume loss is greatest in the first 6 to 8 hours; capillary integrity returns toward normal by 36 to 48 hours after the burn (Demling, 2015). These patients are best served when transferred to a verified burn center as they are candidates for the occurrence of burn shock.

Langerhans cells

are accessory cells of the afferent immune system that play a role in cutaneous (skin) immune system reactions. These cells process invading antigens and transport the antigens to the lymph system to activate the T lymphocytes.

Helper T cells

are activated on recognition of antigens and stimulate the rest of the immune system. When activated, helper T cells secrete cytokines, which attract and activate B cells, cytotoxic T cells, NK cells, macrophages, and other cells of the immune system. Separate subpopulations of helper T cells produce different types of cytokines and determine whether the immune response will be the production of antibodies or a cell-mediated immune response. Helper T cells produce lymphokines, one category of cytokines. These lymphokines activate other T cells (e.g., interleukin-2 [IL-2]), natural and cytotoxic T cells (e.g., IFN-gamma), and other inflammatory cells (e.g., tumor necrosis factor). Helper T cells produce IL-4 and IL-5, lymphokines that activate B cells to grow and differentiate.

Systemic medications

are also prescribed for skin conditions. These include corticosteroids for short-term therapy for contact dermatitis or for long-term treatment of a chronic dermatosis, such as pemphigus vulgaris. Other frequently used systemic medications include antibiotics, antifungals, antihistamines, sedatives, tranquilizers, analgesics, and cytotoxic (destructive of cells) agents.

The sebaceous glands

are associated with hair follicles. The ducts of the sebaceous glands empty sebum onto the space between the hair follicle and the hair shaft. For each hair, there is a sebaceous gland, the secretions of which lubricates the hair and renders the skin soft and pliable.

Seborrheic and actinic keratoses

are benign, wartlike lesions of various sizes and colors, ranging from light tan to black, that are usually located on the face, shoulders, chest, and back. Treatment is removal of the tumor tissue by excision, electrodesiccation, and curettage, or application of carbon dioxide or liquid nitrogen. Aare premalignant skin lesions that develop in chronically sun-exposed areas of the body. They appear as rough, scaly patches with underlying erythema. A small percentage of these lesions gradually transforms into cutaneous squamous cell carcinoma. They are usually removed by cryotherapy or shave excision.

Secondary dressings

are capable of absorbing wound exudate while (1) maintaining a moist environment in the area of the wound and (2) allowing the surrounding skin to remain dry. They include hydrocolloids, alginates, and hydrogels. Secondary dressings are able to modify the physiology of the wound environment by modulating and stimulating cellular activity and by releasing growth factor (Bryant & Nix, 2016).

Immunodeficiencies

are classified as either primary or secondary and are further classified by the affected components of the immune system. Primary immunodeficiency diseases are genetic in origin and manifest most commonly in infancy and childhood as abnormally recurrent infections. About 80% of the patients with primary immunodeficiency are less than 20 years of age. Many primary immunodeficiencies may occur alone or as part of a syndrome

Hydrocolloids

are composed of a water-impermeable, polyurethane outer covering separated from the wound by a hydrocolloid material. They are adherent and nonpermeable to water vapor and oxygen. As water evaporates over the wound, it is absorbed into the dressing, which softens and discolors with the increased water content. The dressing can be removed without damage to the wound. As the dressing absorbs water, it produces a foul-smelling, yellowish covering over the wound. This is a normal chemical interaction between the dressing and wound exudate and should not be confused with purulent drainage from the wound. Most can be left in place for as long as 7 days.

Sweat glands

are found in the skin over most of the body surface, but they are heavily concentrated in the palms of the hands and soles of the feet. Only the glans penis, the margins of the lips, the external ear, and the nail bed are devoid of sweat glands. Sweat glands are subclassified into two categories: eccrine and apocrine.

Antibodies

are large proteins called immunoglobulins (because they are found in the globulin fraction of the plasma proteins). All immunoglobulins are glycoproteins and contain a certain amount of carbohydrate. Each antibody molecule consists of two subunits, each of which contains a light and a heavy peptide chain. Each subunit has a portion, referred to as the Fab fragment, that serves as a binding site for a specific antigen. The Fab fragment (antibody-binding site) binds to the antigenic determinant, similar to a lock-and-key mechanism. The Fab fragment provides the "lock" portion that is highly specific for an antigen. An additional portion, known as the Fc fragment, which contains the c-terminal and does not contain antigen-binding sites, allows the antibody molecule to take part in the complement system (Frank & Hester, 2014; Paul, 2012). Antibodies defend against foreign pathogens in several ways, and the type of defense employed depends on the structure and composition of both the antigen and the immunoglobulin. The antibody molecule has at least two combining sites, or Fab fragments. One antibody can act as a cross-link between two antigens, causing them to bind or clump together. This clumping effect, referred to as agglutination, helps clear the body of the pathogen by facilitating phagocytosis. Agglutination is used in several laboratory tests, such as those for syphilis, to recognize and enumerate the presence of antibody-antigen complexes, indicative of infection. Some antibodies assist in removal of offending organisms through opsonization. In this process, the antigen-antibody molecule is coated with a sticky substance that also facilitates phagocytosis. Antibodies also promote the release of vasoactive substances, such as histamine and slow-reacting substance, two of the chemical mediators of the inflammatory response. Antibodies do not function in isolation; rather, they mobilize other components of the immune system to defend against the pathogen. The typical role of antibodies is to focus components of the natural immune system on the pathogen. This includes activation of both the complement system and phagocytosis (Paul, 2012; Salmon, 2016).

Venous ulcers

are more common than arterial ulcers. They occur due to impaired return of venous blood from the tissue to the heart, also known as chronic venous insufficiency (CVI) or lower extremity venous disease (LEVD). Risk factors are valvular dysfunction caused by obesity, multiple pregnancies, thrombophlebitis, leg trauma (deep vein thrombosis or fractures), and thrombophilic conditions (increased coagulability of the blood). Other risks factors include arthritis or calf muscle dysfunction, IV drug use involving the affected extremity, sedentary lifestyle, or prolonged standing. Healing can be affected by diabetes, smoking, nutrition, and medications (Carmel & Bryant, 2016). Management includes reduction of edema, prevention of complications, and appropriate topical therapy or specialty dressings (Carmel & Bryant, 2016).

Foam dressings

are nonadherent and require a secondary dressing to keep them in place. Moisture is absorbed into the foam layer, decreasing maceration of surrounding tissue. A moist environment is maintained, and removal of the dressing does not damage the wound. Foams are a good choice for exudative wounds. They are especially helpful over bony prominences because they provide contoured cushioning

Stem cells

are potentially immortal cells that are capable of self-renewal and differentiation; they continually replenish the body's entire supply of both RBCs and WBCs. Some stem cells, described as totipotent cells, have tremendous capacity to self-renew and differentiate. Embryonic stem cells, described as pluripotent, give rise to numerous cell types that are able to form tissues (Grossman et al., 2014). Research and clinical trials have shown that stem cells can restore an immune system that has been destroyed. Stem cell transplantation therapy has been developed for numerous types of conditions, such as severe combined immunodeficiency (SCID), acute myeloid leukemia, periodontal disease, and other types of cancer (Klein & Nör, 2015). Clinical trials using stem cells as therapy are underway in patients with a variety of disorders having an autoimmune component, including systemic lupus erythematosus (SLE), rheumatoid arthritis, scleroderma, multiple sclerosis, and heart disease, specifically in the repair of endothelial cells

Merkel cells

are receptors that transmit stimuli to the axon through a chemical synapse and therefore are associated with the sense of touch.

Gels

are semisolid emulsions that become liquid when applied to the skin or scalp. The water-based gels appear to penetrate the skin more effectively, are greaseless and odorless, and cause less stinging on application. They are especially useful for acute dermatitis in which there is weeping exudate (e.g., poison ivy).

Autografts

are the ideal covering for burn wounds because the grafts are the patient's own skin and, therefore, are not rejected by the patient's immune system. The purposes of wound coverage are to decrease the risk of infection; prevent further loss of protein, fluid, and electrolytes through the wound; and minimize heat loss through evaporation. Once the wound is surgically excised, a wound covering is applied to keep the area moist and promote the granulation process. Care of the Graft Site. Occlusive dressings are commonly used initially after grafting to immobilize the graft. Synthetic dressings may be used to protect grafts. The patient is positioned and turned carefully to avoid disturbing the graft or putting pressure on the graft site. If an extremity has been grafted, it is elevated to minimize edema. Care of the Donor Site. A moist gauze dressing is applied at the time of surgery to maintain pressure and to stop any oozing. With all types of covering, donor sites must remain clean, dry, and free from pressure. Because a donor site is usually a partial-thickness wound, it will heal spontaneously within 7 to 14 days with proper care. Donor sites are painful, and additional pain management must be a part of the patient's care.

Melanocytes

are the special cells of the epidermis that are primarily involved in producing the pigment melanin, which colors the skin and hair. Most of the skin of dark-skinned people and the darker areas of the skin on light-skinned people (e.g., the areola) contain larger amounts of this pigment Production of melanin is controlled by a hormone secreted from the hypothalamus of the brain called melanocyte-stimulating hormone. Melanin provides a natural protection against the harmful effects of ultraviolet light; however, it does not provide complete protection from the sun's damaging rays.

Transparent films

are thin, transparent, polyurethane, impermeable adhesive films that are used for partial thickness, minimally draining, or closed wounds. They permit visualization of the wound, promote autolysis, reduce friction, and are sometimes used as a secondary dressing. Examples are Op-Site and Tegaderm.

Antimicrobial dressings

are used for partial and full-thickness wounds. They help to control or decrease the bioburden and odor for minimal and heavy exudating wounds. They are a topical antifungal and antibiotic agent that come in ointments, gels, impregnated gauze, hydrofiber, and pads. Examples are Acticoat 7 and Aquacel Ag (hydrofiber).

Corticosteroids

are widely used in treating dermatologic conditions to provide anti-inflammatory, antipruritic, and vasoconstrictive effects. The patient is taught to apply the product sparingly and rub it into the prescribed area thoroughly. Absorption of topical corticosteroid is enhanced when the skin is hydrated or when the affected area is covered by an occlusive or moisture-retentive dressing. Inappropriate use of topical corticosteroids can result in local and systemic side effects, especially when the medication is absorbed through inflamed and excoriated skin or is used for long periods on sensitive areas. Local side effects may include skin atrophy and thinning, striae (bandlike streaks), and telangiectasia (small dilated blood vessels on the surface of the skin). Thinning of the skin results from the ability of corticosteroids to inhibit the synthesis of skin collagen. The thinning process can be reversed by discontinuing the medication, but striae and telangiectasia are permanent. Systemic side effects may include hyperglycemia and symptoms of Cushing syndrome (refer to Chapter 31). Caution is required when applying corticosteroids around the eyes for two reasons: (1) long-term use may cause glaucoma or cataracts, and (2) the anti-inflammatory effect of corticosteroids may mask existing viral or fungal infections. Concentrated (fluorinated) corticosteroids are never applied on the face or intertriginous areas (i.e., axilla and groin) because these areas have a thinner stratum corneum and absorb the medication much more quickly than do other areas of the body, such as the forearm or legs.

n antigen

can be a small patch of proteins on the outer surface of a microorganism. Some antigens are naturally immunogenic or able to stimulate an immune response directly. Most antigens must be coupled with other molecules to stimulate the immune response. A single bacterium or large molecule, such as a diphtheria or tetanus toxin, may have several antigens, or markers, on its surface, thus inducing the body to produce a number of different antibodies. Once produced, an antibody is released into the bloodstream and carried to the attacking organism. There, it combines with the antigen, binding with it like an interlocking piece of a jigsaw puzzle (Fig. 36-4). There are four well-defined stages in an immune response: recognition, proliferation, response, and effector.

Primary immunodeficiencies,

classified by the main component of the immune system that is dysregulated, include B lymphocytes (or IgG), T lymphocytes, natural killer (NK) cells, phagocytic cells, or complement proteins. More than 50% of primary immunodeficiency is caused by errors in B lymphocytes, causing decreases in production of immunoglobulin and antibodies. The most common B-cell disorder is selective IgA deficiency (Stiehm, 2014).

The epidermis

consists of continuously dividing cells covered on the surface by dead cells that were originally deeper in the dermis but were pushed upward by the newly developing, more differentiated cells underneath. This external layer is almost completely replaced every 3 to 4 weeks. The dead cells contain large amounts of keratin, an insoluble, fibrous protein that forms the outer barrier of the skin and has the capacity to repel pathogens and prevent excessive fluid loss from the body. Keratin is the principal hardening ingredient of the hair and nails.

Occlusive dressings

cover a topical medication that is applied to a skin lesion. The area is kept airtight by using plastic film (e.g., plastic wrap). Plastic film is thin and readily adapts to all sizes, body shapes, and skin surfaces. In general, plastic wrap should be used no more than 12 hours each day.

Cryosurgery

destroys the tumor by deep-freezing the tissue. A thermocouple needle apparatus is inserted into the skin, and liquid nitrogen is directed to the center of the tumor until the tumor base is -40°C to -60°C. Liquid nitrogen has the lowest boiling point of all cryogens, is inexpensive, and is easy to obtain. The tumor tissue is frozen, allowed to thaw, and then refrozen. The site thaws naturally and then becomes gelatinous and heals spontaneously. Swelling and edema follow the freezing. The appearance of the lesion varies. Normal healing, which may take 4 to 6 weeks, occurs faster in areas with a good blood supply.

Acquired or specific immunity

develops after birth. Although each type of immunity plays a distinct role in defending the body against harmful pathogens, the various components usually act in an interdependent manner. —immunologic responses acquired during life but not present at birth—usually develops as a result of exposure to an antigen through immunization (vaccination) or by contracting a disease, both of which generate a protective immune response. Weeks or months after initial exposure to the disease or vaccine, the body produces an immune response that is sufficient to defend against the disease on re-exposure. In contrast to the rapid but nonspecific innate immune response, this form of immunity relies on the recognition of specific foreign antigens. The two components of the immune response are strongly interrelated. Events occurring early in infection dictate the direction of the adaptive response and activate the acquired immune effector mechanisms, which have direct feedback on the cells of the innate (natural) system. The acquired immune response is broadly divided into two mechanisms: the cell-mediated response, involving T-cell activation, and effector mechanisms, involving B-cell maturation and the production of antibodies. With the combination of innate and acquired immune responses, the body is capable of protecting itself immediately as well as against future challenges to its integrity.The two types of acquired immunity are known as active and passive. In active acquired immunity, the immunologic defenses are developed by the person's own body. This immunity typically lasts many years or even a lifetime. This response is best demonstrated by the response of the body to immunizations. Exposure to attenuated virus, such as the influenza vaccine, prompts the production of antibodies against influenza. Re-exposure to influenza initiates a cascade of immune responses that are more rapid and capable of controlling the virus. Patients either eliminate the virus from their system or have a milder case of influenza. Passive acquired immunity is temporary immunity transmitted from a source outside the body that has developed immunity through previous disease or immunization. For example, immune globulin or antiserum, obtained from the plasma of people with acquired immunity, is used in emergencies to provide temporary immunity to certain diseases, such as hepatitis, immediately after exposure. Immunity resulting from the transfer of antibodies from the mother to an infant in utero or through breastfeeding is another example of passive immunity. Active and passive acquired immunity involve immunologic responses that are both humoral (antibodies produced by B cells) and cellular (cell-mediated T lymphocytes that attack pathogens).When the body is invaded or attacked by bacteria, viruses, or other pathogens, it has three means of defense: The phagocytic immune response The humoral or antibody immune response The cellular immune response

Postexposure prophylaxis

in response to the exposure of health care personnel to blood or other body fluids reduces the risk for HIV infection. According to the CDC, there have been only 58 confirmed cases of HIV transmission through occupational exposure (CDC, 2014). The CDC recommends that all health care providers who have sustained a significant exposure to HIV be counseled and offered anti-HIV postexposure prophylaxis, if appropriate (Box 37-4). More clinicians are using postexposure prophylaxis for patients exposed to HIV because of high-risk sexual behavior or possible contact through IV/injection drug use. This use of postexposure prophylaxis is controversial because of concern that it may be substituted for safer sex practices and safer IV/injection drug use. Postexposure prophylaxis should not be considered an acceptable method of preventing HIV infection but used for reducing risk after a possible transmission. The medications recommended for postexposure prophylaxis are those used to treat established HIV infection. Ideally, prophylaxis needs to start immediately after exposure; therapy started more than 72 hours after exposure is thought to offer no benefit due to rapid increases in viral load upon initial infection. Postexposure Prophylaxis for Health Care Providers If you sustain a puncture injury, such as a needle stick, take the following actions immediately: Wash the area thoroughly with soap and water. Alert your supervisor/nursing faculty and initiate the injury- reporting system used in the setting. Identify the source patient who may need to be tested for HIV, hepatitis B, and hepatitis C. State laws will determine whether written informed consent must be obtained from the source patient before his or her testing. Rapid testing should be used, if possible, if the HIV status of the source patient is unknown because results can be available within 20 minutes. Report as quickly as possible to employee health services, the emergency department, or other designated treatment facility. This visit should be documented in the health care worker's confidential medical record. Give consent for baseline testing for HIV, hepatitis B, and hepatitis C. Confidential HIV testing can be performed up to 72 hours after the exposure but should be performed as soon as the health care worker can give informed consent for baseline testing. Get postexposure prophylaxis for HIV in accordance with CDC guidelines. Start the prophylaxis medications within 2 hours after exposure. Postexposure prophylaxis must be initiated within 72 hours of exposure to be effective. Make sure that you are being monitored for symptoms of toxicity. Practice safer sex until follow-up testing is complete. Continue the HIV medications for 4 weeks. Follow up with postexposure testing at 1 month, 3 months, and 6 months. Document the exposure in detail for your own records, as well as for the employer.

Pressure ulcers

involve the breakdown of the skin due to prolonged pressure, friction, and shear forces, and insufficient blood supply, usually at bony prominences. Pressure ulcers are localized areas of infarcted soft tissue that occur when pressure applied to the skin over time is greater than normal capillary closure pressure, which is about 32 mm Hg. Weight-bearing bony prominences are most susceptible to pressure ulcer development because they are covered only by skin and small amounts of subcutaneous tissue. Susceptible areas include the sacrum and coccygeal areas, ischial tuberosities (especially in people who sit for prolonged periods), greater trochanter, heel, knee, malleolus, medial condyle of the tibia, fibular head, scapula, and elbow (Fig. 52-1). Clinical Manifestations and Assessment The initial sign of pressure is erythema (redness of the skin) caused by reactive hyperemia, which normally resolves in less than 1 hour. Unrelieved pressure results in tissue ischemia or anoxia. The cutaneous tissues become broken or destroyed, leading to progressive destruction and necrosis of underlying soft tissue, and the resulting pressure ulcer is painful and slow to heal. The nurse assesses the patient's mobility, sensory perception, cognitive abilities, tissue perfusion, nutritional status, friction and shear forces, sources of moisture on the skin, age, and skin condition Risk Factors for Pressure Ulcers Immobility, compromised mobility Prolonged pressure on tissue Altered skin moisture: excessively dry, excessively moist (perspiration, urine, feces, or drainage produces maceration [softening] of the skin) Equipment: Casts, traction, restraints Impaired sensory perception or cognition Decreased tissue perfusion (seen with diabetes, obesity, and edema). Patients who are critically ill have a lower capillary closure pressure and, thus, higher risk. Decreased nutritional status (anemia, hypoalbuminemia, vitamin deficiency) Friction and shear forces

cellular immune response,

involves the T lymphocytes, which can turn into special cytotoxic (or killer) T cells that can attack the pathogens. Table 36-2 summarizes the types of cells involved in immune response.

phagocytic immune response,

involves the WBCs (granulocytes and macrophages), which have the ability to ingest foreign particles. These cells move to the point of attack, where they engulf and destroy the invading agents. Phagocytes also remove the body's own dying or dead cells. Dying cells in necrotic tissue release substances that trigger an inflammatory response.

Angioneurotic edema

involves the deeper layers of the skin, resulting in more diffuse swelling, rather than the discrete lesions characteristic of hives. On occasion, this reaction covers the entire back. The skin over the reaction may appear normal but often has a reddish hue. The skin does not pit on pressure, as ordinary edema does. The regions most often involved are the lips, eyelids, cheeks, hands, feet, genitalia, and tongue; the mucous membranes of the larynx, the bronchi, and the GI canal also may be affected, particularly in the hereditary type (see discussion in the following section). Swellings may appear suddenly, in a few seconds or minutes, or slowly, in 1 or 2 hours. In the latter case, often their appearance is preceded by itching or burning sensations. Seldom does more than a single swelling appear at one time, although one may develop while another is disappearing. Infrequently, swelling recurs in the same region. Individual lesions usually last 24 to 36 hours. On rare occasions, swelling may recur with remarkable regularity at intervals of 3 to 4 weeks.

HIV

is a bloodborne, sexually transmissible virus. HIV-1 is transmitted in body fluids containing HIV or infected CD4+ T lymphocytes. These fluids include blood, seminal fluid, vaginal secretions, amniotic fluid, and breast milk. Mother-to-child transmission of HIV-1 may occur in utero or through breastfeeding, but most perinatal infections are thought to occur after exposure during delivery (CDC, 2016a). Inflammation and breaks in the skin or mucosa result in the increased probability of exposure to HIV. HIV is not transmitted through casual contact. Because HIV is harbored within lymphocytes, a type of white blood cell (WBC), any exposure to infected blood results in a significant risk of infection. The amount of virus and infected cells in the body fluid, as well as other host factors, is associated with the risk of new infection after exposure to that fluid .Pathophysiology . HIV belongs to a group of viruses known as retroviruses. These viruses carry their genetic material in the form of ribonucleic acid (RNA) rather than deoxyribonucleic acid (DNA). As shown in Figure 37-1, HIV consists of a viral core containing the viral RNA, surrounded by an envelope consisting of protruding glycoproteins (gp). For HIV to enter the targeted cell, the membrane of the viral envelope must be fused with the plasma membrane of the cell, a process mediated by the envelope glycoproteins of HIV and other coreceptors (National Institutes of Health [NIH], 2016). All viruses target specific cells. Lymphocytes (type of WBC) consist of three major populations: T cells, B cells, and NK cells. Mature T cells are phenotypically (characteristics of the cells) composed of two major subpopulations, defined by cell surface reciprocal expression of CD4 or CD8. Approximately two thirds of peripheral blood T cells are CD4+, and approximately one third is CD8+. Most people have about 700 to 1,500 CD4+ cells/mm3, but a count as low as 500 cells/mm3 can be considered "normal." HIV targets cells with the CD4 glycoprotein expressed on the surface of T lymphocytes, monocytes, dendritic cells, and brain microglia. Monocytes and macrophages serve as long-lived reservoirs of HIV. Most primary clinical isolates of HIV use the chemokine coreceptor CCR5 for cell entry. HIV-1 isolates that appear later in the course of infection often use other chemokine receptors, such as CXCR4, in addition to CCR5 (National Institute of Allergy and Infectious Disease [NIAID], 2016). HIV must attach to both the CD4 and the CCR5 coreceptor binding sites in order to infect CD4+ cells. A mutation of CCR5 that is common among Caucasians but not other ethnic groups has been identified. About 1% of Caucasians lack functional CCR5 and are highly protected against HIV infection even if exposed (although protection is not absolute); about 18% are not markedly protected against infection but, if infected, demonstrate significantly slower rates of disease progression The HIV life cycle is complex (see Fig. 37-1) and consists of the following: The HIV gp120 and gp41 attach to the uninfected CD4+ lymphocyte at the CD4 receptor and one of two coreceptors, fusing with the cell membrane. The viral core contents are emptied into the host cell, a process known as uncoating. HIV enzyme reverse transcriptase converts the viral genetic material from RNA into double-stranded DNA. Double-stranded DNA is spliced into the cellular DNA by the action of integrase, another HIV enzyme. During transcription, the integrated DNA or provirus makes new viral proteins and viral RNA. Provirus may remain inactive for months to years within the CD4+ cell and other components of the immune system. HIV protease cleaves the new proteins (polyproteins). The new proteins join the viral RNA into new viral particles. New viral particles bud from the cell and start the process all over. In resting (nondividing) cells, HIV can apparently survive in a latent state as an integrated provirus that produces few or no viral particles. These resting CD4+ T cells as well as monocytes and macrophages can be stimulated to produce new particles if something reactivates them. Activation of the infected cell may be achieved by antigens, mitogens, certain cytokines (tumor necrosis factor-α [TNF] or interleukin-1 [IL-1]), or virus gene products of such viruses as cytomegalovirus (CMV), Epstein-Barr virus, herpes simplex virus, and hepatitis viruses. Consequently, whenever the infected T cell is activated, HIV replication and budding occur, which often destroys the host cell. Then newly formed HIV is released into the blood plasma and infects other CD4+ cells (see Fig. 37-1). If inadequately suppressed, HIV mutates at a relatively constant rate, enabling it to blunt or completely suppress the effects of HIV medications.

A malignant melanoma

is a cancerous neoplasm in which atypical melanocytes are present in the epidermis and the dermis (and sometimes the subcutaneous cells). It is the most lethal of all the skin cancers and is responsible for about 3% of all cancer deaths (Castiglione et al., 2016). Malignant melanoma can occur in one of several forms: superficial spreading melanoma, lentigo-maligna melanoma, nodular melanoma, and acral-lentiginous melanoma. These types have specific clinical and histologic features as well as different biologic behaviors. Most melanomas arise from cutaneous epidermal melanocytes, but some appear in preexisting nevi (i.e., moles) in the skin or develop in the uveal tract of the eye. Melanomas occasionally appear simultaneously with cancer of other organs. Risk Factors The cause of malignant melanoma is unknown, but ultraviolet rays are strongly suspected based on indirect evidence, such as the increased incidence of melanoma in countries near the equator and in people younger than 30 years of age who have used a tanning bed more than 10 times per year. Ethnicity is a risk factor; in general, 1 in 100 Caucasians acquires melanoma each year. As many as 10% of patients with melanoma are members of a family that is more melanoma-prone. They have multiple changing moles (dysplastic nevi), which are susceptible to malignant transformation. Patients with dysplastic nevus syndrome have been found to have unusual moles, larger and more numerous moles, lesions with irregular outlines, and pigmentation located all over the skin.

Systemic Lupus Erythematosus SLE

is a chronic inflammatory multisystem autoimmune disease with variable presentations, courses, and prognoses characterized by remissions and exacerbations. Pathophysiology SLE is a result of disturbed immune regulation that causes an exaggerated production of autoantibodies and antigens. The immune abnormalities that characterize SLE occur in five phases: susceptibility (genes and environmental factors), abnormal innate and adaptive immune responses, autoantibodies immune complexes, inflammation, and damage. Interactions of predisposing factors (genes, female gender, and environment) result in abnormal immune responses, specifically in B cells and T cells. These responses produce pathogenic autoantibodies and immune complexes that activate complement, form in tissue, and cause inflammation. Inflammation stimulates antigens, which, in turn, stimulate additional antibodies. The cycle repeats and, over time, leads to irreversible organ damage. Some individuals do not progress through all phases (Crow, 2013). Clinical Manifestations and Assessment . The most common presenting manifestations are constitutional symptoms (fever, fatigue, and/or weight loss), cutaneous manifestations, and articular manifestations (arthritis and/or arthralgia). Each of these manifestations appears to be present in at least 50% of patients with lupus at the time of diagnosis (Dall'Era & Wofsy, 2013). SLE is an autoimmune systemic disease that can affect any body system. Clinical manifestations can resemble RA and may be mistaken for it, especially early in the course of the disease. Unlike RA, the arthritis is nonerosive and not seen on x-ray. Several different types of skin manifestations are prevalent in 80% to 90% of patients with SLE. Photosensitivity rashes are most common; however, the most characteristic skin manifestation is an acute cutaneous lesion consisting of a butterfly-shaped rash across the bridge of the nose and cheeks (Dall'Era & Wofsy, 2013; Dvorkina & Ginzler, 2015) (Fig. 39-7). This malar rash manifests as an erythematous, flat or raised lesion, pruritic (itchy) or painful, and can be transient and heal without scarring. In some cases of discoid lupus erythematosus (DLE), only skin involvement occurs. Discoid (coinlike) lesions are scarring and ring-shaped that may result in erythematous, scaling plaques, and alopecia (hair loss). In some patients with SLE, the initial skin involvement is the precursor to more systemic involvement. The lesions often worsen during exacerbations (flares) of the systemic disease and possibly are provoked by sunlight or artificial ultraviolet B light. The varied and frequent neuropsychiatric presentations of SLE are now widely recognized. In general, these are demonstrated by subtle changes in behavior patterns or cognitive ability. Headaches, psychiatric disorders (mood disorder, depression, and psychosis), cognitive dysfunction, and seizures are common (Dvorkina & Ginzler, 2015; Hahn, 2015). Pericarditis and pleuritis are the most common cardiopulmonary disorders (refer to Chapters 10 and 16). Women who have SLE are also at risk for early atherosclerosis. About 50% of patients with SLE have kidney disease, such as glomerulonephritis. Serum creatinine levels and urinalysis are used in screening for kidney involvement. Early detection allows for prompt treatment so that kidney damage can be prevented. Kidney involvement may lead to hypertension, which also requires careful monitoring and management. The presence of at least four of the criteria established by the ACR is required to make the diagnosis of SLE. Cutaneous manifestations comprise 4 of the 11 diagnostic ACR criteria (malar rash, discoid rash, photosensitivity, and oral ulcers). When performing an assessment, it is critical to inspect skin for erythematous rashes. No single laboratory test confirms SLE. Laboratory features include both hematologic abnormalities (e.g., hemolytic anemia, leukopenia, thrombocytopenia) and immunologic findings indicative of autoimmunity. Most patients with SLE (more than 98%) demonstrate elevated serum levels of ANA, which is another ACR criterion for SLE diagnosis. A small percent of patients will test negative for ANA but will have antibodies to the nuclear antigen anti-Ro (SSA) (Hahn, 2015). Other diagnostic immunologic tests that support SLE diagnosis in the presence of clinical manifestations are CRP, anti-double-stranded DNA (anti-ds DNA), anti-RNA, anti-La (SSB), anti-Sm (Smith) or antiphospholipid antibodies, and high-titer IgG antibodies. The double-stranded DNA test, C3, and C4 indicate whether there is a genetic component that is common in patients with SLE (Dall'Era & Wofsy, 2013). Medical and Nursing Management The mainstay of SLE treatment is based on pain management and nonspecific immunosuppression. Therapy includes NSAIDs, DMARDs (including antimalarials) alone or in combination with glucocorticoids, and, in severe SLE cases, immunosuppressive agents (azathioprine, mycophenolate mofetil, methotrexate). Hydroxychloroquine has a central role for long-term treatment. In 2011, the biologic, belimumab (Benlysta) for treatment of mild to moderate SLE became the first FDA-approved drug (ACR, 2015d; Lim & Drenkard, 2015). Corticosteroids are the single most important medication available for SLE. These drugs are used topically for cutaneous manifestations in low oral doses for minor disease activity and in high doses for major disease activity. IV administration of corticosteroids is an alternative to traditional high-dose oral use Treatment of moderate to severe SLE consists of a period of intensive immunosuppressive therapy (induction therapy) followed by a longer period of less intensive maintenance therapy. The main objective of the induction therapy is to stop injury, recover function, and induce remission by managing immunologic activity. The combination of high-dose glucocorticoids with pulses of intravenous cyclophosphamide (CYC), a cyctoxic agent, remains the standard of care for severe SLE with major organ involvement. B-cell-depleting therapies, such as the monoclonal antibodies rituximab (Rituxan) and epratuzumab (humanized anti-CD22 antibody), are the newest form of treatment for SLE and are reserved for patients who have serious forms of SLE that have not responded to conservative therapies.

Herpes simplex

is a common skin infection. There are two types of the causative virus, which are identified by viral typing. In general, herpes simplex type 1 occurs on the mouth and type 2 occurs in the genital area, but both viral types can be found in both locations. About 85% of adults worldwide are seropositive for herpes type 1. The prevalence of type 2 is lower; type 2 usually appears at the onset of sexual activity. Herpes simplex type 2 is discussed in detail in Chapter 35. Serologic testing shows that many more people are infected than have a history of clinical disease. Herpes simplex infection is classified as a true primary infection, a nonprimary initial episode, or a recurrent episode. True primary infection is the initial exposure to the virus. A nonprimary initial episode is the initial episode of either type 1 or type 2 in a person previously infected with the other type. Recurrent episodes are subsequent episodes of the same viral type.

The thymus

is a double-lobed organ found in the upper mediastinum. The spleen is located in the left upper quadrant of the abdomen. It is composed of red pulp (where old and injured red blood cells [RBCs] are destroyed) and white pulp (which contains concentrations of lymphocytes), and it acts like a filter. Lymph nodes are distributed throughout the body and connected by lymph channels and capillaries. The lymph nodes remove foreign material from the lymph system before it enters the bloodstream. The lymph nodes are centers for the proliferation of immune cells.

Pemphigus

is a group of serious diseases of the skin characterized by the appearance of bullae (blisters) of various sizes on apparently normal skin (Fig. 52-5) and mucous membranes. Pathophysiology Pemphigus is an autoimmune disease involving immunoglobulin G. It is thought that the pemphigus antibody is directed against a specific cell-surface antigen in epidermal cells. A blister forms from the antigen-antibody reaction. The level of serum antibody is predictive of disease severity. Risk Factors Genetic factors may also have a role in its development, with the highest incidence among those of Jewish or Mediterranean descent. This disorder usually occurs in men and women in middle and late adulthood. The condition may be associated with the use of penicillins and captopril and with the disorder myasthenia gravis. p. 1478 p. 1479 Clinical Manifestations and Assessment Most patients present with oral lesions appearing as irregularly shaped erosions that are painful, bleed easily, and heal slowly. The skin bullae enlarge, rupture, and leave large, painful, eroded areas that are accompanied by crusting and oozing. A characteristic offensive odor emanates from the bullae and the exuding serum. There is blistering or sloughing of uninvolved skin when minimal pressure is applied (Nikolsky sign). The eroded skin heals slowly, and large areas of the body eventually are involved. Bacterial superinfection is common. Complications The most common complications arise when the disease process is widespread. Before the advent of corticosteroid and immunosuppressive therapy, patients were very susceptible to secondary bacterial infection. Skin bacteria have relatively easy access to the bullae as they ooze, rupture, and leave denuded (loss of epidermis) areas exposed to the environment. Fluid and electrolyte imbalance results from fluid and protein loss as the bullae rupture. Hypoalbuminemia is common when the disease process includes extensive areas of the body's skin surface and mucous membranes. Medical and Nursing Management The goals of therapy are to bring the disease under control as rapidly as possible, to prevent loss of serum and the development of secondary infection, and to promote re-epithelization (i.e., renewal of epithelial tissue). Corticosteroids are administered in high doses to control the disease and keep the skin free of blisters. The high dosage level is maintained until remission is apparent. In some cases, corticosteroid therapy must be maintained for life. High-dose corticosteroid therapy has serious toxic effects. Immunosuppressive agents (e.g., azathioprine, cyclophosphamide, gold) may be prescribed to help control the disease and reduce the corticosteroid dose. Plasmapheresis temporarily decreases the serum antibody level and has been used with variable success, although it is generally reserved for life-threatening cases.

Kaposi sarcoma (KS)

is a malignancy of endothelial cells that line the small blood vessels. KS is manifested clinically by lesions of the skin, oral cavity, GI tract, and lungs. The skin lesions consist of reddish-purple to dark-blue macules, plaques, or nodules. KS is subdivided into three categories: Classic KS occurs predominantly in men of Mediterranean or Jewish ancestry between 40 and 70 years of age. Most patients have nodules or plaques on the lower extremities that rarely metastasize beyond this area. Classic KS is chronic, relatively benign, and rarely fatal. Endemic (African) KS affects people predominantly in the eastern half of Africa near the equator. Men are affected more often than women, and children can be affected as well. The disease may resemble classic KS, or it may infiltrate and progress to lymphadenopathic forms. Immunosuppression-associated KS occurs in transplant recipients and people with AIDS. This form of KS is characterized by local skin lesions and disseminated visceral and mucocutaneous diseases. The greater the degree of immunosuppression, the higher the incidence of KS. Immunosuppression-related KS that results from AIDS is an aggressive tumor that involves multiple body organs. Its presentation resembles that of KS associated with immunosuppressive therapy. Most patients are between 20 and 40 years of age. Refer to Chapter 37 for more information about KS and AIDS.

An allergic reaction

is a manifestation of tissue injury resulting from interaction between an antigen and an antibody. Allergy is an inappropriate and often harmful response of the immune system to substances that are normally harmless. In this case, the inappropriate substance is termed an allergen.Mast cells located in tissues throughout the body can be activated by a variety of stimuli, causing immediate allergic inflammation. The binding of the antigen and antibodies on the mast cells causes the release of mediators that effect blood vessel, smooth muscle, and glandular secretions. The powerful chemical mediators released from the mast cells cause a sequence of physiologic events, resulting in symptoms of immediate hypersensitivity. There are two types of chemical mediators: primary and secondary. Primary mediators are preformed and are found in mast cells or basophils. Secondary mediators are inactive precursors that are formed or released in response to primary mediators (e.g., leukotrienes, bradykinin, and serotonin).When in contact with an allergen, the body produces large amounts of IgE, thus causing a hypersensitivity or allergic response (see figure on next page). IgE-producing cells are located in the respiratory and intestinal mucosa. Two or more IgE molecules bind together to an allergen and trigger mast cells or basophils to release chemical mediators, such as histamine and leukotrienes. Maximal intensity of histamine release is reached within about 15 minutes after antigen contact. Effects of histamine release include erythema; localized edema in the form of wheals; pruritus; contraction of bronchial smooth muscle, resulting in wheezing and bronchospasm; dilation of small venules and constriction of larger vessels; and increased secretion of gastric and mucosal cells, resulting in diarrhea. Histamine action results from stimulation of histamine-1 (H1) and histamine-2 (H2) receptors found on different types of lymphocytes, particularly T-lymphocyte suppressor cells and basophils. H1 receptors are found predominantly on bronchiolar and vascular smooth muscle cells; H2 receptors are found on gastric parietal cells.

Natural immunity

is a nonspecific immunity present at birth that provides protection against an infectious agent without ever having encountered it before. provides a nonspecific response to any foreign pathogen, regardless of the pathogen's composition. Because of its lack of specificity, natural immunity maintains a broad spectrum of defense against and resistance to infection. The basis of this defense mechanism is the ability to distinguish between "self" and "nonself." Recent research in transplantation medicine demonstrates that this is a very simplistic differentiation. Natural killer (NK) cells also recognize "missing self" or cells that have been transformed or infected by pathogens and no longer present the usual cell membrane markers (Abbas, Lictman, & Pillai, 2016; Paul, 2012). Natural (innate) immunity coordinates the initial response to pathogens through the production of cytokines, which are hormone-like molecules released by cells; they have a profound impact on the growth, development, and activation of immune system cells and the inflammatory response. Natural immunity also responds to pathogens via other effector molecules, which either activate cells for control of the pathogen (by elimination) or promote the development of the acquired immune response. The cells involved in this response include macrophages, dendritic cells, and NK cells. These cells directly recognize and respond to a wide variety of pathogens long before the development of antigen-specific acquired immunity. The early events in this immune response are critical in determining the nature of the adaptive immune response. Innate immune mechanisms can be divided into two stages: immediate (generally occurring within 4 hours) and delayed (occurring between 4 and 96 hours after exposure).

Autolytic débridement

is a process that uses the body's own digestive enzymes to break down necrotic tissue. The wound is kept moist with occlusive dressings. Eschar and necrotic debris are softened, liquefied, and separated from the bed of the wound.

Radioallergosorbent testing (RAST)

is a radioimmunoassay that measures allergen-specific IgE in the patient's blood. In addition to detecting an allergen, RAST indicates the quantity of allergen necessary to evoke an allergic reaction. Values are reported on a scale from 0 to 5. Values of 2 or greater are considered significant. The major advantages of RAST over other tests include decreased risk of systemic reaction, stability of antigens, and lack of dependence on skin reactivity modified by medications. The major disadvantages include limited allergen selection and reduced sensitivity compared with intradermal skin tests, lack of immediate results, and higher cost. RAST is being replaced by the more sensitive fluorescence enzyme-labeled assays such as ImmunoCAP, a quantitative test for IgE proteins.

Exfoliative dermatitis

is a serious condition characterized by progressive inflammation in which generalized erythema and shedding of the skin occur. It may be associated with chills, fever, prostration, severe toxicity, and a pruritic scaling of the skin. Pathophysiology There is a profound loss of stratum corneum (i.e., outermost layer of the skin), which causes capillary leakage, hypoproteinemia, and negative nitrogen balance. Because of widespread dilation of cutaneous vessels, large amounts of body heat are lost, and exfoliative dermatitis has a marked effect on the entire body. Exfoliative dermatitis has a variety of causes. It is considered to be a secondary or reactive process to an underlying skin or systemic disease. It may appear as a part of the lymphoma group of diseases and may precede the clinical manifestations of lymphoma. Clinical Manifestations and Assessment This condition starts acutely as a patchy or a generalized erythematous eruption accompanied by fever, malaise, and, occasionally, GI symptoms. The skin color changes from pink to dark red. Redness and other color changes are usually not noticed in patients with darker tones. It is recommended that the skin should be compared with the adjacent or opposite area of the body to note skin color changes. The skin should also be assessed for firmness and bogginess when palpated as well as the presence of pain, edema, warmth or cooler temperatures. Medical and Nursing Management The objectives of management are to maintain fluid and electrolyte balance and to prevent infection. The treatment is individualized and supportive and should be initiated as soon as the condition is diagnosed. The patient may be hospitalized and placed on bed rest. All medications that may be implicated are discontinued. A comfortable room temperature should be maintained because the patient does not have normal thermoregulatory control as a result of temperature fluctuations caused by vasodilation and evaporative water loss. Fluid and electrolyte balance must be maintained because there is considerable water and protein loss from the skin surface. Administration of plasma volume expanders may be indicated.

Urticaria (hives)

is a type I hypersensitive allergic reaction of the skin characterized by the sudden appearance of pinkish, edematous elevations that vary in size and shape, itch, and cause local discomfort (Fig. 38-4). They may involve any part of the body, including the mucous membranes (especially those of the mouth), the larynx (occasionally with serious respiratory complications), and the GI tract. Each hive remains for a few minutes to several hours before disappearing. For hours or days, clusters of these lesions may come, go, and return episodically. If this sequence continues for longer than 6 weeks, the condition is called chronic urticaria. Chronic urticaria requires an extensive workup, ruling out numerous autoimmune diseases (e.g., lupus, rheumatoid arthritis, thyroid disease, etc.).

Bullous pemphigoid

is an acquired disease of flaccid blisters appearing on normal or erythematous skin. Clinical Manifestations and Assessment Bullous pemphigoid appears more often on the flexor surfaces of the arms, legs, axilla, and groin. Oral lesions, if present, are usually transient and minimal. When the blisters break, the skin has shallow erosions that heal fairly quickly. Pruritus can be intense, even before the appearance of the blisters. Bullous pemphigoid is common in the elderly, with a peak incidence at about 60 years of age. There is no gender or racial predilection, and the disease can be found in patients throughout the world. Medical and Nursing Management Medical treatment includes topical corticosteroids for localized eruptions and systemic corticosteroids for widespread involvement. Systemic corticosteroids (e.g., prednisone) may be continued for months, in alternate-day doses. The patient needs to understand the implications of long-term corticosteroid therapy. Complications Infection and Sepsis The patient is susceptible to infection because the barrier function of the skin is compromised. Bullae are also susceptible to infection, and sepsis may follow. The skin is cleaned to remove debris and dead skin and to prevent infection. Secondary infection may be accompanied by an unpleasant odor from skin or oral lesions. Candida albicans of the mouth (i.e., thrush) commonly affects patients receiving high-dose corticosteroid therapy. The oral cavity is inspected daily, and any changes are reported. Oral lesions are slow to heal. Fluid and Electrolyte Imbalance Extensive denudation of the skin leads to fluid and electrolyte imbalance because of significant loss of fluids and sodium chloride from the skin. This sodium chloride loss is responsible for many of the systemic symptoms associated with the disease and is treated by IV administration of saline solution. A large amount of protein and blood is also lost from the denuded skin areas. Blood component therapy may be prescribed to maintain the blood volume, hemoglobin level, and plasma protein concentration. Serum albumin, protein, hemoglobin, and hematocrit values are monitored.

Hyperbaric oxygenation (HBO)

is an adjunctive therapy that requires the patient to breathe 100% oxygen while under increased atmospheric pressure in a pressure chamber. It is recommended that hyperbaric therapy be utilized for limb-threatening diabetic wounds of the lower extremities and pressure ulcers. Also, it is used for hypoxic vascular wounds of the lower extremity (Bryant & Nix, 2016). Those who received HBO as part of their wound care regimen healed faster than those who received standard treatment (Ramundo, 2016).

Serum sickness

is an immune-complex type III hypersensitivity. If these type III complexes are deposited in tissues or vascular endothelium, there is an increase in vascular permeability and tissue injury, resulting in a vasculitis (inflammation of blood vessels). Traditionally serum sickness has resulted from the administration of therapeutic antisera of animal sources for the treatment or prevention of infectious diseases, such as tetanus, pneumonia, rabies, diphtheria, and botulism, as well as the bites of venomous snakes and black widow spiders. With the advent of human antitetanus serum and antibiotics, classic serum sickness is much less common now. However, various medications (primarily penicillin) may cause a serum-sickness-like reaction similar to that caused by foreign sera. Clinical Manifestations and Assessment Symptoms are caused by a reaction and immunologic attack on the serum or medication. Antibodies appear to be of the IgE and IgM classes. Early manifestations, beginning 6 to 10 days after administration of the medication, include an inflammatory reaction at the site of injection of the medication, followed by regional and generalized lymphadenopathy and fever. Symptoms may appear as late as 3 weeks afterward. There is usually a skin rash, which may be urticarial or purpuric. Joints are frequently tender and swollen. Vasculitis may occur in any organ but is observed most commonly in the kidney, resulting in proteinuria and, occasionally, casts in the urine. There may be mild to severe cardiac involvement. Peripheral neuritis may cause temporary paralysis of the upper extremities or may be widespread, causing Guillain-Barré syndrome Medical and Nursing Management The primary goal in serum sickness therapy is to treat the clinical syndrome symptomatically. This hypersensitivity reaction lasts for several days to a few weeks if untreated, but the patient responds promptly and completely if treated with antihistamines and corticosteroids (Bope & Kellerman, 2016). Aggressive therapy, including ventilator support, may be necessary if peripheral neuritis and Guillain-Barré syndrome occur. If symptoms are severe enough to warrant ventilator support or if hemodynamic instability ensues, the patient is to be admitted to an intensive care unit. See Chapter 46 for nursing management of Guillain-Barré syndrome.

Contact dermatitis

is an inflammatory reaction of the skin to physical, chemical, or biologic agents. Pathophysiology The epidermis is damaged by repeated physical and chemical irritations. Contact dermatitis may be of the primary irritant type, in which a nonallergic reaction results from exposure to an irritating substance, or it may be an allergic reaction resulting from exposure of sensitized people to contact allergens. Common causes of irritant dermatitis are soaps, detergents, scouring compounds, and industrial chemicals. Predisposing factors include extremes of heat and cold, frequent contact with soap and water, and a pre-existing skin disease (Box 52-6). Clinical Manifestations and Assessment The eruptions begin when the causative agent contacts the skin. The first reactions include pruritus, burning, and erythema, followed closely by edema, papules, vesicles, and oozing or weeping. In the subacute phase, these vesicular changes are less marked, and they alternate with crusting, drying, fissuring, and peeling. If repeated reactions occur or if the patient continually scratches the skin, lichenification (thickening of the horny layer of the skin) and pigmentation occur. Secondary bacterial invasion may follow. Medical and Nursing Management The objectives of management are to rest the involved skin and protect it from further damage. The distribution pattern of the reaction is identified to differentiate between allergic and irritant contact dermatitis. A detailed history is obtained. If possible, the offending irritant is removed. Local irritation should be avoided, and generally soap is not used until healing occurs. Many preparations are advocated for relieving dermatitis. In general, a bland, unmedicated lotion is used for small patches of erythema. Cool, wet dressings also are applied over small areas of vesicular dermatitis. Finely cracked ice added to the water often enhances its antipruritic effect. Wet dressings usually help clear the oozing eczematous lesions. Then a thin layer of cream or ointment containing a corticosteroid may be used. Medicated baths at room temperature are prescribed for larger areas of dermatitis. For severe, widespread conditions, a short course of systemic corticosteroids may be prescribed.

The humoral response

is characterized by the production of antibodies by B lymphocytes in response to a specific antigen. Although the B lymphocyte is ultimately responsible for the production of antibodies, both the macrophages of natural immunity and the special T-cell lymphocytes of cellular immunity are involved in recognizing the foreign substance and in producing antibodies.

Homograft

is donor skin from a cadaver. It is a biologic dressing that has several uses. In extensive burns, it save lives by providing temporary wound coverage and protecting the granulation tissue until autografting is possible. Biologic dressings also provide temporary immediate coverage for clean, superficial burns and decrease the wound's evaporative water and protein loss. They decrease pain by protecting nerve endings and are an effective barrier against water loss and entry of bacteria. Biosynthetic and synthetic skin substitutes continue to be used as temporary wound coverings. In an attempt to develop the ideal burn wound covering product, dermal substitutes have been created. It is believed that skin substitutes enhance the healing process of an open wound when autologous skin is unavailable.

The stratum lucidum

is found only on the skin of the palms and soles (James, Berger, & Elston, 2016a).

Apoptosis

is the body's way of destroying worn-out cells, such as blood or skin cells, or cells that need to be renewed. The cells that have been damaged by infection or genetic change, or cells that are simply in excess of the body's needs, are targeted for removal and destruction by a subgroup of proteases called caspase. Once the process of apoptosis begins, generally it is irreversible (Paul, 2012).Eosinophils are only weakly phagocytic. On activation, eosinophils probably kill parasites by releasing specific chemical mediators into the extracellular fluid. Additionally, eosinophils secrete leukotrienes (discussed later in the chapter), prostaglandins, and various cytokines (Paul, 2012; Salmon, 2016).

Electrosurgery

is the destruction or removal of tissue by electrical energy. The current is converted to heat, which then passes to the tissue from a cold electrode. Electrosurgery may be preceded by curettage (excising the skin tumor by scraping its surface with a curette). Then electrodesiccation is implemented to achieve hemostasis and to destroy any viable malignant cells at the base of the wound or along its edges. Electrodesiccation is useful for lesions smaller than 1 to 2 cm (0.4 to 0.8 in) in diameter. This method takes advantage of the fact that the tumor is softer than surrounding skin and, therefore, can be outlined by a curette, which "feels" the extent of the tumor. The tumor is removed and the base cauterized. The process is repeated twice. Usually, healing occurs within a month.

Rheumatoid Arthritis RA

is the most common inflammatory arthritic disorder and serves as a prototype for the study of many inflammatory and immune-mediated diseases Pathophysiology A variety of predetermined genes (e.g., human leukocyte antigens [HLA]), random events, and environmental (e.g., pathogens, smoking) factors contribute to RA susceptibility and pathogenesis. In RA, numerous cell types are involved, including macrophages, T cells, B cells, fibroblasts, chondrocytes, and dendritic cells. The autoimmune reaction primarily occurs in the synovial tissue. Adaptive and innate immune responses in the synovium have been implicated in the pathogenesis of RA. RF antibodies develop in the synovium against the Immunoglobulin G (IgG) to form immune complexes. The activation of the complement system and release of lysosomal enzymes from leukocytes lead to inflammation. It is unknown why the body produces an antibody (RF) against its own antibody (IgG) and, in consequence, transforms IgG to an antigen or foreign protein that must be destroyed. Phagocytosis produces enzymes (proinflammatory cytokines such as interleukin [IL]-1, interleukin-6 [IL-6], and tumor necrosis factor [TNF]) within the joint. These cytokines are the primary factors that drive the inflammatory response in RA. The enzymes (especially cytokines) break down collagen, causing edema, proliferation of the synovial membrane, and, ultimately, formation of pannus (Fig. 39-5). Pannus, formation of vascular granulation tissue, is a characteristic of RA that differentiates it from other forms of inflammatory arthritis. Pannus has a destructive effect on the adjacent cartilage and bone. If response is not suppressed, the disease progresses and the consequences are loss of articular surfaces and joint motion. Muscle fibers also undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost. Clinical Manifestations and Assessment . Physical signs of RA are associated with the pathophysiology of the disease. The manifestations of RA can be categorized as early or late disease and as articular (joint) or extra-articular. Joint pain, swelling, warmth, erythema (redness), and lack of function are classic symptoms. Palpation of the joints reveals spongy or boggy tissue. Often, fluid can be aspirated from the inflamed joint. The hallmark of RA is synovial proliferation and tenderness in multiple joints, particularly in the small joints of the hands, wrists, and feet. As the disease progresses, the knees, shoulders, hips, elbows, ankles, cervical spine, and temporomandibular joints are affected. In addition to joint pain and swelling, a cardinal sign of inflammatory arthritis that can appear even before pain is morning stiffness, lasting for more than an hour Deformities of the hands and feet are common in RA (Fig. 39-6). Often the PIP and metacarpophalangeal (MCP) joints of the hands are involved initially. The deformity may be caused by misalignment resulting from swelling, progressive joint destruction, or the subluxation (partial dislocation) that occurs when one bone slips over another and eliminates the joint space. RA is a systemic disease with multiple extra-articular features. Most common are fever, weight loss, fatigue, anemia, lymph node enlargement, and Raynaud phenomenon (cold- and stress-induced vasospasm causing episodes of digital blanching or cyanosis). Extra-articular disease manifestations occur in about 40% of patients at some time in the course of the disease (Turesson & Matteson, 2015). Rheumatoid nodules may be noted in patients with more advanced RA in about 20% of patients (Brasington, 2015). These nodules are usually nontender and movable in the subcutaneous tissue. They usually appear over bony prominences, most often on extensor surfaces or pressure points, such as the elbow, are varied in size, and can disappear spontaneously. Nodules occur only in people positive for RF. The nodules often are associated with rapidly progressive and destructive disease. Other extra-articular features include arteritis (inflammation of the walls of arteries), neuropathy, scleritis (inflammation of the sclera), pericarditis, splenomegaly, and Sjögren syndrome (dry eyes and dry mucous membranes). Presence of deformities, such as hyperextension of PIP joints (swan neck), flexion of PIP joints (Boutonniere), and ulnar deviation, in which fingers point toward the ulna, may be noted on examination. The patient is also assessed for extra-articular changes, such as weight loss, sensory changes, lymph node enlargement, and fatigue. Arthrocentesis shows abnormal synovial fluid that is cloudy, milky, or dark yellow and contains numerous inflammatory components, such as leukocytes and complement. The enzyme MMP-3 is increased in the synovial fluid of the patient with RA, and it may be a marker of progressive joint damage. Synovial biopsy can detect inflammatory cells associated with RA. Radiologic studies are not specifically diagnostic in the early stages of RA; however, they do show characteristic bony erosions and narrowed joint spaces occurring later in the disease and help in monitoring the progression of disease and effectiveness of treatment. Medical and Nursing Management . Current guidelines recommend starting a course of DMARDs early, within 3 months of RA diagnosis to delay joint degeneration (O'Dell, 2013). NSAIDs provide fast relief of symptoms but do not prevent joint damage nor slow disease progression. Because the effects of DMARDs take weeks or months to develop, whereas the effects of NSAIDs are immediate, an NSAID is given until the DMARD has had time to act. The use of traditional NSAIDs (salicylates and nonsalicylates) inhibits the production of prostaglandins and provides anti-inflammatory effects as well as analgesia.

Débridement

is the removal of nonviable tissue from pressure and vascular ulcers, burns, surgical or traumatic wounds, and other types of wounds.

Mohs' micrographic surgery

is the technique that is most accurate and that best conserves normal tissue. The procedure removes the tumor layer by layer. The first layer excised includes all evident tumor and a small margin of normal-appearing tissue. The specimen is frozen and analyzed by section to determine if the entire tumor has been removed. If not, additional layers of tissue are shaved and examined until all tissue margins are tumor-free. In this manner, only the tumor and a safe, normal-tissue margin are removed. Mohs' surgery is the recommended tissue-sparing procedure, with extremely high cure rates for both BCC and SCC. It is the treatment of choice and the most effective for tumors around the eyes, nose, upper lip, and auricular and periauricular areas.

The dermis

makes up the largest portion of the skin, providing strength and structure. It is composed of two layers: papillary and reticular. The papillary dermis lies directly beneath the epidermis and is composed primarily of fibroblast cells capable of producing one form of collagen, a component of connective tissue. The reticular layer lies beneath the papillary layer and also produces collagen and elastic bundles. The dermis is also made up of blood and lymph vessels, nerves, sweat and sebaceous glands, and hair roots. The dermis is often referred to as the "true skin." It is especially thick on the palms and soles, while thin over the eyelids and scrotum; thus, it is not surprising that in conditions of fluid volume excess, patients develop edema in thin skinned areas, resulting in periorbital and scrotal edema. An infection of the dermis that spreads rapidly within the skin and subcutaneous structures is termed cellulitis. It is usually caused by staphylococci or streptococci and presents with redness, warmth, swelling, and tenderness, usually of the limbs.

Creams

may be suspensions of oil in water or emulsions of water in oil, with additional ingredients to prevent bacterial and fungal growth. Both may cause an allergic reaction, such as contact dermatitis (discussed on page 1473). Oil-in-water creams are easily applied and usually are the most cosmetically acceptable to the patient. Although they can be used on the face, they tend to have a drying effect. Water-in-oil emulsions are greasier and are preferred for drying and flaking dermatoses.

. Lotions

must be applied every 3 or 4 hours for sustained therapeutic effect because if left in place for a long period, they may crust and cake on the skin. There are two types of lotions: suspensions and liniments. Suspensions are medicines that are mixed with a liquid, usually water, in which it cannot dissolve and, therefore, remains intact in the form of small particles. The important thing to remember about suspensions is to shake the medication before giving each dose so that the medicine particles are evenly distributed throughout the liquid. An example is calamine lotion, which provides a rapid cooling and drying effect as it evaporates, leaving a thin, medicinal layer of powder on the affected skin. Liniments are lotions with oil added to prevent crusting. An example of a liniment is Ben-Gay for muscle aches.

immunity

refers to the body's specific protective response to an invading foreign agent or organism. The immune system functions as the body's defense mechanism against invasion and allows a rapid response to foreign substances in a specific manner. Responses occur at the genetic and cellular levels. Immune function is affected by a variety of factors, such as central nervous system integrity, emotional status, medications, and the stress of illness, trauma, or surgery

Autoimmune reactions

occur when self-antigens are recognized by the body's normal defense mechanisms as foreign. With the presence of these "foreign" antigens, B cells become hyperactive, and increased amounts of immunoglobulin E (IgE) are produced, thus causing a hypersensitivity or allergic response. Hypersensitivity is an amplified or inappropriate response to an antigen (on second exposure, see Pathophysiology), leading to inflammation and destruction of healthy tissue. The cause may result from genetic, hormonal, and environmental factors; many times, the etiology is unclear.

Shock

occurs when oxygen supply does not meet tissue demand. Burn shock develops from several abnormalities of the circulation. The initial systemic event is hemodynamic instability, which results from loss of capillary integrity and a subsequent shift of fluid, sodium, and protein from the intravascular space into the interstitial spaces. This leaky capillary syndrome increases cell permeability at the burn site, as well as throughout the body. In the major burn, this syndrome far exceeds the useful effect of the inflammatory response. Progressive edema develops in unburned tissue and organs, causing hypoperfusion and hypovolemic shock. As fluid loss continues and vascular volume decreases, the cardiac output (CO) and blood pressure (BP) fall. This is the onset of burn shock. The systemic response is caused by the release of cytokines and other mediators into the systemic circulation. The result is overwhelming; there is an increase in peripheral vascular resistance secondary to the edema formation, a decrease in blood volume, and a decrease in CO (Latenser, 2015). Thus, burn shock is characterized by capillary leak, "third spacing" of fluid, severe hypovolemia, and decreased CO. If the burn patient is not resuscitated adequately, circulatory collapse ensues.

Gout,

one of the most common of the inflammatory arthritides, is a metabolic disorder marked by the deposition of monosodium urate crystals within joints and other tissues. Gout is a heterogeneous group of conditions related to a genetic defect of purine metabolism that results in hyperuricemia (excessive uric acid, a purine end product) Primary gout is characterized by hyperuricemia caused by an overproduction of uric acid or a decreased urate excretion in the kidney. Often primary gout is caused by an inherited disorder in purine metabolism, with a 50% incidence (Keenan, Nowatzky, & Pillinger, 2013; McLean & Dalbeth, 2015). Secondary gout is related to a wide number of diseases or drugs that decrease the kidney's ability to excrete uric acid, increase the production of uric acid, or a combination of both. Conditions associated with secondary gout include diabetic ketoacidosis, severe dieting or starvation, and metabolic syndrome. Disorders, such as multiple myeloma and leukemia, result in increased production of uric acid because of a greater cell turnover and an increase in cell breakdown. Altered renal tubular function, either as a major action or as an unintended side effect of certain pharmacologic agents (e.g., diuretics such as thiazides and furosemide), low-dose salicylates, or ethanol, can contribute to uric acid underexcretion. An excessive intake of foods that are high in purines (shellfish, organ meats) may result in symptoms of gout in susceptible persons. Pathophysiology . To define individuals with hyperuricemia, current evidence-based reviews recommend that it is more clinically relevant to use the biologic value of 6.8 mg/dL or 408 μmol/L, a level of serum uric acid above the saturation point for crystal formation When the uric acid precipitates and then deposits within a joint as urate crystals, an inflammatory response occurs, and an attack of gout begins. With repeated attacks, accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as the great toe, the hands, and the ear (lower temperature areas). Renal urate lithiasis (kidney stones), with chronic renal disease secondary to urate deposition, may develop. Clinical Manifestations and Assessment Manifestations of the gout syndrome include acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation), tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage), gouty nephropathy (renal impairment), and uric acid urinary calculi. Four phases (or stages) of gout can be identified: asymptomatic hyperuricemia, acute gouty arthritis, intercritical or interval gout, and chronic tophaceous gout (acute and intercritical gout together are sometimes noted as one phase). Phase 1, asymptomatic hyperuricemia, is when the serum urate level is high, but gout manifested by arthritis or nephrolithiasis has not yet occurred. People can remain asymptomatic throughout their lifetimes. The subsequent development of gout is directly related to the duration and magnitude of the hyperuricemia. Therefore, the commitment to lifelong pharmacologic treatment of hyperuricemia is deferred until there is an initial attack of gout (phase 2). Acute arthritis is the most common early clinical manifestation of gouty arthritis. The first attack usually occurs between 40 and 60 years of age in men and after 60 years of age in women (Burns & Wortmann, 2013). The patient experiences excruciating pain and inflammation in one or more small joints. The metatarsophalangeal (MTP) joint of the big toe is the joint affected most commonly (up to 90% of patients) and is referred to as podagra . The attack is followed by a symptom-free period (the intercritical stage or phase 3) until the next attack, which may not come for months or years. However, with time, attacks tend to occur more frequently, to involve more joints, last longer, and lead to long-term sequelae (phase 4). In general, tophi are associated with more frequent and severe inflammatory episodes. Higher serum concentrations of uric acid also are associated with more extensive tophus formation. Tophi most commonly occur in the synovium, olecranon bursa, subchondral bone, infrapatellar and Achilles tendons, and subcutaneous tissue on the extensor surface of the forearms and overlying joints. Medical Management Treatment of gout is managed in two major phases: management of acute gouty inflammation and long-term management to prevent flare ups and to control hyperuricemia. According to recent ACR guidelines, an acute gout attack should be treated pharmacologically within 24 hours of the onset of symptoms. First-line oral drugs are usually NSAIDs or colchicine. NSAIDs with short half-life are most effective (e.g., indomethacin, naproxen, ibuprofen, and diclofenac). Other agents prescribed to relieve an acute attack of gout are corticosteroids (oral or parenteral) or adrenocorticotropic hormones (ACTH) because of their anti-inflammatory properties and their ability to be used for short periods of time so generally long-term complications can be avoided . Usually management of hyperuricemia, tophi, joint destruction, and kidney disorders is initiated after the acute inflammatory process has subsided. Allopurinol (Zyloprim), a xanthine oxidase inhibitor, is considered the drug of choice for preventing the precipitation of an attack and tophi formation and for promoting the regression of existing tophi.

Epitopes

or antigenic determinants, which are substances that, when introduced into the body, stimulate the production of an antibody. These epitopes are present on foreign materials and initiate a series of actions in a host, including the inflammatory response, the lysis of microbial agents, and the disposal of foreign toxins.

Pain in patients with burn wounds can be divided into four types: (1) Rest pain, constant background, and dull pain; (2) Breakthrough pain, intermittent, short duration, rapid onset (can be excruciating); (3) Procedural, short durations, greatest intensity (wound cleansing, therapy); and (4) Psychogenic pain, anticipatory pain without stimulation (Brookman, 2016). The nurse should be aware that rest pain (background) is best handled by administering regularly scheduled long-acting opioids for continuous coverage; procedural pain requires premedication with analgesic medications before painful procedures (Hall, 2012). Breakthrough pain occurs when blood levels of analgesic agents decrease below the level required to control background pain. Psychogenic pain, which is pain that may be caused by an emotional issue, often fear, depression, stress, or anxiety, may be managed with early psychological evaluation and patient-specific treatment.

pain management in burns

HIV encephalopathy or HIV-associated dementia (HAD)

was formerly referred to as AIDS dementia complex. The clinical syndrome is characterized by a progressive decline in cognitive, behavioral, and motor functions. Substantial evidence exists that HIV encephalopathy is a direct result of HIV infection in brain macrophages and microglia. HIV infection is thought to trigger the release of lymphokines and other inflammatory factors that result in cellular dysfunction or interference with neurotransmitter function rather than cellular damage. Signs and symptoms may be subtle and difficult to distinguish from fatigue, depression, or the adverse effects of treatment for infections and malignancies. Early manifestations include memory deficits, headache, difficulty concentrating, progressive confusion, psychomotor slowing, apathy, and ataxia. Later stages include global cognitive impairments, delay in verbal responses, a vacant stare, spastic paraparesis (a slight weakness or paralysis of both lower extremities), hyperreflexia, psychosis, hallucinations, tremor, incontinence, seizures, mutism, and death. Confirming the diagnosis of HIV encephalopathy can be difficult. Extensive neurologic evaluation includes a computed tomography (CT) scan, which may indicate diffuse cerebral atrophy and ventricular enlargement. Other tests that may detect abnormalities include magnetic resonance imaging (MRI), analysis of CSF through lumbar puncture, and brain biopsy.

The dermis,

which is the thickest layer of skin, is composed principally of collagen, a fibrous protein synthesized primarily by fibroblast cells, which are important in remodeling and repairing skin. This layer is split up into two regions, the papillary dermis and reticular dermis. This connective tissue layer contains nerve endings, sensory receptors, capillaries, and elastic fibers.