disorders of the immune system

DISORDERS OF THE IMMUNE SYSTEM

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)- Lupus erythematosus is an autoimmune disease that affects the connective tissue of the

body.- The course of disease is variable and unpredictable, with episodes of remission and

relapse.- A multisystem inflammatory disease that affects any body system but primarily the

musculoskeletal, cutaneous, renal, nervous, and cardiovascular systems.- The multisystem nature of SLE places the patient at risk for multiple complications, and

the disease is ultimately fatal. The most common causes of death are renal failure and infections, followed by neurological and cardiovascular disorders.

Pathophysiology:

- SLE is a result of disturbed immune regulation that causes an exaggerated production of autoantibodies.

- The immunoregulatory disturbance is brought about by some combination of genetic, hormonal (as evidenced by the usual onset during the childbearing years), and environmental factors (sunlight, thermal burns).

- Certain medications, such as hydralazine (Apresoline, procainamide (Pronestyl), isoniazid (INH), chlorpromazine (Thorazine), and some antiseizure medications, have been implicated in chemical or drug-induced SLE.

- Inflammation stimulates antigens, which in turn stimulate additional antibodies, and the cycle repeats.

- It also results in inflammation of the veins and arteries.

Signs and Symptoms:

Arthritis: joint swelling, tenderness, pain.Skin rash.Butterfly rash across the bridge of the nose and cheeks.Skin lesions that worsen during flares and exposure to sunlight.Alopecia, especially during flare-ups.Oral and nasal ulcers.Pleuritic pain with deep inspiration.Pericarditis, which causes chest pain.

Atherosclerosis. Fatigue.Glomerulonephritis, renal illness. Hypertension.Impaired cognitive function, depression, psychosis.Lymphadenopathy, splenomegaly, hepatomegaly.Anemia, leukopenia, thrombocytopenia

- Involvement of the musculoskeletal system, with arthralgias and arthritis (synovitis), is a common presenting feature of SLE, accompanied by morning stiffness

- The most familiar skin manifestation but occurring in fewer than half of patients with SLE is an acute cutaneous lesion consisting of a butterfly-shaped rash across the bridge of the nose and cheeks

Immunologic Disorders

- Lesions often worsen during exacerbations (flares) of the systemic disease and possibly are provoked by sunlight or artificial ultraviolet light.

- Pericarditis is the most common cardiac manifestation.

Diagnostics:

ANA, positive Decreased complement fixation. Decreased hemoglobin, hematocrit, white blood cells, platelets. Increased erythrocyte sedimentation rate (ESR). Lupus erythematosus cell preparation, positive. Rheumatoid factor, positive. Proteinuria and hematuria on urinalysis

- No single laboratory test confirms SLE

Management:

- Skin is inspected for erythematous rashes. Cutaneous erythematous plaques with an adherent scale may be observed on the scalp, face,or neck. Areas of hyperpigmentation or depigmentation may be noted, depending on the phase and type of the disease.

- The patient should be questioned about skin changes and specifically about sensitivity to sunlight or artificial ultraviolet light.

- The scalp should be inspected for alopecia and the mouth and throat for ulcerations reflecting gastrointestinal involvement

- Cardiovascular assessment includes auscultation for pericardial friction rub- Neurologic assessment is directed at identifying and describing any central nervous

system changes. The patient and family members are asked about any behavioral changes, including manifestations of neuroses or psychosis.

- Generally, management involves periodic monitoring and recognition of meaningful clinical changes requiring adjustments in therapy

- Goals of treatment include preventing progressive loss of organ function, reducing the likelihood of acute disease, minimizing disease-related disabilities, and preventing complications from therapy

- Most common problems include fatigue, impaired skin integrity, body image disturbance, and lack of knowledge for self-management decisions.

Treatment includes:

Aspirin. NSAIDs. Antianemics: ferrous sulfate (Feosol). Antirheumatic: hydroxychloroquine (Plaquenil).


Cytotoxic drugs: methotrexate (Folex). Steroids: prednisone (Deltasone). Immunosuppressants: azathioprine (Imuran). Scheduled rest periods. If renal failure, hemodialysis or kidney transplant. Dietary iron, protein, vitamins. Plasmapheresis

HUMAN IMMUNODEFICIENCY VIRUS (HIV) / ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)

Pathophysiology:

- Viruses are intracellular parasites. 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)

- 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.

- When a T cell becomes activated against HIV or other microbes, the cell replicates and also unwittingly begins to produce new copies of both RNA and viral proteins

- Activation of the infected cell may be achieved by antigens, mitogens, select cytokines (tumor necrosis factor-alpha or interleukin-1), or virus gene products of such viruses as cytomegalovirus (CMV), Epstein-Barr virus, herpes simplex virus, and hepatitis.

- Consequently, whenever the infected T4 cell is activated, HIV replication and budding occur, which often destroys the host cell. Newly formed HIV is then released into the blood plasma and infects other CD4+ cells

- All viruses target specific cells. Lymphocytes consist of three major populations: T cells, B cells, and natural killer cells

- Approximately two thirds of peripheral blood T cells are CD4 and approximately one third are CD8. Most people have about 700 to 1,000 CD4 cells/mm3, but as low as 500/mm3 can be considered “normal.”


Stages of HIV Disease

a. PRIMARY INFECTION - period from infection with HIV to the development of antibodies to HIV

- intense viral replication and widespread dissemination of HIV throughout the body

- During the primary infection period, the window period occurs because a person is infected with HIV but tests negative on the HIV antibody blood test

- By the time neutralizing antibodies are detected, HIV-1 is firmly established in the host). During this period, there are high levels of viral replication and the killing 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 level of at least 800 cells/mm3 of blood.

b. HIV ASYMPTOMATIC (CDC CATEGORY A: MORE THAN 500 CD4+ T LYMPHOCYTES/MM3)

- clinically asymptomatic state begins- on average, 8 to 10 years pass before a major HIV-related complication develops. In this

prolonged, chronic stage, patients feel well and show few if any symptoms. - apparent good health continues because CD4 T-cell levels remain high enough to

preserve defensive responses to other pathogens

c. HIV SYMPTOMATIC (CDC CATEGORY B: 200 TO 499 CD4+ T LYMPHOCYTES/MM3)- CD4 T cells gradually falls

d. AIDS (CDC CATEGORY C: LESS THAN 200 CD4+ T LYMPHOCYTES/MM3)- When CD4 T-cell levels drop below 200 cells/mm3 of blood, patients are said to have

AIDS.- As levels fall below 100, the immune system is significantly impaired

Diagnostics:

EIA (enzyme immunoassay), formerly referred to as ELISA (enzyme-linked immunosorbent assay) - Antibodies are detected, resulting in positive results and marking the end of the window period

Western Blot - Also detects antibodies to HIV; used to confirm EIA


Viral Load - Measures HIV RNA in the plasma

CD4/CD8 ratio

Signs and Symptoms:

Respiratory Manifestations- Shortness of breath, dyspnea (labored breathing), cough, chest pain, and fever are

associated with various opportunistic infections , such as those caused by Pneumocystis carinii, Mycobacterium avium-intracellulare,CMV, and Legionella species.

- The most common infection in people with AIDS is Pneumocystis carinii pneumonia (PCP)

- TB that occurs late in HIV infection is characterized by absence of an immune response to a tuberculin skin test response. This is known as anergy and results because the compromised immune system can no longer respond to the TB antigen.

Gastrointestinal Manifestations- loss of appetite, nausea,vomiting, oral and esophageal candidiasis, and chronic

diarrhea.- Diarrhea is a problem in 50% to 90% of all AIDS patients.- GI symptoms may be related to the direct effect of HIV on the cells lining the intestines.

Oncologic Manifestation- Kaposi’s sarcoma (KS), the most common HIV-related malignancy, is a disease

involving the endothelial layer of blood and lymphatic vessels.

Neurologic Manifestations- HIV encephalopathy was formerly referred to as AIDS dementia complex. It is a clinical

syndrome characterized by a progressive decline in cognitive, behavioral, and motor functions.

- A fungal infection, Cryptococcus neoformans,is another common opportunistic infection among patients with AIDS and causes neurologic disease.

- HIV-related peripheral neuropathy is thought to be a demyelinating disorder; it is associated with pain and numbness in the extremities, weakness, diminished deep tendon reflexes, orthostatic hypotension, and impotence.

Depressive Manifestation- causes of depression are multifactorial and may include a history of pre-existing mental

illness, neuropsychiatric disturbances, and psychosocial factors.


Integumentary Manifestations- Kaposi sarcoma and and infections such as herpes zoster and herpes simplex are

associated with painful vesicles that disrupt skin integrity.- Patients with AIDS may also exhibit a generalized folliculitis associated with dry, flaking

skin or atopic dermatitis, such as eczema or psoriasis. - Patients treated with trimethoprim-sulfamethoxazole (TMP-SMZ) develop a drug-related

rash that is pruritic with pinkish-red macules and papules

Gynecologic Manifestation- Persistent, recurrent vaginal candidiasis may be the first sign of HIV infection in women

Management:- Treatment focuses on maintaining health and improving survival time. No cure has been

found- Administer prescribed medications for AIDS-related opportunistic infections, antiretroviral

therapy, antidiarrheals, and anti-emetics- Maintain skin integrity- Instruct the client about the promotion of normal bowel movements and prevention of

diarrhea- Promote infection prevention- Teach energy conservation techniques- Discuss ways the client and family can assist with mental status problems- Teach methods for airway clearance- Help maintain nutritional status- Monitor and manage complications of opportunistic infections- Teach ways to cope with chronic illness- Provide referrals

PHYSIOLOGY OF ALLERGIC REACTION

- An allergic reaction is a manifestation of tissue injury resulting from interaction between an antigen and an antibody.

- When the body is invaded by an antigen, usually a protein that the body’s defenses recognize as foreign, a series of events occurs in an attempt to render the invader harmless, destroy it, and remove it from the body.

- When lymphocytes respond to the antigen, antibodies (protein substances that protect against antigens) are produced.

- Immunoglobulins of the IgE class are involved in allergic disorders and some parasitic infections, evidenced by elevation of IgE levels

- Two or more IgE molecules bind together to an allergen and trigger mast cells or basophils to release chemical mediators, such as histamine, serotonin, kinins, slow-


reacting substance of anaphylaxis (SRS-A), and the neutrophil factor, which produces allergic skin reactions, asthma, and hay fever.

- When the allergen is absorbed through the respiratory tract, gastrointestinal tract, or skin, allergen sensitization occurs.

Allergen triggers B cell to make IgE antibody, which attaches to mast cell. When that allergen reappears, it binds to the IgE and triggers the mast cell to release its chemicals.

Primary Mediators:

1. Histamine - 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; increased secretion of gastric and mucosal cells, resulting in diarrhea.

2. Eosinophil Chemotactic Factor of Anaphylaxis - inhibit the action of leukotrienes and histamine

3. Platelet-Activating Factor (PAF) - responsible for initiating platelet aggregation at sites of immediate hypersensitivity reactions

o It also causes bronchoconstriction and increased vascular permeability.

4. Prostaglandins – produce smooth muscle contraction as well as vasodilation and increased capillary permeability.

o The fever and pain that occur with inflammation are due in part to the

prostaglandins.


Secondary Mediators:

1. Leukotrienes - chemical mediators that initiate the inflammatory response.o cause smooth muscle contraction, bronchial constriction, mucus secretion in the

airways, and the typical wheal and flare reaction of the skin

2. Bradykinin - polypeptide with the ability to cause increased vascular permeability, vasodilation, hypotension, and contraction of many types of smooth muscle, such as the bronchi

o Increased permeability of the capillaries results in edema

3. Serotonin - released during platelet aggregation, acting as a potent vasoconstrictor and causing contraction of bronchial smooth muscle.

ANAPHYLACTIC (TYPE 1) HYPERSENSITIVITY

- An immune response to an antigen may result in sensitivity to challenge with that antigen; hypersensitivity is a reflection of excessive or aberrant immune responses

- A hypersensitivity reaction is an abnormal, heightened reaction to any type of stimuli. - It usually does not occur with the first exposure to an allergen.- The most severe form of a hypersensitivity reaction is anaphylaxis. - This systemic reaction is characterized by edema in many tissues, including the larynx,

and is often accompanied by hypotension.- Type I or anaphylactic hypersensitivity is an immediate reaction beginning within minutes

of exposure to an antigen.- Primary chemical mediators are responsible for the symptoms of type I hypersensitivity

because of their effects on the skin, lungs, and gastrointestinal tract.

An anaphylactic reaction is characterized by vasodilation, increased capillary permeability, smooth muscle contraction, and eosinophilia


- Smooth muscle spasm, bronchospasm, mucosal edema and inflammation, and increased capillary permeability result. These systemic changes characteristically produce clinical manifestations within seconds or minutes of antigen exposure

- Substances that most commonly cause anaphylaxis include foods, medications, insect stings, and latex

Diagnostics:

1. Eosinophil Count - An actual count of eosinophils may be obtained from blood samples or smears of secretions.

o During symptomatic episodes, smears obtained from nasal secretions,

conjunctival secretions, and sputum of atopic patients usually reveal eosinophils, indicative of an active allergic response.

2. Total Serum Immunoglobulin E Levels - Indications for determining IgE levels include the following:

• Evaluation of immunodeficiency• Evaluation of drug reactions• Initial laboratory screening for allergic bronchopulmonary aspergillosis• Evaluation of allergy among children with bronchiolitis• Differentiation of atopic and nonatopic eczema• Differentiation of atopic and nonatopic asthma and rhinitis

3. Skin Tests - entails the intradermal injection or superficial application (epicutaneous) of solutions at several sites.

o Solutions contain individual antigens representing an assortment of allergens,

including pollen, most likely to be implicated in the patient’s disease. o Positive reactions (wheal and flare) are clinically significant when correlated with

the history, physical findings, and results of other laboratory tests.o The back is the most suitable area of the body for skin testing because it permits

the performance of many tests

4. Provocative Testing - involves the direct administration of the suspected allergen to the sensitive tissue, such as the conjunctiva, nasal or bronchial mucosa, or gastrointestinal tract (by ingestion of the allergen) with observation of target organ response.

o 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.

5. Radioallergosorbent Test - A sample of the patient’s serum is exposed to a variety of suspected allergen particle complexes.


Signs and Symptoms:

Management:

Determine the cause and maintain the airway Patient’s history and signs and symptoms establish the diagnosis. Skin testing may help identify a specific antigen, but can cause severe allergic reaction. Maintain a patent airway. Cardiopulmonary resuscitation (CPR). Oxygen therapy. Endotracheal tube, if needed. Epinephrine 1:1000 aqueous solution, subQ, or IV. Corticosteroids to reduce inflammatory reaction. Diphenhydramine (Benadryl) IV. Vasopressors to support blood pressure. Norepinephrine (Levophed) to restore blood pressure. Volume expander infusions. Dopamine (Dobutrex) to support blood pressure. Aminophylline (Truphylline) IV to dilate bronchi. Antihistamines to counteract histamine reaction. Patients with severe reactions are observed closely for 12 to 14 hours If a patient is experiencing an allergic response, the nurse’s initial action is to assess the

patient for signs and symptoms of anaphylaxis. The nurse assesses the airway, breathing pattern, and other vital signs. The patient is observed for signs of increasing edema and respiratory distress.

Prevention:


- Strict avoidance of potential allergens is an important preventive measure for the patient at risk for anaphylaxis

- Patients at risk for anaphylaxis from insect stings should avoid areas populated by insects and should use appropriate clothing, insect repellent, and caution to avoid further stings.

- If avoidance of exposure to allergens is impossible, administration of epinephrine is a critical measure to prevent an anaphylactic reaction.

- Patients should always carry an emergency kit that contains epinephrine. - Screening for allergies before a medication is prescribed or first administered is an

important preventive measure. - Insulin-allergic diabetic patients and penicillin-sensitive patients may require

desensitization. Desensitization is based on controlled anaphylaxis, with a gradual release of mediators.

- Patients who undergo desensitization are cautioned that there should be no lapses in therapy, because this may lead to the reappearance of an allergic reaction when the medication is reinstituted.

FOOD ALLERGY

- IgE-mediated food allergy, a type I hypersensitivity reaction, occurs in 0.1% to 7.0% of the population.

- Almost any food can cause allergic symptoms. Any food can contain an allergen that results in anaphylaxis.

- The most common offenders are: seafood (lobster, shrimp, crab, clams, fish), legumes (peanuts, tree nuts, peas, beans, licorice), seeds (sesame, cottonseed, caraway, mustard, flaxseed, and sunflower seeds), nuts, berries, egg white, buckwheat, milk, and chocolate

- Peanut and tree nut (cashew, walnut) allergies are responsible for most severe food allergy reactions

- One of the dangers of food allergens is that they may be hidden in other foods and not apparent to those susceptible to the allergen.

Signs and Symptoms:


- Clinical symptoms are classic allergic and gastrointestinal symptoms:

UrticariaAtopic dermatitisWheezingCoughlaryngeal edemaangioedema

ItchingSwelling of lips, tongue, and palateAbdominal painNauseaCrampsVomitingDiarrhea

Management:

- Therapy for food hypersensitivity includes elimination of the food responsible for the hypersensitivity.

- Pharmacologic therapy is necessary in patients who cannot avoid exposure to offending foods or patients with multiple food sensitivities not responsive to elimination measures.

- Medication therapy involves the use of H1- and H2-blockers, antihistamines, adrenergic agents, corticosteroids, and cromolyn sodium.

- Focus on preventing future exposure of the patient to the food allergen.- The patient and family must be knowledgeable about early signs and symptoms of

allergic reactions and must be proficient in emergency administration of epinephrine if a reaction occurs.

- Advise the patient to wear a medical alert bracelet or to carry identification and emergency equipment at all times.

LATEX ALLERGY

- Latex allergy, the allergic reaction to natural rubber proteins, has been implicated in rhinitis, conjunctivitis, contact dermatitis, urticaria, asthma, and anaphylaxis.

- Natural rubber latex is derived from the sap of the rubber tree (Hevea brasiliensis). - The conversion of the liquid rubber latex into a finished product entails the addition of

more than 200 chemicals.- The proteins in the natural rubber latex (Hevea proteins) or the various chemicals that

are used in the manufacturing process are thought to be the source of the allergic reactions.

- Populations at risk include health care workers, patients with atopic allergies or multiple surgeries, people working in factories manufacturing latex products, females, and patients with spina bifida.

- Because more food handlers, hairdressers, auto mechanics, and police are now wearing latex gloves, they may also be at risk for latex allergy.

- Food that has been handled by individuals wearing latex gloves may stimulate an allergic response.


- 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 can settle on skin, mucous membranes, or clothing.

Signs and Symptoms:

Common symptoms of irritant dermatitis:

o Erythema and prurituso Vesicular skin lesionso Papuleso Prurituso Edema,o Crusting and thickening of the skin

Immediate hypersensitivity:

o Urticaria,o Wheezing,o dyspnea,o Laryngeal edema,o Bronchospasm,o Tachycardia,o Angioedema,o Hypotension,o Cardiac arrest

Management:

- Avoidance of latex products; preventing exposure by wrapping BP cuffs and stethoscopes in cloth

- Patients are instructed to wear medical identification.- Antihistamines and an emergency kit containing epinephrine should be provided to

patients, along with instructions about emergency management of latex allergy symptoms.

- Patients should be counseled to notify all health care workers as well as local paramedic and ambulance companies about their allergy.

- 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.

- Individuals with latex allergy should be provided with a list of alternative products and referred to local support groups; they are also urged to carry their own supply of nonlatex gloves.

- People with type I latex sensitivity may be unable to continue to work if a latex-free environment is not possible. This may occur with surgeons, dentists, operating room personnel, or intensive care nurses.

ALLERGIC RHINITIS

- Allergic rhinitis (inflammation of nasal mucosa) is the most common form of respiratory allergy presumed to be mediated by an immediate (type I hypersensitivity) immunologic reaction.


- When untreated, many complications may result, such as allergic asthma, chronic nasal obstruction, chronic otitis media with hearing loss, anosmia (absence of the sense of smell), and, in children, orofacial dental deformities.

- Characterized by the following seasonal occurrences:• Early spring—tree pollen (oak, elm, poplar)• Early summer—rose pollen (rose fever), grass pollen (Timothy, red-top)• Early fall—weed pollen (ragweed)

- Sensitization begins by ingestion or inhalation of an antigen. - On re-exposure, the nasal mucosa reacts by the slowing of ciliary action, edema

formation, and leukocyte (primarily eosinophil) infiltration.

Signs and Symptoms:

nasal congestion clear, watery nasal discharge intermittent sneezing nasal itching. itching of the throat and soft palate headache pain over the paranasal sinuses epistaxis

Management:

Avoidance Therapy- In avoidance therapy, every attempt is made to remove the allergens that act as

precipitating factors. - Simple measures and environmental controls are often effective in decreasing

symptoms. Examples include use of air conditioners, air cleaners, humidifiers and dehumidifiers, and smoke-free environments

Pharmacologic Therapya. Antihistamines - Oral antihistamines, which are readily absorbed, are most effective

when given at the first occurrence of symptoms because they prevent the development of new symptoms by blocking the actions of histamine at the H1-receptors.

o The major side effect is sedation, although histamine H1 antagonists are less

sedating than earlier antihistamineso Antihistamines are contraindicated during the third trimester of pregnancy; for

nursing mothers and newbornso Examples of non-sedtaing antihistamines are loratadine (Claritin), cetirizine

(Zyrtec), and fexofenadine (Allegra)


b. Adrenergic Agents - vasoconstrictors of mucosal vesselso The topical route (drops and sprays) causes fewer side effects than oral

administration; however, the use of drops and sprays should be limited to a few days to avoid rebound congestion.

o Potential side effects include hypertension, dysrhythmias, palpitations, central

nervous system stimulation, irritability, tremor, and tachyphylaxis (acceleration of hemodynamic status).

o Examples are phenylephrine hydrochloride, pseudoephedrine hydrochloride

c. Mast Cell Stabilizers - 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.

d. Corticosteroids - Intranasal corticosteroids are indicated in more severe cases of allergic and perennial rhinitis that cannot be controlled by more conventional medications such as decongestants, antihistamines, and intranasal cromolyn.

- These medications include beclomethasone (Beconase, Vancenase), budesonide (Rhinocort), dexamethasone (Decadron Phosphate Turbinaire), flunisolide (Nasalide), fluticasone (Cutivate, Flonase), and triamcinolone (Nasacort).

Immunotherapy- Allergen desensitization (allergen immunotherapy, hyposensitization) is primarily used to

treat IgE-mediated diseases by injectionsof allergen extracts.- The most common method of treatment is the serial injection of one or more antigens

that are selected in each particular case on the basis of skin tests.- Injections begin with very small amounts and are gradually increased, usually at weekly

intervals, until a maximum tolerated dose is attained.

CONTACT DERMATITIS

- Contact dermatitis (dermatitis venenata), a type IV delayed hypersensitivity reaction, is an acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens.

- Type IV, or delayed-type hypersensitivity, also known as cellular hypersensitivity, occurs 24 to 72 hours after exposure to an allergen.

- Eighty percent of cases are due to excessive exposure to or additive effects of irritants (eg, soaps, detergents, organic solvents)

Four Basic Types:1. Allergic


2. Irritant3. Phototoxic

4. Photoallergic

Signs and Symptoms:- 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 pigmentary

changes (lichenification and pigmentation)

Diagnosis:

1. Use Test – a suspected agent is applied far from the original area of dermatitis o Useful when shampoos, perfumes or other home agents are suspected

2. Patch Testing – indicated for allergic contact dermatitiso Standard contact allergens are applied to the upper back using adhesive-

mounted patches containing minute amounts of allergen or plastic chambers containing allergen held in place with porous tape

o Evaluated 48 to 96 hours after application


Management:

- Study the cycle, occurrence or season of allergy or reaction; reactivity is usually lifelong- Help the patient identify materials possibly causing the reaction and avoid contact with

them or other possible irritants- Advice the patent to wash hands thoroughly immediately after exposure to the

suspected allergen- Cool, wet dressings or cold bath; wet-to-dry dressings to soothe oozing blisters- Avoid sun exposure- Administer prescribed medications such as antihistamines and corticosteroids- Advice patients that antihistamines causes drowsiness, hence the patoent has to avoid

alcohol-containing products

Complications:- Scarring of the skin- Secondary bacterial infection- Anaphylactic reaction

ATOPIC DERMATITIS

- Atopic dermatitis is a type I immediate hypersensitivity disorder.- A family history is common.; common in children- Exact cause is unknown but related factors include depressed cell-mediated

immunity, elevated IgE levels and increased histamine response- Atopic dermatitis is chronic, with remissions and exacerbations.- Also known as eczema

Signs and Symptoms:

- Pruritus and hyperirritability of the skin are the most consistent features of atopic dermatitis and are related to large amounts of histamine in the skin.

- 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

- Lesions develop secondary to the trauma of scratching and appear in areas of increased sweating and hypervascularity.

Management:


- 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)- Avoiding animals, dust, sprays, and perfumes. - Keeping the skin moisturized with daily baths to hydrate the skin- Topical skin moisturizers is encouraged- Topical corticosteroids are used to prevent inflammation- Any infection is treated with antibiotics to eliminate Staphylococcus aureus when

indicated. - Use of low doses of cyclosporine (Neoral, Sandimmune), an immunosuppressive agent,

may be effective- Explore patients coping mechanisms because the appearance of the skin may affect the

patient’s self-esteem

STEVENS-JOHNSON SYNDROME / TOXIC EPIDERMAL NECROLYSIS

- potentially fatal skin disorders and the most severe form of erythema multiforme- drugs, especially sulfa drugs, antiepileptics and antibiotics are the most common

causes- macules rapidly coalesce, leading to epidermal blistering, necrosis and sloughing- Incidence or severity of both disorders may be higher in immunocompromised patients

Pathophysiology:

- Exact mechanism is unknown- One theory holds that altered drug metabolites in some patients causes formation of

reactive metabolites that bind to and alter cell proteins, triggering a T-cell mediated cytotoxic reaction to drug antigens

Signs and Symptoms:

Characterized initially by: conjunctival burning or itching cutaneous tenderness fever, cough, sore throat headache extreme malaise myalgias (aches and pains)

Followed by: rapid onset of erythema involving much of the skin surface and mucous membranes,

including the oral mucosa, conjunctiva, and genitalia


shedding of large sheets of epidermis exposing the underlying dermis shedding of fingernails, toenails, eyebrows, and eyelashes skin is excruciatingly tender loss of skin leaves a weeping surface similar to that of a total-body, partial-thickness

burnDiagnosis:

- Histologic studies of frozen skin cells from a fresh lesion- Immunofluorescent studies may be performed to detect atypical epidermal

autoantibodies- History of ingestion of medications known to precipitate TEN or SJS may confirm

medication reaction as the underlying cause

Complications:

Sepsis Keratoconjunctivitis Pneumonia

Nursing Diagnoses:• Impaired tissue integrity (ie, oral, eye, and skin) related to epidermal shedding• Deficient fluid volume and electrolyte losses related to loss of fluids from denuded skin• Risk for imbalanced body temperature (ie, hypothermia) related to heat loss secondary

to skin loss• Acute pain related to denuded skin, oral lesions, and possible infection• Anxiety related to the physical appearance of the skin and prognosis

Management:

- 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; patients are at high risk for infection, multi-organ failure and death

- All nonessential medications are discontinued immediately.- Tissue samples from the nasopharynx, eyes, ears, blood, urine, skin, and unruptured

blisters are obtained for culture to identify pathogenic organisms. - Intravenous fluids are prescribed to maintain fluid and electrolyte balance.- Prophylactic antibiotics are controversial- Initial treatment with systemic corticosteroids is controversial; some experts argue

for early high-dose corticosteroid treatment.- Plasmapharesis can remove reactive drug metabolites or antibodies- Administer early high-dose IV immune globulins (IVIG)


- Temporary biologic dressings (eg, pigskin, amniotic membrane) or plastic semi-permeable dressings (eg, 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.

Evaluation Outcomes:

Patient outcomes may include:

1. Achieves increasing skin and oral tissue healinga. Demonstrates areas of healing skinb. Swallows fluids and speaks clearly

2. Attains fluid balancea. Demonstrates laboratory values within normal rangesb. Maintains urine volume and specific gravity within acceptable rangec. Shows stable vital signsd. Increases intake of oral fluids without discomforte. Gains weight, if appropriate

3. Attains thermoregulationa. Registers body temperature within normal rangeb. Reports no chills

4. Achieves pain reliefa. Uses analgesics as prescribedb. Uses self-management techniques for relief of pain

5. Appears less anxiousa. Discusses concerns freelyb. Sleeps for progressively longer periods

6. Absence of complications, such as sepsis and impaired visiona. Body temperature within normal rangeb. Laboratory values within normal rangesc. Has no abnormal discharges or signs of infectiond. Continues to see objects at baseline acuity levele. Shows no signs of keratoconjunctivitisf. Shows no signs of pneumonia


disorders of the immune system

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