Assessment and Management of Pt’s w/ Allergic Disorders

 The epithelial cells that coat the skin and make up the lining of the respiratory, gastrointestinal, and genitourinary tracts
provide the first line of defense against microbial invaders.
 The structure and continuity of these surfaces and their resistance to penetration are initial deterrents to invaders.
 One of the most effective defense mechanisms is antibodies, specific protein antigens.
 Antibodies react with antigens in a variety of ways by:
coating the antigens’ surfaces if they are particular substances,
neutralizing the antigens if they are toxins, and
precipitating the antigens out of solution if they are dissolved.
 The antibodies prepare the antigens so that the phagocytic cells of the blood and the tissues can dispose of them.

Physiologic Overview
 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 normally harmless allergens.

Function of Immunoglobulin
 Antibodies that are formed by lymphocytes and plasma cells in response to an immunogenic stimulus constitute a group of
serum proteins called immunoglobulins.
 Grouped into five classes ( IgE, IgD, IgG, IgM, and IgA), immunoglobulins can be found in the lymph nodes, tonsils,
appendix, and Peyer’s patches of the intestinal tract or circulating in the blood and lymphs.
 IgE- producing cells are located in the respiratory and intestinal mucosa.
 Allergic skin reactions, asthma, and hay fever are produced when two or more IgE molecules bind together to an allergen
and trigger mast cells or basophils to release chemical mediators:
histamine
serotonin
kinins
slow- reacting substances of anaphylaxis
neutrophil factor, which produces.
 Atopy refers to IgE-mediated diseases such as allergic rhinitis that have a genetic component.

Role of B Cells
 B lymphocytes, are programmed to produce one specific antibody.
 On encountering a specific antigen, B cells stimulate production of plasma cells, the site of anti-body production.
 The result is the outpouring of antibodies for the purpose of destroying and removing the antigens.

Role of T Cells
 T lymphocytes, assist the B cells in producing antibodies.
 T cells secrete substances that direct the flow of cell activity, destroy target cells, and stimulate the macrophages.
 Unlike a specific antibody, a T cell does not bind free antigens.

Function of Antigens
 Antigens are divided into two groups: complete protein antigens and low- molecular- weight substances.
 Complete protein antigens, such as animal dander, pollen, and horse serum, stimulate a complete humoral response
(humoral immune response: the immune system’s second line of defense; often termed the antibody response )
 Low- molecular-weight substances, such as medications, function as haptens (incomplete antigens), binding to tissue or
serum proteins to produce a carrier complex that initiates an antibody response.

Function of Chemical Mediators

 Mast cells, are located in the skin and mucous membranes, play a major role in IgE- mediated immediate hypersensitivity.
 When mast cells are stimulated by antigens, powerful chemical mediators are released, causing a sequence of physiologic
events which results 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.

Primary Mediators

Histamine
 Histamine, which is released by mast cells, plays an important role in the immune response.
 Its effects, which are greatest within about 15 minutes after antigen contact, 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.
 Histamine action results from stimulation of histamine- 1 ( H1) and histamine- 2 ( H2) receptors.
H1 receptors are found predominantly on bronchiolar and vascular smooth muscle cells;
H2 receptors are found on gastric parietal cells.

Eosinophil Chemotactic Factor of Anaphylaxis

 Affects movement of eosinophils to the site of allergens.
 It is preformed in the mast cells and is released from disrupted mast cells.

Platelet- Activating Factor

 Responsible for initiating platelet aggregation and leukocyte infiltration at sites of immediate hypersensitivity reactions.
 It also causes bronchoconstriction and increased vascular permeability.

Prostaglandins
 Produce smooth muscle contraction as well as vasodilation and increased capillary permeability.
 The fever and pain that occur with inflammation in allergic responses are caused in part by the prostaglandins.

Secondary Mediators

Leukotrienes
 Chemical mediators that initiate the inflammatory response.
 Many manifestations of inflammation can be attributed in part to leukotrienes.
smooth muscle contraction,
bronchial constriction,
mucus secretion in the airways,
the typical wheal and flare reactions of the skin

Bradykinin
 A substance that has the ability to cause:
increased vascular permeability,
vasodilation,
hypotension,
contraction of many types of smooth muscle, such as the bronchi.
 Increased permeability of the capillaries results in edema.
 Stimulates nerve cell fibers and produces pain.
Serotonin
 Acts as a potent vasoconstrictor and causes con-traction of bronchial smooth muscle.

Hypersensitivity

Classified into 4 types (most are either type I or type IV):

Type Description Examples

Increased production of immunoglobulin E
(IgE), an antibody
Type I
Acute inflammation occurs when IgE
Rapid Hypersensitivity Rx
responds to an antigen such as pollen, and
causes the release of histamines and other
vasoactive amines (e.g. basophils,
eosinophils, and mast cells)
anaphylaxis, allergic asthma, atopic allergies
(e.g. allergic rhinitis, hay fever, latex, bee
venom, peanuts, iodine, shellfish, drugs
Causes reactions in (a.) mucus membranes of
nose and eyes (sneezing, itchy watery eyes or
(b) involving all blood vessels and bronchiolar
smooth muscles ( widespread blood vessel
dilation, decreased cardiac output,
bronchoconstriction)

Hemolytic anemias, thrombocytopenia

Body makes special auto-antibodies directed
purpura, hemolytic transfusion reaction, and
against self cells that have some form of
drug induced hemolytic anemia.
Type II foreign protein attached to them. The
Cytotoxic Rx autoantibody binds to the self cell and forms
Treatment includes plasmapheresis (filtering
an immune complex. The self cell is then
the blood) and/or just treating the
destroyed along with the attached protein.
symptoms.
Excess antigens cause immune complexes to
form in the blood. These circulating
Type III
complexes usually lodge in small blood vessel rheumatoid arthritis
Immune Complex Rx
walls especially kidneys, skin, and joints. The systemic lupus erythematosus (SLE).
deposited complexes trigger inflammation,
and tissue or vessel damage.
 Sensitized T-cells from a precious exposure
Type IV PPD injection, contact dermatitis from
respond to an antigen
Delayed Hypersensitivity cosmetics, tape, topical meds, plants
occurs 24-72 hours after exposure to an
Rx symptoms-itching, erythema, raised lesions
allergen
treatment –remove offending antigen
Hypersensitivities/Allergies
 increased response to the presence of an antigen (foreign protein or allergen) the pt has been previously exposed.
 These responses can cause problems from uncomfortable: ( watery, itchy eyes or sneezing) to life-threatening (allergic
asthma, circulatory collapse).

Testing

Total Serum Immunoglobulin E Levels

 High total serum IgE levels support the diagnosis of allergic disease.
 However, a normal IgE level does not exclude the diagnosis of an allergic disorder.
 IgE levels are not as sensitive as the paper radioimmunosorbent test or the enzyme linked immunosorbent assay.

Skin Tests
 Entails the intradermal injection or superficial application of solutions at several sites.
 Solutions contain individual antigens representing an assortment of allergens most likely to be implicated in the pt’s
disease.
 Results indicate which of several antigens are most likely to provoke symptoms and provide some clue to the intensity of
the pt’s sensitization.

Types of Skin Tests

 The methods of 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 pt’s
history to be problematic.
 A negative response on a skin test cannot be interpreted as an absence of sensitivity to an allergen

NURSING ALERT
 Corticosteroids and antihistamines, including over-the- counter allergy medications, suppress skin test reactivity and
should be stopped 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.

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.
 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.

Radioallergosorbent Test
 RAST is a radioimmunoassay that measures allergen-specific IgE.
 A sample of the pt’s serum is exposed to a variety of suspected allergen particle complexes.
 If antibodies are present, they will combine with radio labeled allergens.
 Test results are then compared with control values.
 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,
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,
higher cost

Oral Food Challenge

 Eliminate suspected foods for 7-14 days before test. Then eat foods for one day and monitor reactions

ALLERGIC DISORDERS
 There are two types of IgE mediated allergic reactions.
 Immunologic reactions of the two are the same, the predisposing factors and manifestations are different.
 The atopic disorders are characterized by:
a hereditary predisposition and production of a local reaction to IgE antibodies,
which manifests in one or more of the following three atopic disorders:
allergic rhinitis,
asthma,
atopic dermatitis/ eczema.
 The nonatopic disorders lack the genetic component and organ specificity of the atopic disorders.

Anaphylaxis
 Clinical response to an immediate immunologic reaction between a specific antigen and an antibody.
 The reaction results from a rapid release of IgE mediated chemicals.

Pathophysiology
 Anaphylaxis is caused by the interaction of a foreign antigen with specific IgE antibodies found on the surface membrane of
mast cells and peripheral blood basophils.
 The subsequent release of histamine and other bioactive mediators causes activation of platelets, eosinophils, and
neutrophils.
 Histamine, prostaglandins, and inflammatory leukotrienes are potent vasoactive mediators that are implicated in:
vascular permeability changes,
flushing,
urticaria,
angioedema,
hypotension,
bronchoconstriction
 Clinical manifestations within seconds or minutes after antigen exposure are:
Smooth muscle spasm,
bronchospasm,
mucosal edema and inflammation,
increased capillary permeability result
 Prevention
wear medic alert bracelet
tell health care provider
nurse should ask about known allergies -if allergic to penicillins, likely allergic to cephalosporins.
If allergic to bananas, likely allergic to latex
carry emergency anaphylaxis kit (e.g. EpiPen) -delivers 0.3 mg epinephrine.

Nonallergenic Anaphylaxis (Anaphylactoid Reaction)

 Closely resembling anaphylaxis is an anaphylactoid reaction, which is caused by the release of mast cell and basophil
mediators triggered by non– IgE mediated events.
 Reaction may occur with medications, food, exercise, or cytotoxic antibody transfusions.
 The reaction may be local or systemic.
Local reactions usually involve urticaria and angioedema at the site of the antigen exposure.
 Although possibly severe, nonallergenic anaphylaxis reactions are rarely fatal.
  Systemic reactions occur within about 30 minutes after exposure and involve:
cardiovascular,
respiratory,
gastrointestinal,
integumentary organ systems
 Treatment is identical to that of anaphylaxis

Clinical Manifestations
 Anaphylactic reactions produce a clinical syndrome that affects multiple organ systems.
 Reactions may be categorized as mild, moderate, or severe.
 The time from exposure to the antigen to onset of symptoms is a good indicator of the severity of the reaction: the faster
the onset, the more severe the reaction.
 The severity of previous reactions does not determine the severity of subsequent reactions, which could be the same or
more or less severe.
 The severity depends on the degree of allergy and the dose of allergen
 Mild systemic reactions consist of: (Onset of symptoms begins within the first 2 hours after exposure)
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,
tearing of the eyes can also be expected
 Moderate systemic reactions may include:
flushing, warmth,
anxiety, and
itching
any of the milder symptoms.
 More serious reactions include: (Onset of symptoms begins within the first 2 hours after exposure)
bronchospasm and edema of the airways or larynx with dyspnea,
cough, and wheezing.
 Severe systemic reactions have an abrupt onset, same signs and symptoms described previously but progress rapidly to:
bronchospasm,
laryngeal edema,
severe dyspnea,
cyanosis,
hypotension
Dysphagia ,
abdominal cramping,
vomiting,
diarrhea,
seizures can also occur
Cardiac arrest and coma may follow

Assessment
 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,
VS: < BP, rapid, weak, irreg pulse due to vasodilation and extensive capillary leak can lead to cardiac arrest
 The patient is observed for signs of:
increasing edema and respiratory distress
auscultation -crackles, wheezing, < BS, hoarseness, stridor
 Prompt notification of the physician and preparation for initiation of emergency measures
intubation,
 administration of emergency medications,
insertion of IV lines,
fluid administration,
oxygen
EpiPen important to reduce the severity of the reaction and to restore cardiovascular function.
 The nurse documents the interventions used and the patient’s vital signs and response to treatment.
 The patient who has recovered from anaphylaxis needs an explanation of what occurred and instruction about avoiding
future exposure to antigens and how to administer emergency medications to treat anaphylaxis.
 The patient must be instructed about antigens that should be avoided and about other strategies to prevent recurrence of
anaphylaxis.
 All patients who have experienced an anaphylactic reaction should receive a prescription for preloaded syringes of
epinephrine.
 The nurse instructs the patient and family in their use and has the patient and family demonstrate correct administration

Interventions
 assess resp function
 establish airway
 give epinephrine 0.3 to 0.5 ml SC -constricts blood vessels, improves cardiac contractions, dilates bronchioles. Repeat Q 15-
20 min prn
 antihistamines ( e.g. Benadryl) to tx urticaria, angioedema
 O2 via cannula or face mask
 pulse ox > 90% corticosteroids -long term tx
 suction prn
 HOB 45 degrees
 theophylline IV for bronchospasm
 Medications
Sympathomimetics e.g. epinephrine (Adrenalin), isoproterenol (Isuprel)
action : vasoconstriction, bronchodilation
side effects: pallor, tachy, palpitations, nervousness, sweating, anxiety, > BP

Antihistamines ( diphenhydramine HCL (Benadryl)

action: blocks effects of histamine on bronchioles, GI tract and blood vessels
side effects: drowsiness, confusion, insomnia, H/A, N/V, dry mouth, vertigo, diplopia, photosensitivity

Allergic Rhinitis
 The symptoms are similar to those of viral rhinitis but are usually 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
 The proportion of patients with the allergic form of rhinitis increases with age.
 It often occurs with other conditions, such as:
allergic conjunctivitis,
sinusitis,
asthma.
 If symptoms are severe, allergic rhinitis may interfere with:
sleep,
leisure,
school or work activities
 If left 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),
in children, orofacial dental defomities.
  Allergic rhinitis is induced by airborne pollens or molds
 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)

Pathophysiology
 Sensitization begins by ingestion or inhalation of an antigen.
 On re-exposure,
the nasal mucosa reacts by the slowing of ciliary action,
edema formation,
leukocyte infiltration.
 Histamine is the major mediator of allergic reactions in the nasal mucosa.
 Tissue edema results from vasodilation and increased capillary permeability.
 Primary phase
histamine release causes capillary leak, nasal and conjunctival secretion, pruritis and redness.
symptoms last 10 minutes. Longer if allergen continuously present.
 Secondary phase
release of other proteins that draw more WBCs to the area and stimulate a more general inflammatory
reaction

Clinical Manifestations
 Typical signs and symptoms of allergic rhinitis include
Sudden outburst of sneezing and nasal congestion;
clear, watery nasal discharge; a
nasal itching.
itching of the throat and soft palate is common.
drainage of nasal mucus into the pharynx
dry cough or hoarseness
headache,
pain over the paranasal sinuses,
epistaxis
 Lab assessment
> eosinophils (nl 1-2%)
> IgE (nl 39I U/ml
 Allergic rhinitis can affect quality of life by also producing:
fatigue,
loss of sleep,
poor concentration

Etiology
 based on genetic inheritance
 50% of pts with allergic rhinitis have one parent with type I allergies

 Incidence
affects about 25% of the population of U.S.
men and women affected equally
racial differences have not been documented

Medical Management
 Avoidance therapy
air conditioning units
remove cloth drapes, upholstered furniture, carpeting
cover mattresses and pillows with plastic cover
pets -frequent bathing, keep out of bedroom, or remove completely
  Symptomatic therapy
Drug Therapy
Decongestants-available as oral drugs or nasal sprays
cause vasoconstriction in inflamed tissue reducing edema
SE - dry mouth, > BP, sleep difficulties. Consult with MD before taking if have high BP, glaucoma or urinary
retention

Antihistamines -compete with histamine at receptor site and block histamine from binding to the receptor. May
also < secretions. Older preparations such as Benadryl may induce sedation. Newer preps such as
Zyrtec, Clarinex are less sedating

Corticosteroids -decrease inflammatory response by stabilizing the cell membranes of inflammatory cells thereby
decreasing capillary permeability. Nasal sprays (e.g. Flonase) can < sx of rhinitis. Oral preps have
serious side effects and are used only short term
SE -GI ulceration, poor wound healing, < immune function, > risk for infections, weight gain, hyperglycemia,
personality changes, fluid retention

Mast Cell Stabilizers (Nasalcrom) -prevent mast cell membs from opening when an allergen binds to IgE.
Prevent symptoms from occurring but do not tx sx. Not useful during an acute episode.

Leukotriene Antagonists (Zyflo, Accolate) -work best to prevent allergic rhinitis. Less side effects but more
expensive

Desensitization Therapy -“allergy shots”

SC injections of small amts of the allergen
> dose given weekly or more often
recommended course of tx is 5 years

 The patient must be aware of the effects caused by overuse of the sympathomimetic agents in nose drops or sprays.
 A condition referred to as rhinitis medicamentosa may result
 After topical application of the medication, a rebound period occurs in which the nasal mucous membranes become more
edematous and congested than they were before the medication was used.
 Such a reaction encourages the use of more medication, and a cyclic pattern results.
 The topical agent must be discontinued immediately and completely to correct this problem.

Assessment
 The examination and history of the patient reveals S&S of allergic rhinitis
 The health history includes a personal or family history of allergy.
 The allergy assessment identifies the nature of antigens, seasonal changes in symptoms, and medication history.
 The nurse also obtains subjective data about how the patient feels just before symptoms become obvious.
 Any relationship between emotional problems or stress and the triggering of allergy symptoms is assessed.

Selected Nursing Strategies for Allergy Management

 Identify and document the patient’s known allergens (eg, medications, foods, insects, environmental allergens).
 Describe the patient’s typical allergic reaction and its severity.
 Post allergy alerts appropriately.
 Encourage the patient to wear a medical alert band and to carry information about allergies at all times.
 Monitor the patient closely after administration of new medications and exposure to new foods, contrast agents, latex,
and other allergens.
 Investigate potential for allergic reactions with all new medications through consultation with the pharmacist.
 Instruct the patient to question all medications and new foods.
 Identify early manifestations of allergic reactions.
 Administer emergency treatment for allergic reactions.
 Monitor the patient’s response and status for 12– 14 hours after a severe allergic reaction.
 Instruct the patient and family about emergency home management and avoidance measures from allergens.
Contact Dermatitis
 Type IV delayed hypersensitivity reaction A
 An acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens.
 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.
 There are four basic types:
allergic,
irritant,
phototoxic, and
photoallergic
 Signs & Symptoms
itching, burning, erythema, skin lesions, edema
weeping, crusting dryness and peeling of skin
may become infected
finding cause is difficult -patch tests

Latex Allergy
 type I hypersensitivity reaction in which the allergen is a specific protein found in processed natural latex rubber products
 may be limited to skin or mucous membranes causing contact dermatitis which is a type IV delayed hypersensitivity
reaction
 other people have a mixed type I and Type IV reaction
 others have just a type I reaction
 Ask pts if they have a known latex allergy

Atopic Dermatitis (Eczema)

 type I hypersensitivty
 most common in infants and children
 affects 1-20% of population
 After stroking the skin, immediate redness appears followed in 15-30 seconds by pallor for 1-3 minutes
 lesions develop secondary to trauma of scratching
 chronic with remissions and exacerbations up to age 20

 Signs & Symptoms

pruritis, hyperirritability of skin, excessive dryness
 Treatment
wear cotton fabrics
use mild detergent
humidify air
antihistamines
avoid animals, dust, perfumes
keep skin moisturized
topical corticosteroids
treat infections with antibiotics
teach pt about meds and side effects

Dermatitis Medicamentosa (Drug Reactions)

 type I hypersensitivity disorder
 caused by internal administration of certain meds
 most common reaction is a rash that usually disappear after med is stopped
 may have a systemic reaction
 remind pt to inform all medical personnel of drug allergy
Urticaria and Angioneurotic Edema

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.
 They may involve any part of the body:
mucous membranes (especially those of the mouth),
larynx (occasionally with serious respiratory complications),
gastrointestinal 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.

Angioneurotic Edema
 Involves the deeper layers of the skin, resulting in more diffuse swelling than 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, tongue;
hands, feet, genitalia,
mucous membranes of the larynx, the bronchi, and the gastrointestinal canal, mainly in the hereditary type
 Swellings may appear in a few seconds or minutes, or in 1 or 2 hrs 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.
 Angiotensin converting enzyme (ACE) inhibitors and penicillin, may cause angioedema.