Nursing Care of Clients with Allergic

Allergic Reaction Disorders

 Manifestation of tissue injury resulting from interaction between an antigen and antibody.
 ALLERGY – is an inappropriate and often harmful response of the immune system to normally
harmless substances (allergens)
Allergy Reaction
 In allergic reactions, the body encounters allergens body’s defenses recognize as foreign
destroy them, and remove them from the body.

Functions of Immunoglobulins

 Immunoglobulins of the IgE class

 Involved in allergic disorders and some parasitic infections
 IgE-producing cells are located in the respiratory and intestinal mucosa.
 Two or more IgE molecules bind together to an allergen and trigger the mast cells or basophils to
release chemical mediators.
 ATOPY – refers to IgE-mediated diseases, such as allergic rhinitis.

ROLE OF B CELLS
 Production of plasma cells (site of antibody production) -> destroy and remove antigens

ROLE OF T CELLS
 Assis B cells: directs flow of cell activity; destroy and digest antigens; remove cells and other
debris.
 Does not bind free antigens

Functions of Antigens

Two groups:
 Complete protein antigens
 Stimulate a complete humoral response.
 Example: Animal dander, Pollen, Horse serum
 Low molecular-weight substances
 Function as haptens (incomplete antigens) binding to tissue or serum proteins to produce
a carrier complex that initiates an antibody response.
 Example: Medications
 When the allergen is absorbed through the respiratory tract, GIT or skin, allergen sensitization
occurs.
 Macrophages process the antigen & present it to the appropriate cells.
 These cells mature into allergen-specific secreting plasma cells that synthesize & secrete
antigen-specific antibodies.

Function of Chemical Mediators

 Mast cells: located in skin and mucous membrane
 Major role in IgE-mediated immediate hypersensitivity
 Releases powerful chemical mediators:
o Primary mediators – preformed; found in mast cells or basophils
o Secondary mediators – inactive precursors formed or released in response to
primary mediators.
 Primary Chemical Mediators

 Histamine
 1st chemical mediator in immune and inflammatory responses.
 effects peak 5 to 10 minutes after antigen contact.
 erythema, localized edema in the form of wheals: pruritus; contraction of bronchial smooth
muscle -> wheezing and bronchospasm; dilation of small venules and constriction of large
vessels; increased secretion of gastric and mucosal cells -> diarrhea
 stimulates H1 (bronchiolar and vascular smooth muscle cells) and H2 receptors (gastric
parietal cells)
 Eosinophil Chemotactic Factor of Anaphylaxis
 Affects the movement of eosinophils to the site of allergens
 Preformed in the mast cells and is released from disrupted mast cells.
 Platelet-Activating Factor
 Responsible for initiating platelet aggregation & leukocyte infiltration at sites of immediate
hypersensitivity reactions.
 Also causes bronchoconstriction and increased vascular permeability.
 Prostaglandins
 Produce smooth muscle contraction as well as vasodilation & increased capillary
permeability.
 Causes fever and pain in allergic responses.

Secondary Chemical Mediators

 Leukotrienes
 Initiate the inflammatory response
 Cause smooth muscle contraction, bronchial constriction, mucus secretion in the airways,
& typical wheal-and-flare reactions of the skin.
 100 to 1,000 times more potent in causing bronchospasm
 Bradykinin
 Has the ability to cause increased vascular permeability, vasodilation, hypotension &
contraction of many types of smooth muscle.
 Stimulates nerve cell fibers and produces pain.
 Serotonin
 Acts as a potent vasoconstrictor & causes contraction of bronchial smooth muscle.

Hypersensitivity
 Is a reflection of excessive or aberrant immune response to any type of stimulus
 Usually does not occur with the first exposure to an allergen
 Reaction follows a re-exposure after sensitization, or buildup of antibodies in a predisposed
person.
4 SPECIFIC TYPES OF REACTIONS:
 Anaphylactic (type 1) Hypersensitivity
- MOST SEVERE TYPE of hypersensitivity
- An immediate reaction beginning within minutes of exposure to an antigen
- Primary chemical mediators are responsible for the symptoms
- Characterized by edema in many tissues, including the larynx
- Often accompanied by hypotension, bronchospasm & cardiovascular collapse.
- Clinical symptoms are determined by the amount of the allergen, the amount of mediator
released, the sensitivity of the target organ, and the route of allergen entry
- May include both local & systemic anaphylaxis

 Cytotoxic (type 2) Hypersensitivity

- Occurs when the system mistakenly identifies a normal constituent of the body as
foreign
- May be the result of cross-reacting antibody, possibly leading to cell & tissue damage.
- Example:
o Myasthenia gravis – the body mistakenly generates antibodies against normal nerve
ending receptors.
o Goodpasture syndrome – generates antibodies against lung & renal tissue thereby
producing lung damage & renal failure

 Immune Complex (type 3) Hypersensitivity

- Involves immune complex that are formed when the antigens bind to antibodies.
 - Normally, these immune complexes are cleared through phagocytosis
- This type of hypersensitivity, the immune complexes are deposited in tissues or vascular
endothelium.
- 2 factors that contribute to injury:
o Creased amount of circulating complexes
o Presence of vasoactive amines
- Result:
o Increase vascular permeability
o Tissue injury
- Example:
o Systemic Lupus Erythematosus, serum sickness, nephritis, and rheumatoid arthritis
- Signs & Symptoms
o Urticaria, joint pain, fever, rash and adenopathy (swollen glands)

 Delayed-type (type 4) Hypersensitivity

- Also known as cellular hypersensitivity; delayed type
- Occurs 24 to 72 hours after exposure to an allergen
- Mediated by sensitized T cells that cause cell & tissue damage
- Symptoms include itching, erythema and raise lesions
- Subcutaneous injection of antigen
- Is often used as an assay for cell-mediated immunity (e.g., the purified)
- Assay for cell-mediated immunity: purified protein derivative skin test for immunity to
Mycobacterium tuberculosis.

Assessment of Clients with Allergic Disorders

- Comprehensive allergy history

- Thorough physical examination
- Use of an allergy assessment form
- Take note of:
 Degree and difficulty experienced
 Degree of improvement of symptoms with or without treatment
 Relationship of symptoms to exposure to possible allergens

Health History (Allergy)

- Allergies
o Types of allergens
o Symptoms experienced
o Seasonal variations in occurrence or severity in the symptoms
- History of testing & treatments
- Prescribed OTC medications
o Previously taken
o Currently taking for these allergies
o Effectiveness of the treatments
- Continued assessment for potential allergic reactions in the patient is vital
NOTE: All medication & food allergies are listed on an allergy alert sticker & placed on the front of the
patient’s health record or chart to alert others.
Diagnostic Evaluation for Allergic Disorders
 Blood tests
 CBC with Differential
o Eosinophils (n=2% - 5%)
o 5% to 10% for patients with allergic disorders
 Eosinophil Count
o Blood samples or Smears of secretions (nasal, I & sputum)
 Total Serum IgE levels
o Increased levels may support diagnosis of allergic disease
 Smears of body secretions
 Skin tests (MOST ACCURATE)
- Intradermal injection or superficial application (epicutaneous) of solutions at several
sites
- Positive (wheal-and-flare) reactions are clinically significant when correlated with the
history, physical findings, and results of other laboratory tests
- Results complement the data obtained from history
- Dosage of the antigen (allergen) injected is also important

Precautionary Steps before Skin Testing

1. Testing must not be performed during periods of bronchospasm
2. Epicutaneous tests are performed before other testing methods
3. Emergency equipment must be readily available to treat anaphylaxis
4. Corticosteroids & antihistamines should be stopped 48 – 96 hours before testing

Types of Skin Tests

 Prick skin tests
 Scratch tests
 Intradermal skin test
o Positive reaction (urticarial wheal, localized erythema, pseudopodia [irregular
projection at the end of the wheal])

The following guidelines are used for the interpretation of skin test results:
 Skin tests are used most frequently with the dx of allergic rhinitis
 Negative test results are helpful in ruling out food allergy
 Positive skin tests correlative highly with food allergy
Diagnostic Evaluation for Allergic Disorders (Continuation)
 Provocative Testing
- Direct administration of suspected allergen to the sensitive tissue (conjunctiva, nasal
& bronchial mucosa or GIT)
- Helpful who have large no. of positive tests
- Disadvantages:
o Limitation of 1 antigen per session
o Risk for producing severe symptoms
 Serum-Specific IgE Test
- Formerly known as Radioallergosorbent Test (RAST)
- Radioimmunoassay that measures allergen-specific IgE
- Patient’s serum is exposed to a variety of suspected allergen particle complexes
- If antibodies are present, they combine with radiolabeled antigen
- Test results are compared with control values; reported on a scale of 0 to 5
(significant ≥ 2)
- Advantages:
o Decreased risk of systemic reaction
o Stability of antigens
o Lack of dependence on skin reactivity modified by medications
- Disadvantages:
o Limited allergen selection
o Reduced sensitivity compared with intradermal skin tests
o Lack of immediate results, and higher cost

Medical Management
Goal: Provide relief symptoms
 Avoidance therapy
- Every attempt is made to remove allergens that act as precipitating factors
- Examples:
o Use of air conditioners & air cleaners
o Removal of dust-catching furnishings
o Removal of pets from home
o Use of high-efficiency particulate air (HEPA) purifiers
- Changing clothing when coming in from outside
- Showering to wash allergens from hair and skin
- Using an over-the-counter nasal irrigation device or saline nasal spray to reduce
allergens in the nasal passages
 Pharmacologic Agents
- Antihistamines (H1 receptor antagonist/ H1 blockers)
o Bind selectively to H1 receptors, preventing the action of histamine at these
sites
o FOR MILD ALLERGIC DISORDERS
o They do not prevent the release of histamine from mast cells or basophils
o Oral antihistamines are most effective when given at the first occurrence of
symptoms
o Effectiveness is limited to certain patients with hay fever, vasomotor rhinitis,
urticarial, & mild asthma
 o Major class of medications prescribed for the symptomatic relief of allergic
rhinitis
o Major side effect: DROWSINESS AND DRY MOUTH
o Other side effects
Anxiety
Agitation
Urinary retention
Blurred vision
Anorexia
Nausea and vomiting
o Contraindications
Intake during the third trimester
In nursing mothers
Newborns & children
Older patients
Patient with asthma, urinary retention, open-angle glaucoma, HPN &
prostatic hyperplasia
o Second-generation H1-receptor antagonists
 Nonsedating (does not cross the blood-brain barrier)
 Examples: Loratadine, Cetirizine, fexofenadine
 May be combined with decongestants to reduce nasal congestion
 Examples: Loratidine/Pseudoephedrine (Claritin-D) and
Cetirizine/Pseudoephedrine (Zyrtec-D)
 Decongestants can cause increase in blood pressure
- Adrenergic agents
o Vasoconstrictor of the mucosal muscles
o Reduces local blood flow, fluid exudation, mucosal edema
o Used for relief of nasal congestion
o Activate the alpha-adrenergic receptor sites of the smooth muscle of the
nasal mucosal blood vessels causing reduction of:
Local blood flow
Fluid exudation
Mucosal edema
o Used topically in nasal (Afrin) & ophthalmic (Alphagan P) formulations in
addition to oral route (pseudoephedrine (Sudafed))
o Topical preparations have less side effects
o However, should be limited to a few days to avoid rebound congestion
o Potential side effects:
Hypertension
Dysrhythmias
Palpitations
CNS stimulation
Irritability
Tremor
Tachyphylaxis (acceleration of hemodynamic status)
- Mast cell stabilizers
o Stabilizes the mast cell membrane thus reducing the release of histamine &
other mediators
o Inhibits macrophages, eosinophils, monocytes & platelets involved in the
immune response
o Used prophylactically to prevent the onset of symptoms & to treat the
symptoms once they appear
o Used therapeutically for chronic allergic rhinitis
o E.g. Intranasal cromolyn sodium
 Effective as antihistamines but less effective than nasal
corticosteroids in the treatment of seasonal allergic rhinitis
 Beneficial effects may have a week to manifest
o Mild adverse effects:
Sneezing
Local stinging
Burning sensations
- Corticosteroids
o Anti-inflammatory action
o Indicated for more severe cases of allergic & perennial rhinitis
o Examples:
Beclomethasone (Beconase, Qnasl)
Budenoside (Rhinocort)
 Flunisolide (AeroSpan)
Triamcinolone (Nasocort)
o Full benefit may not be achieved for several days to 2 weeks
o Adverse effects
Drying of the nasal mucosa
Burning & itching sensations
o Systemic effects are more likely with DEXAMETHASONE
o Use of this medication should be limited only up to 30 days
o Suppresses the host defenses, must be used with caution in patients with
tuberculosis or untreated bacterial infections
o Inhaled corticosteroids DO NOT affect the immune system to the same
degree as systemic corticosteroids
o Because the response to corticosteroids is delayed, they have little or no
value in acute therapy for severe reactions such as anaphylaxis
o Patients who receive high-dose or long-term corticosteroid therapy must be
cautioned not to stop taking the medication suddenly. Doses are tapered
when discontinuing this medication to avoid adrenal insufficiency
o Side effects:
Fluid retention
Weight gain
Hypertension
Gastric irritation
Glucose intolerance
Adrenal suppression
- Leukotriene modifiers
o Block the action of leukotriene; prevent the signs & symptoms of asthma
o For long term use
o Should be taken daily
o Examples:
Zileuton
Zafirlukast (Accolate)
Montelukast
- Immunotherapy
o “allergen desensitization”/ “ allergen immunotherapy” / “hyposensitization” /
“allergen vaccine therapy”
o 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
o Used when avoidance of allergen is impossible
o Most common method: serial injection of one or more antigen
o Goal:
Reduce level of circulating IgE
Increase level of blocking IgG
Reduce mediator cell sensitivity
o Effective for ragweed pollen, grass, tree pollen, cat dander, & house dust
mites
o Evidences of failure:
No decrease in symptoms within 12 to 24 months
Failure to develop increased tolerance to known allergens
Failure to decrease the use of medications to reduce symptoms
o Begin with very small amount
o Gradually increased. Usually on a weekly interval, until a maximum tolerated
dose is achieved
o Maintenance booster injections are administered at 2-4-week interval
o Contraindications:
Patients using beta-blocker or ACE inhibitors
With significant pulmonary or cardiac disease or organ failure
Inability of the patient to recognize/report signs of systemic reaction
Non-adherence of the patient
Absence of any equipment or adequate personnel to respond to
allergic reaction
Should not be initiated during pregnancy
o Nursing responsibilities:
Monitor patient after administration of immunotherapy
Should not be administered by a lay person/patient
Patient must remain in the office or clinic for 30 minutes
 If patient develops local swelling, the next dose should not be
increased

Allergic Disorders
 Anaphylaxis
- A clinical response to an immediate immunologic reaction between a specific antigen and an
antibody
- Results from a rapid release of IgE-mediated chemicals, which can induce a severe, life-
threatening allergic reaction
- Most commonly caused by:
Foods
Medications
Insect stings
Latex
 Antibiotics and radiocontrast agents – cause the most serious anaphylactic reactions
 Penicillin – most common cause of anaphylaxis
- Diagnosis:
Prick test
Intradermal skin testing
- Clinical manifestations: (CATEGORIES)
NOTE: “the faster the onset, the more severe reaction”
 Mild
Peripheral tingling
Sensation of warmth Onset of
Sensation of fullness in the mouth or throat symptoms begins
Nasal congestion within the first 2
Periorbital swelling hours after
Pruritus exposure
Sneezing
Tearing of the eyes

 Moderate
Symptoms in the mild category plus:
Flushing
Warmth Onset is the
Anxiety same as the
Itching mild category
Bronchospasm
Edema of the airways or larynx with dyspnea,
coughing & wheezing

 Severe
Symptoms previously described then 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
NOTE: “the severity of previous reactions does not determine the severity of the subsequent reactions”
- Prevention:
 Strict avoidance of potential allergens
Insect stings
o Should avoid areas populated by insects
o Use appropriate clothing
o Use of insect repellant
o Caution to avoid further stings
 If avoidance of exposure is impossible, an auto-injector system for
epinephrine should be prescribed
EpiPen Auto-Injector
o A commercially available first aid device that delivers premeasured doses of
0.3 mg (EpiPen) or 0.15 mg (EpiPen Jr.) of epinephrine
 o Requires no preparation
o Self-administration is not complicated
o Who should ALWAYS carry it?
o Those who are sensitive to insect bites & stings
o Those who have experienced food or medication reactions
o Those who have experienced idiopathic or exercise-induced anaphylactic
reactions

 Screening of allergies before a medication is prescribed or first administered

o Careful history of any sensitivity must be obtained
o Ask about previous exposure to contrast agents, medications, food, insect
stings & latex
o If predisposed, should wear medical identification (i.e. bracelets/necklace)
 Immnunotherapy/desensitization
o Those who are allergic to insect venom
o Very effective in the reduction of risk of anaphylaxis in future stings
o Honeybees, fire ants & wasps
o Effective also for insulin-allergic patients with diabetes
o Allergic to penicillin
NOTE: **used as a control measure, not cure**
- Medical management
 CPR if cardiac arrest is noted
 Supplemental oxygen
o Provided during CPR or if the patient is cyanotic, dyspneic or wheezing
 Administer epinephrine
o 1:1,000 dilution; administered SC in the upper extremity or in the thigh
o May also be followed through continuous intravenous infusion
 Antihistamines & Corticosteroids
o To prevent recurrence of the reaction
o Treat urticaria & angioedema
 Intravenous fluids, volume expanders & vasopressor agents
o To maintain BP & normal hemodynamic status
 Aminophylline + Corticosteroids
o To improve airway patency, esp. those with bronchospasm & history of
asthma & COPD
 Patients should also be transported immediately to the local emergency department
for observation and monitoring because of the risk of “rebound” or delayed reaction 4
to 10 hours after the initial reaction
 Monitoring should be done for the next 12 of 14 hours
- Nursing Management
 Assess for S/S of anaphylaxis
o Airway, breathing pattern & vital signs
o Increasing edema
o Respiratory distress
 Prompt notification of the rapid response team and/or provider
 Rapid initiation of emergency measures
o Intubation
o Administration of emergency medications
o Insertion of intravenous lines
o Fluid administration
o Oxygen administration
 Documentation of interventions done, patient’s vital signs & response to the
treatment
 Explanation to the patient of what has occurred
 Give instructions about avoiding future reactions and about how to administer
emergency medications
 Make sure the patient has received a prescription of preloaded syringes of
epinephrine

 Allergic Rhinitis
- “hay fever”
- Most common form of respiratory allergy
- Presumed to belong to the Type I hypersensitivity reaction
- Occurrence increases as one ages
- Occurs with other conditions:
Allergic conjunctivitis
 Sinusitis
Asthma
- Induced by airborne pollens or molds
 In temperature areas that do not experience freezing teperatures, molds can persist
throughout the year
- Pathophysiology
 Begins by inhalation or ingestion of antigen
 On re-exposure, the nasal mucosa reacts by:
Slowing of ciliary action
Edema formation – results from vasodilation & increased tissue permeability
Leukocyte (eosinophil) infiltration
NOTE: HISTAMINE is the major mediator of allergic reactions in the nasal mucosa
- Clinical Manifestations
Sneezing
Nasal congestion
Clear watery discharge
Nasal itching
Itching of the throat & soft palate
Dry cough
Headache
Pain over the paranasal sinuses
Epistaxis
- Complications
Allergic asthma
Chronic nasal obstruction
Chronic otitis media with hearing loss
Anosmia (absence of the sense of smell)
- Assessment & Diagnostics
History & PE
Nasal smears
Peripheral blood smears
Total serum IgE – increased
Epicutaneous & intradermal testing
RAST – presence of IgE
Food elimination & challenge
Nasal provocation test
 Results indicative of allergy as the cause of allergy:
Increased IgE
Increased eosinophil levels
Positive reactions to allergen testing
- Medical Management
 Avoidance therapy
 Pharmacologic therapy
Antihistamines adrenergic agents
Mast cell stabilizers
Corticosteroids
Leukotriene modifiers
 Immunotherapy
- Nursing diagnoses
 Ineffective breathing pattern r/t allergic reaction
 Deficient knowledge about allergy and the recommended modifications in lifestyle &
self-care practices
 Ineffective coping with chronicity of condition & need for environmental modifications
- Nursing Interventions
 Assist in modifying environment
 Reduce exposure to people with respiratory infections
 If with upper respiratory infection, instruct deep breaths & to cough frequently
 Reinforce adherence to medication schedules & other treatment regimen
 Instruct to seek medical attention if both upper respiratory infection & allergic rhinitis
are present
 Remind about the desensitization schedules
 Explain the difference of each medication
 Encourage client to verbalize feelings & concerns

 Contact Dermatitis
- An acute or chronic skin inflammation that results from direct skin contact with chemical or
allergens
- A delayed-type hypersensitivity reaction
 - Skin sensitivity may develop after brief or prolonged periods of exposure
 Clinical picture may appear hours or weeks after sensitized skin has been exposed
- 4 basic types:
 Allergic
o Results from contact of skin and allergenic substance
o Has sensitization period of 10-14 days
o Clinical manifestations:
Vasodilation & perivascular infiltrates on the dermis
Intracellular edema
Usually seen on the dorsal aspects of hand
 Irritant
o Results from contact with substance that chemically or physically damages the
skin on a nonimmunologic basis
o Occurs after first exposure to irritant or repeated exposure to milder irritants over
an extended time
o Clinical manifestations:
Dryness lasting days to months
Vesiculation, fissures, & cracks
Most common areas: hands & lower arms
 Phototoxic
o Resembles the irritant type but requires sun & chemical in combination to
damage to epidermis
 Photoallergic
o Resembles allergic dermatitis but requires light exposure in addition to
allergen contact to produce immunologic reactivity
- Clinical manifestations:
Itching
Burning
Erythema
Skin lesions
Edema
Followed by: weeping, crusting and drying & peeling of the skin
Hemorrhagic bullae may develop
Repeated reactions may be accompanied by thickening of the skin
Secondary infection may develop
- Assessment & diagnostic findings
History
Patch Test
Thin-layer Rapid Use Epicutaneous Test (T.R.U.E) [commonly used]
- Treatment
 Allergic type
o Avoidance of offending material
o Aluminum acetate (Burrow’s solution or Domeboro powder) or cool water
compress
o Systemic corticosteroids (prednisone) for 7-10 days
o Topical corticosteroids for mild cases
o Oral antihistamines to relieve pruritus
 Irritant
o Identification & removal of source of irritation
o Application of hydrophilic cream or petrolatum to soothe & protect
o Topical corticosteroids & compresses for weeping lesions
o Antibiotics for infection & oral antihistamines for pruritus
 Phototoxic & Photoallergic
o Same as with allergic and irritant types of contact dermatitis

 Atopic Dermatitis
- Characterized by inflammation & hyperreactivity of the skin
- Other name: ATOPIC ECZEMA
- A type I immediate hypersensitivity disorder
- Clinical manifestations:
o Most consistent features: pruritus & hyperirritability of the skin
Related to large amounts of histamine in the skin
o Excessive dryness of the skin with resultant itching
o In response to stroking of the skin, redness appears immediately
Pallor follows in 15 to 30 seconds and persists for 2-3 minutes
Lesions develop secondary to trauma from scratching;
 Appears in areas of increased sweating & hypervascularity
 - Chronic
 Has a tendency to recur, with from adolescence to 20 years of age
- Medical Management
 Decrease itching & scratching
o Wear cotton fabrics
o Wash with mild detergent
o Humidify dry heat in winter
o Maintain room temperature at 20⁰C to 22.2⁰
o Use antihistamines such as diphenhydramine
o Avoid animals, dust, sprays & perfumes
o Keep skin moisturize with daily baths & moisturizers
o Topical corticosteroids for inflammation
o Antibiotics for infection
o Immunosuppressives such as cyclosporine, tacrolimus, pimecrolimus
- Nursing Management
 Provide instructions & counseling about strategies to incorporate preventive
measures & treatments into the lifestyle
 Teach the signs secondary infection
 Teach about the side effects of the medications used

 Dermatitis Medicamentosa
- “drug reaction”
- Term applied to skin rashes associated with certain medications
- A type I hypersensitivity reaction
- Rashes appear suddenly and have a particular vivid in color
o Disappear rapidly after the medication is withdrawn
- On the discovery of a medication allergy,
o Patient is warned against the medication & should be advised never to take it again
o Always advise to let the patient carry information identifying the hypersensitivity with
them