Practice
nursing care for Clients with Immune Function Excess (Allergy)
The
inflammatory and immune responses are normally beneficial. They not only protect the body against
microorganism invasion and
cancer development, but they also stimulate tissue growth and repair after
injury. However, when inflammation or immune responses are prolonged,
excessive, or occur at an
inappropriate time, normal tissues can be damaged instead of protected. These responses are considered
"over-actions" to
invaders and foreign antigens and are known as hypersensitivity or allergic
responses. In addition, inflammatory and immune responses can fail to recognize self-cells and
literally attack normal body tissues. This type of reaction is known as an autoimmune
response. Both hypersensitivity and autoimmune responses can damage cells, tissues, or organs and have
serious consequences.
HYPERSENSITIVITY/ALLERGY
A hypersensitivity or
allergy is a state of increased or excessive response to the presence of an antigen (foreign
protein or allergen) to which the client has been previously
exposed. These responses
cause symptoms that range from uncomfortable (e.g., itchy, watery eyes or sneezing) to life
threatening (e.g., allergic
asthma, anaphylaxis, bronchoconstriction, or circulatory collapse). The terms hypersensitivity and
allergy are synonymous and
are used interchangeably. Hypersensitivity or allergy reactions are classified into five basic
types, which are determined by differences in timing, mechanism, pathophysiology, and clinical manifestations. Each
type may occur alone or in
combination with one or more other types.
Figure *
There are four types of hypersensitivity reaction mediated by immunological mechanisms
that cause tissue damage. Types I–III are
antibody-mediated and are distinguished by the different types of antigens
recognized and the different classes of (more...)
TYPE I: RAPID HYPERSENSITIVITY REACTIONS
Figure * IgE-mediated
reactions to extrinsic antigens. All IgE-mediated
responses involve mast-cell degranulation, but the
symptoms experienced by the patient can be very different depending on whether
the allergen is injected, inhaled, or eaten, and depending (more...)
Type I (rapid) hypersensitivity, sometimes called atopic allergy,
is the most common type of
hypersensitivity. This type results from increased production of the
immunoglobulin E (IgE) antibody class. An acute inflammatory reaction occurs when
IgE responds to an otherwise
harmless antigen (e.g., pollen) and causes
the release of histamine and other vasoactive amines from basophils, eosinophils
and mast cells. Clinical examples of type
I reactions include systemic anaphylaxis, allergic asthma, and
atopic (genetic tendency)
allergies such as hay fever, allergic rhinitis, and allergies to specific allergens such as latex, bee venom,
peanuts, iodine, shellfish,
drugs, and thousands of other environmental antigens. Allergens can be encountered in the following ways:
•
Inhaled
(plant pollens, fungal spores, animal dander,
house dust, grass, ragweed)
•
Ingested
(foods, food additives, drugs)
•
Injected
(bee venom, drugs, biologic substances such as
contrast dyes and adrenocorticotropic hormone)
• Contacted (pollens, foods, environmental
proteins)
Some reactions are confined to
the areas exposed to the antigen,
such as the mucous membranes of the nose and eyes, causing symptoms of rhinorrhea, sneezing, and itchy,
red, and watery eyes. Other
reactions may involve all blood vessels and bronchiolar smooth muscle, causing widespread vasodi-lation, decreased cardiac output, and severe bronchoconstric-tion; this condition is known as anaphylaxis.
Allergic Rhinitis
OVERVIEW
Allergic rhinitis,
often called "hay fever," is triggered by hypersensitivity reactions to airborne allergens,
especially plant pollens, molds, dust, animal
dander, wool, food, and industrial
pollutants. Some acute episodes are "seasonal" in that they tend to recur at the same time each year;
they coincide with the timing of
large environmental exposure and last only a few weeks. Chronic rhinitis, or perennial rhinitis, tends to occur intermittently (with no predictable seasonal
pattern) or continuously on exposure to certain allergens. In "nonallergic rhinitis,"
the same clinical manifestations are present although no allergic cause is identified and the immune system does not appear to be involved.
Figure * Antibody Fc (fragment, crystalline) receptors
on basophils and mast cells.
Pathophysiology
On first
exposure to an allergen (an antigen that provokes allergic sensitization with IgE),
the person responds by making antigen-specific
IgE. This antigen-specific IgE
binds to the surface of basophils and
mast cells. These cells have large numbers of granules
containing vasoactive amines (including
histamine) that are released when stimulated. Once the
antigen-specific IgE has formed, the person is
sensitized to that allergen.
In a type I hypersensitivity reaction, the previously sensitized person
is re-exposed to the provoking allergen. The resulting response has a primary phase and a secondary
phase. In the primary phase, the allergen binds to two adjacent IgE molecules
on the surface of a basophil or mast cell, which breaks or distorts the cell membrane. These membrane
changes cause the cell to degranulate
and release the vasoactive amines within
the granules into the tissue fluids.
The most abundant vasoactive amine is histamine, a short-acting biochemical.
Histamine causes increased capillary permeability, nasal and conjunctival mucous secretion, and itching (pruritus), sometimes accompanied by erythema
(redness). These
symptoms last for approximately 10 minutes after the histamine is released. When
the allergen is continuously
present, mast cells continuously release histamine and other vasoactive amines,
thus prolonging the response.
The secondary phase results from the secretion of other vasoactive amines during the primary phase. These
other vasoactive amines draw more white blood cells to the area and stimulate
a more general inflammatory reaction through the action
of the biochemicals leukotriene
and prostaglandins. This reaction occurs in
addition to the allergic reaction stimulated
in the primary phase. The resulting inflammation increases the clinical manifestations and is
probably responsible for continuing
the response.
Etiology
The tendency to produce IgE in response to antigen exposure is based on genetic
inheritance, but no single gene has been found to be responsible. Specific
allergies are not inherited. Approximately 50% of clients with allergic rhinitis have one parent with type I
hypersensitivities/allergies.
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Figure * Degranulation and histamine release. Top, Mast cell with immunoglobulin E (IgE).
Bottom, Mast cell degranulation and histamine release when allergen binds to IgE.
LABORATORY ASSESSMENT
A complete blood
count and differential may be ordered. An increase in the percentage of eosinophils is consistent with allergic rhinitis. A client with severe seasonal
allergic rhinitis may have an eosinophil count as high as 12% (with
normal being 1% to
2%). Some clients have an increased total white blood cell count, but the percentage of
neutrophils remains normal (55%
to 70%). If
an acute infection accompanies allergic rhinitis, both the total white blood
cell count and the number of neutrophils may increase.
Other laboratory tests that indicate the presence of a hypersensitivity reaction include serum
immunoglobulin E (IgE)
levels and the Radioallergosorbent Test (RAST). Normal levels of IgE for nonallergic adults is approximately 39 IU/mL
(or less than 100 IU/mL). This level can increase many times in the presence of allergies. The usual IgE test does not indicate the specific allergen—only the tendency
to have allergic responses.
The RAST can determine the blood concentration of IgE
directed against a specific antigen and thus can determine specific allergies. However, the expense of
this study limits its use in allergy testing.
Incidence/Prevalence
Atopic allergies,
including allergic rhinitis, affect approximately
10% of the population in
COLLABORATIVE
MANAGEMENT
Assessment
HISTORY
An accurate
and detailed history may provide insight into the possibility of allergic rhinitis. The client is asked
to describe the onset and
duration of symptoms in relation to possible allergen exposure. The nurse asks about work, school,
home environments, and
possible exposures through hobbies, leisure time, or sports activities. Because
a tendency toward type I hypersensitivities can
be inherited, the client is asked about the
presence of allergies among close relatives.
PHYSICAL
ASSESSMENT/CLINICAL MANIFESTATIONS
The client with
allergic rhinitis usually has rhinorrhea (a "runny"
nose), a "stuffy" nose sensation, and itchy, watery eyes. Mouth breathing may be evident, and the
voice can have a nasal sound. Drainage
from the nose is usually clear or white.
The nasal mucosa appears swollen and pink on inspection. The client may have a
headache or feel pressure over the frontal
and maxillary sinuses. Transillumination of the sinuses may be decreased. If nasal secretions drip
posteriorly, the client may have a dry, scratchy throat and the appearance
ALLERGY TESTING
SKIN TESTING. With
most type I hypersensitivities, skin
testing can reveal which specific allergens are causing the reaction. Skin
testing can be performed as scratch testing and intradermal testing. Patch
testing is generally reserved
for contact dermatitis and other manifestations of type IV hypersensitivities.
SCRATCH
TESTING. A scratch or prick test results in an immediate
hypersensitivity reaction to an
allergen. Scratch tests are used in routine
allergy testing to determine the possible
cause of allergic rhinitis, asthma, urticaria
(hives), or any other type I
hypersensitivity/allergic reactions. Allergens introduced through a superficial scratch or prick cause a localized
reaction (wheal) when the test result is positive. Results are usually
determined after 15 to
20 minutes.
CLIENT PREPARATION. For best results, systemic corti-costeroids
or antihistamines are discontinued for 5 days before the test; this prevents
suppression of the inflammatory response
to an allergen. Nasal sprays to reduce mucous membrane swelling are
permitted, except for antihistamine sprays such as azelastine
(Astelin). Some allergists recommend that aspirin and other nonsteroidal
anti-inflammatory agents be withheld before allergy testing.
PROCEDURE. The
preferred site for scratch testing is the inside of the arm or the back.
Alternate sites may be used if a rash or other skin
problem is present in these areas. The skin is
gently cleaned with soap and water, and surface oils are removed with alcohol.
Small drops of sera containing
different known allergens are
placed on the skin approximately
Control drops are also applied during the scratch test. Normal saline drops are negative controls, and histamine drops are positive controls. A variation from the
expected response to the controls can
invalidate the skin test results. If a positive reaction to the saline control
occurs, the client may have very sensitive skin or a condition called dermographism. In such cases, the reddened test areas may
be skin reactions to the scratch or prick
rather than an allergic response to the sera. If the histamine control produces a negative reaction, the client may have
used an antihistamine recently.
Serious reactions in response to scratch testing are rare. However, the nurse ensures that emergency
equipment is readily available
during a scratch test.
FOLLOW-UP CARE. After testing is completed, the nurse washes the solution from the skin. Topical
steroids and oral antihistamines may be administered to reduce itching and
increase client comfort. If the administered antihistamine can cause sedation, the client will need to have another person drive him or her home.
INTRADERMAL TESTING. Intradermal testing is reserved for substances
that are strongly suspected of causing allergy but did not test positive during
scratch testing. Intradermal testing increases the
risk for a greater adverse reaction,
including anaphylaxis, but it is a relatively safe procedure. The nurse ensures
that emergency equipment is in the room with the client. Small amounts
of testing sera (0.1 mL)
are injected intradermally on the client's upper arm,
and the area is observed for erythema and
wheal formation. The degree of
hypersensitivity is grossly estimated by the size of the response. Client preparation and follow-up care
are the same as for scratch testing.
ORAL
FOOD CHALLENGE. Some clients
experience allergic rhinitis (and other
hypersensitivity manifestations) when the
allergen does not come into direct contact with the nasal mucosa but is ingested orally. The oral
food challenge has been effective for
some individuals in identifying specific allergens when skin testing has been inconclusive and keeping a food diary has failed to determine the offending
food items. This test requires the
client to eliminate suspected foods for 7 to 14 days
before testing. After this time, the client is directed to eat a defined food for at least one day and
to monitor for clinical
manifestations. When many food allergies are present, the client may need to eat only one food type per
day of testing.
IN VITRO TESTING.
Hypersensitivity to specific allergens can be tested using an in
vitro method. One method, the ALCAT, is available in some areas of the
Allergy Management: Identification,
treatment, and prevention
of allergic responses to food, medications, insect bites, contrast material, blood, or other substances
• Identify known allergies and usual reaction
(e.g., med
ication, food, insect, environmental).
• Notify caregivers and health care providers of
known
allergies.
• Document all allergies in clinical record,
according to
protocol.
• Place an allergy band on client, as appropriate.
• Monitor client for allergic reactions to new
medications,
formulas, foods, and/or test
dyes.
• Encourage client to wear a medical alert tab,
as
appropriate.
• Provide medication to reduce or minimize an
allergic
response.
• Assist with allergy testing, as appropriate.
• Administer allergy injections, as needed.
• Instruct client to avoid allergic substances,
as
appropriate.
• Instruct client to avoid further use of
substances caus
ing allergic responses.
• Discuss methods to control environmental
allergens
(e.g., dust, mold, and pollen).
• Instruct client and caregiver(s) on how to avoid
situa
tions that put them at risk and how to respond if an ana-
phylactic reaction should occur.
• Instruct client and caregiver on use of epinephrine
pen.
Anaphylaxis Management: Promotion of adequate
ventilation and tissue perfusionfor a client with a severe allergic (antigen-antibody) reaction
• Place client in Fowler's or high Fowler's
position.
• Apply tourniquet immediately proximal to the allergen
point of entry (e.g., injection
site, IV site, insect bite,
etc.), when possible.
• Administer aqueous epinephrine 1:1000 (0.3-0.5 mL)
subcutaneously at the contact
site, if applicable, and
proximal to the tourniquet and
repeat every 3 minutes,
as needed.
• Establish and maintain a patent airway.
• Administer oxygen by mask.
• Start an IV infusion of normal saline, lactated
Ringer's,
or a plasma volume expander, as appropriate.
• Reassure the client and family members.
• Monitor for signs of shock, airway obstruction,
cardiac
arrhythmia, aspiration of
gastric contents, and seizures.
• Administer spasmolytics,
antihistamines, or cortico-
steroids as indicated if urticaria, angioedema, or bron-
chospasm present.
• Monitor for recurrence of anaphylaxis within 24 hours.
NIC intervention
activities selected from McCloskey, J.C., & Bulechek, G.M. (Eds.). (2000). Nursing interventions classification
(NIC) (3rd ed.).
Interventions
Chart lists NIC
interventions for allergy management. Common interventions include avoidance therapy, desensitization therapy,
and symptomatic therapy. Many clients use a combination of all three interventions for the
effective management of allergic
rhinitis and other manifestations of type I hypersensitivity.
AVOIDANCE
THERAPY. When specific environmental allergens have been identified, the client is encouraged
to avoid direct or close contact
with these agents. For example:
Many airborne allergens can be minimized by the use of air-conditioning/air-cleaning units. Removing
cloth drapes, upholstered furniture, and carpeting reduces airborne allergens.
Covering mattresses and pillows with plastic or ultra-fine mesh hypoallergenic covers also reduces exposure
to dust mites and mold.
Pet-induced
allergies pose special challenges. Sometimes even simple interventions (e.g.,
keeping pets out of the bedroom,
thoroughly cleaning the room to remove animal hair/dander) may help reduce symptoms. Bathing the pet
frequently or keeping the pet outdoors can decrease allergen exposure. Depending on the severity of the
allergy and how well other methods provide relief, pets with feathers or dander
may need to be removed
from the household.
SYMPTOMATIC THERAPY. When avoidance therapy is impractical, symptomatic therapy can be very effective
in reducing the intensity
of the allergic response and making the client more comfortable.
DRUG THERAPY. Drug
therapy involves the use of steroidal
and nonsteroidal agents (to reduce inflammation), vasoconstrictors, antihistamines, mast cell
stabilizers, and new agents that
inhibit the release or action of leukotrienes. Some
drugs reduce the response, and others actually prevent the response. Chart 23-2 lists
common agents used for symptomatic
therapy of allergic rhinitis.
Decongestants.
Decongestants are
available in systemic oral
medications or nasal sprays. These agents do not clear the allergen or prevent the release of histamine or
leukotrienes. They often have actions similar to
those of adrenergic drugs and generally work by
causing vasoconstriction in the inflamed
tissue, thereby reducing the edema. Common vasoconstrictors used in decongestant preparations are ephedrine, phenylephrine, phenylpropanolamine, and
pseudoephedrine. Secretions are inhibited
when the vasoconstrictor is combined with
an anticholinergic agent such as scopolamine or at-ropine. Numerous combination decongestants are available by prescription and as over-the-counter cold and
allergy medications. Common side
effects include dry mouth, increased blood pressure, and sleep alterations.
Because the effects are systemic,
clients with hypertension, glaucoma, and urinary
DRUG THERAPY for Allergic Rhinitis
Drug |
Usual Dosage |
Nursing Interventions |
Rationale |
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LEUKOTRIENE ANTAGONISTS |
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Zafirlukast (Accolate) |
20 mg bid |
Take 1 hr before or 2 hr after eating. |
Drug absorption is slowed by the presence of food. |
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There is an increased incidence of upper respiratory infections
when coadministered with inhaled corticosteroids. |
Drugs reduce local inflammatory and immune responses. |
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Reduce dose in clients who are also taking aspirin. |
Aspirin increases plasma concentration of drug. |
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Zileuton (Zyflo) |
600 mg qid |
Do not take with terfenadine
or theophylline. |
Drug increases plasma concentrations of terfenadine and theophylline. |
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CORTICOSTEROIDS |
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Beclomethasone (Beconase) |
1 -2 metered sprays per nostril, 1 -2 times/day (approximately 50 g/metered spray) |
Use daily as directed. |
Effectiveness depends on regular use. |
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Symptoms may persist for 2-3 days after initial administration. |
Maximum effectiveness requires continued
use for 48-72 hr. |
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Fluticasone (Flonase) |
2 metered sprays pernostril qd (approximately 50 (g/metered spray) |
Same as for beclomethasone. |
Same as for beclomethasone. |
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MAST CELL STABILIZERS (NASAL) |
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Cromolyn sodium (Nasalcrom) |
1 spray/nostril 4-6 times/day |
Use daily as directed. |
Effectiveness depends on
regular use. |
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Start therapy 3-4 wk before expected allergy season. |
Requires regular use for prophylactic
effect. |
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DECONGESTANTS (NASAL) |
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Phenylephrine (Neo-Synephrine, dozens of others) |
1 spray/nostril 4-6 times/day |
Caution client not to use more frequently
than directed or for longer
than 4 days. |
Overuse or continued use causes a rebound nasal congestion and worsens symptoms. |
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Oxymetazoline |
1 spray/nostril bid |
Same as for phenylephrine. |
Same as for phenylephrine. |
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(Afrin, many others) |
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Additional drugs include Nasacort, Nasonex,
and many others.
Antihistamines. Antihistamines
compete with histamine at the
histamine receptor site and essentially block it from binding to its receptor. This
action prevents vasodilation and capillary leak. Many antihistamines also have some
anticholinergic effects, which
assists in relief by decreasing secretions. First-generation antihistamines, which include
diphenhydramine (Allerdryl, Benadryl) and chlorpheniramine
(Chlor-Trimeton, Chlor-Tripolon) often induce sedation.
Second-generation antihistamines,
which include loratadine (Claritin), cetirizine (Zyrtec), and fexofenadine (Allegra), are less sedating.
Corticosteroids. Corticosteroids decrease inflammatory and immune responses in many ways, one of which
is preventing the synthesis
of mediators. Local corticosteroids in the form of nasal sprays can be helpful in preventing
the symptoms of rhinitis. Systemic corticosteroids can produce severe side effects. Therefore they are avoided
for rhinitis and are used only on a short-term basis for other problems associated with type I hypersensitivities.
Mast Cell Stabilizers. Nasal sprays containing mast cell stabilizers, such as
cromolyn sodium (Nasalcrom),
prevent
mast cell membranes
from opening when an allergen binds to IgE. Thus these agents are helpful in preventing the
symptoms of allergic rhinitis
but are not useful during an acute episode. Leukotriene Antagonists. Two leukotriene antagonists are currently available to treat allergic rhinitis. Zileuton (Zyflo) prevents leukotriene synthesis. Zafirlukast
(Accolate) blocks the leukotriene receptor. Both are oral agents and work best in the prevention of allergic rhinitis.
COMPLEMENTARY AND ALTERNATIVE
THERAPY.
Some clients with
allergic rhinitis have found relief through the use of aromatherapy. Possible
mechanisms of action include competition and
desensitization. Some clients with pollen-induced allergic rhinitis report
decreased sensitivity after ingesting
unprocessed honey.
DESENSITIZATION
THERAPY. Desensitization therapy, commonly called "allergy shots," may be needed when allergens have been identified but cannot be avoided
consistently. The most common form
of desensitization involves subcutaneous injections of small amounts of the allergen. After the allergen has been identified, a very dilute
injection solution(1:100,000 or 1:1,000,000)
of the allergen is compounded. A 0.05-mL dose of the initial solution is injected subcuta-neously. An increasing dose is usually given weekly (or
more frequently) until
the client is receiving a 0.5-mL dose. The client is then started on the lowest dose of the next
higher concentration of
allergen solution. This process is repeated with increasing concentrations of allergen solutions until
the client is receiving the
maximum dose of the greatest concentration determined to be needed (usually 1:100), depending
on his or her response. In general, injections are given at weekly intervals during the first year, every other week for
the second year, and every 3 to 4 weeks
for the third year. The recommended course of treatment is approximately 5 years.
The mechanism of action to reduce allergic responses by desensitization is thought to be competition. In
theory, the very small amounts
of allergen initially injected are too low to bind to the immunoglobulin E (IgE)
already present but are enough
to induce the immune system to make immunoglobulin G (IgG) against that
allergen. Because IgG is not associated with either mast cells or basal cells,
allergens that bind to IgG do not trigger degranulation and are removed from the body by precipitation (see Chapter 20). By
gradually increasing the amount and concentration of
the allergen injection, large amounts of IgG are generated specifically against the allergen. When the client is exposed to the
allergen, IgG will bind to it and clear it from the body before IgE
can bind to it and trigger a
hypersensitivity reaction. Because so much more IgG
can be produced compared with IgE, IgG is successful in the competition to bind the allergen.
Desensitization
can also be accomplished orally. Oral desensitization (sometimes called oral
immunotherapy) is more common
in Europe and is not yet widely available in the
Example
of desensitization:
Anaphylaxis
OVERVIEW
Anaphylaxis, the most
dramatic and life-threatening example of a type I hypersensitivity reaction, occurs rapidly and systemically. It affects multiple organs within
seconds to minutes of exposure to
an allergen. Anaphylaxis is not common, and the episodes can vary in severity
and symptom. It can be fatal.
Many substances can trigger anaphylaxis in a susceptible person (Table).
COLLABORATIVE
MANAGEMENT
Assessment
Typically, a client
experiencing an anaphylactic reaction first complains of feelings of
uneasiness, apprehension, weakness, and impending doom. The nurse notes that the client is anxious and frightened. These feelings are
followed, often quickly, by a
generalized pruritus and urticaria (hives). The nurse sees erythema and sometimes angioedema
(diffuse swelling) of the
eyes, lips, or tongue.
TABLE
• COMMON AGENTS THAT CAUSE ANAPHYLAXIS
DRUGS/FOREIGN PROTEINS
Antibiotics
(penicillin, cephalosporins, tetracycline, sulfon-amides,
streptomycin, vancomycin, chloramphenicol, am-photericin B, others)
Adrenocorticotropic
hormone, insulin, vasopressin, protamine
Allergen
extracts, muscle relaxants, hydrocortisone, vaccines, local anesthetics (lidocaine, procaine)
Whole blood, cryoprecipitate, immune serum
globulin
Radiocontrast media
Opiates
FOODS |
OTHER
AGENTS |
Shellfish |
Pollens |
Eggs |
Exercise |
Legumes, nuts |
Heat/cold |
Grains |
Other |
Berries |
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Preservatives |
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INSECTS/ANIMALS |
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Hymenoptera: bees, |
wasps, hornets |
Fire ants |
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Snake venom |
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Anaphylaxis
caused by these substances is probably a result of direct mast cell degranulation rather than an IgE-mediated
hypersensitivity event.
Intensely praritic skin wheals or hives commonly appear, and these
sometimes merge together in a large, red blotch.
Histamine
and other biochemicals cause bronchoconstriction, mucosal edema, and excess mucus production. On
respiratory assessment, the
nurse notes congestion, rhinorrhea, dyspnea, and increasing respiratory distress with audible
wheezing.
On auscultation
the nurse detects crackles, wheezing, and diminished breath sounds. Clients may
experience laryngeal edema
as a "lump in the throat," hoarseness, and stridor (a crowing sound). Distress increases as the
tongue and larynx become more edematous and excess mucous secretion continues.
The nurse may note increasing stridor and anxiety as the airway begins to
close. Respiratory failure may follow quickly as a complication of laryngeal edema, suffocation, or lower
airway bronchoconstriction causing hypoxemia (insufficient oxygenation of blood) and hypercapnia
(increased carbon dioxide in
the blood).
The client is usually hypotensive and has a rapid, weak, and irregular pulse. These findings are due to
vasodilation and increased
capillary permeability with a resultant leakage of intravascular fluids. The
nurse notes faintness and diaphoresis, increasing anxiety, confusion and, if
the client is not treated immediately,
loss of consciousness. Dysrhythmias, shock, and cardiac arrest may occur within minutes as
intravascular volume is lost.
Abdominal cramping, diarrhea, or vomiting is less common. Respiratory failure or shock and cardiac
dysrhythmias account for 70% of
deaths from anaphylaxis.
Interventions
NIC interventions for clients with anaphylaxis
are listed in Chart.
EMERGENCY RESPIRATORY MANAGEMENT. Emergency respiratory management is critical for
clients experiencing an anaphylactic reaction, because the severity of the reaction and consequences increases with time. An airway must be established or stabilized immediately. The
nurse may need to initiate cardiopulmonary resuscitation. Epinephrine (1:1000) 0.3 to 0.5 mL should be given subcutaneously as soon as
possible after the appearance of symptoms of systemic anaphylaxis. This drug constricts the blood
vessels, increases myocardial contraction, and
dilates the bronchioles. The same dose may be repeated every 15 to 20 minutes if needed. Other commonly
administered drugs are listed in Chart.
Antihistamines such as diphenhydramine (Allerdryl,
Benadryl) 25 to 100 mg
are usually given intravenously, intramuscularly, or orally to treat
angioedema and urticaria. This agent blocks the
histamine receptor site (H,) in vascular and bronchiolar smooth muscle. If
necessitated by the extent of upper
airway narrowing, the physician may insert a small endotracheal tube or perform an emergency tracheostomy.
If the client can breathe
independently, the nurse administers oxygen to minimize hypoxemia. Oxygen is
started via nasal cannula at 2 to 6 L/min
or via face mask at 40% to 60% before arterial blood gas results are obtained.
The nurse monitors pulse oximetry to determine oxygenation adequacy, with the goal of maintaining an oxygen
saturation greater than 90%.
If pulse oximetry readings
are not satisfactory, arterial blood gases may be tested to determine the
effectiveness of therapy. Suction is used to remove excess mucous secretions if indicated. The client's rate,
rhythm, and depth of respirations, as well as the presence of bronchospasm and abnormal breath sounds, are assessed
continually. The nurse or other assistive
nursing personnel elevates the client's bed to 45 degrees unless contraindicated because of hypotension.
For severe bronchospasm, the client is given
aminophylline 6 mg/kg
IV over 20 to 30 minutes. If the client is tak-400 with diphenhydramine (Allerdryl,
Benadryl). The
substance is given
first intradermally, then subcutaneously, and then
intramuscularly in increasing doses at 20- to 30-minute intervals so the initial dose by the next route
does not exceed the final dose
by the previous route. When carefully performed, this procedure is fairly safeing
aminophylline regularly, no more than 3 mg/kg
is given. Maintenance
aminophylline (0.3 to 0.5 mg/kg/hr) is initiated. The client may be given an inhaled beta-adrenergic
agonist such as metaproterenol (Alupent) or
albuterol (Proventil) via high
flow nebulizer every 2 to 4 hours. Corticosteroids are added to emergency interventions, but they are
not effective immediately. To prevent the late recurrence of symptoms, tapered doses of oral steroids are started after
the anaphylaxis is under control.
The nurse's primary role in caring for the client with anaphylaxis is to assess for changes in any body system
or for adverse effects of drug
therapy. For severe anaphylaxis, the client is admitted to a critical care unit for cardiac, pulmonary arterial, and capillary wedge pressure
monitoring. The nurse carefully
observes for fluid overload from the rapid administration of medications and IV fluids and reports
changes to the physician
immediately. The client may be discharged from
the hospital when respiratory and cardiovascular systems have returned to baseline.
PREVENTION. Because of the rapid onset of life-threatening symptoms and the potentially fatal
outcome of this condition,
sometimes even with appropriate medical intervention, preventing anaphylaxis is critical. The
nurse teaches the client
with a history of allergic reactions to avoid allergens
whenever possible, wear a medical alert bracelet, and alert health care personnel about specific allergies. Some clients must carry an emergency anaphylaxis kit
(e.g., a bee sting kit with
injectable epinephrine) or an epinephrine injector such as the EpiPen automatic injector (Dey Laboratories,
The
medical record of clients with a history of anaphylactic symptoms should
prominently display the list of allergens to which they are sensitive. A careful history is
obtained before administering any drug or therapeutic agent. Skin tests should be performed before administering any
substance with a highly
associated incidence of anaphylactic reactions, such as iodine-containing dyes. Physicians and nurses must
be aware of common cross-reacting
agents. For example, a client with
a history of penicillin sensitivity is also likely to react to cephalosporins because both have a similar chemical structure. Clients with an allergy to bananas are
also likely to have a latex sensitivity.
Precautionary
measures must be taken if an agent must be used despite a history of allergenic reactions. An IV
solution is started, and intubation equipment and a
tracheostomy set are placed at the bedside.
The client is often premedicated
CRITICAL THINKING CHALLENGE
The client is a
52-year-old woman with type 1 diabetes who comes to an urgent care center. She fell 1 day
ago and scraped her left
shin. She now has a large, red, and indurated area around the abrasion. She is
diagnosed with cellulitis and is to begin her first dose of penicillin
intravenously because of her
diabetes. The client explains that she is allergic to penicillin. When asked
what type of reaction she has to penicillin, the client says she gets a severe
rash over most of her body. The physician changes the order to cephalothin (Keflin) to be given intravenously for the first dose, followed
by oral cephalexin (Keflex).
With
the client in an examination room, you start an IV with normal saline and hang a 50-mL piggyback
containing
Approximately 5 minutes after the infusion begins, the client
says she is having a hard time catching her breath. She feels dizzy and scared. You find her pulse to be thready and
too rapid to count. Her lips are dusky, and she begins to wheeze.
• What should you do with the IV?
• What is your next response?
• Why should you or should you not start oxygen on
this
client?
• Would epinephrine be helpful in this situation?
Why or why
not? Where, how much, and by what
route would you ad
minister it?
• Would diphenhydramine (Benadryl) be helpful in
this situa
tion? Why or why not?
• What is the explanation for this reaction to cephalothin?
Latex Allergy
OVERVIEW
Latex allergy or hypersensitivity is a
type I hypersensitivity reaction in which the specific allergen is a protein
found in processed natural latex rubber products. When the allergen enters the body through inhalation or direct
contact with blood vessels (such as might occur during surgery), interaction with immunoglobulin E (IgE)
occurs and causes clinical manifestations of type I hypersensitivity
reactions, including anaphylaxis.
For some people, contact with the latex allergen is limited to the skin or mucous membranes. This causes
contact dermatitis, a type IV delayed hypersensitivity
reaction. Others may have
a "mixed" hypersensitivity response to the latex allergen and
experience symptoms of both type I and type
IV hypersensitivities. Others may express only one or the other type of
reaction.
The incidence of latex hypersensitivity is increasing (Becker, 2000; Floyd, 2000). The individuals most at risk are those
with a high exposure to natural latex products, such as health care workers (Karvonen,
1999), clients with spina bifida, and people who routinely use latex condoms.
COLLABORATIVE
MANAGEMENT
The nurse
questions all clients regarding the use of and known reactions to natural latex products. In addition, the
nurse and other health care
workers need to consider their own exposure and
risk for hypersensitivities to natural latex products.
Avoiding products containing natural latex proteins can prevent
reactions and initial sensitivity. More elastomeric products such as surgical gloves, tubing, and vial
closures are now being made
from synthetic substances containing no latex proteins. One such product is the thermoplastic
elastomer glove, ElastyLite. It is essential that latex-free products be used in the care of a client with a known latex
allergy. Interventions for
the client experiencing a type I or type IV hypersensitivity reaction to latex
are the same as for hypersensitivities caused by other allergens.
TYPE II: CYTOTOXIC REACTIONS
OVERVIEW
In a type II (cytotoxic)
reaction, the body makes special au-toantibodies directed against self-cells or tissues that have some form of foreign protein attached to them.
The autoanti-body
binds to the self-cell and forms an antigen-antibody complex, or immune complex (Figure). The
self-cell is then destroyed by phagocytosis or complement-mediated lysis. Clinical
examples of type II reactions include
Coombs'-positive hemolytic anemias, thrombocytopenic purpura,
hemolytic transfusion reactions (when an individual
receives the wrong blood type during a transfusion), hemolytic disease of the newborn, Goodpasture's
syndrome, and drug-induced hemolytic anemia.
COLLABORATIVE
MANAGEMENT
Treatment of
type II cytotoxic reactions begins with discontinuing
the offending drag or blood product. Plasmapheresis (filtration of the plasma to remove specific
substances) to remove autoantibodies may be beneficial. Otherwise, treatment is symptomatic. Complications such as hemolytic crisis and renal failure
can be life threatening.
TYPE III: IMMUNE COMPLEX REACTIONS
OVERVIEW
In a type III
reaction, soluble immune complexes are formed, usually with antigen excess (Figure). These
circulating immune complexes
are usually deposited in the walls of small blood vessels. Common sites include
the kidneys, skin, joints, and
other small blood vessels. The deposited immune complex activates complement, resulting in tissue or
vessel damage.
There
are many immune complex disorders (mostly connective tissue disorders) in
which the type III reaction is the major mechanism of disease. For example, the
clinical manifestations of
rheumatoid arthritis are caused by immune complexes that lodge in joint
spaces; this is followed by tissue destruction and, later, scarring and fibrous changes. Similarly, the clinical manifestations of systemic lupus
erythematosus result from the
deposition of immune complex in the vessels (vasculitis), glomeruli (nephritis), joints (arthralgia, arthritis), and other organs and tissues. In this disorder,
the immune complex is composed
of cellular deoxyribonucleic acid (DNA) and anti-DNA antibodies.
Serum sickness is a complex of symptoms that occurs after the administration of a foreign serum or
certain drugs. It is caused by the collection of immune complexes deposited in the walls of blood vessels in the skin, joints,
and kidney. The most common causes
of serum sickness today are penicillin and
related drags and some animal serum antitoxins. Serum sickness used to be quite common when vaccines were madewith horse or rabbit serum, but now most vaccines
are made with human serum or antigen
fragments. Currently used agents that can cause
serum sickness are antilymphocyte globulin and antithymocyte
globulin, which are used to suppress the immune response in organ
transplantation.
COLLABORATIVE MANAGEMENT
The client with serum
sickness has symptoms of fever, arthralgia (achy
joints), rash, lymphadenopathy (enlarged lymph nodes), malaise, and possibly polyarthritis and
nephritis. These symptoms usually appear
approximately 7 to 12 days after receiving
the causative agent. The nurse alerts the client to the possibility of serum sickness and what
symptoms to look for. When administering a foreign
serum to a client, the nurse is also prepared for a type I anaphylactic
reaction and has emergency equipment and
medications close at hand. Serum sickness is usually self-limiting, and
symptoms subside after several days.
Treatment is usually symptomatic; antihistamines are given for pruritus, and
aspirin is given for arthralgias.
Prednisone is given if symptoms are severe.
TYPE IV: DELAYED HYPERSENSITIVITY
OVERVIEW
In a type IV
reaction, the reactive cell is the T-lymphocyte. Antibodies
and complement are not involved. Sensitized T-lymphocytes
(from a previous exposure) respond to an antigen by producing and releasing certain lymphokines
(chemical mediators), and they
recruit, retain, and activate macrophages
to destroy the antigen. Unlike with a type I hypersensitivity reaction, which occurs immediately, a type IV response typically occurs hours to days after
exposure. A type IV reaction is
characterized by an accumulation of lymphocytes and macrophages, which causes
edema, ischemia, and tissue destruction at the site.
An
example of a small type IV reaction is a positive purified protein derivative
(PPD) test for tuberculosis. In a client previously
exposed to tuberculosis, an intradermal injection of this agent causes sensitized T-cells to accumulate at the injection site, release lymphokines,
and recruit and activate macrophages. Induration and erythema at the site of
the injection appear after approximately 24 to 48 hours.
Other
clinical examples of type IV hypersensitivity reactions include contact
dermatitis, poison ivy skin rashes, a local response to insect stings,
allograft (tissue transplant) rejections, and granulomatous diseases in which
the antigen is unknown (e.g., sarcoidosis).
COLLABORATIVE MANAGEMENT
Intervention
Removal of the
offending antigen is the major focus of management. The reaction is self-limiting in 5 to 7 days,
and the client is treated symptomatically.
Nursing responsibilities include monitoring the reaction site and sites distal
to the reaction for circulation adequacy. Diphenhydramine (Benadryl) is of
minimal benefit for type IV reactions because histamine is not the main mediator. In addition, IgE does not appear to play a role in this type of reaction, and therefore
desensitization does not diminish the response. Corticosteroids or other anti-inflammatory agents can reduce the
discomfort and help resolve the
reaction more quickly.
Identification
of Allergen
Patch testing
can be used to identify the allergen. This type of testing involves skin contact with substances to which
the client is
potentially allergic. Contact with a specific allergen results in a delayed
hypersensitivity reaction that develops in 48 to 96 hours.
Test
chemicals are applied to uninvolved skin under occlusive tape patches. After the patches are removed, the
skin areas in contact with the chemical are examined closely for indications of localized erythema, swelling, and vesicular
(blister) eruption.
For a positive patch test result to have clinical relevance, a history of
exposure to substances containing the chemical is required.
CLIENT PREPARATION. To prevent suppression of the inflammatory response to an allergen, systemic corticosteroids or antihistamines are discontinued for
at least 48 hours before the test. Topical steroid therapy may be continued as long as the agent is not applied on the area to
be tested. To allay the client's anxiety, the nurse explains
that patch testing does not involve pricking
the skin with needles. The client is informed
that testing will involve three separate visits to the allergist or dermatologist: one to apply the test
patches, a second for an initial reading,
and a third for detection of any delayed hypersensitivity reactions.
PROCEDURE. The
upper back is the preferred site for the application of test patches. After the client has
disrobed, the back is inspected for
evidence of rash and the presence of hair. If a rash is present, alternative test sites are the flanks, the
lower back, and the upper arms. Any hair in the area is shaved to prevent poor contact and subsequent
false-negative results. Removing skin oils with alcohol allows better adhesion
of the patches.
Small quantities of
chemicals and solutions in standardized
concentrations are placed in separate metal chambers that are backed with hypoallergenic adhesive tape.
The tape is carefully applied to the
skin so each chemical is held in contact with the skin surface. Each chamber
is marked for later identification.
As many as 60 or more chemicals may be tested simultaneously.
The
nurse instructs the client to keep the test sites dry at all times. Baths are substituted
for showers until testing is complete. The client is
instructed to use caution when washing the
hair to avoid getting the patches wet. Excessive physical activity that results in sweating is discouraged. Reapplying patches that come loose can interfere
with an accurate interpretation of true allergic reactions. Thus the nurse
reinforces the necessity of removing loose or nonad-herent
test patches for later reapplication by the allergist or nurse.
The initial reading is performed 2 days after application. The tape
containing the chemical-filled chambers is peeled away from the skin, and each
area of contact is marked with indelible
ink for future reading. The nurse documents any initial allergic or irritant reactions in the
client's medical record. The final reading occurs in 2 to 5 days.
FOLLOW-UP CARE. If a potential allergen is identified, the client is given a list of items containing that chemical. These items are to be avoided.
TREATMENT
ANTTHISTAMINES |
||
Diphenhydramine (Benadryl, Allerdryl- Hyrexin) |
25-50 mg q4-6h |
Instruct client not to drive
or operate heavy machinery. |
|
||
|
Do not give during an acute asthma attack. |
|
|
|
|
Chlorpheniramine (Chlor-Trimeton, Telachlor, Teldrin, Phenetron) |
2-8 mg 1
-3 times/day |
Avoid alcoholic beverages. |
|
Same as for diphenhydramine. |
|
|
|
|
|
|
|
Loratadine (Claritin) |
10 mg q/d |
Give every other day to
clients with renal or hepatic dysfunction. |
|
||
|
|
|
Cetirizine (Zyrtec) |
5-10 mg qd |
Reduce dose for clients with renal or hepatic dysfunction |
|
||
Fexofenadine (Allegra) |
60 mg bid or 180 mg qd |
Same as for loratadine. |
|
|
|
CORTICOSTEROIDS (ORAL) |
||
(may be given as a "taper" or "short-term burst") |
||
Prednisilone (Cotolone) |
5-40
mg/day |
Not recommended unless symptoms
are severe |
|
Drug can cause significant sedation.
Sedation decreases the voluntary muscle contractions needed for breathing.
Drug potentiates the effects of alcohol.
Renal or
hepatic dysfunction reduces drug clearance.
Same as for loratadine.
Systemic side effects are common and serious:
• GI ulceration
• Poor wound healing
• Decreased immune function
• Increased risk for infections
• Weight gain
• Hyperglycemia
• Personality changes
• Fluid retention
Same as for prednisilone.
CRITICAL THINKING CHALLENGE
The
client is a 25-year-old man who was stung by a wasp on the right hand yesterday
while hiking. He experienced
no problem except for pain at the site. When he woke up today, however, his right hand was twice the size
of his left hand, and it was red, nontender, and very warm. He wonders if he has an infection.
• What additional assessment data should you
obtain?
• Why should you or should you not start oxygen on
this
client?
• Would epinephrine be helpful in this situation?
Why or why
not? Where, how much, and by what
route would you ad
minister it?
• Would diphenhydramine (Benadryl) be helpful in
this situa
tion? Why or why not?
Additionaly:
TYPE V of HYPERSENSITIVITY
OVERVIEW
This relatively new category of
hypersensitivity reactions involves
inappropriate stimulation of a normal cell surface receptor by an autoantibody, resulting in a continuous "turned-on" state for the cell. The
classic example of a stimulatory reaction is Graves' disease, a form of hyperthyroidism. In
Graves' disease an autoantibody binds to thyroid-stimulating hormone (TSH) receptor sites on the thyroid gland. This
binding continually stimulates the thyroid cells to produce thyroid hormones, causing the client to have symptoms of severe
hyperthyroidism. These symptoms occur even though the thyroid
gland itself is completely normal. In a sense, the tissue responding to the autoantibody is "out of
control" from the body's
normal feedback system of checks and balances.
COLLABORATIVE
MANAGEMENT For type V reactions
involving only one organ, management focuses on removing enough of the
responding (stimulated) tissue
to return the function to normal. With Graves' disease, thyroid tissue is usually either surgically
removed or destroyed with
radiation. If more than one tissue is being stimulated by the autoantibodies or if the tissue is
widespread, the focus of
treatment is on reducing the production of autoantibodies through
immunosuppression.
AUTOIMMUNITY
Autoimmunity is
a process whereby a person develops and expresses an inappropriate immune response. In this
response, antibodies and/or
lymphocytes are directed against healthy normal cells and tissues. For unknown reasons, certain
cells or tissues of the body
are recognized as non-self-cells or are no longer tolerated as self-cells, and immune reactions
occur. The resulting
antibody-mediated and cell-mediated responses are similar
to normal immune responses against non-self-cells, but they are inappropriate and sometimes excessive.
TABLE * KNOWN OR
PROBABLE AUTOIMMUNE DISORDERS |
|
Disorder |
Autoantigen |
SYSTEMIC OR NON-ORGAN SPECIFIC |
|
Systemic lupus erythematosus |
DNA, DNA proteins |
Rheumatoid arthritis |
IgG, possibly cartilage |
Progressive systemic sclerosis |
DNA proteins |
Mixed connective tissue Disorder |
DNA proteins |
|
|
ORGAN SPECIFIC |
|
Autoimmune hemolytic anemia |
Erythrocytes |
Autoimmune thrombocytopenic Purpura |
Platelets |
|
|
Diabetes mellitus, Type 1 |
Islet cells, insulin, insulin receptor |
|
|
Dermatomyositis |
Unknown |
Glomerulonephritis |
Glomerular basement membranes |
|
|
Goodpasture's syndrome |
Glomerular basement membranes, pulmonary basement membranes |
|
|
|
|
Graves' disease |
Thyroid-stimulating hormone receptor |
|
|
Hashimoto's thyroiditis |
Thyroid cell surface |
Idiopathic Addison's disease |
Adrenal cell |
Myasthenia gravis |
Acetylcholine receptor, acetylcholine |
Pernicious anemia |
Intrinsic factor, parietal cell, B12 complexes |
|
|
Psoriasis |
Stratum corneum |
Reiter's syndrome |
Possibly collagen, conjunctival cells |
|
|
Sjogren's syndrome |
Salivary gland cells, vaginal mucous cells, lacrimal gland cells |
|
|
|
|
Uveitis |
Uveal tract cells (eye) |
Vasculitis |
Unknown, possibly collagen or endothelial cells |
|
|
IgG, Immunoglobulin G. |
|
The causes of alterations in self-tolerance are not
known, but there are multiple
theories.
Autoimmunity research is ongoing, and there are few confirmed, established data. Not only is the cause
of autoimmunity uncertain, but there is also a lack of consensus regarding
which diseases are truly autoimmune. Examples of diseases generally believed to
be autoimmune include systemic lupus erythematosus, polyarteritis
nodosa, rheumatoid arthritis, autoimmune hemolytic anemia, rheumatic fever, and
Hashimoto's thyroiditis (Table). Other diseases, such as type I diabetes
mellitus, may have multiple
causes, one of which is autoimmune.
Connective tissue disorders, sometimes referred to as collagen disorders or rheumatic disorders, are characterized by changes in connective tissue. Many of these
diseases are considered autoimmune; autoantibodies have been detected
for most of these disorders. Connective
tissue disorders include systemic lupus erythematosus, rheumatoid
arthritis, sclero-derma, and polyarteritis
nodosa. Most of these tissue disorders are
characterized as organ-nonspecific autoimmuni-ties, which
means that the autoantibodies and the tissue damage are not limited to a
specific organ. In organ-specific autoimmunities, tissue
damage occurs in a specific organ.
Cost of Care
• Drug therapy with nonsteroidal
anti-inflammatory drugs
(NSAIDs) remains a standard for
autoimmune disorders that
are associated with chronic
inflammation or chronic pain
(e.g., fibromyalgia, rheumatoid
arthritis, and systemic lupus
erythematosus).
• Aspirin is the oldest and most widely used NSAID.
• Side effects of chronic aspirin therapy include gastrointesti
nal ulceration and bleeding, increased bleeding
tendency,
and liver toxicities.
• Newer NSAIDs, especially the COX-2 selective
inhibitors,
have main effects similar to
aspirin and were thought to
have fewer side effects.
• The cost for 50 tablets
of newer NSAIDs, especially the
COX-2 selective inhibitors,
ranges from 10 to 30 times more
than the cost of aspirin.
• Recent studies using large sample sizes indicate
that all
NSAIDs, including COX-2 selective
drugs, have serious side
effects when taken chronically.
• The major side effect for which hospitalization
and interven
tion may be required is gastrointestinal ulceration.
In addi
tion, some NSAIDs are known to significantly reduce
kidney
function to the point that intervention is necessary.
• The major benefit to the use of NSAIDs other than
aspirin
may be solely in the convenience
of once- or twice-per-day
dosing.
Implications
for Nursing
There may be little
advantage to using the newer, more expensive NSAIDs for inflammation and pain.
The nurse must caution any
client using NSAIDs for more than just a couple of days that these drugs are
not harmless. Teaching priorities include
administration of the drugs with meals, prophylactic use of antacids or H2 histamine blockers,
and the clinical manifestations
of gastrointestinal, liver, or kidney function changes.
Management of autoimmunities depends on the
organ or organs affected.
Anti-inflammatory drugs and immunosuppressive drugs are commonly used along
with symptomatic treatment.
WOMEN'S HEALTH
CONSIDERATIONS Virtually all
autoimmune disorders, especially rheumatic disorders, occur much more commonly among women than men (Cotran, Kumar, & Collins, 1999; Workman, 2000). The risk for autoimmune disease among women
compared to men ranges from 5:1 to 20:1. In addition, most autoimmune disorders are more common among Caucasian women than among women of any other race.
SJOGREN'S SYNDROME
OVERVIEW
Sjogren's syndrome (SS) is a group of problems that often
appear in association with other
autoimmune disorders. Problems
include dry eyes (keratoconjunctivitis sicca), dry mucous membranes of
the nose and mouth (xerostomia), and vaginal dryness. These problems are thought to be
caused by autoimmune destruction of the lacrimal, salivary, and vaginal mucus-producing glands. Most commonly, the client
with Sjogren's syndrome also has rheumatoid arthritis. Fibromyalgia
also is associated with SS.
Ninety percent of clients with Sjogren's
syndrome are women between 35 and 45 years
of age. SS is more common among
clients with certain tissue types, specifically HLA-DRW52, HLA-DR3, and HLA-B8.
Although an exact triggering
agent has yet to be identified, viral infection is strongly suspected. The three viruses thought to be possible triggers for the
autoimmune changes leading to Sjogren's syndrome are human immunodeficiency virus type 1 (HIV-1),
human T-cell lymphotrophic virus type 1 (HTLV-1),
and Epstein-Barr Virus (EBV).
Insufficient tears cause inflammation and ulceration of the cornea.
Insufficient saliva decreases the digestion of carbohydrates, promotes tooth decay, and increases the
incidence of oral/nasal
infections. Vaginal dryness increases the incidence of infection and may cause pain during sexual
intercourse (dyspareunia).
COLLABORATIVE MANAGEMENT
Assessment
The client with
SS usually has blurred vision, burning and itching of the eyes, and thick
mattering in the conjunctiva. Difficulty swallowing food is common, and the
client often experiences changes in taste sensation.
The nurse asks the client about the presence of nosebleeds (epistaxis) and frequent upper respiratory infections.
Physical
examination reveals enlarged lymph nodes. If rheumatoid
arthritis (RA) accompanies SS, the client has swollen,
painful joints and limited joint mobility (see Chapter 21 for
a complete discussion of RA). Laboratory assessment may show an increased presence of general antinuclear
antibodies, anti-SS-A or
anti-SS-B antibodies, and elevated levels of IgM rheumatoid factor.
Interventions
IMMUNOMODULATION. Currently, there is no cure for SS. The intensity and progression of the
disorder can be slowed by suppressing immune and
inflammatory responses. The agents often
used to modulate the immune system in clients with SS include low-dose chemotherapy with methotrexate (Rheumatrex) or cyclophosphamide (Cytoxan). Both agents can have serious long-term detrimental effects,
especially on liver and bone marrow
function. Other immunosuppressive agents
that have shown benefit in managing SS are cortico-steroids, cyclosporine (Neoral,
Sandimmune), and hydroxy-chloroquine (Plaquenil).
SYMPTOMATIC
THERAPY. A variety of artificial tears and artificial saliva can help reduce symptoms of dry
eye and dry mouth. Clients
are instructed to use humidifiers in the home to increase the environmental moisture content.
The use of water-soluble
vaginal lubricants and moisturizers can increase comfort and reduce the
incidence of vaginitis. Some clients have obtained
significant relief from dry mouth with the
use of systemic pilocarpine (Salagen).
This agent is acholinergic agonist that mimics the effects of the parasympa-thetic nervous system, including increased salivation.
A nonpharmacologic intervention for dry eyes is to block the tear outflow channel (nasal punctum). The punctum can be blocked
temporarily with small plugs or closed surgically. Either method allows the scant amount of tears
produced to have longer contact with the eye.
Pain control is an issue for clients who have both SS and either rheumatoid arthritis or fibromyalgia. Nonsteroidal anti-inflammatory drugs
(NSAIDs), rather than pure analgesics, are most commonly used to decrease
inflammation and reduce the associated
pain. Many different types and strengths of NSAIDs are available by prescription and over-the-counter. The mechanism of action and side effects are
similar for all NSAIDs, although the duration of action and cost can vary considerably.
GOODPASTURE'S SYNDROME
OVERVIEW
Goodpasture's
syndrome is an autoimmune disorder in which autoantibodies are made against the
glomerular basement membrane and
neutrophils. The two organs sustaining the most damage are the lungs and the kidney. Lung damage
is manifested as pulmonary
hemorrhage. Kidney damage manifests
as glomerulonephritis, which may rapidly progress to complete renal failure. Unlike
other autoimmune disorders,
Goodpasture's syndrome is more common among males and generally occurs in
adolescents or young adults (Cotran,
Kumar, & Collins,
1999). The exact cause or
triggering agent(s) is unknown.
COLLABORATIVE MANAGEMENT
The client with Goodpasture's syndrome usually is not diagnosed until significant pulmonary and/or kidney
problems are evident. Clinical
manifestations include shortness of breath, hemoptysis (bloody sputum), decreased urine output, weight gain, generalized nondependent edema, hypertension,
and tachycardia. A chest
x-ray study reveals multiple areas of consolidation. The most common cause of
death is uremia as a result
of renal failure.
Spontaneous resolution of
Goodpasture's syndrome has been known to occur but is rare. Interventions focus on reducing immune-mediated damage and in performing
some type of renal supportive
therapy.
Immunomodulation
DRUG
THERAPY. The mainstay of drug
therapy for Goodpasture's syndrome is high-dose corticosteroids. Additional drug therapy to suppress the autoimmune response is the same as
that for Sjogren's syndrome.
OTHER
THERAPY. Additional therapy
to modulate the immune
responses with this autoimmune disorder involves plasmapheresis (filtration of the plasma to remove some proteins) to remove the autoantibodies. If the
lungs and kidneys have not sustained permanent damage, clients undergoing plasmapheresis have shown clinical improvement. Some clients using plasmapheresis
need supplemental administration
of IV immunoglobulin (IVIG) to maintain antibody protection against infection.
■ Renal Support Therapy
Depending on the level of remaining renal function,
the client may need ongoing dialysis. Therapy usually begins with he-modialysis. For chronic therapy, peritoneal or hemodialysis
may be instituted depending on
the client's health status, ability
to self-manage the infusion and drainage systems, and lifestyle.
Renal transplantation is an option for some
clients with Goodpasture's syndrome. After transplantation, renal function is normal. In rare instances, clients are disease free after transplantation. In others, the renal problems are
improved but pulmonary destruction
continues. Some of the drugs required
for immunomodulation for the transplanted kidney also suppress the autoimmune response.