24.1 Allergic Response

Immunoglobins

When the body’s immune system is first exposed to an allergen, lymphocytes and plasma cells produce immunoglobulins. An immunoglobulin is a protein capable of acting as an antibody. Immunoglobulins can be grouped into five classes: IgG, IgA, IgM, IgD, and IgE. They are commonly found in the tonsils, appendix, lymph nodes, and Peyer patches (small groupings of lymphoid follicles) of the intestinal tract; they also circulate in lymph and blood.

The IgE immunoglobulins are involved in producing an allergic disorder, a common pathological condition due to IgE-dependent immunological reactions to an allergen. This particular class of immunoglobulin is found in the respiratory and intestinal mucosa. IgE molecules bind together to an allergen and trigger mast cells of the tissues or white blood cells in the bloodstream, called basophils, to release chemical mediators like histamine, kinins, serotonin, slow-reacting anaphylaxis substances, and the neutrophil factor that produces allergic skin reactions, hay fever, and asthma. IgE-mediated diseases have a genetic component. The genetic tendency to develop allergic diseases such as allergic rhinitis, asthma, and atopic dermatitis is called atopy. It refers to a hypersensitivity response to an allergen.

Antigens

Examples of complete protein antigens include horse serum, pollen, and animal dander. Active communication between cells is necessary in allergic reactions in order for the physiologic process involved in an allergic response to be triggered (Abbas et al., 2023). When an allergen is engulfed through the gastrointestinal tract, skin, or respiratory tract, allergen sensitization occurs. Macrophages manage the antigen and allow it access to the proper cells. These cells develop into allergen-specific secreting plasma cells that produce and secrete antigen-specific antibodies.

Primary Mediators

Primary mediators include histamine, eosinophil chemotactic factor, platelet activating factor, and prostaglandins. Histamine plays a key role in immune responses; it is usually the first chemical mediator to be released in both immune and inflammatory responses. This chemical mediator is produced and kept in high concentrations in body tissues exposed to environmental substances. Effects of histamine include erythema, pruritus, localized edema (wheals), contraction of bronchial smooth muscle (resulting in bronchospasms and wheezing), and enhanced secretion of mucosal and gastric cells (diarrhea), as the role of histamine is to create vasodilation, which promotes oxygen and white blood cells to the area of attack. The histamine’s effects peak 5 to 10 minutes after antigen interaction. Histamine-1 receptors are found primarily on vascular smooth and bronchiolar muscle cells. Histamine-2 receptors are found primarily on gastric parietal cells.

The eosinophil chemotactic factor of anaphylaxis impacts the movement of granular leukocytes, particularly eosinophils, to allergen sites. An eosinophil is a leukocyte that protects the body from parasites, allergens, and other organisms. This chemical mediator is pre-formed in the mast cells and released from disrupted mast cells.

Platelet activating factor is chemically derived from arachidonic acid and is responsible for stimulating the platelet aggregation and leukocyte permeation in immediate hypersensitivity reactions. This chemical mediator causes bronchoconstriction, increased vascular permeability, and vasodilation.

A prostaglandin, or an unsaturated fatty acid with a wide range of biologic activity, produces smooth muscle contraction, increased capillary permeability, and vasodilation. This chemical mediator sensitizes pain receptors and increases pain from inflammation. Prostaglandins also prompt inflammation and boost the effects of mediators in inflammatory responses. Local indications include edema, heat, and erythema.

Secondary Mediators

Secondary mediators include leukotrienes, bradykinin, and serotonin. A leukotriene is a chemical mediator that initiates the inflammatory response. Indications of inflammation may be in part due to leukotrienes. Leukotrienes also cause smooth muscle contraction, bronchial constriction, smooth muscle contraction, mucus airway secretions, and wheal-and-flare skin reactions. In comparison to histamine, leukotrienes are 100 to 1,000 times more powerful in triggering bronchospasm. The chemical mediator bradykinin is a substance that stimulates nerve fibers and causes pain. It can cause vasodilation, hypotension, increased vascular permeability, and smooth muscle contraction (for example, of the bronchi). Edema results from increased capillary permeability. The chemical mediator serotonin acts as a forceful vasoconstrictor and bronchoconstrictor and is formed in platelets.

Pathophysiology

Type I hypersensitivity, or anaphylactic response, is facilitated by IgE antibodies produced by the immune system in response to allergens like dust mites, animal dander, and pollens. These IgE antibodies attach to mast cells and basophils that release histamine granules, which cause inflammation. This type of reaction can be seen in allergic rhinitis, allergic dermatitis, bronchial asthma, food allergy, anaphylactic shock, and conjunctivitis (Vaillant et al., 2023).

Type II hypersensitivity involves cytotoxic-mediated responses against cell surface and extracellular matrix proteins. These reactions are facilitated by IgG and IgM antibodies. The immunoglobulins damage cells by phagocytosis or by triggering the complement system. This type of reaction can be seen in autoimmune hemolytic anemia, autoimmune neutropenia, and immune thrombocytopenia (Vaillant et al., 2023).

Type III hypersensitivity, or immunocomplex reactions, are also facilitated by IgG and IgM antibodies that react with soluble antigens to create antigen-antibody complexes. The complement system is triggered and issues chemotactic agents that attract neutrophils and cause tissue damage and inflammation, as seen in glomerulonephritis and vasculitis. This type of reaction can be seen in an Arthus reaction and serum sickness (Vaillant et al., 2023). An Arthus reaction refers to an acute, localized inflammatory response that typically occurs after vaccination. It is classified as a type III hypersensitivity reaction, which is when antigen-antibody clusters, also known as immune complexes, are formed due to an abnormal immune system response.

Type IV, or delayed-type, hypersensitivity is a reaction where tissue damage is the result of T cell–dependent macrophage activation and inflammation. The pathophysiology of this type of reaction depends on the underlying cause.

• Granulomatous type reactions occur when T cells are triggered by antigen-presenting cells that are not able to terminate engulfed antigens. Macrophages are recruited to the site and accumulate intracellularly, forming a granuloma. An example is sarcoidosis.
• Drug hypersensitivity occurs when various drug particles join T cell receptors.
• Contact hypersensitivities occur when haptens invade the skin with vicinity to the cells of the epidermis and dermis and trigger an inflammatory reaction. A hapten is an incomplete antigen. The dendritic and Langerhans cells play a key role in antigen presentation and sensitization of these haptens to CD4 and CD8 T cells. The T cells exude cytokines and other enzymes to enlist other immune cells to the hapten exposure sites. Keratinocytes also help in recruiting immune cells by secreting cytokines like IL-8 (Marwa & Kondamudi, 2023).

Diagnostics and Laboratory Values

Diagnostic tests for hypersensitivity include complete blood count (CBC) with differential, eosinophil count, total serum IgE, and skin tests. A complete blood count with differential frequently reveals white blood cells are elevated with infection or inflammation. Eosinophils are elevated in an allergic response and may be tested from either blood samples or smears of nasal secretions. High total serum IgE levels are indicative of an allergy disorder.

Other simple blood tests that are commonly used to detect a general state of inflammation include the C-reactive protein (CRP) and homocysteine level tests. These are commonly tested for in autoimmune conditions such as Hashimoto thyroiditis and even to detect cardiac risk for heart attacks. High levels of CRP or homocysteine have been shown to be correlated with early cardiac death.

Skin Tests

Skin tests may be performed as an intradermal injection or a superficial application of solutions at various sites (Figure 24.3). This is commonly done on a patient’s back. Some allergy tests may have several solutions applied at different locations in one sitting. The solutions contain various antigens that represent an assortment of allergens known to cause reactions. Positive reactions are indicated by a wheal-and-flare reaction at the site. Depending on the severity of the reaction, some patients may also exhibit other symptoms like facial swelling or difficulty breathing.

Figure 24.3 This patient is undergoing a skin test for allergies: (a) patches with a variety of allergens are applied to her back; (b) when the patches are removed, red marks indicate reactions to specific allergens. (credit a: modification of “Skin patch allergy test 01” by “Smirkybec”/Wikimedia Commons, CC BY 4.0; credit b: modification of “Skin patch allergy test 02” by “Smirkybec”/Wikimedia Commons, CC BY 4.0)

Skin test results should be combined with patient history, physical findings, and other lab tests like serum IgE, CBC with differential, and an eosinophil count in order for the physician to make a proper diagnosis. Not every person will react to a specific allergen. Precautions are necessary when performing skin tests. For example, avoid testing during times of bronchospasm, have emergency equipment available in the event of anaphylaxis, and perform scratch or prick tests before other methods in order to limit the risk of a systemic reaction. Other physical testing may include muscle testing, which is less invasive.

Clinical Safety and Procedures (QSEN)

QSEN Competency: Safety

Definition: “Minimizes risk of harm to patients and providers through both system effectiveness and individual performances” (Quality and Safety Education for Nurses, 2020, table 5).

Knowledge: The nurse will analyze basic safety principles, understand evidence-based practice standards, and reflect on unsafe nursing practices.

Skill: Demonstrate effective strategies to reduce the risk of harm. The nurse will:

• educate the patient (and guardian if patient is a minor) of the process and ensure consent has been obtained
• be aware of signs and symptoms related to allergic reactions
• be aware of signs and symptoms of anaphylaxis
• assess the patient is safe to proceed with testing; for example, ruling out current signs of bronchospasms or other signs of current allergic response
• remain with the patient
• have the appropriate equipment nearby in the event emergency intervention warranted
• perform scratch or prick tests before other methods in order to limit the risk of a systemic reaction

Attitude: The nurse will respect individual role in preventing errors by adhering to safe, evidence-based practice standards.

(QSEN Institute, n.d.)

Recognizing and Analyzing Cues

Per the Clinical Judgment Measurement Model, part of the nursing process includes recognizing and analyzing cues. When it comes to hypersensitivity reactions in an acute care setting, the nurse should assess for signs of dyspnea, anaphylaxis, rashes, fever, wheals or hives, erythema, flushing, pruritus, and edema. The nurse should also ask the patient if they are experiencing any difficulty breathing, any sudden changes in how they feel, or any other type of discomfort. The nurse should also be aware of when the symptoms started and when medication was given. The nurse should document the symptoms and onset after a medication has been administered. For patients reporting an allergy to a medication, the nurse must ask for onset, symptoms, and type of medication taken in order to assess if the patient is experiencing hypersensitivity or a side effect of the medication.

Prioritizing Hypotheses, Generating Solutions, and Taking Action

If after analyzing cues the nurse determines the patient is having a reaction to a medication, the nurse must quickly prioritize interventions. Immediate interventions include discontinuing or removing the medication, managing the airway, administering oxygen as ordered, administering medications like epinephrine or diphenhydramine as ordered, and activating a rapid response in the event of anaphylaxis. The medication should also be documented as an allergy in the patient’s chart, and the patient should be educated about the allergy, any related medications, and the need to report this medication at other health care facilities. For example, penicillin and amoxicillin are in the same drug category, so a patient who has an allergic reaction to one medication is likely to have a similar reaction to the other. If a patient was told they had a reaction to a medication as a child, but they are unsure of the reaction type, the nurse should err on the side of caution and document the medication as an allergy. Any interventions performed should also be documented.

Evaluating Outcomes

Evaluating is not a one and done procedure; it is ongoing and multifactorial. The nurse should evaluate the effectiveness of every intervention. For example, if the patient experienced difficulty breathing, and the nursing intervention was to apply supplemental oxygen as ordered, the nurse should reassess the patient’s respiratory status for improvement. The nurse should also assess whether any medications administered had the desired effect. For example, if diphenhydramine was given to aid in relieving pruritus, the nurse should ask the patient if itching has improved or gotten worse. The nurse should also watch for cues like scratching or grimacing. The nurse should document the evaluation of the interventions provided as well.