7.1.1 Type I (anaphylaxis)
  • A type I hypersensitivity (allergic) reaction between an allergenic antigen and immunoglobulin E (IgE) bound to mast cells, which stimulates the sudden release of immunological mediators locally or throughout the body.
  • The first symptoms occur within minutes, and a recurrence may follow hours later (late-stage response). Anaphylaxis can only occur in an individual previously sensitized to an allergen, as it is the initial exposure that causes immunoglobulin E (IgE) to bind to mast cells. It is categorized as local or systemic. Local anaphylactic reactions include hay fever, hives, and allergic gastroenteritis. Systemic anaphylaxis, which produces peripheral vasodilation, bronchospasm, and laryngeal edema, can be life- threatening.

    • ETIOLOGY: IgE antibodies bound to mast cells throughout the body as the result of previous exposure to an allergenic antigen (sensitization) react when the allergen is introduced a second time. The mast cells release packets containing chemical mediators (degranulation) that attract neutrophils and eosinophils and also stimulate urticaria, vasodilation, increased vascular permeability, and smooth muscle spasm, esp. in the bronchi and gastrointestinal tract. Chemical mediators involved in anaphylaxis include histamine, proteases, chemotactic factors, leukotrienes, prostaglandin D, and cytokines (e.g., TNF-aand interleukins 1, 3, 4, 5, and 6). The most common agents triggering anaphylaxis are drugs, food, and insect stings. Local anaphylactic reactions are also commonly triggered by pollens (e.g., hay fever, allergic rhinitis, allergic asthma).
    • SYMPTOMS: Local anaphylaxis causes signs to appear at the site of allergen- antibody interaction including urticaria (hives), edema, warmth, and erythema. In systemic anaphylaxis the respiratory tract, cardiovascular system, skin, and gastrointestinal system are involved. The primary signs are urticaria, angioedema, flushing, wheezing, dyspnea, increased mucous production, nausea and vomiting, and feelings of generalized anxiety. Systemic anaphylaxis may be mild or severe enough to cause shock when massive vasodilation is present.
    • TREATMENT: Local anaphylaxis is treated with antihistamines and occasionally epinephrine, if the reaction is severe. Treatment for systemic anaphylaxis includes protection of the airway and administration of oxygen; antihistamines (e.g., diphenhydramine or cimetidine to block histamine H1 and H2 receptors); IV fluids to support blood pressure) and vasopressors (e.g., epinephrine or dopamine) to prevent or treat shock. Epinephrine also is used to treat bronchospasm. Generally, drugs are given intravenously; drugs may also be given intramuscularly (e.g., diphenhydramine) or endotracheally (e.g., epinephrine). In mild cases they may be given subcutaneously. Corticosteroids may be used to prevent recurrence of bronchospasm and increased vascular permeability.
    • PATIENT CARE: Prevention: A history of allergic reactions, particularly to drugs, blood, or contrast media, is obtained. The at- risk patient is observed for reaction during and immediately after administration of any of these agents. The patient is taught to identify and avoid common allergens and to recognize an allergic reaction.
      Patients also should be taught to wear tags identifying allergies to medications, food, or insect venom at all times to prevent inappropriate treatment during an emergency. Individuals who have had an anaphylactic reaction and are unable to avoid future exposure to allergens should carry a kit containing a syringe of epinephrine and be taught how to administer it. Patients who are allergic to the venom of Hymenoptera insects (bees, wasps, hornets) can receive desensitization.
      • active anaphylaxisAnaphylaxis resulting from injection of an antigen.
      • exercise-induced anaphylaxisanaphylactoid reaction.
      • local anaphylaxis A reaction between IgE antibodies bound to mast cells and an allergen that is limited to a small part of the body.Localized edema and urticaria (hives) result and may vary in intensity.
      • passive anaphylaxis Anaphylaxis induced by injection of serum from a sensitized animal into a normal one. After a few hours the latter becomes sensitized.
      • passive cutaneous anaphylaxis ABBR: PCA.. A laboratory test of antibody levels in which serum from a sensitized individual is injected into the skin. Intravenous injection of an antigen accompanied by Evans blue dye at a later time reacts with the antibodies produced in response to the antigen, creating a wheal and blue spot at the site, indicating local anaphylaxis.
      • systemic anaphylaxis A reaction between IgE antibodies bound to mast cells and an allergen that causes the sudden release of immunological mediators in the skin, respiratory, cardiovascular, and gastrointestinal systems. The consequences may range from mild (e.g., itching, hives) to life- threatening (airway obstruction and shock).
graphic
Fig. 5-7 Sequence of events leading to type I hypersensitivity. APC, antigen- presenting cell; GM- CSF, granulocyte- macrophage colony-stimulating factor; TCR, T-cell receptor; TH2 cell, CD4+ helper T cell.