SEMINAR ON ANAPHYLAXIS

BY LIDIYAMOL.P.V 1ST YEAR M.SC NURSING GOVT. CON , THRISSUR

HISTORY OF IMMUNOLOGY: Immunology is a science that examines the structure and function of the immune system. The earliest known reference to immunity was during the plague of Athens in 430 BC. . Thucydides noted that people who had recovered from a previous bout of the disease could nurse the sick without contracting the illness a second time.

HISTORY OF IMMUNOLOGY:CONTD
Immunology made a great advance towards the end of the 19th century, through rapid developments, in the study of humoral immunity and cellular immunity. Particularly important was the work of Paul Ehrlich, who proposed the side-chain theory to explain the specificity of the antigen-antibody reaction

FACTORS THAT DETERMINE AN ALLERGIC RESPONSE: Responsiveness of the host to the allergen: Amount of allergen: Nature of the allergen: Route of entrance of the allergen Timing of exposure to the allergen Site of the allergen immune mediator reaction

FACTORS THAT DETERMINE AN ALLERGIC RESPONSE:- CONTD

Hosts threshold of reactivity The hosts immune system can be changed by factors such as stress, fatigue, or infection, all of which can decrease the responsiveness of immune system to potential allergens.

CLASSIFICATION OF HYPERSENSITIVITY REACTIONS:IMMEDIATE HYPERSENSITIVITY (B-CELL OR ANTIBODY MEDIATED) Anaphylaxis Atopy Antibody mediated cell damage Arthus phenomenon Serum sickness DELAYED HYPERSENSITIVITY (T- CELL MEDIATED) Infection (tuberculin) Contact dermatitis

Coombs and Gell (1963) classification of hypersensitivity reactions

Type I (anaphylactic, IgE or reagin dependent): Antibodies (cytotropic IgE antibodies ) are fixed on the surface of tissue cells ( mast cells and basophils ) in sensitised individuals. The antigen combines with the cell fixed antibody leading to release of vasoactive amines which produces clinical reactions.

Coombs and Gell (1963) classification of hypersensitivity reactions

Type II (cytotoxic or cell stimulating): This type of reaction is initiated by IgE (OR rarely IgM) antibodies that reacts with the cell surface or tissue antigen. Cell or tissuedamage occurs in the presence of complement or mononuclear cells. Type II reactions are intermediate between hypersensitivity and auto immunity.

Coombs and Gell (1963) classification of hypersensitivity reactions

Type III ([mmune complex or toxic complex disease) Here the damage is caused by antigen antibody complexes. These may precipitate in and around small blood vessels, causing damage to cells secondarily, or on membranes, interfering with their function

Coombs and Gell (1963) classification of hypersensitivity reactions

Type IV (ddelayed or cell mediated ) This is a cell mediated response. The antigen activates specifically sensitised CD4 AND CD8 T cells, leading to the secretion of lymphokines, with fluid and phagocyte accumulation.

DEFINITION
Type I Reactions: These occur in two forms : the acute, potentially fatal, systemic form called anaphylaxis and the chronic or recurrent, nonfatal, typically localised form called atopy.

DEFINITION: . Anaphylaxis is defined as "a serious allergic reaction that is rapid in onset and may cause death". It typically results in a number of symptoms including an itchy rash, throat swelling, and low blood pressure. Common causes include insect bites, foods, and medications.

DEFINITION
. Anaphylaxis is an acute, potentially fatal, multiorgan system reaction caused by the release of chemical mediators from mast cells and basophils. The classic form involves prior sensitization to an allergen with later reexposure, producing symptoms via an immunologic mechanism.

DEFINITION
Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunological reaction between a specific antigen and antibody. The reaction result from IgE antibody.

ETIOLOGY
Food Medication Venom Risk factors People with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex, and radiocontrast

immune system
LAYERED DEFENSE: physical barriers prevent pathogens such as bacteria and viruses from entering the organism. If a pathogen breaches these barriers, the innate immune system provides an immediate, but non-specific response

immune system
If pathogens successfully evade the innate response, vertebrates possess a second layer of protection, the adaptive immune system, which is activated by the innate response.

IMMUNE SYSTEM
SURFACE BARRIERS Mechanical, chemical, and biological barriers. INNATE IMMUNE SYSTEM The innate response is usually triggered when microbes are identified by pattern recognition receptors

 Humoral and chemical barriers Inflammation Inflammation is one of the first responses of the immune system to infection. The symptoms of inflammation are redness, swelling, heat, and pain, which are caused by increased blood flow into tissue.

 . Complement system The complement system is a biochemical cascade that attacks the surfaces of foreign cells Complement is the major humoral component of the innate immune response

 In humans, this response is activated by complement binding to antibodies that have attached to these microbes or the binding of complement proteins to carbohydrates on the surfaces ofmicrobes. This recognition signal triggers a rapid killing response

Adaptive immune system

The adaptive immune response is antigenspecific and requires the recognition of specific "non-self" antigens during a process called antigen presentation. Antigen specificity allows for the generation of responses that are tailored to specific pathogens or pathogen-infected cells.

Adaptive immune system

Lymphocytes The cells of the adaptive immune system are special types of leukocytes, called lymphocytes. B cells and T cells are the major types of lymphocytes and are derived from hematopoietic stem cells in the bone marrow. B cells are involved in the humoral immune response, whereas T cells are involved in cell-mediated immune response

Adaptive immune system

Killer T cells Killer T cell are a sub-group of T cells that kill cells that are infected with viruses (and other pathogens), or are otherwise damaged or dysfunctional.

Adaptive immune system

Helper T cells Helper T cells regulate both the innate and adaptive immune responses and help determine which immune responses the body makes to a particular pathogen. These cells have no cytotoxic activity and do not kill infected cells or clear pathogens directly. They instead control the immune response by directing other cells to perform these tasks.

Adaptive immune system

T cells T cells possess an alternative T cell receptor (TCR) as opposed to CD4+ and CD8+ () T cells and share the characteristics of helper T cells, cytotoxic T cells and NK cells. The conditions that produce responses from T cells are not fully understood

Adaptive immune system

B lymphocytes and antibodies A B cell identifies pathogens when antibodies on its surface bind to a specific foreign antigen. This antigen/antibody complex is taken up by the B cell and processed by proteolysis into peptides. The B cell then displays these antigenic peptides on its surface MHC class II molecules. This combination of MHC and antigen attracts a matching helper T cell, which releases lymphokines and activates the B cell.

Adaptive immune system

Immunological memory When B cells and T cells are activated and begin to replicate, some of their offspring become long-lived memory cells. Throughout the lifetime of an animal, these memory cells remember each specific pathogen encountered and can mount a strong response if the pathogen is detected again.

PATHOPHYSIOLOGY: Type I hypersensitivity are mediated by the IgE class of immunoglobulin. In genetically, pre disposed people, initial exposure to an allergen prompts B lymphocytes to produce IgE antibodies, which sensitize the person to the allergen. This initial contact with the allergen is known as the sensitizing dose

PATHOPHYSIOLOGY
Once the person is fully sensitized, subsequent exposure ( termed the shocking dose or challenging dose) results in the allergen combined with the specific IgE antibodies that are bound to receptor sites on tissue mast cells and blood basophils. This antigen antibody reaction results in a rapid release of potent vaso active mediators such as histamines, kinins, chemo tactic factors, and active products of arachidonic acid metabolism

PATHOPHYSIOLOGY
Anaphylaxis is caused by the interaction of a foreign antigen with specific IgE antibodies found on the surface membrane of mast cells and peripheral blood basophils. The subsequent release of histamine and other bioactive mediators cause activation of platelets, eosinophils, and neutrophils and coagulation cascade. Smooth muscle spasm, bronchospasm, mucosal eddema, and inflammation, and increased capillary permeability

CLINICAL FEATURES
Localised reactions:Hives angioedema Systemic anaphylaxis:Apprehension Edema of the hands, face, or other parts of the body Dyspnoea Respiratory collapse Vascular collapse with shock
Rapid, regular pulse Falling blood pressure Cyanosis

Death

DIAGNOSTIC MEASURES
The health history including an environmental assessment, Skin testing and radio allergo sorbent test (RAST) may be helpful

MEDICAL MANAGEMENT
Management depends on the severity of the reaction. Initially, respiratory and cardiovascular functions are evaluated

TREATMENT
Simple BLS (O2, position, etc) Anti Histamines
Benadryl (IV 25-50 mg, PO 50 mg adult, 25 mg ped)

Corticosteroids
Decadron, Solu-medrol, etc

Treat Hypotension
IV fluids
Dopamine 5-20 mcg/min Epi Drip 2-10 mcg/min

TREATMENT
Broncheodiators
Albuterol MDI or Neb

Observe for a minimum 8-12 hours

Benadryl for 24 hours.

Rebound or persitant S/S

Repeat epinephrine if Sx persist or increase after 10-15 minutes

Repeat antihistamine H2 blocker if Sx persist

TREATMENT
Avoidance therapy, in which the patient is thought to reduce exposure to trigerring antigens, is the most effective treatment to decrease allergic attacks Immunotherapy is often useful in reducing symptoms in patients who cannot avoid antigens such as dust mites or pollen

PREVENTION
EDUCATE

Teach avoidance measures

Accidents are never planned Stress importance of:
Immediate treatment

Emphasize the need for follow-up care

NURSING MANAGEMENT
ASSESSMENT: Health history: Assessment data to be collected as part of the health history of a patient with allergy includes: History of allergic reactions in the past ( e.g., type, frequency or perceived causes) Familial history of allergies Recent exposure to sensitizing substances (chemicals, drugs) Changes in living, working, or environmental conditions

NURSING MANAGEMENT
Characteristics of present environment (house, clothing, plants, trees or animals) Increased stress in recent past ( stress aggrevates asthmatic response) Types of symptoms experienced: respiratory, dermal, gastrointestinal or general Alleviating factors, either prescribed, herbal, or over the counter All patients should be questioned about allergies and sensitivities to drugs before any drug therapy is initiated. If there is a positive history, the physician is consulted before a new drug is given, the patient is monitored closely for allergic responses.

Physical examination: Important aspects of the physical examination of the patient with allergy include inspection and observation for : Rashes (location, and colour) Mouth breathing (nasal obstruction) Flaring nares Difficulty hearing (plugged Eustachian tubes) Pale, bluish turbinates that are oedematous with clear secretions

PHYSICAL EXAMINATION
Tearing Dark areas under the eyes ( venous dilation of the skin) Scleral or conjunctival infections Increased respiratory rate Audible wheezing Use of accessory muscles for breathing Anxious depression

NURSING DIAGNOSES: Ineffective airway clearance related to excess secretion production and bronchoconstriction. Decreased cardiac output related to inadequate venous return to heart, peripheral vasodilation. Deficient knowledge related to inadequate information about allergy control and treatments.

 Airway clearence: Cardiac output: Nurse should be alert for the clinical manifstatios of anaphylactic shock. At the first sign of anaphylaxis, the patient is given epinephrine 1:1000 solution 0.3 to 0.5 ml s/c or im Risk for allergy response: High risk patients are instructed to wear a identification bracelet.

INTERVENTIONS
Provide supplemental oxygen and observe. If hypoxia continues, prepare to help insert an artificial airway. Insert an I.V. line for giving emergency drugs and volume expanders. Continually reassure the patient and explain all tests and treatments to reduce fear and anxiety. If the patient undergoes skin or scratch testing. Keep emergency resuscitation equipment nearby during and after the test.

INTERVENTIONS
Continuously assess the patients response to treatment. Monitor vital signs and cardiopulmonary and neurologic function. Observe for complications associated with anaphylaxis, such as vascular collapse and acute respiratory insufficiency or obstruction. Closely observe a patient with known allergies for anaphylaxis when giving a drug with high anaphylactic potential.

COMPLICATIONS
The primary complication of type I hypersensitivity are anaphylactic shock, which can leads to death within minutes without emergency treatment.