This document discusses allergies and anaphylaxis, including their pathophysiology, assessment findings, and management. It describes anaphylaxis as a life-threatening allergic reaction caused by exposure to an allergen, which results in widespread histamine release and affects multiple body systems. Key treatments for anaphylaxis include epinephrine, antihistamines, corticosteroids, oxygen, IV fluids and airway management. Allergic reactions involve similar symptoms but are typically less severe. Patient education focuses on prevention, recognition of symptoms and self-treatment options.
2. Sections
Pathophysiology
Assessment Findings in
Anaphylaxis
Management of Anaphylaxis
Assessment Findings in Allergic
Reaction
Management of Allergic Reactions
Patient Education
3. Allergies and Anaphylaxis
Allergic Reaction
An exaggerated response by the immune
system to a foreign substance
Anaphylaxis
An unusual or exaggerated allergic reaction
A life-threatening emergency
5. Pathophysiology
Immune Response
Exposure to antigen produces primary response with
general antibodies.
Immune system develops antigen-specific antibodies
and memory.
Future exposures generate a faster secondary
response.
Natural and Acquired Immunity
Induced Active Immunity
Active and Passive Immunity
6. Allergies
Sensitization
Hypersensitivity
Delayed
Results from cellular immunity and does not involve
antibodies.
Commonly results in skin rash.
Results from exposure to certain drugs or chemicals.
Immediate
Exposure quickly results in secondary response.
More severe than delayed hypersensitivity.
7. Allergies
Allergen
Exposure generates secondary response.
Large quantities of IgE are released.
Allergen binds to IgE, causing chemical release.
• Release is “allergic reaction.”
• Includes histamines, heparin, and other substances that
are designed to minimize the body’s exposure to an
antigen.
• Histamine causes bronchoconstriction, vasodilation,
increased gastric motility, and increased vascular
permeability.
• Angioneurotic edema.
9. Anaphylaxis
Causes
Injections
Most anaphylaxis results from the injected route.
Allergen rapidly distributed throughout the body,
resulting in massive histamine release.
• Parenteral penicillin injections and insect stings.
• Affects cardiovascular, respiratory, gastrointestinal, and
integumentary systems.
• Significant plasma loss through increased vascular
permeability.
• Slow-reacting substance of anaphylaxis.
10. Assessment Findings
in Anaphylaxis
Focused History & Physical Exam
Focused History
SAMPLE & OPQRST History
• Rapid onset, usually 30–60 seconds following exposure.
• Speed of reaction is indicative of severity.
• Previous allergies and reactions.
Physical Exam
Presence of severe respiratory difficulty is key to
differentiating anaphylaxis from allergic reaction.
11. Assessment
Findings in
Anaphylaxis
Physical Exam
Facial or laryngeal
edema
Abnormal breath
sounds
Hives and urticaria
Hyperactive bowel
sounds
Vital sign deterioration
as the reaction
progresses
12. Management of
Anaphylaxis
Scene Safety
Consider the possibility of trauma.
Protect the Airway.
Use airway adjuncts with care.
Intubate early in severe cases to prevent total
occlusion of the airway.
Be prepared to place a surgical airway.
13. Management of
Anaphylaxis
Support Breathing
High-flow oxygen or assisted ventilation if
indicated.
Establish IV Access
Patient may be volume-depleted due to “third
spacing” of fluid.
Administer crystalloid solution at appropriate rate.
Place a second IV line if indicated.
14. Management of
Anaphylaxis
Administer Medications:
Oxygen
Epinephrine
Antihistamines
Corticosteroids
Vasopressors
Beta-agonists
Other agents
Psychological Support
16. Management of Allergic
Reactions
Scene safety
Protect the
airway.
Support
breathing.
Establish IV
access.
Administer
medications:
Antihistamines
Epinephrine
17. Patient Education
Prevention of Reactions
Recognition of Signs/Symptoms
Patient-initiated treatment
Epinephrine auto-injectors
Desensitization
18. Summary
Pathophysiology
Assessment Findings in
Anaphylaxis
Management of Anaphylaxis
Assessment Findings in Allergic
Reaction
Management of Allergic Reactions
Patient Education
Notas del editor
Pathogen – a disease producing agent or invading substance that causes an immune response. Anitgen – any substance capable of producing an immune response. Including toxins released by bacteria. The body has 2 mschanisma to destroy and illiminate these antigens Cellular immunity – results from a direct attack by specialized cells of the immune system Humoral immunity – reults from the attack of antibodies (immunoglobins) IgA, Igd, IgE, IgM. Manufactured by B cells.
Primary response – initial response to an antigen Secondary response – If the body is exposed a second time, antibodies specific to the antigen are released. Natural Immunity – present at birht Aquired immunity – developed over time resulting from an exposure Active immunity – aquired following exposeure, results in production of antibodies Induced active immunity – vacination Passive Immunity – administration of immunity Natural passive – placental barrier from mother to child Induced passive – tetanus
Sensitization is the initial exposure of a person to an antigen that results in an immune response. Subsequent exposures result in a much stronger secondary response. Hypersensitivity or Allergy Delayed hypersensitivity – result of cellular immunity, days and hours following exposure, skin rash ie poison ivy Immediate hypersenitivity – ex hay fever, drug allergies, asthma,
Allergen, a substance capable of inducing allergic reaction ie drugs, food, animals, insects, fungi molds IgE is released following exposure – IgE binds to basophil (special white blood cells) and mast cells (granulocytes), these cells release histamine and heparin , which are stored in granules, into the sourounding tissues. This process is called degranulation or allergic reaction. Histamine caues bronhoconstriction, vasodilation, increased vascular permeability, increased intestinal motility. Angioedema – swelling of hands and face and upper airway from increased vascular permeability. Histamine receptors (H1 and H2) – the goal of histamine response is to limit bodies exposure to antigens. Broncoconstriction reduses antigens entering resiratory track, vascular permiability removes antigens from circulatory system etc.
epi – sympathetic agonist, causes increased heart rate inotropic peripheral vasoconstriction reverse bronchospasm reverse capilary permebility .3 to .5 1:1,000 subQ, .3 - .5 mg 1:10,000 IV, peds .01 mg/kg, antihistamines – benadryl non selective H1 H2 blocker 25 – 50 mg IV, zantac ex selective H2 used for ulcers but also effects vascular syst corticosteroids – of little benefit in the intial stages but help suppress the inflammatory response ie solu-medrol vasopressors – dopamine beta agonist – albuterol to reduce bronchospasm and laryngeal edema