Anaphylaxis

Definition of Anaphylaxis

ASCIA define Anaphylaxis as:

• Any acute onset illness with typical skin features (urticarial rash or erythema/flushing, and/or angioedema), plus involvement of respiratory and/or cardiovascular and/or persistent severe gastrointestinal symptoms; or
• Any acute onset of hypotension or bronchospasm or upper airway obstruction where anaphylaxis is considered possible, even if typical skin features are not present.

Source: https://www.allergy.org.au/hp/papers/acute-management-of-anaphylaxis-guidelines

Pathophysiolgy

Primary Immune Response

Happens first time patient is exposed to the allergen

Remember:

• Mast cells: WBC present in most tissue, very prevalent around lungs, skin, nose, mouth, GI tract and other mucosal tissue
• Basophils: WBC found in blood, act in a simiar way to mast cells (i.e. they degraunlate)

The most common type of reaction and the one we’re most interested in is the Type 1 IgE mediated reaction, the process for which goes like this:

1. Antigen is either external (examples below) or internal
2. Antigen enters body (if external)
3. Body, in particular the immune system, triggers immune response to produce antibodies to defend against this ‘thing’
4. Antigen stimulates B lymphocytes to produce antigen specific IgE antibodies
5. These IgE antibodies attach to Mast Cells and Basophils and are stored

Secondary Immune Response

1. Re-exposed to same allergen
2. Allergen attaches to IgE antibody on the mast cell
3. This attachment stimulates release of chemical mediators such as histamine from granules within mast cells (degranulation)
4. Other chemical mediators including Luekotrienes, Bradykinins, Prostaglandins and Thromboxanes released
5. The systemic reaction we’re familiar with occurs

Why does the systemic reacion occur?

Histamine is a vasodilator and in combination with the other chemical mediators we get massively increased vascular permiability hence the fluid shift, edema, redness etc.

Chemical mediators and what they do

Mediators

• Bradykinin:
  • Cardiovascular (increased vascular permiability, vasodilation)
  • Constriction of uterine and GI smooth muscle (hence the nausea and vomiting [in combo with diverted blood flow from shunting])
  • Bronchoconstriction
• Histamine:
  • Cardiovascular (vasodilation, increased vascular permiability, increased HR)
  • Skin (irriate sensory nerves)
  • Glandular secretions
• Leukotrienes:
  • Bronchoconstriction
  • Increased vascular permiability
  • Promotes airway remoddeling
• Prostoglandin:
  • Bronchoconstrictor
  • Pulmonary and coronary vasoconstrictor
  • Peripheral vasodilator

Effects

• Cardiovascular effects: Systemic vasodilation and increased capillary permiability -> Decreased circulating volume (as its shifted) -> Decreased BP -> Faint/dizzy
• Respiratory effects: Constriction of bronchioles and mucus production in respiratory tract -> Airway becomes obstructed -> Cough & dyspnea
• Skin effects: Histamine irritates nerve endings causing itchiness

Routes for allergen

Routes with some examples for each type

• Ingestion: Medication, nuts, shellfish
• Inhalation: Pollen, animal dander, dust, mould/mildew
• Injection: Medication, bee sting
• Skin Contact / Absorption: Latex, poisonous plants, pollen

Graphical versions

Pathogenesis

Signs and Symptoms

Type 1 Hypersensitivity