ANAPHYLAXIS

Anaphylaxis:

Anaphylaxis, or anaphylactic shock as it is more accurately termed, occurs when an environmental trigger causes a systemic inflammatory response, leading to distributive shock. Following sensitization to a given substance, the body creates antibodies in the form of IgE, which are the active agents in initiating a true anaphylactic reaction. IgE, in conjunction with mast cells, release histamines, bradykinin, leukotrienes and other inflammatory mediators. In contrast, there do exist “anaphylactoid” reactions that do not involve IgE, and are driven by mast cells alone. As the end result is the same, there is no real reason to separate these 2 reactions in the prehospital setting.

Once inflammatory agents are released into systemic circulation, profound vasodilation and systemic inflammation occur. This can manifest in any of the following ways:

-Angioedema

-Hypotension

-Nausea and vomiting

-Urticaria

-Larygospasm and bronchoconstriction

-Generalized itching

-Rhinorhea

-Tachycardia, which can progress to bradycardia

-Confusion due to cerebral hypoperfusion

-Hypoxemia

In order to diagnose anaphylaxis, 2 or more body systems must be symptomatic, with or without a known allergy exposure.

The major threats to life are:

-Airway obstruction

-Distributive shock and vascular collapse

Prehospital medications: 

-Epinephrine 1:1000: Triggers bronchodilation, elevated heart rate, and causes systemic vasoconstriction. Epinephrine also stops the action of histamine. 

-Benadryl: Works to stop the action of systemic inflammatory mediators. 

-Salbutamol: Triggers beta 2 adrenergic response, leading to bronchodilation.

Treatment Plan: 

-Give epinephrine 1:1000 IM per local protocol 

-Provide supplemental oxygen if needed 

-Establish IV access 

-Give benadryl with IV as preferred route 

-Provide salbutamol by MDI or nebulizer if brochoconstriction is present