Anaphylaxis

Anaphylaxis can be defined as an exaggerated, life-threatening hypersensitive reaction to a previously encountered antigen. As a paramedic, responding to a patient who is having a genuinely anaphylactic reaction is one of the very few situations when your treatment as a paramedic will clearly save a person’s life in front of you. It is because of this that it is paramount for any paramedic to thoroughly understand the pathophysiology and management of anaphylaxis.

Anaphylaxis can occur after a person is exposed to any antigen such as: bites and stings, medications (medical or herbal), foods, chemicals, or plants/pollens.

Paramedic Assessment and Treatment of Anaphylaxis

Airways may be compromised due to laryngeal and eppiglotic oedeama. Good airway management is critical! This includes insertion of nasopharyngeal airways and, if laryngeal or eppiglotic oedema develop, immediate intubation, as a golden standard of airway management.

Breathing may become difficult and should be assisted with intermittent positive pressure ventilation (IPPV) if necessary via bag valve mask

Circulation may be compromised as a result of relative hypovolaemia, and should be treated accordingly with adrenaline and fluid resuscitation.

Administration of the patient’s own “Epipen” if available.

Posturing should depend on the patient’s comfort. Normally, we lie hypovolaemic patients supine or with their legs raised, but this is unlikely to be possible if the person is have severe breathing problems which is often the more likely response to anaphylaxis than the hypotension.

Drugs: 500mcgs Intramuscular Injection of Adrenaline repeated every 5 minutes until desired result. Evidence based practice has indicated that IV adrenaline has no greater benefits to the patient, but many more potentially lethal risks associated with it. Oxygen should be administered. IV fluids should be given if the patient is hypovolaemic. Nebulisers should be considered as a secondary priority in patients with severe breathing difficulties (after adrenaline administration). Nebulisers should include: salbutamol and atrovent.

Any patient given adrenaline should always have a cardiac monitor applied (in case the adrenaline exacerbates a previous known or unknown underlying cardiac condition or dysrhythmia).

Understanding Anaphylaxis Pathophysiology

In order to understand the pathophysiology of anaphylaxis it is important to review the lines of defence that the human body utilises against bacterial, viral or microbial attack. This is important because anaphylaxis is just an exaggerated response by the immune system to target a particular antigen.

Lines of Defence in the Human Body

First line – intact skin, mucous membranes and their secretions

Second line – phagocytic white blood cells, inflammation and fever, antimicrobial substances, natural killer cells

Third line – immune response, specialized lymphocytes and antibodies

First line: surface defences and non-specific resistance factors

1. Physical barriers, such as skin, mucous membranes and secretions

2. Mechanical removal, such as macrophages

3. Chemical inhibitors

4. Anti-microbial substance

5. Fever, lysozyme

Second line: inflammation

1. Metabolic changes to the injured cell

2. Cellular organelles leak and release hydrolytic enzymes, causing the inflammatory response

3. Decreased cellular energy and Na+K+ activity pump, acidosis and decreased membrane integrity (leading to oedema)

4. Chemotactic factors assist the migrating leucocytes (neutrophils and monocytes) to collect along vascular endothelial lumen

5. Localised hyperaemia develops as microvasculature dilates

6. Increased filtration pressures and capillary permeability causes fluid to pass into the interstitium (this causes oedema)

7. Leucocytes engulf, digest and destroy pathogens

8. Circulating macrophages clear dead cells and debris

9. Eventually leukocytes are lysed by the release of certain chemicals

Third line: immune response

1. Primary and secondary responses

2. Lymphatic system

3. Innate (also known as natural immunity) and acquired (or developed) immunity

4. Humoral (antibody dependent) and Cell mediated immunity
B and T cells
Lymphocytes are developed through stem cells within bone marrow. They then differentiate into two distinct classes of lymphocytes. These are called T cells and B cells.

B-cells, also known as the human bursal equivalent, (thus the name B-cells) mature in bone marrow and are essential for humoral or antibody mediated immunity.

T cells are lymphocytes which complete maturation in the thymus (thus the name T-cell) and function to produce cell-mediated immunity, as well as aiding in antibody production.

Characteristics of Immunoglobulin?

There are five immunoglobulins:

IgG – displays antiviral antitoxin, and antibacterial properties

IgA – is the predominant Ig in body secretions

IgM – forms natural antibodies

IgD – is used in the maturation of B cells

IgE – binds to mast cells and basophils, and the binding of an antigen to the bound IgE causes the release of histamine and other mediators of inflammations and allergies

For a person to have an anaphylactic reaction they must first be exposed to a specific antigen to develop type I hypersensitivity. In the first exposure, the antigen enters the body by injection, ingestion, inhalation, or absorption and activates the immune system. Normally T-suppressor cells stop B-cells from proliferating, but sometimes suppression is not sufficient. In the susceptible individuals, large amounts of IgE antibodies are produced. IgE binds to mast cells and basophils and are involved in parasitic infections, allergic reactions and hypersensitive reactions.

Then IgE antibodies leave the lymphatic system and bind to the cell membranes of basophils circulating in the blood and to the mast cells in the tissues surrounding the blood vessels. They then remain there and are inactive until the same antigen is introduced into the body a second time (This is why it normally takes at least two exposures to an antigen to cause anaphylaxis).

With subsequent exposures to the specific antigen, the allergen crosslinks at least two of the cell-bound IgE molecules, resulting in the degrannulation (release of internal substances) of the mast cells and basophils and the onset of an anaphylactic reaction.

What is released on degranulation?

The degranulation of the target cell is associated with the release of pharmacologically active chemical mediators from inside the affected basophils and mast cells. These include histamines, leukotrienes, eosinophil chemotactic factors of anaphylaxis, heparin, kinins, prostaglandins, and thromboxanes. All of which, trigger an internal systemic response, which can lead to anaphylaxis.

What does this cause?

Histamines promote vascular permeability and cause dilation of capillaries and venules and contraction of vascular smooth muscle, especially in the GIT and the bronchial tree.

The increased capillary permeability allows plasma to leak into the interstitial space (causing oedema), decreasing the intravascular volume available for the heart to pump (decreasing pre-load). The profound vasodilatory effect results in further decreases in cardiac preload, compromising stroke volume and cardiac output.

These physiological effects lead to cutaneous flushing, urticaria, angioedema, and hypotension.

What are common antigens that lead to anaphylaxis?

Any antigen can cause an anaphylactic reaction, but many common ones include:

1. Bee stings, wasps, ants

2. Penicillan, morphine, and aspirin

3. Soy beans, peanuts, eggs

4. Latex gloves

There are four types of hypersensitive reactions to allergens

Type I is an IgE-mediated allergic reaction

Type II is a tissue-specific reaction

Type III is an immune complex-mediated reaction

Type IV is cell-mediated reaction

Type One

Type I reaction, or anaphylactic reaction, occurs soon after exposure to an antigen. It occurs when the specific type of antibody (IgE) attaches to mast cells. This causes the chemical substances in the mast cell, including histamine, and slow reactive substance of anaphylaxis to be released

Type two

Type II reactions, or cytotoxic reactions, are delayed reactions that involve certain cytotoxic antibodies of the IgG class. These antibodies are capable of lysing cells and commonly cause haemolytic reactions and the destruction of platelets. This causes swelling and can lead to potentially fatal anaphylaxis and airway obstructions.

Type three

Type III reactions are usually delayed reactions described as serum sickness. Like type II reactions, specific antibodies usually are involved. These antibodies, often IgGs, bind with the antigens in the blood stream and form complexes. These complexes filter out into various anatomical locations and produce an inflammatory response.

Type four

Type IV reactions are those in which contact dermatitis is produced by topical application of an antigen. These reactions are caused by T-lymphocytes, not the humoral antibodies and usually require more than 24 hours for their signs and symptoms to manifest.

There are two types of IgE mediated reactions

These include atopic and non-atopic disorders

The term atopic refers to a genetically determined hypersensitivity to common environmental antigens mediated by an IgE- mast cell reaction

The most common atopic disorders include allergic rhinitis and allergic asthma

The term non-atopic refers to disorders that lack genetic components

Non-atopic disorders include anaphylactic reactions, urticaria and angio-oedema.

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