The protocol for Anaphylaxis:Anaphylaxis
Let’s break it down!
Anaphylaxis is defined as a “serious allergic or hypersensitivity reaction that is rapid in onset and may cause death”. It’s a multisystem syndrome caused by the sudden release of mast cell mediators into the systemic circulation, most often from immunoglobulin E (IgE)-mediated reactions to foods, drugs, and insect stings.
The diagnosis for anaphylaxis is primarily a clinical one. A basic allergic reaction becomes “anaphylaxis” when you have an acute onset of an illness (minutes to several hours) involving the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) and at least one of the following:
- Respiratory Compromise (Airway swelling)
- Reduced blood pressure or symptoms of end-organ dysfunction (Low BP, incontinence syncope, etc.)
The term “Anaphylactic Shock” specifically refers to hypotension caused by anaphylaxis, but they’re often used interchangeably. The video below provides a great explanation on the pathophysiology of anaphylaxis:
Anaphylaxis is a multi-system problem, so we’re going to see multiple problems arise. Specifically in the skin, respiratory, cardiovascular systems,
The first notable symptoms will likely occur on the skin or mucous membranes, specifically urticaria (hives) and angioedema (mucous membrane swelling; tongue, face, larynx). These symptoms occur in up to 87% of all cases of anaphylaxis.
Swelling in the upper airways will cause the patient to become short of breath (dyspnea) as well as produce an audible stridor sound as air attempts to pass through the narrowed airway. In addition, spasms in the bronchioles produce a wheezing sound that can be auscultated as trapped air tries to escape. These symptoms occur in about 50% of patients. The video below demonstrates what stridor and wheezing actually sound like:
The most dangerous consequence of anaphylaxis is its effect on the blood vessels in the body. Anaphylaxis causes a systemic dilation of the vessels and increases their permeability, thus allowing for fluid to be pushed out into the interstitial spaces. This creates hypotension in the form of a distributive shock that can be very difficult to treat. In 25% of cases, tachycardia (increase in heart rate) will occur either as a compensatory mechanism or as a result of catecholamine release.
Although not included in the protocol, approximately 50% of patients will also experience gastrointestinal symptoms such as nausea, vomiting, or abdominal pain. These symptoms are more likely to occur in food-allergy patients.
By far the best treatment for anaphylaxis is early administration of Epinephrine. Epinephrine is the perfect medication for this condition because of it’s following properties:
- Alpha-1-adrenergic agonist effects – It increases vasoconstriction, which helps by countering the distributive shock as well as decreasing the amount of edema in the mucous membranes of the upper airway
- Beta-1-adrenergic agonist effects – Increases inotropy (force of heart contractions) and chronotropy (rate of contractions) to further help with countering hypotension.
- Beta-2-adrenergic agonist effects – Increases bronchodilation; helping the patient breathe and oxygenate more effectively.
The gold standard method for administering epinephrine is via the intramuscular route. This allows for a slower, safer absorption of the drug. It can be done via epi-pen or it can be drawn up. The video below shows how you can manually draw up epinephrine for use:
After epinephrine is given, the next step is to support the patient’s hemodynamics. Due to airway swelling and bronchoconstriction, we can expect the patient to be hypoxic. High flow o2 via a non-rebreather mask is recommended.
In addition, the airway will also have to be managed if the epinephrine is not enough to control the swelling. In many cases, this could require oral or nasopharyngeal airways, although this may be difficult to achieve if massive angioedema is present. The decision to intubate should be made early on in the illness to avoid problematic swelling. Although scary to think about, an emergency cricothyroidotomy may be indicated in a minority of cases. These are the links for airway procedures:
Fluid resuscitation is likely to be needed to offset severe hypotension, although it should be used with caution. The increased “leakiness” of vessels may only allow for a transient benefit of crystalloid fluids and end up exacerbating tissue edema. In anaphylaxis, up to 35% of the intravascular volume may shift into the extravascular space within minutes.
Aside from Epinephrine, there are a TON of other drugs that we can give the patient. Let’s run through each one by one:
Diphenhydramine is a Histamine 1 antagonist that works by competitively binding to histamine receptors found in smooth muscles, vascular endothelial cells, in the heart, and central nervous system. Since anaphylaxis is primarily caused by dumping of histamine into the body, diphenhydramine may help limit this effect. Although it’s commonly effective for reducing pruritus (itchiness) and hives, it hasn’t actually been proven to relieve airway obstructions or hypotension in anaphylaxis. While it’s still recommended in treatment protocols, do not expect amazing results.
Dexamethasone is a glucocorticoid that is commonly given in the treatment of anaphylaxis, although there is little evidence of any clear benefit. The rationale behind using steroids is that it may help by reducing the incidence of biphasic reactions (A “second wave” of anaphylaxis). While it hasn’t proven to be overly beneficial in this aspect, a case can be made for relieving bronchospasms in anaphylaxis.
Ranitidine is an antihistamine like diphenhydramine, but instead of binding to H1 receptors, it binds to H2 receptors (commonly found in the gut). The rationale for ranitidine is that it may have a synergistic effect with diphenhydramine to reduce the overall progression of anaphylaxis, but these effects are not likely to occur for at least 30-45 minutes. And again, it does not have any proven benefit for airway obstruction or shock.
Albuterol is a beta-2 agonist that works by dilating the bronchioles, thus relieving bronchospasms in anaphylaxis. It’s best used in conjunction with epinephrine, which also helps relieve bronchospasms in addition to relieving mucosal edema. Albuterol’s effectiveness is mostly extrapolated from its use in asthma.
The mortality rate for anaphylaxis is only 0.7%, but these patients can be very difficult to manage for a field medic, especially if airway management or continued epinephrine is needed. These patients will always need an Urgent evacuation.
Good luck out there!
- UpToDate: Anaphylaxis Emergency Treatment
- EMRAP Corependium: Allergy, Hypersensitivity, & Anaphylaxis
- UpToDate: Pathophysiology of Anaphylaxis
- Advanced Tactical Paramedic Protocols Handbook. 10th ed., Breakaway Media LLC, 2016.