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Anaphylaxis Module


AuthorKat Priddis
DurationUp to 2 hours
Equipment requiredAdrenaline auto-injector if planning a demonstration on a model
  • Basics (10 mins)
  • Main session: (2 x 15 minute) case discussions covering the key points and evidence
  • Advanced session: (2 x 20 minutes) case discussions covering grey areas, diagnostic dilemmas; advanced management and escalation
  • Sim scenario (30-60 mins)
  • Quiz (10 mins)
  • Infographic sharing (5 mins): 5 take home learning points

We also recommend printing/sharing a copy of your local guideline.

Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction.

Anaphylaxis is described as

  • Sudden onset and rapid progression of symptoms 
  • Life-threatening Airway and/or Breathing and/or Circulation problems 

*Skin and/or mucosal changes (flushing, urticarial, angioedema) are absent 20% of cases*

Angioedema is similar to urticaria but involves swelling of deeper tissues, most commonly in the eyelids and lips, and sometimes in the mouth and throat.

There can also be gastrointestinal symptoms (e.g. vomiting, abdominal pain, incontinence).

Fatality <1%, increased in those with pre-existing asthma. Approximately 20 anaphylaxis-related deaths in the UK every year. 

From a case-series (resus council), fatal food reactions cause respiratory arrest typically after 30–35 minutes; insect stings cause collapse from shock after 10–15 minutes; and deaths caused by intravenous medication occur most commonly within five minutes. Death never occurred more than six hours after contact with the trigger. 


What is an allergy?

It is the body’s response to an external ‘allergen’. An unnecessary immune response to an innocuous substance. 

Common allergens/triggers include: • Food: nuts, milk, fish • Venom: wasp, bee • Drugs: antibiotics, anaesthetic drugs • Contrast media • Latex

Reactions are either delayed type IV or immediate type I. IgE-mediated allergy is broadly characterised as a Type 1 hypersensitivity. Other hypersensitivity reactions (II, III and IV) are mediated by other antibody classes, immune cells or cellular components. Non-IgE mediated reactions typically cause symptoms to appear more slowly, sometimes several hours after exposure. 

Allergy is increasing in prevalence. Theories for this include the ‘Hygiene Hypothesis’, the idea that increased exposure to microorganisms correlates with a decreased tendency to develop allergy and more recently the ‘Old Friends Mechanism’ which links the tendency to develop allergy to an individual’s microbiome (collection of microorganisms living in and on an person’s body). 

Interestingly, kids in developing countries have a decreased allergy prevalence, thought to be because of less sanitation, more exposure to microbes and increased time spent outdoors. 

How do we develop allergic reactions? 

Part 1: Sensitisation

An allergen enters the body and is captured by an antigen presenting cell, that scoops it up and nicely presents it immune cells, particularly T cells (in a similar manner as if the allergen was a foreign invading microbe). Through a number of immune interactions between T cells and B cells, B cells produce allergen-specific IgE antibodies. These get released into the blood, where they bind to mast cells (the major allergy immune cell) as well as other friends like basophils. In some individuals, this can cause a ‘sensitisation’ i.e. the next time their body meets that particular allergen it’s going to go on the offensive. 

Part 2: Re-exposure

Our patient is now carrying allergen-specific IgE bound mast cells. Upon re-exposure, the offensive allergen binds to IgE, causing the mast cells to initiate an aggressive and immediate immune response. 

Mast cells on the attack: 

Mast cells are granular cells, containing many secretory granules that all get released on activation. The binding of IgE causes rapid degranulation, and a shower of inflammatory compounds, including histamine. Result? Local inflammations, and allergy symptoms (see presentation of the patient in anaphylaxis below). 

An 8 year old girl presents after collapsing following attendance at a friend’s birthday party. She was noted to have been eating a sandwich, then promptly developed respiratory distress. On admission with the ambulance crew she is audibly wheezy, with swelling of the tongue and lips.

How would you assess this child?

What is your immediate management?

How much adrenaline do you give and how? Any adjunct therapies to consider?


Manage according to APLS

Adrenaline dosing (early and often)

Adrenaline – mechanism of action

Adrenaline – side effects

Adrenaline – duration of action

Adrenaline – can I go again?

The patient isn’t getting better. What else do I do?

Extra tips

A 3 year old presented with a localised erythematous rash after being stung by a bee at a family picnic. His family attended PED where he subsequently developed respiratory distress and he was treated with IM adrenaline. After a couple of hours he was playful and appeared well and his parents want to take him home.

What would you say to the parents?

How would you manage this patient?

What key points make up the discharge planning? 

Biphasic reactions

Discharging home (RCPCH Pathway)

Can you administer IM adrenaline? (8 minutes)

A 6 year old patient with spina bifida is currently admitted with an LRTI. She has been having a course of amoxicillin for the last week. You are crash bleeped to the ward where she is having her urinary catheter changed by a bank nurse. She is pale and cool to touch, with increased respiratory rate.

What’s going on? Is this allergy? Is this anaphylaxis?

How would you treat it?

What allergy avoidance advice do you give?

  • Initial management: Observations and assess (BP)
  • Initial presentation of anaphylaxis – high safety margin for IM adrenaline
  • Hypotension as a warning sign (absence of a rash) – is it fluid responsive? May require large volumes of fluids. No evidence for crystalline vs colloid. Give 0.9% saline or Hartmanns. 
  • Explore medical history for triggers, explore unusual or uncommon triggers (e.g. exercise as a trigger, consider co-existing triggers e.g. prawns and exercise)

Risk factors for latex allergy

Common food triggers for fatal anaphylaxis

An 8 year old girl presents after collapsing following attendance at a friend’s birthday party. She was noted to have been eating a sandwich, then promptly developed respiratory distress. She has had two epipens with the ambulance crew, and a further dose in PED. You are called as senior support. Her sats are dropping and she is becoming bradycardic.

If the patient isn’t improving after IM adrenaline, what are your next management plans?

How do you prepare for intubation?

What do you do next?

Advanced management

Does this child need to be intubated?

IV adrenaline

Reporting a reaction

Question 1

Answer 1

Question 2

Answer 2

Question 3

Answer 3

Please download our Facilitator and Learner guides


  • Kat is a PEM Consultant and Trauma Director in North-West London. She has an MSc in Trauma Sciences and is an honorary senior lecturer on the PEM MSc at QMUL. An executive member of the Don't Forget the Bubbles team, Kat loves high fid-sim, VR and all things tech.


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