Anaphylaxis

Anaphylaxis may be defined as a severe, life-threatening, generalised or

systemic hypersensitivity reaction.

Common identified causes of anaphylaxis:

 food (e.g. nuts) - the most common cause in children

 drugs
 venom (e.g. wasp sting)

Features - the sudden onset and rapid progression of symptoms

 Airway and/or Breathing and/or Circulation problems

 Airway problems may include:
o swelling of the throat and tongue →hoarse voice and stridor
 Breathing problems may include:
o respiratory wheeze
o dyspnoea
 Circulation problems may include:
o hypotension
o tachycardia

=> This means that if there are no ABC problems then the patient is technically not
having anaphylaxis.

Around 80-90% of patients also have skin and mucosal changes:

 generalised pruritus
 widespread erythematous or urticarial rash
 Treatment
A&B

o The airway should be opened, cleared and maintained

o 100% O2 using a reservoir bag

o After assessing the circulation, commence chest compressions if

there is no detectable cardiac output

o Connect an ECG monitor

o Treat non-perfusing arrhythmias according to standard protocols

o Treat bradycardia with atropine

o If ↓BP - Give IM Adrenaline (see flow diagram)

o If hypotensive, do not sit the patient up

o Repeat Adrenaline as necessary (every 5 minutes)

o Intravenous fluids to counteract hypovolaemic shock

o Rarely (in extremis) titrated intravenous doses of dilute adrenaline

may be required

Once cardiac output has been restored, treat as below.

o The patient must be admitted to hospital

o IV fluid, (10ml/Kg) as a bolus

o Bronchodilator by volumatic/nebuliser

o Consider IV Aminophylline, 250 mg over 5 mins. (or IV Salbutamol

@ 250ug slow loading dose followed by 5-10ug per minute)

o Antihistamines (Chlorpheniramine 10 mg IV over 2 min ) for itch

o H2 antagonist ( PO or IV Ranitidine) are unproven

o Steroids generally not indicated

Patients who present with simple urticaria, minimal airway
involvement and who have a rapid response to Piriton or Histek
(Certirizine) ± ranitidine (itch again) can be discharged.

Patients must be admitted if:

o There is any degree of bronchospasm

o Hypotension

o Airway oedema

Even with good initial responses these patients are at risk of a

biphasic anaphylactic response where the same problems can
arise again.
Follow up
Patients requiring Adrenaline resuscitation warrant admission
(CDU) for 12 hours (rebound phenomenon has been reported -
but rare).
Prescribe an epinephrine auto-injector on discharge (15-30Kg =
150µg dose, >30kg = 300µg dose).
All patients who require Adrenaline should attend their GP for on-
going referral and management.
Anaphylaxis is one of the few times when you would not have time to look up the
dose of a medication. The Resuscitation Council guidelines on anaphylaxis have
recently been updated. Intramuscular adrenaline is by far the most important drug
in anaphylaxis and should be given as soon as possible. Previously IV hydrocortisone
was also recommended but the evidence base for this was poor and it was removed
in the 2021 update.

The recommended doses for adrenaline are as follows: BNF

Age Adrenaline dose

< 6 months 100 - 150 micrograms (0.1 - 0.15 ml 1 in 1,000)
6 months - 6 years 150 micrograms (0.15 ml 1 in 1,000)
6-12 years 300 micrograms (0.3ml 1 in 1,000)
Adult and child > 12 years 500 micrograms (0.5ml 1 in 1,000)

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM
injection is the anterolateral aspect of the middle third of the thigh.

Refractory anaphylaxis

 defined as respiratory and/or cardiovascular problems persist despite 2

doses of IM adrenaline
 IV fluids should be given for shock
 expert help should be sought for consideration of an IV adrenaline infusion
Management following stabilisation:

 non-sedating oral antihistamines, in preference to chlorphenamine, may be

given following initial stabilisation especially in patients with persisting skin
symptoms (urticaria and/or angioedema)
 sometimes it can be difficult to establish whether a patient had a true episode
of anaphylaxis. Serum tryptase levels are sometimes taken in such patients as
they remain elevated for up to 12 hours following an acute episode of
anaphylaxis
 all patients with a new diagnosis of anaphylaxis should be referred to
a specialist allergy clinic
 an adrenaline injector should be given an interim measure before the
specialist allergy assessment (unless the reaction was drug-induced)
o patients should be prescribed 2 adrenaline auto-injectors
o training should be provided on how to use it
 a risk-stratified approach to discharge should be taken as biphasic reactions
can occur in up to 20% of patients

The Resus Council UK recommend the following risk-stratified approach to discharge:

 fast-track discharge (after 2 hours of symptom resolution):

o good response to a single dose of adrenaline
o complete resolution of symptoms
o has been given an adrenaline auto-injector and trained how to use it
o adequate supervision following discharge
 minimum 6 hours after symptom resolution
o 2 doses of IM adrenaline needed, or
o previous biphasic reaction
 minimum 12 hours after symptom resolution
o severe reaction requiring > 2 doses of IM adrenaline
o patient has severe asthma
o possibility of an ongoing reaction (e.g. slow-release medication)
o patient presents late at night
o patient in areas where access to emergency access care may be difficult
o observation for at 12 hours following symptom resolution
 PAEDS – ANAPHYLAXIS

Anaphylaxis is a life-threatening medical emergency. It is caused by a severe type 1

hypersensitivity reaction. Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and
other pro-inflammatory chemicals. This is called mast cell degranulation. This causes a rapid onset of
symptoms, with airway, breathing and/or circulation compromise.

The key feature that differentiates anaphylaxis from a non-anaphylactic allergic reaction is compromise of
the airway, breathing or circulation.

Presentation
Patients present with a history of exposure to an allergen (although it can be idiopathic). There will be
rapid onset of allergic symptoms:

 Urticaria

 Itching

 Angio-oedema, with swelling around lips and eyes

 Abdominal pain

Additional symptoms that indicate anaphylaxis are:

 Shortness of breath

 Wheeze

 Swelling of the larynx, causing stridor

 Tachycardia

 Lightheadedness

 Collapse

Principles of Management
Anaphylaxis requires immediate medical attention and management. It should be managed by an
experienced paediatrician. Call for help early. Refer to the resuscitation guidelines for full management
guidelines.

Initial assessment of acutely unwell child is with an ABCDE approach, assessing and treating:

 A – Airway: Secure the airway

 B – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.

 C – Circulation: Provide an IV bolus of fluids

 D – Disability: Lie the patient flat to improve cerebral perfusion

  E – Exposure: Look for flushing, urticaria and angio-oedema

Once a diagnosis of anaphylaxis is established, there are three medications given to treat the reaction:

 Intramuscular adrenalin, repeated after 5 minutes if required

 Antihistamines, such as oral chlorphenamine or cetirizine

 Steroids, usually intravenous hydrocortisone

After the Event

All children should have a period of assessment and observation after an anaphylactic reaction, as biphasic
reactions can occur, meaning they can have a second anaphylactic reaction after successful treatment of
the first. Children should be admitted to the paediatric unit for observation.

Anaphylaxis can be confirmed by measuring the serum mast cell tryptase within 6 hours of the
event. Tryptase is released during mast cell degranulation and stays in the blood for 6 hours before
gradually disappearing.

Education and follow-up of the family and child is essential. They need to be educated about allergy, how
to avoid allergens and how to spot the signs of anaphylaxis. Parents should be trained in basic life support.
Specialist referral should be made in all children with anaphylaxis for diagnosis, education, follow up and
training in how to use an adrenalin auto-injector.

TOM TIP: Remember to measure mast cell tryptase within 6 hours of an anaphylactic reaction. This is
a common exam question and also something that will impress senior colleagues if it is part of your
management plan when managing children with anaphylaxis.

Indications for an Adrenalin Auto-Injector

Epipen, Jext and Emerade are trade names for adrenalin auto-injector devices.

They are given to all children and adolescents with anaphylactic reactions. They may also be considered
in children with generalised allergic reactions (without anaphylaxis) with certain risk factors:

 Asthma requiring inhaled steroids

 Poor access to medical treatment (e.g. rural locations)

 Adolescents, who are at higher risk

 Nut or insect sting allergies are higher risk

 Significant co-morbidities, such as cardiovascular disease

How to Use an Adrenalin Auto-Injector
The first step is to confirm the diagnosis of anaphylaxis.

Prepare the device by removing the safety cap on the non-needle end. There is a blue cap on EpiPen and a
yellow cap on Jext.

Grip the device in a fist with the needle end pointing downwards. The needle end is orange on EpiPen and
black on Jext. Do not put your thumb over the end, because if the device is upside down you will inject
your thumb with adrenalin and could risk losing it.

Administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the
device clicks. This can be done through clothing. EpiPen advise holding it in place for 3 seconds and Jext
advise 10 seconds before removing the device.

Remove the device and gently massage the area for 10 seconds.

Phone an emergency ambulance. A second dose may be given (with a new pen) after 5 minutes if
required.

TOM TIP: You may be asked to show a parent or child how to use an adrenalin auto-injector, either in
exams or in clinical practice. It is worth familiarising yourself with a Jext and EpiPen device. The drug
companies often provide dummy devices that are usually lying around the paediatric wards. Check the
draws and shelves in the doctors office and ask a friendly senior nurse. They are useful to help you get
familiar with the device and practice explaining to your peers.
 ALLERGY + HYPERSENSITIVITY

Hypersensitivity occurs when the immune system over-responds to harmless antigens that result in harm to
the body. There are four types of hypersensitivity reaction:

 Type I: Classical allergy, mediated by the inappropriate production of specific IgE antibodies to
harmless antigens
 Type II: Caused by IgG and IgM antibodies that bind to antigens cells or tissues leading to cell or
tissue damage
 Type III: Caused by antibody-antigen complexes being deposited in tissues, where they activate
the complement system and cause inflammation
 Type IV: A delayed type hypersensitivity reaction caused by T helper cells traveling to the site of
antigens, recruiting macrophages and causing inflammation

Type I Hypersensitivity (allergy)

Allergens are antigens that produce allergic reactions (e.g. peanuts, penicillin, pollen, house dust mite).

IgE mediated allergy is responsible for a number of atopic conditions:

 Food or drug allergy

 Asthma
 Allergic rhinitis
 Hayfever
 Eczema

Sensitisation is the term to describe the initial event that lead to the specific IgE being developed for that
allergen

 CD4 cells recognise the allergen

 They proliferate and differentiate into T Helper 2 cells
 These Th2 cells release IL-4, that stimulates the production of IgE by B Cells specific to that
allergen
 The IgE then circulates the blood and binds to mast cells

The Allergic Response involve activation of mast cells

  On re-exposure to the allergen, it binds to the IgE and causes mast cell degranulation, releasing
cytokines including histamine and TNF-α.
 Histamine causes vasodilation, increased vascular permeability and broncho-constriction, causing
symptoms of allergy (itch, flushing, rash, angioedema and wheeze). This happens within minutes
of exposure to the allergen.
 TNF-α causes a localised inflammatory process at the site of exposure. This takes a few hours and
is called the late phase reaction.
 The allergic response can vary from mild reactions involving itch, mild swelling and hives to
severe reactions called anaphylaxis that can lead to systemic shock (from severe vasodilation) and
complete airway closure from broncho-constriction and oedema.
 Allergic responses to allergens tend to get worse on repeat exposures due to increased
sensitisation.
 Mast cell tryptase can be measured to confirm the diagnosis of anaphylaxis, and will be raised
after an anaphylactic reaction.

Type II Hypersensitivity
This involves IgG and IgM antibodies that bind to the antigens on cells or tissues that result in a reaction
that is damaging to the person. Here are three examples:

 Blood transfusion reactions: When blood is transfused and the ABO group of the donor does not
match the recipient, the antibodies in the recipients blood attack the donors blood causing
haemolysis of the donor red blood cells, rapidly releasing the contents of those cells and causing a
toxic reaction.
 Haemolytic Disease of the Newborn: When a rhesus negative mother has a rhesus positive baby,
exposure to the babies blood during birth will cause the mother to produce IgG to rhesus. If she
has another rhesus positive baby, that IgG will cross the placenta into the babies bloodstream and
cause haemolysis of the babies red blood cells.
 Goodpastures Syndrome: antibodies specific to a type of collagen in the the glomerular
basement membrane in the kidneys and lungs lead to inflammation and destruction of the
basement membrane leading to pulmonary haemorrhage and kidney failure.

Type III Hypersensitivity

This involves antibodies (mainly IgG and IgM) binding to antigens, which forms immune complexes.
These immune complexes then become deposited in tissues, where they activate the complement system
and cause inflammation.

The difference compared with Type II, is that in Type II it is the antibodies binding to the target that causes
inflammation and damage of the target, whereas in type III, the antibodies bind to antigens, and it is the
antibody-antigen complexes that travel to their target organs where they cause inflammation and damage.

Here are two examples:

 Rheumatoid arthritis: Rheumatoid factor is IgM antibody that recognises IgG antibodies as an
antigen, specifically the Fc portion. It is IgM against IgG. This leads to formation of antibody-
antigen complexes in the blood. These become deposited in joints, skin, lungs and other organs
where they activate the complement system and lead to chronic inflammation.
 Farmers lung: Mould and hay spores are breathed into the lungs. Antibodies against the mould or
hay antigens form antibody-antigen complexes. These are deposited in the lung tissues and alveoli
where they activate the complement system and lead to inflammation of the lung tissue.
Type IV Hypersensitivity
This is also called delayed type hypersensitivity. This is because it takes 24-72 hours for a reaction to
occur. It is a “cell mediated” hypersensitivity reaction. This is what happens:

 Antigens enter tissues

 They get picked up by dendritic cells
 Dendritic cells deliver the antigens to the relevant CD4 cell
 CD4 cells proliferate and differentiate into T helper cells
 T helper cells travel to the tissues where to original antigen presented
 T helper cells release cytokines that recruite macrophages and both cells release proinflammatory
cytokines that result in localised inflammation
 In skin this presents as a contact dermatitis

Some examples of this are:

 Poison Ivy: contact with poison ivy antigens leads to a delayed contact dermatitis via the
 Nickel and gold: some people react to nickel or gold. Small chemicals from the metal enter the
skin and alter proteins in a way that turns them into antigens. These antigens then lead to contact
dermatitis
 Mantoux test: this is a test for TB contact. TB antigens are injected superficially into the skin. If
the person has had previous TB contact, these antigens stimulate an immune response from T cells
in the way described above, leading to a localised inflammation around the infection site.
Urticaria are also known as hives. They are small itchy lumps that appear on the skin. They may be
associated with a patchy erythematous rash. This can be localised to a specific area or widespread. They
may be associated with angioedema and flushing of the skin. Urticaria can be classified as acute
urticaria or chronic urticaria.

Pathophysiology
Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the
skin. This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic
idiopathic urticaria.

Causes of Acute Urticaria

Acute urticaria is typically triggered by something that stimulates the mast cells to release histamine. This
may be:

 Allergies to food, medications or animals

 Contact with chemicals, latex or stinging nettles

 Medications

 Viral infections

 Insect bites

 Dermatographism (rubbing of the skin)

Chronic Urticaria
Chronic urticaria is an autoimmune condition, where autoantibodies target mast cells and trigger them to
release histamines and other chemicals. It can be sub-classified depending on the cause:

 Chronic idiopathic urticaria

 Chronic inducible urticaria

 Autoimmune urticaria

Chronic idiopathic urticaria describes recurrent episodes of chronic urticaria without a clear underlying
cause or trigger.

Chronic inducible urticaria describes episodes of chronic urticaria that can be induced by certain triggers,
such as:

 Sunlight

 Temperature change
  Exercise

 Strong emotions

 Hot or cold weather

 Pressure (dermatographism)

Autoimmune urticaria describes chronic urticaria associated with an underlying autoimmune condition,
such as systemic lupus erythematosus.

Management
Antihistamines are the main treatment for urticaria. Fexofenadine is usually the antihistamine of choice
for chronic urticaria. Oral steroids may be considered as a short course for severe flares.

In very problematic cases referral to a specialist may be required to consider treatment with:

 Anti-leukotrienes such as montelukast

 Omalizumab, which targets IgE

 Cyclosporin
 Anaphylaxis – paediatrics emergency
Basics – what is anaphylaxis:
Anaphylaxis is a severe allergic response manifest by typical skin features and involvement
of one or more of the:
 Respiratory system
 Cardiovascular system
 Gastrointestinal system
OR
Any acute onset episode of bronchospasm or hypotension or upper airway obstruction
where anaphylaxis is considered a possibility. Serum tryptase levels in consultation with a
paediatric allergy specialist can be helpful when the diagnosis of anaphylaxis is uncertain

What is an allergy:
An allergy refers to an inappropriate, exaggerated immune response against ordinarily
harmless substances present in the environment.
Anaphylaxis marks the most extreme endpoint of the spectrum of allergy. It is defined as a
“serious systemic hypersensitivity reaction that is usually rapid in onset and may lead to
death if not recognised and treated promptly”.

What type of reaction is anaphylaxis + how does it occur/ steps:

 Anaphylaxis is a type I hypersensitivity reaction, meaning it is mediated by IgE
antibodies.
Step 1: On first exposure to an allergen, the individual produces IgE antibodies specific to
the antigen. This does not cause symptoms of allergy. These antibodies then remain
attached to receptors on basophils and mast cells.
Step 2: On a subsequent exposure, binding of the antigen (the allergen) to IgE antibodies
triggers basophils and mast cells to degranulate, releasing their contents, including
histamine, tryptase, and chymase.
Step 3: These inflammatory mediators cause vasodilation, increase vascular permeability,
stimulate smooth muscle contraction and increase mucus secretion, which contributes to
the clinical manifestations of anaphylaxis.

Outline the difference between - Anaphylaxis vs anaphylactoid reactions

Anaphylaxis should not be confused with anaphylactoid reaction, also called non-
immunological anaphylaxis. Anaphylactoid reactions produce a similar presentation as
anaphylaxis but are caused by non-IgE-mediated triggering events.
 don't require previous exposure to the allergen. They occur when certain substances
directly cause the release of these same chemicals, particularly histamine, without
involving the immune system's IgE antibodies. These substances can include
medications (like certain antibiotics and NSAIDs), contrast dyes used in medical
imaging, and certain foods.

Triggers for anaphylaxis

 Food: any food could be a trigger but peanut, tree nuts and cow’s milk are the most
common ones.
 Medication: antibiotics (especially penicillin), neuromuscular blocking agents,
chlorhexidine
 Insect sting: particularly bees and wasps.
 Latex: found in some medical and dental supplies
 Exercise: rare (2%)
 Idiopathic: cause of anaphylaxis can remain unknown despite extensive investigations.
 The most common triggers of anaphylaxis are food in children and medication in adults.

Risk factors
o Previous episodes of anaphylaxis: the risk of another episode in the future is
approximately 1 in 12 per year
o Known allergies of any kind
o Concurrent allergic conditions such as allergic asthma, allergic rhinitis, and atopic
dermatitis (eczema)
o Regular exposure to allergens

factors predispose an individual to develop a more severe anaphylactic reaction:

o Advancing age
o Asthma and other chronic lung diseases
o Cardiovascular diseases
o Mast cell disease
o Previous biphasic anaphylaxis
o Individuals who take beta-blockers or angiotensin-converting enzyme inhibitors
 Clinical features:
1. History
A key suggestive feature of anaphylaxis is the sudden onset and rapid progression of
symptoms after exposure to the allergen. Typical symptoms predominately result from
airway and cardiorespiratory issues:

 A feeling of the throat closing up = angio-oedema, swelling around eyes + lips

 Dyspnoea => SOB, wheeze, swelling of larynx an cause stridor
 Chest tightness
 Nausea and vomiting
 Abdominal pain (especially if caused by food allergies)
 Urticaria + itch

If patients present late, they may be confused and obtunded because of cerebral hypoxia.

2. Examination
Airway problems

 Difficulty in breathing and/or swallowing

 Hoarse voice
 Stridor
 Swollen tongue and lips +/- saliva drooling

Breathing problems

 Dyspnoea and tachypnoea

 Wheeze (widespread)
 Cyanosis

Circulation problems

 Tachycardia, typically a rapid, weak, thready peripheral pulse

 Hypotension
 Cold, clammy skin with prolonged capillary refill time
Skin and/or mucosal changes

 Widespread urticarial/erythematous rash

 Generalised pruritus
 Angioedema
 Flushing

Differences in presentation according to the trigger

The onset and the primarily affected organ system can vary depending on the trigger of
anaphylaxis:7

 Food: less rapid onset and breathing problems typically predominate

 Medication: rapid onset and circulation problems typically predominate
 Insect sting: rapid onset and circulation problems typically predominate

3. Investigations
 Life threatening condition so manage with ABCDE approach but some inx are useful
also
i. Bedside:
Observations
12 lead ECG
ii. Bloods
Routine set
ABG
Serum mast cell tryptase level
iii. Imaging
Chest Xray to rule out resp pathologies – only if possible after stabilised etc.

Serum mast cell tryptase in anaphylaxis

This is recommended in all patients with suspected anaphylaxis where the diagnosis is
uncertain and in children <16 years old if the cause is thought to be venom-related, drug-
related, or idiopathic. However, it should never delay life-saving treatments.3,12

At least one sample should be taken within 2 hours of symptom onset and no longer than 4
hours later.3,7

Although an elevated serum mast cell tryptase level confirms the diagnosis of anaphylaxis,
a normal result does not rule out anaphylaxis.
Diagnosis
Anaphylaxis is a severe allergic response manifest by typical skin features
and involvement of one or more of the:

o Respiratory system
o Cardiovascular system
o Gastrointestinal system

OR

o Any acute onset episode of bronchospasm or hypotension or upper

airway obstruction where anaphylaxis is considered a possibility.
Serum tryptase levels in consultation with a paediatric allergy
specialist can be helpful when the diagnosis of anaphylaxis is
uncertain

+ differential diagnosis
The top differential diagnoses of anaphylaxis include simple allergy and other causes of
sudden onset shortness of breath.

In a simple allergic reaction, skin changes like a widespread pruritic urticarial rash are
often present, which can also be seen in anaphylaxis. The key differentiating factor from
anaphylaxis is the absence of airway, breathing, and circulation problems.

Common causes of sudden onset shortness of breath include:

 Foreign body aspiration

 Acute epiglottitis in a child
 Acute exacerbation of asthma or COPD
 Pulmonary embolism
 Pneumothorax
 Panic attack
Oral allergy syndrome is also a potential mimic of anaphylaxis. It is also a type I
hypersensitivity reaction initiated by cross-reaction with a non-food allergen, such as
pollen or latex, involving plant-based foods only.

Unlike anaphylaxis, it usually only causes oropharyngeal symptoms like itching and a
tingling sensation, with or without mild swelling of the lips and tongue. Symptoms tend to
fully resolve within one hour post-contact and rarely develop into anaphylaxis, although it is
sometimes possible.

Other causes of skin rashes or cutaneous flushing should also be considered as differential
diagnoses of anaphylaxis, such as:3,4

 Carcinoid syndrome
 Red neck syndrome (from rapid vancomycin infusion)
 Scombroid food poisoning (from contaminated fish)
 Monosodium glutamate poisoning
Management

1. Assess ABC
 Assess airway
 Breathing – give o2 if required
 Circulation – IV Bolus of fluids
 Disability – lie flat to improve cerebral perfusion
 Exposure – look for flushing, urticaria + angioedema
2. High flow oxygen
3. IM Adrenaline (flow diagram for dose)
4. REPEAT IM Adrenaline @ 3-5 mins if required
5. Nebulised Adrenaline if airway obstruction
6. Treat ↓ BP with 20ml/kg fluid bolus
7. Consider Salbutamol nebs if wheeze
8. Antihistamines given for itch (not "collapse") => chlorphenamine or
cetirizine
9. Early anaesthetic involvement if airway obstruction
10. Early ENT involvement if possibility surgical airway required

Insert flow chart

The child should be admitted overnight if:

o Two or more adrenaline injections were required

o Lives a significant distance from medical services

o Poorly controlled asthma

o Ongoing symptoms

Discharge criteria

o Patients should be observed for 6 hours following administration of

adrenaline. The child must be symptom free at the time of
discharge
o Fill in the allergy clinic referral form
o Prescribe 2 epipens (junior <30kg, or epipen >30kg)
 o Contact allergy CNS during working hours for education.
Afterhours – educate using epipen trainer found in CNF office
o Give anaphylaxis action plan

Complications of anaphylaxis include:3,4,7

 Anaphylactic shock: leading cause of death

 Respiratory failure: leading cause of death
 Refractory anaphylaxis
 Biphasic anaphylaxis: recurrence of symptoms within 72 hours after complete
recovery of anaphylaxis, in the absence of further exposure to the trigger
 Myocardial infarction: cardiac ischaemia may occur from hypotension associated with
anaphylaxis, or from hypertension and tachycardia following adrenaline
administration
 Death: usually occurs shortly after contact with the trigger

After the Event

All children should have a period of assessment and observation after an anaphylactic reaction, as biphasic
reactions can occur, meaning they can have a second anaphylactic reaction after successful treatment of
the first. Children should be admitted to the paediatric unit for observation.

Anaphylaxis can be confirmed by measuring the serum mast cell tryptase within 6 hours of the
event. Tryptase is released during mast cell degranulation and stays in the blood for 6 hours before
gradually disappearing.

Education and follow-up of the family and child is essential. They need to be educated about allergy, how
to avoid allergens and how to spot the signs of anaphylaxis. Parents should be trained in basic life support.
Specialist referral should be made in all children with anaphylaxis for diagnosis, education, follow up and
training in how to use an adrenalin auto-injector.

TOM TIP: Remember to measure mast cell tryptase within 6 hours of an anaphylactic reaction. This is
a common exam question and also something that will impress senior colleagues if it is part of your
management plan when managing children with anaphylaxis.