Anaphylaxis

Question 1

Steps of anaphylaxis management

Answer 1

1. Shout for help
2. Call anaesthetist and request difficult airway trolley
3. If necessary put out 222 call - cardiac arrest
4. Remove allergen if possible
5. Lie patient flat and raise legs
6. Give adrenaline - 0.5mL 1:1000 IM (adults)
7. ABCDE assessment
8. Maintain patent airway: manouevres, adjuncts, supraglottic or definitive airway as indicated
9. Evidence of impending airway compromise: give nebulised adrenaline
10. Maintain sats 94-98%
11. Attach monitoring: BP cuff, oximeter, 3 lead ECG
12. IV access: take blood, give fluid challenge (500-1000mL crystalloid)
13. Give chlorphenamine and hydrocortisone IM or slow IV
14. Consider nebulised salbutamol or ipatropium bromide if evidence of wheeze

Question 2

Define anaphylaxis

Answer 2

A severe, life threatening, generalised or systemic type 1 hypersensitivity reaction characterised by rapidly devloping life thretening airway and or breathing and or circulatory problems

Question 3

What is biphasic anaphylaxis?

Answer 3

After complete recovery of anaphylaxis a recurrence of symptoms within 72hrs occurs following no further exposure to the allergen

Question 4

What is suspected anaphylaxis?

Answer 4

The diagnosis prior to assessment by a specialist allergist for people who present with symptoms of anaphylaxis

Question 5

Common anaphylaxis triggers

Answer 5

• Insect venom
• Food
• Latex
• Drugs
• Idiopathic

*Presentation and timing depends on the route that the allergen has been encountered via

Question 6

Pathophysiology of type 1 hypersensitivity reactions

Answer 6

Type 1 hypersensitivity is IgE mediated

AKA immediate hypersensitivity

Allergies occur in 2 phases:

1. first exposure/ sensitisation
2. subsequent exposure
3. Individual exposed to allergen
4. Allergen taken up by APCs and presented to a T-cell which changes it into a Th2 cell (type of CD4+ cell)
5. Th2 cell makes cytokines which cause B-cells to class switch and produce IgE antibodies rather than IgM
6. Th2 also causes eosinophils to degranulate, they release substances that can damage host and invading cells
7. IgE attaches to mast cells via Fce receptor
8. Second exposure: specific IgE antibodies bound to mast cells bind the allergen and cause mast cells to degranulate and release inflammatory mediators

Pro inflammatory mediators:

• Histamine: binds to H1 receptors, causes smooth muscle contraction in airway and increases vessel permeability causing swelling, oedema and urticaria
• Mediatorys that activate eosinophils
• Proteases

Cytokines are produces and more immune cells are recruited

• Leukotrienes also cause smooth muscle contraction and attract even more immune cells
• Eosinophils release peroxidases which cause further tissue damage

Question 7

What happens when mast cells degranulate following 2nd exposure to allergen?

Answer 7

GI tract: increased fluid secretion, increased peristalsis >> diarrhoea and vomiting

Eyes, nose and airways: decreased airway diameter, increased mucous secretion >> congested, constricted airways

Skin: vasodilation + histamine release >> itching and flushing

Blood vessels: increased blood flow, increased permeability, increased fluid and protein in the tissue >> BP drops because effective crculating volume is low

Cardiac: hypotension, tachycardia, syncope

The above culminate in an allergic reaction which, if severe enough, results in anaphylactic shock

Question 8

Which factors may modulate the onset of allergic and non-allergic immediate hypersensitivity

Answer 8

• Stress
• Infection
• Dose of allrgen
• Rate of drug injection
• Host factors

Question 9

What is the ring and mesmer grading scale?

Answer 9

Scale used to grade anaphylactic reactions

Grade 1:

Skin itching, flushing, urticaria, angioedema

Grade 2:

Skin + nausea, cramps

Grade 3:

Skin+ N&V, defecation, laryngeal oedema, brochospasm, cyanosis, shock

Grade 4: cardiac arrest

Skin + N&V and defecation, repsiratory arrest, circulatory arrest

Patients can rapidly progress along the scale hence rapid treatment being essential

Question 10

Factors that indicate anaphylaxis is severe

Answer 10

1. Sudden onset + rapid progression
2. Life threatening ABC problems
3. Skin and or mucosal changes (flushing, oedema)

Question 11

Important to document re anaphylaxis

Answer 11

Document acute clinical features of suspected reaction

Record the circumstances immediately before the onset of symptoms

Record time of onset

Question 12

Airway considerations during anaphylaxis

Answer 12

Swelling: tongue or throat

Difficulty breathing/ swallowing

Hoarse voice

Stridor

Patient reporting they feel throat is closing

Question 13

Breathing considerations during anaphylaxis

Answer 13

SOB

RR

Wheeze

Patient becoming tired

Confusion due to hypoxia

Cyanosis - central cyanosis is a late sign

Respiratory arrest

Question 14

Circulatory considerations during anaphylaxis

Answer 14

Signs of circulatory shock: pale and clammy

Tachycardia

Low BP

Decreased consciousness

MI due to loss of circulating volume

Cardiac arrest

**DO NOT STAND PATIENT UP - can cause dangerous BP drop**

Question 15

Disability considerations during anaphylaxis

Answer 15

Sense of impending doom

Anxiety and panic

Decreased consciousness

Question 16

Exposure considerations during anaphylaxis

Answer 16

Sking changes are often the first feature

80% show skin changes

Erythema/ rash

Urticaria

Angioedema: swelling of deeper tissue e.g. throat, lips, eyelids

Question 17

Dose of adrenaline in anaphylaxis

Answer 17

Give 0.5ml of 1 in 1000 INTRAMUSCULAR

This means 1g of adrenaline in 1000mls (i.e. 1g in 1L) but we give 0.5ml of this solution

>> Repeat after 5 mins if no response <

LEAVE IV TO EXPERTS

Question 18

Management of a patient with anaphylaxis

Answer 18

Call for help

Lie patient flat

Raise their legs

GIVE ADRENALINE BEFORE O2 AND FLUID

Airway: establish

B: O2 sats probe, 15L O2 non-rebreathe

C: BP cuff, ECG, IV access, adrenaline (1:1000 0.5mL)

Fluids

ADULT - 500-1000mL bolus crystalloid (0.9% w/v sodium chloride)

CHILD - 20mL/ kg bolus crystalloid (0.9% w/v sodium chloride)

**Avoid colloids because they can be a source of reaction**

Question 19

Use of chlorphenamine and hydrocortisone in anaphylaxis

Answer 19

Take longer to act, these drugs can wait - adrenaline and ABC is priority

Chlorphenamine = antihistamine >> given for 24-48hrs after adrenaline to reduce severity & duration of symptoms and to prevent relapse

Hydrocortisone >> dampens down immune response, reduced swelling and inflammation >> reduces risk of relapse/ biphasic anaphylaxis

Question 20

Differentials for anaphylaxis

Answer 20

Asthma attack

Sepsis

Vasovagal

Panic attack

Idiopathic urticaria/ angioedema

Question 21

What is mast cell tryptase testing?

Answer 21

Tryptase is an enzyme released when mast cells degranulate - the level of tryptase is used to indicate the level of mast cell activation

The test is used to confirm diagnosis of anaphylaxis and to diagnose mastocytosis (too many mast cells)

Question 22

When are samples taken for mast cell tryptase testing?

Answer 22

1st sample: after initial resus started

2nd sample: 1-2hrs after symptom onset

3rd: 24hrs later or at follow up

Question 23

What are auto injectors?

Answer 23

Used by patients or carers with severe reactions or those who have trouble avoiding triggers

Question 24

Management of a patient following anaphylaxis when stable

Answer 24

Adults and those 16+: observe for 6-12hrs from symptom onset

Children <16hrs: admit under paeds

Question 25

Risk factors for anaphylaxis

Answer 25

Allergic rhinitis Asthma Eczema

Question 26

Brief summary of anaphylaxis pathophysiology

Answer 26

Allergen previously encountered binds to IgE on mast cells, causes them to degranulate and release histamine Histamine mediates inflammatory response causing bronchospasm, vasodilation, increased capillary permeability and tissue oedema