Paediatric Anaphylaxis Flashcards

1
Q

Definition of Anaphylaxis as per AV CPG

A

Severe, potentially life-threatening systemic hypersensitivity reaction

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2
Q

Common Allergens

A

Exposure to an allergen may be known or unknown.
Insect stings: Bees, wasps, jumping jack ants
Food: Peanuts/treenuts, egg, fish/shellfish, dairy products, soy, sesame seeds, wheat
Medications: Antibiotics, anaesthetic drugs, contrast media
Exercise-induced: Typically affecting young adults (rare)
Idiopathic anaphylaxis: No external trigger (rare)

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3
Q

RASH Criteria

A

Respiratory
Abdominal
Skin
Hypotension

Isolated Hypotension with known exposure OR
Isolated Severe Resp Distress with known exposure

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4
Q

Respiratory S+S

A

Respiratory distress, shortness of breath, wheeze, cough, stridor

Due to inflammatory bronchoconstriction or upper airway oedema

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5
Q

Abdominal S+S

A

Pain / cramping
Nausea / vomiting / diarrhoea
- Particularly to insect bites and systemically administered allergens (e.g. IV medications)

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6
Q

Skin S+S

A

Hives, welts, itching, flushing, angioedema (e.g. lips, tongue)

Due to vasodilation and vascular hyperpermeability

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7
Q

Cardiovascular (Hypotension) S+S

A

Hypotension

Due to vasodilation and vascular hyperpermeability

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8
Q

Anaphylaxis and Asthma considerations

A

Asthma, food allergy and high risk of anaphylaxis frequently occur together, often in adolescence.
Bronchospasm is a common presenting symptom in this group, raising the likelihood of mistaking anaphylaxis for asthma. A history of asthma increases the risk of fatal anaphylaxis.

Maintain a high index of suspicion for anaphylaxis in patients with a history of asthma or food allergy

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9
Q

Other causes of angiodema

A

Several types of non-allergic angioedema exist including hereditary angioedema (HAE) and its more broad categorisation: bradykinin-mediated angioedema.

These may present with similar symptoms to anaphylaxis including abdominal signs and symptoms
and laryngeal swelling however will not respond to anaphylaxis management.

Where HAE or bradykinin-mediated angioedema is identified AND the patient has their own
medication to manage this, follow the patient’s treatment plan and use the patient’s own medication.

Otherwise strongly consider standard anaphylaxis management if indicated.

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10
Q

Food Protein Induced Enterocolitis (FPIES)

A

FPIES is a non-immunoglobulin E mediated paediatric allergy that usually presents with nausea and
vomiting, and in severe cases may present with collapse, confusion or altered consciousness. These patients should not be treated with adrenaline under this guideline. If the patient has a positive diagnosis of FPIES and a care plan, treat symptomatically (e.g. ondansetron, IV fluid) and transport to hospital. Consider consultation with paediatric receiving hospital regarding steroid administration.

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11
Q

Risk factors for refractory anaphylaxis or deterioration

A

Expected clinical course (e.g. history of refractory anaphylaxis / ICU admission / multiple adrenaline
doses)
Hypotensive
Medication as precipitating cause (e.g. antibiotics, IV contrast medium)
Respiratory symptoms / respiratory distress
History of asthma or multiple co-morbidities/medications
OR
No response to initial dose of IM Adrenaline

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12
Q

Adrenaline in Anaphylaxis (CPG)

A

Adrenaline is the primary treatment agent for anaphylaxis.
Administration site: anterolateral mid-thigh.
Deaths from anaphylaxis are far more likely to be associated with delay in management rather than
inadvertent administration of Adrenaline.
Patients with known anaphylaxis may carry their own Adrenaline autoinjector. If the patient responds
well to their own autoinjector dose, further Adrenaline may not be required. Closely monitor for
deterioration and transport to hospital.
Patients should carry their Adrenaline auto-injector with them to hospital.

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13
Q

Adrenaline toxicity:

A

Where the patient develops nausea, vomiting, shaking, tachycardia or arrhythmias but has some improvement in symptoms and a normal or elevated BP, consider the
possibility of adrenaline toxicity rather than worsening anaphylaxis. Consider whether further doses of adrenaline are appropriate.

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14
Q

Bronchospasm in Anaphylaxis

A

Where bronchospasm persist despite the administration of adrenaline, administer salbutamol, ipratropium bromide and dexamethasone. These medications should never be the first line treatment for bronchospasm associated with anaphylaxis.

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15
Q

Hypotension in Anaphylaxis

A

Where hypotension persists despite initial Adrenaline therapy, large volumes of fluid may be extravasating. IV fluid therapy is indicated to support vasopressor administration.

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16
Q

Mgx of Anaphylaxis for SD

A

1) R+R
2) Pos - Semi-recumbent/supine
3) MICA
4) O2 NRB 15L/min
5) Stop trigger - cease infusion, remove food, wash exposed skin
6) Adrenaline 10mcg/kg IM @5/60 intervals
(consider antiemetic if N/V - Ondans oral)
7) Sitrep, up/downgrade MICA
***
8) Extrication - wheelchair to stretcher
9) Reassess 5/60
10) Load sig 1 with notification

** if airway oedema/stridor
a) adrenaline 5mg nebulised - consult for further doses at RCH
**
if bronchospasm
b) salbutamol nebulised or pMDI at 20/60
c) ipratropium bromide neb or pMDI
d) dex 600mcg/kg oral

17
Q

Bronchospasm Salbutamol Neb and pMDI doses

A

6-11 yrs: NEB 2.5-5mg pMDI 4-12 puffs
2-5yrs: NEB 2.5mg pMDI 2-6 puffs

18
Q

Bronchospasm Ipratropium Bromide Neb and pMDI doses

A

6-11yrs: NEB 250mcg pMDI 8 puffs
2-5yrs: NEB 250mcg pMDI 4 puffs

19
Q

Anaphylaxis Patho

A
  • IgE mediated hypersensitivity response to antigen
  • Degranulation of mast cells, leading to histamine release
  • Histamine mediated vasodilatation/increased vessel permeability, leading to hypotension and urticaria
  • Histamine mediated GI tract smooth muscle contraction leading to nausea/vomiting/abdo cramps
  • Histamine mediated bronchial smooth muscle contraction leading to bronchospasm
    `
20
Q

Adrenaline Alpha and Beta Effects

A

Alpha
* ↑ PVR (peripheral vascular resistance) thus ↑venous return and CO and BP
* ↓peripheral vasodilation
* ↓ angio-oedema
* ↓ urticaria (hives)
Beta 2
* Bronchodilation
* ↑ monophosphate production with decreases degranulation – further reduces release of inflammatory mediators)
* Interrupts the positive feedback mechanism – stops enhancing the OG stimulus

21
Q

Adrenaline Pharmacology

A

A naturally occurring alpha and beta-adrenergic stimulant
Actions:
Increases HR by increasing SA node firing rate (Beta 1)
Increases conduction velocity through the A-V node (Beta 1)
Increases myocardial contractility (Beta 1)
Increases the irritability of the ventricles (Beta 1)
Causes bronchodilatation (Beta 2)
Causes peripheral vasoconstriction (Alpha)

22
Q

Adrenaline Metabolism

A

By monoamine oxidase and other enzymes in the blood, liver and around nerve
endings; excreted by the kidneys

23
Q

Adrenaline Indications

A
  1. Cardiac arrest - VF/VT, Asystole or PEA
  2. Inadequate perfusion (cardiogenic or non-cardiogenic/nonhypovolaemic)
  3. Bradycardia with poor perfusion
  4. Anaphylaxis
  5. Severe asthma - imminent life threat not responding to nebulised
    therapy, or unconscious with no BP
  6. Croup
24
Q

Adrenaline Contras

A
  1. Hypovolaemic shock without adequate fluid replacement
25
Q

Adrenaline Precautions

A

Consider reduced doses for:
1. Elderly / frail patients
2. Patients with cardiovascular disease
3. Patients on monoamine oxidase inhibitors
4. Higher doses may be required for patients on beta blockers

26
Q

Adrenaline Side Effects

A

Sinus tachycardia
Supraventricular arrhythmias
Ventricular arrhythmias
Hypertension
Pupillary dilatation
May increase size of MI
Feeling of anxiety/palpitations in the conscious patient

27
Q

Adrenaline IV Effects

A

Onset: 30 seconds
Peak: 3 – 5 minutes
Duration: 5 – 10 minutes

28
Q

Adrenaline IM Effects

A

Onset: 30 – 90 seconds
Peak: 4 – 10 minutes
Duration: 5 – 10 minutes

29
Q

Why can a patient with anaphylaxis present with Urticaria/Rash?

A
  • The degranulation of mast cells result in histamine release increasing capillary
    permeability
  • This increase in permeability causes the capillaries to leak and urticaria appears
30
Q

Why is adrenaline the first line of management for Anaphylaxis?

A

Anaphylaxis is primarily caused by mast cells degranulation leading to release of
inflammatory mediators

Adrenaline stabilises the mast cells effectively halting the anaphylactic reaction

31
Q

What are most deaths from anaphylaxis associated with?

A

Delays in treatment/management

32
Q

What actions of adrenaline relate specifically to the treatment of anaphylaxis and how?

A
  • Stabilises mast cells (& basophils) membrane and prevents further release of mediators
    (primary indication for use)
    Secondary effects:
    α effects
     Contraction of smooth muscle → vasoconstriction leading to improved venous return
    → increased cardiac output → increased BP
    β1 effects
     Positive inotrope → increases force contraction → increases cardiac output
     Positive chronotrope (increases heart rate) → increases cardiac output
    β2 effects
     Bronchodilation
33
Q

Explain why anaphylaxis can cause hypotension?

A
  • Inflammatory mediators increase the permeability of vessels
  • This means fluid moves from the intravascular compartment into the extravascular compartment
  • This leads to hypotension
34
Q

Why is the anterolateral thigh the preferred site of IM injection in the patient with Anaphylaxis?

A

International guidelines recommend this due to improved absorption

35
Q

Inadequate Perfusion in Anaphylaxis

A

Due to inflammatory mediators causing permeability of vessels, there is a fluid shift from intravascular space to the extravascular compartment.
This leads to decreased BP, with the potential for compensatory tachycardia

36
Q

IM indications

A
  • Medications that, as per the AV CPG’s, are required to be administered via the intra-muscular route
37
Q

IM Contras

A

Nil

38
Q

IM Preceutions

A
  • Safety – Ensure correct technique for administration, anatomical location, and disposal of sharps technique is
    used at all times
  • Larger volumes may be painful. Dilution should be avoided