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Folio edition · Set in Instrument Serif & Archivo

Paeds Vivasallergy-and-immunology

Paeds Vivas · allergy-and-immunology

Food allergy management and prevention — branching viva

Branching viva on acute food-allergy management, adrenaline dosing, biphasic risk, and early-allergen-introduction prevention in a high-risk infant.

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On this page & tools

Target exams

RACP General PaediatricsRACP DCEMRCPCH ClinicalRCPSC Pediatrics

Target exams

RACP General PaediatricsRACP DCEMRCPCH ClinicalRCPSC Pediatrics
Prompt
You are the paediatric registrar at the acute-allergy and preventive interface. The examiner will test emergency response, the action-plan ladder, and early-introduction prevention in a high-risk infant.

Stem

The examiner moves from a definition, to an acute reaction, to the action-plan ladder, and finishes on prevention in a high-risk infant. [6] [14]

Branch 1 — Definition and classification

Examiner: Distinguish a food allergy from a food intolerance, and classify food allergy by mechanism. Why does the mechanism change management? [6]

Strong answer: A food allergy is an immune-mediated reproducible reaction to a food protein; intolerance is non-immune (e.g. lactase deficiency). Classify by mechanism: IgE-mediated (rapid, mast-cell driven, can cause anaphylaxis) versus non-IgE or mixed (delayed, T-cell or eosinophil-driven). IgE reactions can need adrenaline; non-IgE reactions are managed with diet, so the mechanism dictates the treatment. [6]

Branch 2 — Acute reaction

Examiner: A seven-year-old with peanut and mild asthma develops lip swelling, wheeze and pallor minutes after a biscuit. What is your first action? [14]

Strong answer: This is anaphylaxis — a clinical diagnosis. Give IM adrenaline into the anterolateral thigh first, not an antihistamine. Call for help, lie flat with legs elevated if shocked, high-flow oxygen, IV fluids for shock, bronchodilator adjunctive. Adrenaline works because its alpha effect reduces oedema and its beta effect opens bronchi. Repeat at five minutes if no response. [14]

Branch 3 — Dose, biphasic risk, disposition

Examiner: How do you dose adrenaline by weight, and when can you send the child home? [14]

Strong answer: Roughly 0.01 mg/kg of 1:1000 (1 mg/mL) IM; autoinjector doses 0.15 mg under about 20 kg, 0.30 mg at about 20 kg and over. Observe for biphasic reaction — at least six hours for moderate reactions. This child should be admitted: co-existing asthma, a severe reaction, and the chance of needing more than one adrenaline dose all raise the risk. [14] [6]

Branch 4 — The action-plan ladder

Examiner: The child is settled. What do you put in place before discharge? [6]

Strong answer: The five rungs — avoid the confirmed allergen precisely (without over-restricting tolerated foods); a written action plan with photo, allergen and stepwise response; two adrenaline autoinjectors by weight, with expiry checked and carer and child trained; education of school and childcare including an anaphylaxis policy; and a plan for specialist review and re-challenge to detect tolerance. [6] [14]

Branch 5 — Prevention in a high-risk infant

Examiner: A separate parent of a four-month-old with severe eczema asks whether to delay allergenic foods. [1] [4]

Strong answer: Do not delay. Introduce common allergens around four to six months and sustain them in the diet. LEAP showed early sustained peanut cut peanut allergy by roughly 80% relative risk; LEAP-ON showed tolerance largely persisted. For this high-risk infant (severe eczema), risk-stratify with a skin-prick test first: introduce peanut early if low or negative, and arrange specialist-led introduction if positive. Do not restrict the maternal diet. [1] [2] [4]

Examiner extras

  • A positive skin-prick or IgE with no reaction history is sensitisation, not allergy — do not over-restrict the diet. [6]
  • Most children outgrow milk and egg; peanut, tree nut, seed and seafood more often persist. [6]
  • FPIES is non-IgE — supportive care with IV fluids, not adrenaline. [6]
  • The Ierodiakonou meta-analysis gives moderate-certainty evidence for early egg and peanut and no signal of autoimmune harm. [8]
  • Adolescents with co-existing asthma are the highest fatal-anaphylaxis group — focus on self-carry and peer awareness. [14]

References

  1. [1]Du Toit G Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med, 2015.PMID 25705822
  2. [2]Du Toit G Effect of Avoidance on Peanut Allergy after Early Peanut Consumption. N Engl J Med, 2016.PMID 26942922
  3. [4]Togias A Addendum guidelines for the prevention of peanut allergy in the United States: Report of the NIAID-sponsored expert panel. J Allergy Clin Immunol, 2017.PMID 28065278
  4. [6]Sicherer SH Food allergy: A review and update on epidemiology, pathogenesis, diagnosis, prevention, and management. J Allergy Clin Immunol, 2018.PMID 29157945
  5. [8]Ierodiakonou D Timing of Allergenic Food Introduction to the Infant Diet and Risk of Allergic or Autoimmune Disease. JAMA, 2016.PMID 27654604
  6. [13]Halken S EAACI guideline: Preventing the development of food allergy in infants and young children (2020 update). Pediatr Allergy Immunol, 2021.PMID 33710678
  7. [14]Simons FE World Allergy Organization Anaphylaxis Guidelines: 2013 update of the evidence base. Int Arch Allergy Immunol, 2013.PMID 24008815