Food allergy and anaphylaxis in children

• A food allergy is an immune reaction to a food. In children it is most often driven by IgE antibodies and starts within minutes of eating, but delayed, non-IgE reactions are also common, especially in infants. ^[1]
• Cow's milk, hen's egg, peanut and tree nuts are the allergens most often responsible, but the list of important allergens varies by country and age.
• Anaphylaxis is a rapidly developing, life-threatening reaction involving the airway, breathing or circulation. Adrenaline injected into the outer thigh is the first treatment, and children at risk carry two adrenaline auto-injectors at all times. ^[2][5]
• Diagnosis rests on a careful allergy-focused history. IgE-mediated allergy is confirmed with skin prick or specific IgE blood tests, used only after that history; non-IgE allergy is diagnosed by a supervised elimination and reintroduction.
• Prevention has changed: avoiding common allergens in pregnancy, lactation or infancy is no longer recommended, and peanut and well-cooked egg can be introduced during weaning, with precautions in high-risk infants.

By the end of this page you should be able to:

1. Distinguish IgE-mediated, non-IgE-mediated and mixed food allergy and give the typical timing and features of each.
2. Take an allergy-focused clinical history that points to either IgE or non-IgE disease and recognise when referral is needed.
3. Plan investigation: skin prick or specific IgE testing, the role of elimination and reintroduction, and the safety limits of oral food challenge.
4. Recognise and treat paediatric anaphylaxis in the community and hospital, including adrenaline dosing and observation after the event.
5. Counsel families on adrenaline auto-injectors, avoidance, label reading, action plans and follow-up.
6. Apply current guidance on early allergen introduction to prevent food allergy.

A food allergy is an adverse reaction to a food that is caused by an immune mechanism and is reproducible on re-exposure. ^[1] It is different from food intolerance (for example lactose intolerance), in which no immune sensitisation is present and the dose that causes symptoms is larger and more predictable. ^[1] This distinction matters because the management is different: intolerance is managed by reducing the amount or using an enzyme preparation, whereas allergy requires identifying and avoiding a specific allergen and planning for possible anaphylaxis. ^[1]

Food allergy is also different from coeliac disease. Coeliac disease is an immune reaction to gluten, but it is a chronic enteropathy, not an acute allergy; it is investigated with serology and biopsy under its own guideline. ^[1]

Food allergy is usefully divided by timing and mechanism. ^[1]

• IgE-mediated (immediate) allergy. Symptoms usually begin within minutes of eating the food, and almost always within a short time. ^[1] The mechanism is sensitisation to food proteins with production of allergen-specific IgE, which coats mast cells and basophils; on re-exposure the allergen cross-links IgE, releasing histamine, tryptase and other mediators. ^[1] Urticaria, angioedema, wheeze, rhinitis, vomiting and anaphylaxis are typical.
• Non-IgE-mediated (delayed) allergy. Symptoms usually appear hours to days after the food. ^[1] The mechanism is T-cell driven rather than IgE driven and often affects the gastrointestinal tract and skin. Presentations include food protein-induced enterocolitis (FPIES), food protein-induced proctocolitis, food protein-induced enteropathy, atopic dermatitis flares and some cases of constipation with perianal redness.
• Mixed IgE and non-IgE allergy. Conditions such as eosinophilic oesophagitis and atopic dermatitis with eczema exacerbations can have both mechanisms operating together. ^[1]

In childhood the most common allergens differ by age. Cow's milk and hen's egg predominate in infants, peanut and tree nuts become prominent from the toddler years, and fish and shellfish matter more in older children. Peanut, tree nuts, sesame and seeds are more common in countries with high prevalence, and shellfish is important in adolescents. ^[7]

IgE-mediated food allergy is estimated to affect roughly 5 to 10% of children in the United States, and prevalence has risen over recent decades. ^[7] Boys are slightly more often affected in early childhood. Severity varies: most reactions are mild, but adolescents with asthma and those with peanut, tree nut and sesame allergy have a higher risk of severe reactions.

Diagnosis lags behind disease. Many people who report an adverse reaction to a food do not have a true allergy; most confirmed reactions are mild, but non-IgE-mediated disease is also common. ^[1] This is why a structured history comes before any testing.

Food allergy arises when the immune system responds to a food protein as though it were dangerous. The "dual allergen exposure hypothesis" explains the main modifiable pathway: early exposure to food through the gut usually induces tolerance, whereas early exposure through an inflamed, eczematous skin barrier favours sensitisation. ^[7] Infants with early or severe atopic dermatitis and those with a previous food allergy (for example egg allergy in a baby) are at increased risk of developing further food allergies. ^[7]

Other associations include personal or family history of atopy (asthma, eczema, allergic rhinitis), and, for individual foods, country of birth and feeding practices. ^[1] There is no evidence that avoiding allergens during pregnancy or breastfeeding prevents allergy (see prevention below). ^[3]

The IgE pathway proceeds in two phases. During sensitisation, antigen-presenting cells in the gut or skin process food proteins and drive Th2-cell responses; interleukins-4 and -13 promote class switching to IgE. Allergen-specific IgE binds to high-affinity Fc-epsilon-RI receptors on mast cells and basophils. On re-exposure, the food protein cross-links bound IgE, triggering degranulation. Histamine causes urticaria, angioedema, rhinorrhoea and gut cramping; lipid mediators (leukotrienes, prostaglandins) cause bronchospasm and hypotension; tryptase and cytokines drive the systemic inflammation of anaphylaxis. ^[1] Because sensitisation is necessary before reaction, a first clinical reaction to a food is not usually anaphylaxis unless the person has been silently sensitised (for example through skin contact or cross-reactive foods).

The non-IgE pathway is less well characterised. Food-specific T cells infiltrate the gut mucosa and produce inflammation without IgE. In FPIES, a large protein load triggers massive neutrophil and mononuclear activation, leading to profuse vomiting and lethargy a few hours after ingestion, sometimes with shock. In food protein-induced proctocolitis, small amounts of blood and mucus pass per rectum in an otherwise well breastfed or formula-fed infant.

Anaphylaxis is the extreme end of a spectrum defined not by the mechanism but by severity: a rapidly developing, life-threatening reaction involving the airway, breathing or circulation, usually with skin or mucosal changes. ^[2]

The table below groups allergens by the age at which they usually matter. It is a guide, not a list of probabilities for any one child.

In the UK and several other countries these are among the foods that must be clearly declared on labels.

IgE-mediated food allergy produces acute, multisystem symptoms, often to very small amounts of food. A useful rule is that onset is within minutes to, at most, a few hours. ^[1] NICE divides the possible features by system. ^[1]

In infants the first and sometimes only clues are skin (urticaria, flaring eczema), lip or eye angioedema and vomiting. Respiratory symptoms usually accompany rather than replace other findings; isolated rhinitis after food is uncommon and should be interpreted cautiously. ^[1]

These develop after a delay, so families rarely connect them to a specific food unless prompted. Look for:

• Food protein-induced proctocolitis: small amounts of fresh blood and mucus in the stool of a well infant, usually in the first months of life while milk or soy is in the diet; growth is preserved.
• Food protein-induced enterocolitis (FPIES): repetitive vomiting a few hours after the protein, often with lethargy, pallor and diarrhoea; can lead to shock and dehydration. Rice, oats, cow's milk, soy and egg are common triggers.
• Enteropathy: chronic diarrhoea, malabsorption and faltering growth.
• Eczema flares and reflux-like symptoms: some infants have worsening atopic dermatitis or unsettled behaviour with feeds.
• Constipation with perianal redness can also be associated with cow's milk in some children.

Because these features are also common in babies without allergy, the diagnosis is clinical and should be reassessed after a trial elimination. ^[1]

Anaphylaxis is the end of the spectrum that demands immediate action. Suspect it when there are rapidly developing, life-threatening problems involving one or more of the airway (pharyngeal or laryngeal oedema), breathing (bronchospasm with tachypnoea) or circulation (hypotension or tachycardia, or both), usually with skin or mucosal changes. ^[2] Record the time of onset and the circumstances immediately before symptoms, because these help to identify the trigger. ^[2]

In practice the presentation can be sudden collapse, severe wheeze, hoarse voice, throat tightness, pallor, or a rapidly spreading rash. Not every anaphylaxis has obvious skin findings, so do not wait for a rash before treating respiratory or circulatory features. ^[9] Progress is usually fast enough that there is time to act if adrenaline is given early, but not time to wait for investigations.

The key distinction is between food allergy and other causes of the same symptoms.

• Non-allergic reactions. Lactose intolerance, other carbohydrate malabsorption, and reactions to food additives or natural toxins (for example scombroid fish poisoning) can mimic allergy. The history helps: symptoms are dose-dependent, tolerance is present in small amounts, and there is no urticaria or anaphylaxis. ^[1]
• Coeliac disease. Gluten-triggered, chronic, with autoantibodies; not an acute allergy. ^[1]
• Eosinophilic oesophagitis and gastroenteritis. Mixed IgE/non-IgE disease with dysphagia, food impaction or reflux; diagnosis needs endoscopy. ^[1]
• Mast cell disorders and idiopathic anaphylaxis. Consider in recurrent episodes without an obvious trigger; mast cell tryptase and allergist referral help. ^[2]
• Other causes of acute urticaria, wheeze or collapse, such as viral wheeze, venom sting, drug reaction or exercise-induced anaphylaxis.

For an individual child the main task is not to label but to decide whether the story is convincing enough to test, and whether the next exposure could be dangerous. If there is any suspicion of anaphylaxis, manage the risk first: avoid the suspected food, prescribe adrenaline if indicated, and refer.

An allergy-focused clinical history is the single most important step and should be taken before any testing. ^[1] For IgE-mediated disease the history should cover atopy in the child and family, foods avoided and why, symptoms with their speed of onset after the food, severity, frequency, reproducibility, dose and setting, and the feeding history including breastfeeding, formula and age of weaning. ^[1] For non-IgE disease, ask about eczema, reflux, stool blood or mucus, constipation, colic, feeding difficulties and growth.

Examine growth and signs of undernutrition, eczema, asthma and allergic rhinitis. ^[1]

If the history suggests IgE-mediated allergy, offer skin prick testing and/or blood tests for specific IgE antibodies to the suspected foods and likely co-allergens. ^[1] Tests must be chosen and interpreted by professionals with the right competencies, in the context of the history; never order broad panels without clinical reasoning. ^[1] Skin prick tests are only done where treatment for anaphylaxis is available. ^[1] Do not use atopy patch testing or oral food challenges for IgE diagnosis in primary care or community settings. ^[1]

A positive test shows sensitisation, not disease. Many children have specific IgE to a food they tolerate, so a test without a compatible history leads to unnecessary and nutritionally harmful avoidance. ^[1]

For suspected non-IgE food allergy, the standard approach is an elimination diet for the suspected allergen, normally 2 to 6 weeks, followed by reintroduction while watching symptoms. ^[1] A dietitian with allergy competencies should guide nutrition, timing and follow-up, especially where staples such as milk or egg are removed. ^[1] IgE blood tests and skin prick tests are not helpful here because the mechanism is not IgE driven. ^[1]

After a suspected anaphylactic reaction, mast cell tryptase can support the diagnosis. In adults and young people aged 16 years or older, NICE recommends a sample as soon as possible after emergency treatment and a second sample ideally within 1 to 2 hours (and no later than 4 hours) from symptom onset. ^[2] In children younger than 16 years the same timing should be considered when the cause is thought to be venom-related, drug-related or idiopathic. ^[2] Baseline tryptase may be measured later at follow-up with the allergy service. ^[2] Tryptase is less often raised in children than in adults, and the result does not replace the history. ^[2]

There is no biomarker that defines food allergy. Diagnosis is confirmed when the history, examination and testing converge, and, when needed, an oral food challenge.

Anaphylaxis is recognised clinically by ABC symptoms, as above. ^[2] For severity of non-IgE reactions there is no universally accepted score; FPIES is diagnosed by characteristic timing and exclusion of other causes, sometimes after a supervised challenge.

A medically supervised oral food challenge (OFC) is the reference test for confirming or excluding IgE-mediated food allergy when the history and tests do not settle the diagnosis, and it is used to check for tolerance development over time. ^[8] It should never be done in primary care or the community for IgE-mediated disease. ^[1]

Common reasons to perform an OFC:

• a convincing history with negative or inconclusive tests;
• positive tests with a vague history, where sensitisation may exist without clinical allergy;
• assessment of tolerance before reintroduction after a period of avoidance;
• determining the threshold dose for an allergen.

The challenge starts from a very low dose and progresses in increments. Published protocols use increments of 3, 10, 30, 100, 300, 1000 and 3000 mg of food protein, with about 20 to 30 minutes between doses in clinical practice (and at least 30 minutes between doses in research challenges); the final dose should approximate an age-appropriate portion of the food. ^{[8] [4]} Lower starting doses are safer, and longer intervals between doses reduce the chance of a reaction to a cumulative dose. ^[8] For challenge foods that are less protein-dense (fruit and vegetables) or more dense (meat, fish, shellfish) the increments and top dose are adjusted so that the final dose is realistic. ^[8]

An OFC is stopped if objective symptoms appear. Continuing absorption can cause late symptoms, so minimum observation after the final dose is needed (commonly 2 hours for a challenge where adrenaline was not used, and longer if symptoms occurred). NICE also allows discharge after 2 hours from resolution following a supervised allergy challenge, even if two doses of IM adrenaline were needed. ^[2]

Safety planning is as important as the dose plan. Challenges require trained staff, emergency medication (including adrenaline, antihistamine, bronchodilator and steroid), intravenous access preparedness, resuscitation equipment, and observation space. Children with unstable asthma or a recent severe reaction need individualised risk assessment before challenging. ^[8]

Adrenaline is the first-line treatment for anaphylaxis in every guideline cited here. ^{[6] [4] [9]} Give it intramuscularly into the anterolateral aspect of the middle third of the thigh as soon as airway, breathing or circulation problems are recognised. ^{[9] [6]} Delays in adrenaline worsen outcomes; a single IM dose is well tolerated and carries minimal risk, so if in doubt, give it. ^[9]

Use the ABCDE approach alongside adrenaline: secure the airway, give high-flow oxygen to saturation 94 to 98%, and give rapid intravenous or intraosseous fluid (10 mL/kg in children, 500 to 1000 mL in adults) for hypotension or shock. ^[9] Nebulised adrenaline can be used as an adjunct for laryngeal oedema only after IM adrenaline. ^[9] Intravenous adrenaline is reserved for experienced specialists in monitored settings and is used for refractory anaphylaxis. ^[9] Patients on beta-blockers may respond poorly to adrenaline. ^{[9] [4]}

Position matters as much as drugs. The child should lie flat with the legs raised; a sitting position can be used if respiratory distress dominates; pregnant adolescents lie on the left side with the bed head-down. ^{[4] [9]} Avoid a sudden move to upright even if the child feels better, because postural change can restart collapse. ^{[4] [9]} Remove the trigger where possible (stop an infusion, spit out the food).

Post-reaction care prevents biphasic (repeat) reactions and sets up long-term management. NICE recommends a risk-stratified observation period, adapted from RCUK guidance: ^[2]

• Discharge after 2 hours of observation from resolution may be considered if there was a good response (within 5 to 10 minutes) to a single dose of IM adrenaline given within 30 minutes of onset, symptoms have completely resolved, the child already has 2 in-date auto-injectors and knows how to use them, and adequate supervision after discharge is available. ^[2]
• Observe for at least 6 hours after resolution of all symptoms if 2 doses of IM adrenaline were needed, or there is a history of biphasic reaction. ^[2]
• Observe for at least 12 hours after resolution if the reaction was severe (more than 2 doses of adrenaline), involved severe respiratory compromise or occurred in severe asthma, if allergen absorption may continue (for example slow-release medicines), if care access is difficult, or in similar risk situations. ^[2]
• After a supervised allergy challenge, discharge after 2 hours may be considered even if 2 doses of IM adrenaline were needed. ^[2]

NICE NG258 sets those risk-stratified minimums. Resuscitation Council UK and UK defence anaphylaxis guidance may recommend longer in-hospital observation for severe presentations (commonly 6 to 24 hours), so when in doubt observe the longer period and follow local protocol. ^{[2] [9]}

Food allergy is managed long term by:

• Avoidance of the confirmed allergen, with practical label-reading training, awareness of cross-contamination and advice about eating away from home. ^[1]
• Nutritional support from a dietitian when staples are removed (milk, egg, wheat, soy) or multiple foods are avoided, to prevent deficiencies and support growth. ^[1]
• Comorbidity control, especially asthma: poorly controlled asthma is the main risk factor for fatal food anaphylaxis, so asthma action plans and inhaler technique matter as much as the food allergy plan. ^[6]
• Follow-up and re-evaluation. Children are retested (skin prick or specific IgE, sometimes followed by challenge) every 1 to 2 years to see whether the allergy has been outgrown. Cow's milk and hen's egg are often outgrown; peanut, tree nut, fish and shellfish allergy usually persists. ^[7]
• Education and action plans. Children, parents and school staff need written emergency plans, training in auto-injector use and refreshers as devices and guidelines change. ^[6]

Adrenaline auto-injectors allow a child or caregiver to give a dose of adrenaline early, outside a healthcare setting, while emergency help is on the way. They should be prescribed at discharge after anaphylaxis and used as an interim measure for children at risk. ^{[2] [9]}

• Prescribe two in-date devices and make sure the family carries both at all times. ^{[2] [5]} Two are needed because a second dose may be required and a device can fail or be discharged by mistake.
• Do not prescribe after anaphylaxis due to a drug if the drug has been identified and can be easily avoided. ^[2]
• Train by brand. Show the exact device prescribed (EpiPen, Jext, etc.) with an auto-injector trainer, so the child and caregivers are confident to press the device into the outer thigh through clothing, hold for the required time, and call emergency services. ^{[2] [6]}
• Action plans and reminders. Give written guidance: use the device if breathing or circulation problems start, lie down and raise legs, do not stand suddenly, and go to hospital. ^{[2] [6]} Check expiry dates and replace in advance; an expired device is better than none, but is not reliable. ^[6]
• Storage: keep at room temperature, not frozen, and out of direct sunlight. ^[6]
• Weight-based prescribing. Devices deliver fixed doses (150, 300 and, for some, 500 micrograms), which may not match a child's weight exactly. EAACI suggests 0.15 mg auto-injectors for children from 7.5 kg to 25-30 kg and 0.3 mg for children from 25-30 kg upward. ^[6] Product licences differ: EpiPen Jr is licensed 150 micrograms for body weight up to 15 kg (with 300 micrograms sometimes used for 15-24 kg) and EpiPen 300 micrograms for 25 kg and above, whereas BNF presents the bands as up to 15 kg, 15-24 kg and 25 kg and above. ^{[5] [9]} Use the dose card for the device prescribed, which ever authority is cited, and reassess as the child grows: moving from a 150 microgram to a 300 microgram device is commonly needed around 25 kg. ^{[5] [9]}
• In hospital give adrenaline from an ampoule by syringe and needle, not from an auto-injector, because it cannot be titrated. ^[9]

The thinking about prevention has changed completely. Older advice to avoid allergens in pregnancy, during breastfeeding and in infancy did not prevent allergy and may have increased risk by removing the chance for oral tolerance. Current guidance is:- No routine avoidance. The EAACI 2020 update advises against avoiding dietary food allergens during pregnancy or breastfeeding and against using soy protein formula in the first 6 months of life as a prevention strategy. ^{[3] [7]}

• Start early. Introduce peanut and well-cooked egg as part of complementary feeding. The evidence is strongest for starting from 4 to 6 months of age in infants who are developmentally ready. ^{[3] [7]} Recent guidelines recommend early introduction of egg- and peanut-containing products from around 6 months (but not before 4 months) for all infants and advise not deliberately delaying other potentially allergenic foods. ^[7]
• High-risk infants need a plan. Infants with severe eczema or an existing egg allergy are at highest risk of peanut allergy. They should ideally be evaluated (skin prick test or specific IgE) before the first introduction, and if needed the first feed should be medically supervised, without delaying weaning past the window of opportunity. ^[7]
• Regular, not one-off. In the LEAP study, regular peanut consumption from 4 to 10 months in infants at increased risk cut the development of peanut allergy by more than 80% by age 5 years, and tolerance persisted even when peanut was then avoided. ^[7]
• Breastfeeding remains recommended for its general benefits; hydrolysed or amino-acid formula is not a prevention strategy and should not be advised for that purpose. ^[3]

Regulation also matters locally: several European and North American programmes now support early introduction, and national infant-feeding guidance should be followed alongside this.

Where specialist allergy services, skin prick reagents or auto-injectors are limited:

• Diagnose from the history using the NICE symptom list, and treat with a period of supervised elimination and reintroduction rather than broad, unsupervised exclusion. ^[1]
• Protect nutrition. Removing milk, egg or wheat without dietetic support causes faltering growth; a dietitian (or trained community worker) should advise on alternatives. ^[1]
• Treat anaphylaxis with the resources you have. Adrenaline ampoules and syringes are preferred in hospital; where auto-injectors are unavailable or unaffordable, train families in drawing up and using adrenaline from an ampoule is not recommended for home use, so an ampoule-based emergency plan needs local adaptation and escalation pathways. ^[9]
• Challenge only where safe. Oral challenges should be performed in settings with resuscitation capacity and post-challenge observation; defer non-urgent diagnostic challenges rather than perform them unsafely. ^[8]
• Refer into networks. Even a single visit to a regional allergy service can establish the diagnosis and a safe first challenge. ^[2]

• Food allergy in children is either IgE-mediated (minutes, urticaria, angioedema, wheeze, anaphylaxis) or non-IgE-mediated (hours to days, gut and skin), and the two need different tests.
• Cow's milk and hen's egg dominate in infants; peanut, tree nuts and sesame matter more with age and are important causes of anaphylaxis.
• Diagnosis begins with an allergy-focused clinical history taken before any test; skin prick or specific IgE testing only confirms sensitisation in the right clinical context.
• Non-IgE allergy is diagnosed by 2 to 6 weeks of supervised elimination followed by reintroduction, with dietetic support.
• Anaphylaxis is a rapidly developing airway, breathing or circulation problem, usually with skin changes, treated first with intramuscular adrenaline in the outer thigh, repeated every 5 minutes.
• After anaphylaxis, observe 2 hours if the response to one dose was rapid, at least 6 hours if two doses were needed or there is a biphasic history, and at least 12 hours for severe cases.
• Every child discharged after anaphylaxis needs 2 in-date adrenaline auto-injectors, training by brand, a written action plan and referral to a specialist allergy service.
• Prevention has shifted to early introduction: avoid unnecessary maternal or infant restriction, and introduce peanut and well-cooked egg from 4 to 6 months (with evaluation of high-risk infants first).
• Cow's milk and egg allergy are often outgrown; peanut, tree nut, fish and shellfish allergy usually persist but should be reassessed.

Food allergy crosses several disciplines: anaphylaxis and its management, atopic dermatitis and eczema, asthma control, infant feeding and nutrition, gastro-oesophageal reflux, growth faltering, vaccines and allergy. (Although the broader MedGrasp network contains topics on these subjects, links to planned topics are deliberately not embedded here.)

References are listed in the front matter and are cited in the text with the corresponding number.