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• Severe food allergy in childhood
  Andrew T Clark
  Published on: 9 January 2022
• Food allergy in childhood
  Allan F Colver
  Published on: 9 January 2022
• Co-existence of asthma and mild food allergy a strong indication for epinephrine autoinjector
  Onajite M Oyaide
  Published on: 9 January 2022

• Published on: 9 January 2022

  Severe food allergy in childhood

  • Andrew T Clark, Paediatrician
  • Other Contributors:
    • Pamela W. Ewan

  Dear Editor

  We thank Colver, MacDougall and Cant for their response to our paper.[1] The message underpinning our paper was that severe allergic reactions to foods are not as uncommon as MacDougall et al. suggested.[2] However, we are not comparing like with like and the problem lies in the definition of a severe food reaction. MacDougall et al. only identified the extreme end of the clinical s...

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  Dear Editor

  We thank Colver, MacDougall and Cant for their response to our paper.[1] The message underpinning our paper was that severe allergic reactions to foods are not as uncommon as MacDougall et al. suggested.[2] However, we are not comparing like with like and the problem lies in the definition of a severe food reaction. MacDougall et al. only identified the extreme end of the clinical spectrum (children who have suffered cardio-respiratory arrest, received at least 2 doses of epinephrine (adrenaline), a fluid bolus, inotropic support or at least 2 doses of nebulised bronchodilator- all unvalidated and unreferenced outcome measures). Having set the threshold for inclusion so high, it is hardly surprising that the incidence of this extreme outcome is so low. What was the authors’ purpose in identifying this extreme population? If it was reassurance about the low incidence of life- threatening reactions, then it should be appreciated that in a recent American series [3] 8/10 children who died of food allergy had previously reacted to the food that caused the fatality. Also, in a UK survey, 21/92 (23%) of peanut allergic patients with a history of a mild reaction subsequently had a severe reaction to peanut.[4] MacDougall’s data should not be used to dilute care given to children with less severe food allergy.

  MacDougall et al. have failed to identify the much larger population, of the most interest to paediatricians, allergists and parents i.e. children who have suffered a less extreme but still severe food allergy reaction (or anaphylaxis) characterised by airway narrowing.[5] It is important to identify and study this large group as there is no consensus on how they should be managed. We have shown that intervention with a structured management plan, incorporating assessment of severity, avoidance advice and tailored medication for self treatment, together with a patient-held treatment plan, reduces the risk and severity of further reactions, in both adults and children.[6]

  It is clear that the British Paediatric Surveillance Unit (BPSU) survey missed children referred to allergy centres, not run by paediatricians. MacDougall et al. studied only inpatient admissions and not outpatient referrals. It is erroneous to assume that children referred to an allergy clinic would have been seen by a paediatrician. We look after over 790 outpatient referrals of children with nut allergy, 218 (29%) have had reactions involving respiratory symptoms and 58 (8%) severe dyspnoea and collapse. This number would be much larger is all foods were considered, and this effect is repeated for other allergy centres around the country. These children with severe reactions are derived from approximately 1/30th of the UK population. The majority were referred directly from their general practitioner and have had no contact with a paediatrician and therefore would not have been notified to the BPSU. The fact that the number of inpatient admissions in MacDougall's paper matched that from a previous survey is irrelevant, as neither considers the large number of children who present to allergy out-patient clinics via their general practitioner.

  We present data to estimate the incidence of those severe reactions that were missed by MacDougall’s paper, using a different and more appropriate definition of severity. We compare them to MacDougall’s estimate of 0.19 severe food reactions per 100,000 children per year. We have data from 791 children with nut allergy, 58 of whom had at least one severe nut induced reaction and the data were collected over six years, giving an incidence of at least 1.93 severe reactions per 100,000 children per year for nut allergy alone: a figure 10 fold higher than MacDougall’s data for all food allergy. This estimate is a minimum, as each child has had at least one severe reaction (possibly more) and is for nut allergy alone, rather than all food allergies.

  The estimate of the incidence of deaths due to food allergy produced by MacDougall et al. is an underestimate, as the authors did not consider asthmatic deaths, where no allergenic cause was suspected and we thank Colver for acknowledging this. There are sixty fold more deaths due to asthma, than those identified as due to a severe food reaction by MacDougall et al. If only a few of these were due to food allergy, it would alter the figures dramatically.

  Colver has citied Bock’s important series of fatal food reactions,[3] which showed 80% (8/10) of deaths in under 16 year olds were due to peanuts or nuts, the youngest being 2 years old. It is not clear, however, why we should be reassured by MacDougall’s finding of no peanut allergy induced deaths in children under 13 years. Do the authors not consider tree nut allergy induced deaths in 2 year olds, or peanut allergy induced deaths in 14-16 year olds relevant?

  Finally, we agree that the issues surrounding provision of adrenaline autoinjectors require good data on the clinical features and natural history of nut allergy. However, to consider adrenaline autoinjectors in isolation is missing the point. The provision of adrenaline autoinjectors should be seen in the broader context of a comprehensive management plan for all children with food allergy. Children with mild food allergy reactions can go on to have more severe reactions.[4] We have shown that enrolment of children with nut allergy of all severities in such a management plan, consisting of repeated specialist advice on allergen avoidance, together with tailored medication including oral antihistamine with or without inhaled adrenaline or injectable adrenaline, results in reduced number and severity of further reactions.[6] Colver has emphasised the efficacy of this treatment plan in children, by highlighting that only three adults (aged 27-41 years) and no children had further severe reactions.

  References

  (1) Clark AT, Ewan PW. Food allergy in childhood: Have the dangers been underestimated? Arch Dis Child 2003;88:79-81.

  (2) MacDougall CF, Cant AJ, Colver AF. How dangerous is food allergy in childhood? The incidence of severe and fatal allergic reactions across the UK and Ireland. Arch Dis Child 2002:86:236-239.

  (3) Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol 2001;107:191-3.

  (4) Hourihane JO’B, Kilburn SA, Dean P, Warner JO. Clinical characteristics of peanut allergy. Clin Exp Allergy 1997;27:634-9.

  (5) Project team of the Resuscitation Council, UK. Emergency medical treatment of anaphylactic reactions. J Accid Emerg Med 1999;16:243-7.

  (6) Ewan PW, Clark AT. Long-term prospective observational study of patients with peanut and nut allergy after participation in a management plan. Lancet 2001;357:111-15.

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  Conflict of Interest:
  None declared.

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• Published on: 9 January 2022

  Food allergy in childhood

  • Allan F Colver, Senior Lecturer Community Child health
  • Other Contributors:
    • Colin Macdougall, Andrew Cant

  Dear Editor

  We were surprised by some of the content of Clark and Ewan’s paper [1] and their interpretation of our data.[2]

  As death certification of allergy deaths is problematic, we collected reports through the prospective BPSU mechanism and other sources as listed in our article. No additional deaths in the study period have been brought to our attention since publication. Our finding of no deaths due t...

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  Dear Editor

  We were surprised by some of the content of Clark and Ewan’s paper [1] and their interpretation of our data.[2]

  As death certification of allergy deaths is problematic, we collected reports through the prospective BPSU mechanism and other sources as listed in our article. No additional deaths in the study period have been brought to our attention since publication. Our finding of no deaths due to peanut under the age of 13 is supported rather than refuted by the study of Bock,[3] cited by Clark and Ewan. In Bock’s study, which looked at all ages, there were 10 childhood deaths (c.f. 8 in ours) and they found no deaths due to peanut allergy under the age of 12. The death of a child aged two years was due to brazil nut, not peanut.

  Clark and Ewan were concerned that we did not put sufficient weight on respiratory presentations. Of the 55 non-fatal severe cases, 30 had only upper or lower airway problems. Of the 173 children admitted to hospital not classified by us as severe, 60 had an upper or lower airway presentation for which adrenaline or bronchodilator or both were administered. Even if all these are added to our severe group, the rate of non-fatal severe events only changes from 0.2 to 0.4 per 100,000 children per year.

  Allergic deaths indistinguishable from asthma are potentially important but if a child’s symptoms are only asthmatic and no allergen is suspected, then there is no means for attributing such reactions to food or for knowing if a causal link exists. The possibility of an unrecognised link is a key area for further research.

  It is misleading to state that the mechanisms of the British Paediatric Surveillance Unit will miss children referred to allergy centres not run by paediatricians. We studied hospital admissions, not outpatient referrals, and all such children should be admitted under the care of paediatricians. The effectiveness of our reporting mechanisms is supported rather than refuted by the study of Alves and Sheikh,[4] cited by Clark and Ewan. Alves and Sheik report all hospital admissions for anaphylaxis in children aged 0-15 years over a four-year period in England and Wales. There were 60 for food allergy and a further 240 with no cause coded. If, as Clark and Ewan suggest, 94% of the un-coded cases were due to food then there were 288 admissions from 10.6 million children (denominator from Office of National Statistics, personal communication) over four years or 0.68 admissions per 100,000 children per year. This is comparable to our reported 231 admissions over 2 years in a population of 13 million, equivalent to 0.89 admissions per 100,000 children per year.

  The inclusion of Clark and Ewan’s own data in their Table 1 is inappropriate. Two concerns are that their data are extrapolations and use a completely different definition of severity. But more importantly, their figures are numbers of children with severe allergy per 100,000 child population; whereas our figures, and those of Alves,[4] are numbers of severe reactions per year per 100,000 child population. Clark and Ewan therefore confuse prevalence of severely allergic children with incidence of severe allergic reactions. Such data cannot be tabulated against each other and their suggestion that our figures are a 62-fold underestimate is therefore without meaning.

  We all want to know which children should have an adrenaline auto- injector and what the indications should be for administering it. However in seeking such knowledge, we must be careful not to extrapolate from adult studies. In Clark and Ewan’s own study,[5] the high percentage (70%) of children in the study is stated but the median age of a moderate or severe reaction on follow up was 18 years and the three severe cases referred to in which adrenaline was used were actually aged between 27 and 41 years.

  We agree with Clark and Ewan’s assertion that problems over the decision to prescribe adrenaline “highlight the need for good data on the clinical features and natural history of nut allergy in children” but would add that studying the epidemiology is also fundamental.

  References

  (1) Clark AT, Ewan PW. Food allergy in childhood. Arch Dis Child 2003:88:79-81

  (2) Macdougall CF, Cant AJ, Colver AF. How dangerous is food allergy in childhood? The incidence of severe and fatal allergic reactions across the UK and Ireland. Arch Dis Child 2002:86:236-9.

  (3) Bock SA, Munaz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. Journal of Allergy and Clinical Immunology 2001:107:191-3.

  (4) Alves B, Sheikh A. Age specific aetiology of anaphylaxis. Arch Dis Child 2001:85:349.

  (5) Ewan PW, Clark AT. Long-term prospective observational study of patients with peanut and nut allergy after participation in a management plan. Lancet 2001:357:111-115.

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  Conflict of Interest:
  None declared.

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• Published on: 9 January 2022

  Co-existence of asthma and mild food allergy a strong indication for epinephrine autoinjector

  • Onajite M Oyaide, Clinical Fellow, Paediatric Intensive Care Unit
  • Other Contributors:
    • Fiona Reynolds, Consultant Paediatric Intensivist, Birmingham Children's Hospital

  Dear Editor

  Following two recent articles on food allergy in childhood by Macdougall et al,[1] Clark and Ewan,[2] we report a case of near fatal food allergic reaction in a child with a history of asthma and mild food allergy.

  This 14-year-old girl with life-long asthma also had a history of angioedema associated with ingestion of eggs and fish. She experienced sudden severe breathing difficulties a...

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  Dear Editor

  Following two recent articles on food allergy in childhood by Macdougall et al,[1] Clark and Ewan,[2] we report a case of near fatal food allergic reaction in a child with a history of asthma and mild food allergy.

  This 14-year-old girl with life-long asthma also had a history of angioedema associated with ingestion of eggs and fish. She experienced sudden severe breathing difficulties at a party following ingestion of a variety of foods. Attempts to obtain relief of symptoms using her salbutamol metred- dose inhaler was unsuccessful and unconsciousness ensued. On arrival to the accident and emergency department, she had severe respiratory distress with severely decreased air entry to her lungs generally. On presentation SaO₂ was 77% in 15l/min oxygen flow via mask and reservoir bag , she had a low volume pulse with a rate of 160/min, blood pressure 125/65 mmHg, Glasgow Coma Scale was 4. SaO₂ improved to 95% with concomitant application of positive-end expiratory pressure via mask and T-piece with bag and the administration of intravenous salbutamol. She needed intubation and anaesthesia was induced using ketamine, known to have bronchodilator effects. During the resuscitation an urticarial rash on her trunk and angioedema became evident. This prompted the administration of adrenaline, hydrocortisone and chlorpheniramine. Salbutamol infusion was then commenced. Air entry to her lungs, chest compliance and ease of ventilation improved gradually and significantly over the following hour. Chest Xray showed hyperinflated lungs and a small basal pneumothorax on the right side. Her treatment was complicated by a short run of ventricular tachcardia followed by bigeminy in association with serum potassium level of 2.9 mmol/l. Salbutamol infusion was discontinued at this stage and potassium was given intravenously. Following stabilisation, ventilation was weaned with ease and she was extubated 5 hours after hospital presentation.

  Fatal anaphylactic reactions are often mislabelled as asthma deaths. This near-fatal case described was initially managed as a severe asthma attack in the absence of a complete patient history, until cutaneous signs of an allergic reaction became obvious. The rapid improvement of our patient after treatment for anaphylaxis is contrary to what is often seen with a severe asthma attack needing intubation. We agree with both sets of authors that the child with food allergy, however mild previous reactions have been, and asthma is at particular risk of severe food allergic reaction. We advocate a management package for the child at risk to include administration of salbutamol by inhalation, together with intramuscular epinephrine and rapid transfer to hospital as suggested by Macdougall et al.[1] The possibility of anaphylaxis should always be considered in a child presenting to hospital with an apparent severe asthma attack.

  References

  (1) Macdougall CF, Cant AJ, Colver AF. How dangerous is food allergy in childhood? The incidence of severe and fatal allergic reactions across the UK and Ireland. Arch Dis Child 2002; 86:236-239.

  (2) Clark AT, Ewan PW. Food allergy in childhood. Arch Dis Child 2003; 88: 79-81.

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  Conflict of Interest:
  None declared.

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