Quick Guide to Anaphylaxis

© Springer Nature Switzerland AG 2020

C. Cingi, N. Bayar MulukQuick Guide to Anaphylaxishttps://doi.org/10.1007/978-3-030-33639-4_1

1. Anaphylaxis: Definition, History, and Epidemiology

Cemal Cingi¹  and Nuray Bayar Muluk²

(1)

ENT Department, Faculty of Medicine, Eskişehir Osmangazi University, Eskisehir, Turkey

(2)

ENT Department, Faculty of Medicine, Kırıkkale University, Kırıkkale, Turkey

1.1 Definition of Anaphylaxis

Anaphylaxis can lead to death, but even so, rates of diagnosis and levels of treatment remain low. In part, not understanding that anaphylaxis covers more than simply anaphylactic shock, and that treating the disorder depends upon identifying the syndrome rapidly and stopping, by judicious use of epinephrine, the potentially lethal cardiovascular and respiratory complications, may be to blame [1].

Anaphylaxis lies at the severe end of a spectrum of acute allergy responses which affect multiple body systems. In clinical practice, anaphylactic signs are observed in several organs, usually beginning with skin signs before next involving the respiratory system, also reacting on the gut and producing cardiovascular alteration, until the heart and breathing are arrested in the last phase. Anaphylaxis, strictly speaking, refers to the immunological response working through IgE and, to a lesser extent, IgG and IgM (Coombs and Gell Type 3 reactions). Anaphylactoid (pseudo-allergic) is, by contrast, the term used in cases showing a similar clinical profile but not attributable to antibody formation. Some recent classification attempts have put such syndromes under the anaphylactic label, extending usage to mean any acute reaction involving hypersensitivity and affecting the whole body [2].

Anaphylaxis is definable as a life-threatening response, acute in onset, involving many organs and initiated by mast cell and basophilic degranulation [3, 4]. Archetypally, previous exposure to an allergen induces sensitivity, which, upon second exposure, incites an immunological response [5]. The main culprits are allergens in food, implicated in 33–56% of incidences overall and approaching 81% in paediatric cases [6–8].

The principal systems with involvement in anaphylaxis are the skin, gut, respiratory, and cardiovascular systems. Fully developed anaphylaxis features urticarial, angioedematous (with consequent hypotension), and bronchospastic responses [5]. However, no one clinical definition is agreed upon by all authorities. Clinicians rely on the habitual systemic features and, frequently, documented exposure to an antigenic stimulus, to make the diagnosis [5].

Laboratory confirmation is seldom necessary or beneficial in what is, in essence, a purely clinical diagnosis. In case of unclarity, particularly where a chronic element is present, or other conditions need to be considered, the laboratory may be of some limited assistance in the provision of IgE serology, as may dermal prick tests [5]. Immediate action to recognise and treat anaphylaxis is essential—it is an emergency, but the actual treatment varies according to the initial severity and how the patient responds clinically to intervention [5].

Whilst anaphylaxis is most frequently attributable to medications, food or additives, other sources of allergens as well as non-chemical initiators (temperature extremes or ultraviolet irradiation) exist. How anaphylaxis unfolds clinically and how severely, hinges upon both the level to which the patient is sensitised and other elements present at the time of exposure: infection, physical exercise, emotional pressure, and other medicinal drug use, such as beta adrenoceptor antagonists. A high percentage of otherwise unexplained (idiopathic) anaphylactic reactions may conceivably be due to this summation anaphylaxis. Cases due to insect stings have levels of angiotensin in blood that are inversely correlated with the degree of reaction, a severe reaction showing lower angiotensin and vice versa [2].

1.2 History

Anaphylaxis as a term dates to Portier and Richet’s study in 1902 in which a dog died as a result of receiving two consecutive doses of sea anemone toxin, the second after a delay. It is made up of the Greek terms ana- (again, up) and -phylaxis (protection, immunity) [5].

Paul Portier and Charles Richet did the key study, but in fact, Megendie had also noted that a substance which one would not normally expect to be lethal could cause a generalised reaction ending in death. He injected egg albumin sequentially into rabbits, which suddenly collapsed and died [9]. For the following few decades, researchers observed that laboratory animals could have a life-threatening reaction to non-self-materials, even when at levels that previously caused no apparent problem. Richet, in concert with Portier, isolated the toxin found in tentacles of the genus Physalia (the Portuguese man-of-war) as well as the venom of the Actinia sulcata, an anemone found in prolific numbers at the French seaside, and closely related to the Physalia toxin. They were attempting to establish what constituted a lethal dosage of the toxin in dogs, and, assuming that those animals who survived being given a first dose would now carry immunity to the toxin, they were astonished instead to discover that lower levels of the toxin given subsequently were in fact lethal in a short space of time [10]. In explaining the finding as an apparent lack of immunity following innoculation with toxin, Richet coined the term aphylaxis, subsequently settling on anaphylaxis as a more euphonious combination of letters [11]. But, even though the terminology dates to over a century ago, defining the actual phenomenon it denotes in a consistent way has been less straightforward [12].

Anaphylaxis is archetypally a severe reaction, affecting skin, gut, lungs, and heart [13]. Generally, such a picture is readily identified by doctors, but the presence of few or less severe symptoms can complicate diagnosis. An immediate systemic reaction caused by rapid, IgE [immunoglobulin E]-mediated immune release of potent mediators from tissue mast cells and peripheral basophils is how the 1998 Joint Task Force of the American Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) describe an anaphylactic reaction [14]. However, since some reactions can mimic signs and symptoms of anaphylaxis but are caused by non-IgE-mediated release of potent mediators from mast cells and basophils, they are described as anaphylactoid rather than anaphylactic, a complicated situation for the clinician working in a clinic or Accident and Emergency, who may recognise the syndrome but be unaware of the underlying mechanism, which the above scheme bases the distinction upon. The definition of anaphylaxis as a serious allergic reaction that is rapid in onset and may cause death [15] emerged from two later symposia. Criteria to diagnose anaphylaxis in clinical settings were outlined by the Second Symposium on the Definition and Management of Anaphylaxis [12, 15].

1.3 Epidemiology of Anaphylaxis

It is unknown what the actual incidence of all-cause anaphylaxis in the general population is [16–18]. Estimates based upon occurrence in communities are complicated by low rates of diagnosis and incomplete documentation, coupled with erroneous coding practice, concomitant use of differing case definitions, and ways to quantify the incidence [18–20]. Nonetheless, anaphylaxis is evidently not a seldom-seen phenomenon and incidence is on the rise, particularly in childhood and early adulthood [21–23].

Anaphylaxis occurs 30 times in every 100,000 person-years [24, 25], with the most severe forms put at the level of 5–15 per 100,000 [26]. Using data gathered routinely when admitting patients to hospital in the UK, some studies recorded a 700% increase in anaphylactic incidence between 1990/1 and 2003/4, noting the incidence to be highest in children of school age [27, 28]. Quantification of paediatric risk of anaphylaxis is hampered by a paucity of relevant data. Since different ways were used for defining anaphylaxis in the data that are available, this presents methodological issues to researchers. To illustrate the problem, whilst incidence in children equals that of adults in some studies [29, 30], elsewhere it is quoted as a mere 0.19 in 100,000 [31], although this figure is likely to be on the low side due to the method used to calculate it [32]. A variety of techniques have been employed to reveal the epidemiological aspects of anaphylaxis. One study looking at all school students in France gauged that 1 in 1000 had a plan to manage their anaphylaxis. The increasing rate of epinephrine prescription mirrors the increase in awareness of risks attributable to allergies: in the UK, children born between 1990 and 1992 were seven times more likely to have an Epipen than those born 9 years earlier [33]; in Canada, 1% of the population is in possession of a prescription for epinephrine, rising to 5% in boys between 1 year and 17 months old [34].

Anaphylaxis incidence is on the rise, especially in patients up to the age of 20, most frequently triggered by foodstuffs, medicinal drugs, or insect venom. To make the diagnosis, a careful history establishing that the patient has been exposed to the putative offending agent, with a typical symptomatic and clinical pattern ensuing, needs to be recorded. On occasion, serum tryptase elevation may be indicative. It is worth investigating atypical presentations of anaphylaxis as a way of identifying unsuspected causes and ways for anaphylaxis to develop. Cases determined to be idiopathic on account of negative dermal tests and IgE serology may be due to an unsuspected allergen or may be a manifestation of mastocytosis or clonal mast cell disorder, so these possibilities must be entertained [35].

The variety of criteria used in the diagnosis of anaphylaxis ensures that the actual incidence of the disorder continues to be unknown. Hospital—or health maintenance organization—(HMO)-based studies have given results ranging between 30–60 cases per 100,000 and 2000 events per 100,000, equating to 0.03–2.0% risk of developing the disease in a lifetime [36]. Anaphylaxis may in fact still be underreported due to the diagnosis of allergic reaction being used where several physiological systems are involved, in place of the more precise anaphylaxis descriptor [20]. An audit of case notes for Accident and Emergency revealed that in 678 cases, anaphylaxis had been wrongly classified as food allergy. Another research team found that 617 cases in which an insect had stung the patient and which reached the threshold for a diagnosis for anaphylaxis had not been so diagnosed [37, 38]. The reasons why neither victims nor clinicians consider the anaphylaxis diagnosis may be multifactorial. Where episodes are unique and repetition in symptomatology is not observed, the involvement of IgE may be overlooked. Although the majority of anaphylactic reactions triggered by food happen in minutes from the exposure, meat of mammalian animals may not trigger a reaction for a number of hours post ingestion [39]. If the victim is a small child or one with communication problems arising from disease, neither the patient nor carer may realise what has happened. Symptoms may be masked by drugs used for other conditions, such as classical H1 antagonists. If clinicians do not take a full history and examine the patient carefully, anaphylaxis will pass unnoticed, and even where this is undertaken, if urticaria or other dermal signs are not present, the clinician may miss the diagnosis [16, 20].

A cohort study made feasible by the Rochester Epidemiology Project and conducted retrospectively revealed doubling of anaphylactic incidence between the 1980s and 1990s (21 in 100,000 to 49.8 in 100,000) [21]. The peak incidence was situated in those under the age of 19 (70 in 100,000). Comparable results have emerged from other research [22, 23]. Up to their 15th year, boys are more likely to be affected than girls, but this pattern then reverses after age 15. The most common trigger in children, adolescents, and younger adults is food, but in midlife and beyond, drug treatments and insects assume greater significance, alongside unknown causes [17].

Anaphylaxis seldom results in death, it seems [40–44], but this may be an artefact, since missing clinical details, not performing a careful search of the surrounding area where a death has occurred, non-specific post-mortem results, the non-existence of perfectly specific and sensitive diagnostic pathological tests and a tendency to misclassify the condition all probably contribute to a falsely low incidence [19, 20].

A clinical audit in the west of the USA undertaken in a big healthcare provider discovered that 35% of cases labelled anaphylactic shock (ICD9-CM 995.0) as well as 87.3% anaphylactic shock secondary to adverse food reaction (ICD9-CM 995.3) lacked supporting clinical details for anaphylaxis to be confidently diagnosed [45]. If no signs are present, a symptomatic history only (e.g. abdominodynia or pruritus) may not alert the clinician to anaphylaxis. Since there is symptomatic overlap with other conditions, the history needs to be precisely taken to be sure it represents anaphylaxis and not factitious disorder imposed on self or another, or seafood poisoning [20]. In spite of the limitations on the data arising from lack of recognition or confounding with other disorders, it can be demonstrated that there has been a significant rise in anaphylaxis episodes [12, 21, 22, 27, 46–48].

Children who suffer anaphylaxis usually have the reaction triggered by food allergies [49–51]. A study which looked back over 3 years’ worth of children’s Accident and Emergency records in Australia showed three main causes of anaphylaxis: food, medication, and insect venom (56%, 5%, and 5%, respectively), with the remaining cases lacking a documented trigger [30]. The medications most frequently cited as cause to the Allergy Vigilance Network are anti-microbials, especially penicillin-class and β-lactams [26]. Severe anaphylaxis occurring under anaesthesia is still most often attributable to muscle relaxants [52, 53]. Paediatric patients with known allergic problems, spina bifida, or having repeat surgery are especially prone to anaphylaxis triggered by latex [54, 55]. Specific immunotherapy is also known to trigger anaphylaxis [56]. Finally, there are reactions which do not fit into the above schema and are therefore termed idiopathic. The paediatric incidence is unknown [57].

Severe anaphylaxis has an associated mortality of 0.65–2% [6, 58], translating to 1–3 deaths annually per million population. An American review of 32 deaths caused by anaphylaxis triggered by allergy to food [50] found an age range of 2–33 years, acute severe spasm of the bronchi having happened in the majority (96%) of these. Similar figures have emerged from the UK [59]. Of the 32 US deaths, 63% were caused by peanut, whilst other nuts from trees explained a further 31%. The remainder were attributed to dairy products or fish. It is calculated that anaphylaxis triggered by food claims 150 lives every year in the USA [50].

References

1.

Campbell RL, Kelso JM. Anaphylaxis: emergency treatment. In: Walls RM, Randolph AG. Feldweg AM, editors. UpToDate. Last updated: Jun 07, 2016. http://​www.​uptodate.​com/​contents/​anaphylaxis-emergency-treatment. Accessed online at 24 June 2016.

2.

Ring J, Brockow K, Behrendt H. History and classification of anaphylaxis. Novartis Found Symp. 2004;257:6–16; discussion 16–24, 45–50, 276–85.PubMed

3.

Kemp SF, Lockey RF. Anaphylaxis: a review of causes and mechanisms. J Allergy Clin Immunol. 2002;110(3):341–8.PubMed

4.

Simons FE, Anaphylaxis J. Allergy Clin Immunol. 2008;121(2 Suppl):S402–7; quiz S420.

5.

Mustafa SS. Anaphylaxis. In: Kaliner MA, editor. Medscape. http://​emedicine.​medscape.​com/​article/​135065-overview#showall. Accessed online at 24 June 2016.

6.

Ben-Shoshan M, Clarke AE. Anaphylaxis: past, present and future. Allergy. 2011;66:1–14.PubMed

7.

Cianferoni A, Novembre E, Mugnaini L, Lombardi E, Bernardini R, Pucci N, et al. Clinical features of acute anaphylaxis in patients admitted to a university hospital: an 11-year retrospective review (1985-1996). Ann Allergy Asthma Immunol. 2001;87:27–32.PubMed

8.

Wang J, Sampson HA. Food anaphylaxis. Clin Exp Allergy. 2007;37:651–60.PubMed

9.

Megendie F. Lectures on blood. Philadelphia: Aswell, Barrington and Haswell; 1839.

10.

Cohen SG, Mazzullo JC. Discovering anaphylaxis: elucidation of a shocking phenomenon. J Allergy Clin Immunol. 2009;124:866–869. e1.PubMed

11.

May CD. The ancestry of allergy: being an account of the original experimental induction of hypersensitivity recognizing the contribution of Paul Portier. J Allergy Clin Immunol. 1985;75:485–95.PubMed

12.

Boden SR, Burks AW. Anaphylaxis: a history with emphasis on food allergy. Immunol Rev. 2011;242(1):247–57.PubMedPubMedCentral

13.

Sampson HA, et al. Symposium on the definition and management of anaphylaxis: summary report. J Allergy Clin Immunol. 2005;115:584–91.PubMedPubMedCentral

14.

Joint Task Force on Practice Parameters, American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology, and the Joint Council of Allergy, Asthma and Immunology. The diagnosis and management of anaphylaxis. J Allergy Clin Immunol. 1998;101:S465–528.

15.

Sampson HA, Muñoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A, et al. Second symposium on the definition and management of anaphylaxis: summary report—Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol. 2006;117(2):391–7.PubMedPubMedCentral

16.

Tejedor-Alonso MA, Moro-Moro M, Múgica-García MV. Epidemiology of anaphylaxis: contributions from the last 10 years. J Investig Allergol Clin Immunol. 2015;25(3):163–75; quiz follow 174–5. Review.

17.

Lieberman PL. Anaphylaxis. In: Adkinson Jr NF, Bochner BS, Busse WW, Holgate ST, Lemanske Jr RF, Simons FER, editors. Middleton’s allergy: principles and practice. 7th ed. St Louis: Mosby, Inc; 2009. p. 1027–49.

18.

Clark S, Camargo CA Jr. Epidemiology of anaphylaxis. Immunol Allergy Clin N Am. 2007;27(2):145–63.

19.

Clark S, Gaeta TJ, Kamarthi GS, Camargo CA. ICD-9-CM coding of emergency department visits for food and insect sting allergy. Ann Epidemiol. 2006;16(9):696–700. Epub 2006 Mar 3.PubMed

20.

Simons FER, Sampson HA. Anaphylaxis epidemic: fact or fiction? J Allergy Clin Immunol. 2008;122:1166–8.PubMed

21.

Decker WW, Campbell RL, Manivannan V, Luke A, St Sauver JL, Weaver A, et al. The etiology and incidence of anaphylaxis in Rochester, Minnesota: a report from the Rochester Epidemiology Project. J Allergy Clin Immunol. 2008;122(6):1161–5.PubMedPubMedCentral

22.

Lin RY, Anderson AS, Shah SN, Nurruzzaman F. Increasing anaphylaxis hospitalizations in the first 2 decades of life: New York State, 1990-2006. Ann Allergy Asthma Immunol. 2008;101:387–93.PubMed

23.

Sheikh A, Hippisley-Cox J, Newton J, Fenty J. Trends in national incidence, lifetime prevalence and adrenaline prescribing for anaphylaxis in England. J R Soc Med. 2008;101(3):139–43. https://​doi.​org/​10.​1258/​jrsm.​2008.​070306.​CrossrefPubMedPubMedCentral

24.

Muraro A, Roberts G, Clark A, Eigenmann PA, Halken S, Lack G, Moneret-Vautrin A, Niggemann B, Rancé F. EAACI Task Force on Anaphylaxis in Children. The management of anaphylaxis in childhood: position paper of the European Academy of Allergology and Clinical Immunology. Allergy. 2007;62(8):857–71. Epub 2007 Jun 21PubMed

25.

Yocum MW, Butterfield JH, Klein JS, Volcheck GW, Schroeder DR, Silverstein MD. Epidemiology of anaphylaxis in Olmsted Country: a population-based study. J Allergy Clin Immunol. 1999;104:452–6.PubMed

26.

Moneret-Vautrin DA, Morisset M, Flabbee J, Beaudouin E, Kanny G. Epidemiology of life-threatening and lethal anaphylaxis: a review. Allergy. 2005;60:443–51.PubMed

27.

Sheikh A, Alves B. Hospital admissions for acute anaphylaxis: time trend study. BMJ. 2000;320:1441.PubMedPubMedCentral

28.

Gupta R, Sheikh A, Strachan DP, Anderson HR. Time trends in allergic disorders in the UK. Thorax. 2007;62:91–6.PubMedPubMedCentral

29.

Bohlke K, Davis RL, De Stefano F, Mary SM, Braun MM, Thompson RS. Epidemiology of anaphylaxis among children and adolescents enrolled in a health maintenance organization. J Allergy Clin Immunol. 2004;113:536–42.PubMed

30.

Braganza SC, Acworth JP, Mckinnon DR, Peake JE, Brown AF. Paediatric emergency department anaphylaxis: different patterns from adults. Arch Dis Child. 2006;91:159–63.PubMed

31.

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.PubMedPubMedCentral

32.

Clark AT, Ewan PW. Food allergy in childhood. Arch Dis Child. 2004;89:197.PubMedPubMedCentral

33.

Morritt J, Aszkenasy M. The anaphylaxis problem in children: community management in a UK National Health Service district. Public Health. 2000;14:456–9.

34.

Simons F, Peterson S, Black CD. Epinephrine dispensing patterns for an out of-hospital population: a novel approach to studying the epidemiology of anaphylaxis. J Allergy Clin Immunol. 2002;110:647–51.PubMed

35.

Simons FE. Anaphylaxis: recent advances in assessment and treatment. J Allergy Clin Immunol. 2009;124(4):625–36.; ; quiz 637–8. https://​doi.​org/​10.​1016/​j.​jaci.​2009.​08.​025.CrossrefPubMed

36.

Lieberman P, Camargo CA Jr, Bohlke K, Jick H, Miller RL, Sheikh A, Simons FE. Epidemiology of anaphylaxis: findings of the American College of Allergy, Asthma and Immunology Epidemiology of Anaphylaxis Working Group. Ann Allergy Asthma Immunol. 2006;97:596–602.PubMed

37.

Gaeta TJ, Clark S, Pelletier AJ, Camargo CA. National study of US emergency department visits for acute allergic reactions, 1993 to 2004. Ann Allergy Asthma Immunol. 2007;98:360–5.PubMed

38.

Clark S, Long AA, Gaeta TJ, Camargo CA Jr. Multicenter study of emergency department visits for insect sting allergies. J Allergy Clin Immunol. 2005;116:643–9.PubMed

39.

Commins SP, Satinover SM, Hosen J, Mozena J, Borish L, Lewis BD, et al. Delayed anaphylaxis, angioedema, or urticaria after consumption of red meat in patients with IgE antibodies specific for galactose-alpha-1,3-galactose. J Allergy Clin Immunol. 2009;123:426–33.PubMed

40.

Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med. 1992;327(6):380–4.PubMed

41.

Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007;119(4):1016–8. Epub 2007 Feb 15.PubMed

42.

Pumphrey RS, Gowland MH. Further fatal allergic reactions to food in the United Kingdom, 1999-2006. J Allergy Clin Immunol. 2007;119(4):1018–9.. Epub 2007 Mar 8.PubMed

43.

Greenberger PA, Rotskoff BD, Lifschultz B. Fatal anaphylaxis: postmortem findings and associated comorbid diseases. Ann Allergy Asthma Immunol. 2007;98(3):252–7.PubMed

44.

Liew WK, Williamson E, Tang ML. Anaphylaxis fatalities and admissions in Australia. J Allergy Clin Immunol. 2009;123(2):434–42. https://​doi.​org/​10.​1016/​j.​jaci.​2008.​10.​049. Epub 2008 Dec 30.CrossrefPubMed

45.

Bohlke K, Davis RL, DeStefano F, Marcy SM, Braun MM, Thompson RS, et al. Epidemiology of anaphylaxis among children and adolescents enrolled in a health maintenance organization. J Allergy Clin Immunol. 2004;113(3):536–42.PubMed

46.

Gupta R, et al. Time trends in allergic disorders in the UK. Thorax. 2007;62:91–6.PubMedPubMedCentral

47.

Poulos LM, Waters AM, Correll PK, Loblay RH, Marks GB. Trends in hospitalizations for anaphylaxis, angioedema, and urticaria in Australia, 1993–1994 to 2004–2005. J Allergy Clin Immunol. 2007;120(4):878–84.PubMed

48.

Simon MR, Mulla BD. A population-based epidemiologic analysis of deaths from anaphylaxis in Florida. Allergy. 2008;63:1077–83.PubMed

49.

Novembre E, Cianferoni A, Bernardini R, Mugnaini L, Caffarelli C, Cavagni G, et al. Anaphylaxis in children: clinical and allergologic features. Pediatrics. 1998;101:8–16.

50.

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

51.

Mehl A, Wahn U, Niggemann B. Anaphylactic reactions in children—a questionnaire based survey in Germany. Allergy. 2005;60:1440–5.PubMed

52.

Mertes PM, Laxenaire MC. Adverse reactions to neuromuscular blocking agents. Curr Allergy Asthma Rep. 2004;4:7–16.PubMed

53.

Karila C, Brunet-Langot D, Labbez F, Jacqmarcq O, Ponvert C, Paupe J, et al. Anaphylaxis during anesthesia: results of a 12-year survey at a French pediatric center. Allergy. 2005;60:828–34.PubMed

54.

Beaudouin E, Prestat F, Schmitt M, Kanny G, Laxenaire MC, Moneret-Vautrin DA. High risk of sensitization to latex in children with spina bifida. Eur J Pediatr Surg. 1994;4:90–3.PubMed

55.

Tucke J, Posch A, Baur X, Rieger C, Rauf-Heimsoth M. Latex type I sensitization and allergy in children with atopic dermatitis evaluation of crossreactivity to some foods. Pediatr Allergy Immunol. 1999;10:160–7.PubMed

56.

Berstein DI, Wanner M, Borish L, Immunotherapy Committee, American Academy of Allergy, Asthma and Immunology. Twelve-year survey of fatal reactions to allergen injections and skin testing: 1990–2001. J Allergy Clin Immunol. 2004;113:1129–36.

57.

Lenchner K. Idiopathic anaphylaxis. Curr Opin Allergy Clin Immunol. 2003;3:305–11.PubMed

58.

Brown A, Mckinnon D, Chu K. Emergency department anaphylaxis: a review of 142 patients in a single year. J Allergy Clin Immunol. 2001;108:861–6.PubMed

59.

Pumphrey RS. Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy. 2000;30(3):1144–50.PubMedPubMedCentral

© Springer Nature Switzerland AG 2020

C. Cingi, N. Bayar MulukQuick Guide to Anaphylaxishttps://doi.org/10.1007/978-3-030-33639-4_2

2. The Aetiology of Anaphylaxis

Cemal Cingi¹  and Nuray Bayar Muluk²

(1)

ENT Department, Faculty of Medicine, Eskişehir Osmangazi University, Eskisehir, Turkey

(2)

ENT Department, Faculty of Medicine, Kırıkkale University, Kırıkkale, Turkey

2.1 Food Allergy

2.1.1 Background

Allergy to food is a harmful reaction, involving immune mechanisms, to a foodstuff. On occasion, the harmful reaction may occur very quickly after the offending food has been swallowed, such