INTRODUCTION — Food allergy affects approximately up to 8 percent of children and 10.8 percent of adults in the United States [1-3]. Anaphylaxis is "a serious allergic reaction that is rapid in onset and may cause death," a definition developed by a consensus of international experts [4].
This topic will review unique features of anaphylaxis caused by food, the characteristics of patients at risk for such reactions, and the foods that most often induce anaphylaxis. Differences between food-induced anaphylaxis in children and adults and important issues in the diagnosis and management of this disorder are also discussed.
Aspects of anaphylaxis that are not unique to food-induced reactions, such as diagnosis, acute treatment, and pathophysiology, are presented elsewhere. (See "Anaphylaxis: Emergency treatment" and "Pathophysiology of anaphylaxis" and "Anaphylaxis: Confirming the diagnosis and determining the cause(s)".)
A detailed discussion of the use of skin testing and in vitro testing to diagnose food allergy is found separately. (See "Diagnostic evaluation of IgE-mediated food allergy".)
TYPES OF FOOD-INDUCED ANAPHYLAXIS — Food-induced anaphylaxis refers to a serious allergic reaction following the ingestion of a food, which is generally rapid in onset and may progress to death.
IgE-mediated anaphylaxis — The most common form of food-induced anaphylaxis is that caused by the ingestion of a food to which the patient has immunoglobulin E (IgE) mediated allergy. Symptoms typically appear within a few seconds to two hours after food ingestion and are believed to arise from massive mediator release from mast cells and basophils. (See 'Signs and symptoms' below.)
IgE-mediated, food-induced anaphylaxis accounts for the vast majority of reactions in older children and adults. The remainder of this topic review refers to IgE-mediated reactions, except where specifically noted.
Anaphylaxis caused by food exposures other than ingestion, such as physical contact between food and skin or inhalation of aerosolized food proteins, has not been convincingly demonstrated. Inhalation of steam/vapors from cooking food (eg, fish and shellfish) rarely induces anaphylactic reactions. Intimate oral contact with others who have been eating the culprit food is a rare cause of food-allergic reactions. These and other issues in food allergen avoidance are reviewed in detail separately. (See "Management of food allergy: Avoidance".)
Food-dependent, exercise-induced anaphylaxis — A variant of food-induced anaphylaxis is food-dependent, exercise-induced anaphylaxis (FDEIA), which refers to an IgE-mediated, food-induced anaphylactic reaction that develops only when exercise is undertaken within a few hours of ingesting a food [5-7]. If the food is consumed without subsequent exercise or if exercise is performed without associated ingestion of the food, the patient does not develop allergic symptoms [5,6].
In most patients, FDEIA only develops if a certain food, such as wheat, seafood, or nuts, is eaten in association with exercise/exertion [5-7]. (See "Exercise-induced anaphylaxis: Management and prognosis".)
Hypotensive reactions in infants with enterocolitis — Infants with food protein-induced enterocolitis, a form of non-IgE-mediated food allergy, often present with chronic illness, characterized by diarrhea, vomiting, and failure to thrive [8]. These symptoms improve once the culprit food is identified and removed from the diet. Reintroduction of the food, however, may precipitate acute vomiting beginning approximately two hours after ingestion, sometimes accompanied by diarrhea, lethargy, hypotension or shock, and acidosis. There may be an associated peripheral blood leukocytosis and thrombocytosis, which typically peaks within a few hours of allergen ingestion. Therapy involves fluid resuscitation and supportive care.
Food protein-induced enterocolitis is reviewed in more detail elsewhere. (See "Food protein-induced allergic proctocolitis of infancy".)
PREVALENCE — Food is the most common trigger for anaphylaxis resulting in admission to hospitals, although it is not the most common cause of anaphylaxis-related fatalities [9]. Rates of emergency department visits and hospitalizations for food-induced anaphylaxis have been increasing in developed countries, particularly within the pediatric population [10-12]. Obtaining absolute figures on the prevalence of food-induced anaphylaxis is difficult, however, because there have been no universally accepted diagnostic criteria, presenting symptoms are frequently misdiagnosed, and there are no central reporting agencies in most countries [4,13]. The following represents estimates based on limited data:
●Episodes of anaphylaxis (from all causes) occur 50 to 2000 times per 100,000 persons, for a lifetime prevalence of 0.05 to 2 percent [14].
●A systematic review and meta-analysis from North America, Europe, and Australia estimated the incidence of fatal food anaphylaxis in a food-allergic individual as 1.81 (95% CI 0.94-3.45) per million person-years, equivalent to approximately 25 deaths per year in the United States [15].
●A systematic review and meta-analysis noted that, among food-allergic people, hospital admission for food anaphylaxis had an incidence rate of 9 per 100,000 person-years (for ages zero to four years it was 50 per 100,000 person-years) [16].
●Utilizing the National Electronic Injury Surveillance System, it was estimated that food allergy accounted for approximately 125,000 emergency department visits per year and 3100 hospitalizations in the United States [10].
●The United States Centers for Disease Control and Prevention estimated that there was a 3.5-fold increase in hospital discharges among children less than 18 years of age with any diagnosis related to food allergy between 1998 and 2006 [17].
CAUSATIVE FOODS — Any food can cause anaphylaxis in a susceptible individual, although in the United States and Germany [18] peanuts and tree nuts (walnuts, pecans, pistachios, cashews, and others) are responsible for the majority of severe anaphylactic reactions, followed by shellfish (crustaceans and mollusks) and fish. In other parts of the world, foods that are prominent in the regional diet are leading culprits, including sesame in Israel and seafood in China [19,20].
Additional observations include the following:
●Cow's milk, hen's egg, and sesame are more frequent culprits in children [21-23].
●Fatal food-induced anaphylactic reactions are most commonly induced by peanuts, tree nuts, seafood, and cow's milk, based upon a few small series [21,24,25]. (See "Fatal anaphylaxis".)
●Wheat sensitivity is one of the most common causes in food-dependent, exercise-induced anaphylaxis (FDEIA), although shellfish, celery, other cereal grains, and a variety of foods have been implicated [5-7].
●Certain mammalian meats (specifically beef, lamb, and pork that contain galactose-alpha-1,3-galactose) can cause anaphylaxis that is delayed in onset by several hours, sometimes waking patients in the middle of the night. Although meat is not a common cause of food-induced anaphylaxis, awareness of its unique presentation is critical to identifying the responsible food [26]. (See "Allergy to meats", section on 'Clinical reactions'.)
RISK FACTORS — Anyone with IgE-mediated food allergy may develop food-induced anaphylaxis, although most food-allergic individuals will experience lesser reactions without ever developing anaphylaxis. In a comprehensive review regarding risk factors for severe reactions to foods [27], the following were identified (with low certainty of evidence) as drivers of increased risk:
●Poorly controlled asthma
●Inappropriate or delayed treatment
●Cofactors including exercise
●Medications (beta blockers or angiotensin-converting enzyme [ACE] inhibitors)
●Specific food allergy phenotypes (persistent cow's milk allergy, monosensitization to lipid transfer proteins)
Factors that were not identified as drivers or predictors of severe reactions included having any asthma severity (if not poorly controlled), level of IgE sensitization, or history of past reaction severity (alone).
PATHOPHYSIOLOGY — Food-induced anaphylactic reactions occur when sufficient amounts of food allergen cross the oral or gastrointestinal mucosal barrier (or the respiratory mucosal barrier in rare cases of inhalation of steam or particulates containing food allergen proteins) in a susceptible individual. Once food allergen has traversed a mucosal barrier, it circulates throughout the body and cross-links food allergen-specific IgE antibodies bound to circulating basophils and tissue mast cells in the skin, gastrointestinal tract, respiratory tract, and/or the cardiovascular system [28]. Activation of these cells results in their release of a variety of proinflammatory mediators. The pathophysiology of anaphylaxis is reviewed in greater detail separately. (See "Pathophysiology of anaphylaxis".)
CLINICAL FEATURES
Time course — Anaphylaxis from food or other triggers usually progresses in a rapid and uniphasic manner, although a subset of individuals experience biphasic reactions or protracted reactions. In a United States registry of 5149 individuals with peanut or tree nut allergy, the median time of symptom onset postexposure was three minutes [29]. In a European anaphylaxis registry [30] of 793 food-allergic reactions, onset of symptoms following ingestion was approximately 50 percent at <10 minutes, 23 percent at 10 to 30 minutes, 14 percent at 30 to 60 minutes, 8 percent at 1 to 2 hours, and 5 percent over 2 hours.
Biphasic anaphylaxis — Biphasic anaphylaxis is defined as a recurrence of symptoms that develop following the apparent resolution of the initial anaphylactic event. Biphasic reactions have been reported to develop in up to 5 percent of anaphylactic reactions and typically occur within one to four hours following the resolution of the initial symptoms, although some cases have been reported up to 78 hours later. (See "Biphasic and protracted anaphylaxis", section on 'Biphasic reactions'.)
Protracted anaphylaxis — Protracted anaphylaxis is defined as an anaphylactic reaction that lasts for hours or even days in extreme cases. (See "Biphasic and protracted anaphylaxis", section on 'Protracted reactions'.)
Signs and symptoms — Food-induced anaphylactic reactions provoke signs and symptoms similar to anaphylactic reactions induced by other causes, although gastrointestinal symptoms tend to be more prominent (table 1).
Gastrointestinal manifestations may include the following:
●Nausea
●Abdominal pain or colic
●Vomiting (large amounts of "stringy" mucus)
●Diarrhea
Other signs and symptoms, in order from mild to severe, include pruritus, flushing, urticaria/angioedema, periorbital edema, conjunctival injection, rhinorrhea, nasal congestion, cough, wheezing, dyspnea, change of voice quality, sense of choking, tachycardia (or bradycardia less commonly), dizziness, hypotension, sense of impending doom, and cardiovascular collapse. (See "Anaphylaxis: Emergency treatment".)
Evolution of symptoms during reactions — The symptoms that present when a patient is first seen may be quite variable and not immediately suggestive of an anaphylactic reaction. In most cases, however, a careful history and attention to the evolution of symptoms should enable the clinician to make the correct diagnosis.
As an example, a six-year-old boy with a history of asthma presents with wheezing and cough since arriving home from school, although his mother states that he was well that morning, and she received no calls from his teacher during the day. He then begins to vomit while receiving nebulized albuterol. He has never had any problems with albuterol in the past. On closer examination, the boy is flushed and has scattered urticaria on his neck and in his axillae. Further questioning reveals that he shared a candy bar during the bus ride home. The mother then recalls a previous "asthma attack" a few months earlier after he had eaten trail mix, although she did not make a connection between the two events at the time. The evolution of this patient's symptoms should alert the clinician to the correct diagnosis of anaphylaxis, possibly triggered by peanuts or tree nuts.
The symptoms and temporality of symptoms in anaphylaxis can vary in an individual from time to time, although a study of patients having experienced two or more anaphylactic reactions found that individual patients were likely to experience reproducibly stereotypic patterns in their anaphylactic reactions over time [31].
Differences between children and adults — In infants and young children experiencing food-allergic reactions, gastrointestinal and cutaneous symptoms tend to be most prominent, and shock is less common than in adults.
The frequency of presenting symptoms in anaphylaxis differs somewhat between children and adults, with children manifesting cardiovascular symptoms less often and respiratory symptoms more often than their adult counterparts [18,32,33]. In infants <2 years, cutaneous and gastrointestinal symptoms are most common [23,34], and, in young children, cutaneous, gastrointestinal, and respiratory symptoms were most prominent. In these series, fatal anaphylaxis was primarily due to respiratory compromise in children, in contrast to cardiovascular complications in adults.
Factors affecting presentation — In most cases, it is unclear why a specific food-allergic individual may ingest a food allergen on a number of occasions and experience only mild symptoms, whereas on another occasion, a life-threatening reaction develops.
There are several factors specific to particular incidents, however, which are believed to impact the onset and severity of symptoms, such as the nature of the food or concomitant augmentation or cofactors that exacerbate allergic reactions [5,21,35-38]:
●The quantity of food allergen ingested. The larger the dose, the more rapid and pronounced the onset of symptoms.
●The composition of the food containing the allergen. Fatty foods tend to be absorbed more slowly, delaying the onset of or prolonging symptoms.
●The concomitant ingestion of alcohol, which leads to more rapid and pronounced symptoms.
●The concomitant administration of nonsteroidal antiinflammatory drugs, which may increase gastric permeability to food allergens.
●Sleep deprivation.
●Illness (eg, viral).
●Accidental ingestion. In one series, 87 percent of patients were aware of their food allergy but ingested the food unknowingly [21].
FATAL REACTIONS — Less than 1 percent of anaphylaxis cases (from all causes) prove fatal. A more general discussion of fatal anaphylaxis from all causes is found separately. (See "Fatal anaphylaxis".)
Epidemiology — In a systematic review, the incidence of fatal food-induced anaphylaxis among food-allergic people was estimated to be between 1.4 to 2.7 per million person-years and 3.25 per million person-years in those 0 to 19 years of age [15]. While such studies have limitations, these findings suggest that the incidence of fatal food anaphylaxis in food-allergic people is lower than the incidence of accidental death in the general population [25]. These reactions are most common in adolescents and young adults, although patients of all ages may succumb [21,39]. Possible contributing factors among young people include increasing independence in decision-making, risk-taking behaviors, susceptibility to peer pressure, and ingesting risky foods at social and sporting events [40]. In an internet-based anonymous survey of 176 adolescents and young adults with food allergy, more than one-half reported purposefully ingesting a potentially unsafe food [40]. In addition, 17 percent both ate foods that "may contain" allergens and did not consistently carry epinephrine autoinjectors.
Features of fatal food reactions — Most individuals dying from a food-allergic reaction had experienced previous reactions, although these reactions were rarely severe, illustrating the important concept that the severity of previous reactions cannot be relied upon to predict the severity of future reactions [21,24,39].
Fatal food-induced anaphylaxis typically progresses rapidly, with symptoms appearing a median of 25 to 35 minutes following ingestion of the allergen and death ensuing in less than one hour [21,24,39]. Cutaneous signs and symptoms were less common in fatal food-induced anaphylaxis compared with reactions in which patients survived [39]. The reasons for this phenomenon are not known, although it may reflect the rapid development of hypotension in the fatal reactions such that there was not enough time or intravascular pressure for the allergen to reach mast cells in peripheral tissues.
Three reviews of food-induced fatal anaphylaxis comprising a total of 111 deaths indicated that 76 percent occurred outside of the victim's home [21,24,41].
Delayed administration of epinephrine — Epinephrine should be administered as soon as possible in the setting of anaphylaxis. Delayed administration of epinephrine is believed to be a contributing factor in some fatal reactions [21,24,35,39]. In a study of 13 fatal or near-fatal food-induced anaphylactic reactions in children, six of the seven children who survived received epinephrine within 30 minutes of ingesting the allergen, whereas only two of the six children who died received epinephrine within the first hour [39].
ISSUES IN DIAGNOSIS — The diagnosis of food-induced anaphylaxis is made clinically, based upon a detailed history of clinical events, including the consumption of any food or drink prior to the episode, associated exertion or exercise, progression of clinical signs and symptoms, and response to treatment.
Application of diagnostic criteria to food-induced anaphylaxis — Anaphylaxis is often misdiagnosed and underreported [4]. Diagnosis has been hampered by a lack of agreement on the exact criteria that constitute anaphylaxis. To address this problem, the National Institutes of Health and the Food Allergy and Anaphylaxis Network convened two symposia of international experts who proposed a definition and a set of three criteria for diagnosing anaphylaxis (table 2) [4]. These criteria reflect the fact that the pattern of target organ involvement in anaphylaxis is quite variable. These criteria have been validated in a prospective study [42].
The first criterion requires the presence of cutaneous signs or symptoms, in combination with respiratory symptoms, cardiovascular symptoms (or associated end-organ dysfunction due to low blood pressure), or both (table 2). Cutaneous involvement is present in the vast majority of anaphylactic reactions, and the first criterion, therefore, will be used most frequently. However, up to 20 percent of cases lack skin symptoms.
The second criterion incorporates less obvious symptoms, although it is applied to patients with known food allergy. This criterion requires signs/symptoms in two or more of the following categories: cutaneous, respiratory, cardiovascular/hemodynamic, or gastrointestinal (table 2).
The third criterion is intended to capture uncommon episodes of food-induced anaphylaxis that consist of isolated cardiovascular symptoms. This criterion applies to individuals with known exposure to a food allergen (table 2). Uncommon cases of food-induced anaphylaxis presenting as isolated hypotension have been reported in adults [43]. Isolated cardiovascular symptoms are rare in children, although hypotension may lead to nausea, vomiting, dyspnea, diaphoresis, hypoxia, dizziness, syncope, and seizures.
Laboratory tests — There are no reliable laboratory markers of anaphylaxis. Plasma histamine levels may be fleetingly elevated, returning to normal within one hour in most cases. Elevations in serum tryptase, which are sometimes detectable in anaphylaxis caused by non-food triggers, are usually normal in food-allergic reactions for unclear reasons [44,45]. However, one study in adults with peanut allergy, which evaluated the rise in tryptase against baseline, found an increase in 63 percent of 160 reactions, with a median 71 percent rise in those with anaphylaxis [46]. Therefore, the absence of an elevated plasma histamine or serum tryptase level never excludes the diagnosis of anaphylaxis but may support it. The use of laboratory studies to support the clinical diagnosis of anaphylaxis is reviewed in detail elsewhere. (See "Laboratory tests to support the clinical diagnosis of anaphylaxis".)
Differential diagnosis — Examples of commonly encountered conditions that may mimic food-induced anaphylaxis in the emergency setting include the following [47]:
●Acute exacerbation of asthma
●Foreign body aspiration (especially in the pediatric population)
●Myocardial infarction
●Acute urticaria
●Vocal cord dysfunction
●Scombroid poisoning
●Vasovagal response
●Panic attack
Each of these alternative diagnoses is reviewed in detail elsewhere. (See "Differential diagnosis of anaphylaxis in adults and children".)
ISSUES IN PREVENTION AND LONG-TERM MANAGEMENT — Prevention and long-term management of food-induced anaphylaxis involve accurate identification of the culprit food trigger, education in food allergen avoidance, and preparation for recurrent episodes [48].
All patients who have experienced anaphylaxis should be supplied with epinephrine autoinjectors and trained in self-administration for treatment of a possible recurrence. Referral to an allergy specialist who is experienced in the diagnosis and management of food-allergic disorders is strongly recommended [28,49]. (See "Anaphylaxis: Confirming the diagnosis and determining the cause(s)".)
Verification of the culprit allergen — It is absolutely essential that patients with food-induced anaphylaxis receive an in-depth evaluation to identify and verify the culprit food allergen. Defining the patient's food allergies with certainty allows for the following:
●Effective avoidance without undue dietary restrictions
●Improved patient compliance with avoidance recommendations
●Reduction of patient/caregiver anxiety associated with an unidentified trigger
Definitive diagnosis of food allergy is often not straightforward. It usually requires skin testing and/or in vitro testing, sometimes followed by supervised food challenges to ensure that the correct food has been implicated. The techniques utilized in the diagnosis of food allergy are reviewed separately. (See "History and physical examination in the patient with possible food allergy" and "Diagnostic evaluation of IgE-mediated food allergy".)
Allergen avoidance education — The clinician must assist the patient and/or caregiver in food allergen avoidance once the trigger has been identified with certainty. Strict food avoidance is extremely difficult, which is reflected in the fact that most patients experiencing food-induced anaphylaxis have known food allergy but were unable to avoid exposure.
Effective avoidance requires ongoing education, meticulous attention to food labeling, and avoidance of situations where foods are frequently cross-contaminated (eg, buffets), minor allergenic ingredients are often present (eg, Asian cuisine restaurants), or where food allergens may become aerosolized (eg, seafood restaurants). These and other issues concerning food allergen avoidance are presented in detail elsewhere. (See "Management of food allergy: Avoidance".)
Issues surrounding the safety of children with food allergies in schools and camps, including specific forms for use in those settings, are reviewed separately. (See "Food allergy in schools and camps".)
Preparation for recurrent reactions — Recurrent episodes of food-induced anaphylaxis are common despite patients' best efforts at avoidance [50]. The patient/caregiver must learn to recognize the earliest signs and symptoms of a pending anaphylactic reaction and initiate emergency medical management without delay.
Patients should be provided with a written anaphylaxis emergency action plan that specifies clearly what should be done if a food-allergic reaction develops again. Action plan forms are available in English and Spanish from Food Allergy Research and Education (Food Allergy & Anaphylaxis Emergency Care Plan) and the American Academy of Pediatrics (Allergy and Anaphylaxis Emergency Plan English and Spanish). These plans are appropriate for patients with anaphylaxis from any cause.
A form specifically designed for children is also available (form 1). This should include individualized advice about when to self-administer epinephrine based upon the characteristics of past reactions.
Epinephrine — Epinephrine is the primary treatment of anaphylaxis, and first aid management of food-induced anaphylaxis in the community requires prompt administration [51]. All patients who have experienced food-induced anaphylaxis or are at increased risk should have access to self-injectable epinephrine at all times [48]. Epinephrine should be administered immediately in patients meeting any of the three criteria that define anaphylaxis (table 2).
Immediate epinephrine self-administration in the setting of a food-induced allergic reaction is recommended for patients experiencing the following symptoms:
●Respiratory symptoms – Difficulty breathing, chest tightness, wheezing, repetitive dry cough
●Signs/symptoms of laryngeal edema – Sensation of throat swelling, change of voice quality (eg, hoarseness)
●Sign/symptoms of low blood pressure – Dizziness, lightheadedness, or presyncope
In addition, children should be treated if they display the following during a food-allergic reaction:
●Lethargy or change in mental status
●Vomiting repeatedly shortly after eating, especially if these symptoms are accompanied by flushing or hives
Areas of uncertainty — There are circumstances, however, in which the optimal advice regarding epinephrine self-administration for first-aid management is not known [52-54]. In such cases, decisions may depend upon the capabilities of the caregiver/patient to identify symptoms, clinical judgment, and knowledge of the patient's past reactions. The author's approach, based upon clinical experience, is described below [52]:
●If a patient experienced severe food-induced anaphylaxis in the past and has a known ingestion of the trigger food, we suggest self-administration of epinephrine at the first sign of symptoms, regardless of the severity of those symptoms.
●We educate patients about the severe symptoms, like those mentioned above, where epinephrine should be administered. We also find that it may be simpler to instruct patients that they should administer epinephrine if they are experiencing more than mild symptoms (mild symptoms being itchy nose, sneezing, itchy mouth, a few hives, mild stomach nausea/discomfort). We also emphasize "if in doubt, give epinephrine." These instructions match those on the pediatric allergy and anaphylaxis action plan [52].
Patients with severe symptoms of anaphylaxis should be transported immediately to an emergency facility, preferably by ambulance, for observation and management since approximately 5 percent of reactions will result in a recurrence of symptoms (biphasic anaphylaxis), which may be more refractory to standard therapy [55]. (See 'Time course' above.)
Medical identification — Patients at risk for food-induced anaphylaxis should consider having some form of emergency medical identification stating that they are food allergic (eg, Medic Alert bracelet or other identification jewelry). There are also smart phone apps that can be set to allow first responders to access emergency health information.
EXTERNAL RESOURCES — Additional information is available through Food Allergy Research and Education, which provides helpful manuals, videos, and informational brochures for patients, including age-appropriate materials for children.
Other external sources of accurate patient information include the American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Anaphylaxis".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Anaphylaxis (The Basics)" and "Patient education: How to use an epinephrine autoinjector (The Basics)")
●Beyond the Basics topics (see "Patient education: Anaphylaxis symptoms and diagnosis (Beyond the Basics)" and "Patient education: Anaphylaxis treatment and prevention of recurrences (Beyond the Basics)" and "Patient education: Using an epinephrine autoinjector (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Types of food-induced anaphylaxis – Food can trigger anaphylaxis in an individual with immunoglobulin E (IgE) mediated allergy following ingestion or when food ingestion is also associated with exertion (food-dependent, exercise-induced anaphylaxis [FDEIA]). Food protein-induced enterocolitis, a type of non-IgE-mediated allergy, can cause hypotensive reactions in infants and young children. (See 'Types of food-induced anaphylaxis' above.)
●Prevalence – Food allergy is the leading cause of anaphylaxis outside of the hospital in children and young adults in developed countries, although patients of any age may be affected. Rates of emergency department visits and hospitalizations for food-induced anaphylaxis have been increasing in resource-rich countries. (See 'Prevalence' above.)
●Common triggers – Foods that commonly cause IgE-mediated anaphylaxis include peanuts, tree nuts, hen's egg, cow's milk, crustacean shellfish, fish, and sesame, although any food can cause anaphylaxis in a susceptible individual. (See 'Causative foods' above.)
●Risk factors – Risk factors for food-induced anaphylaxis include poorly controlled asthma, allergies to certain high-risk foods (peanuts, tree nuts, seafood, and sesame), and extreme sensitivity. The severity of previous reactions does not predict the severity of future reactions. (See 'Risk factors' above.)
●Fatal reactions – Fatal food-induced anaphylaxis disproportionately affects adolescents and young adults for reasons that may be largely related to risk-taking behaviors. Deaths most often occur in individuals who have had only mild previous reactions. Delayed administration of epinephrine appears to be an important and potentially correctable risk factor. (See 'Fatal reactions' above.)
●Signs and symptoms – Food-induced anaphylactic reactions provoke signs and symptoms similar to anaphylactic reactions caused by non-food allergens, although gastrointestinal symptoms tend to be more prominent (table 1). (See 'Clinical features' above.)
●Diagnosis – Food-induced anaphylaxis is diagnosed clinically, based upon a detailed history of antecedent events and characteristic signs and symptoms. A panel of experts from different specialties has established clinical criteria for the diagnosis of anaphylaxis, which define three distinct presentations (table 2) [4]. (See 'Issues in diagnosis' above.)
●Epinephrine autoinjectors and allergy referral – All patients who have experienced anaphylaxis should be supplied with injectable epinephrine and trained in self-administration for treatment of a possible recurrence. Referral to an allergy specialist who is experienced in the diagnosis and management of food-allergic disorders should be arranged. (See 'Issues in prevention and long-term management' above.)
●Long-term management – Prevention and long-term management of food-induced anaphylaxis involve accurate identification of the culprit food trigger, education in allergen avoidance, and preparation for recurrent episodes (which are common). (See 'Issues in prevention and long-term management' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Hugh A Sampson, MD, who contributed to an earlier version of this topic review.
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