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Quandaries in prescribing an emergency action plan and self-injectable epinephrine for first-aid management of anaphylaxis in the community.

Anaphylaxis often occurs in the community in the absence of a health care professional. Prompt administration of self-injectable epinephrine as first-aid treatment in the context of a personalized emergency action plan is the key to survival. There is little argument that physicians should prescribe self-injectable epinephrine for individuals who have already experienced anaphylaxis involving respiratory distress or shock triggered by allergens that might be encountered in the community. A quandary faced by physicians is that additional individuals with identified allergy who have no recognized prior history of anaphylaxis or who have a history of mild symptoms after exposure to a known trigger might also be at risk for subsequent life-threatening anaphylaxis and might also warrant prescription of self-injectable epinephrine. Prescribing for the latter individuals requires considerable clinical judgment and has led to controversy regarding possible overprescription or underprescription of self-injectable epinephrine. A second quandary for physicians occurs with regard to the advice they should give to at-risk individuals about actual use of their self-injectable epinephrine. It is difficult for health care professionals, let alone persons with no health care training, to predict whether anaphylaxis symptoms will occur in an at-risk individual after exposure to a known trigger. Moreover, at the onset of an acute allergic reaction, it is difficult to predict the symptoms that will ultimately develop. We examine these 2 common quandaries and provide examples of clinical scenarios and potential pitfalls in the management of persons identified as being at risk for anaphylaxis in the community. Additional studies of the recognition and treatment of anaphylaxis in the community are needed to develop comprehensive, evidence-based recommendations for its management in this setting.

Anaphylaxis↗

Level of exhaled nitric oxide during human anaphylaxis.

BACKGROUND: Nitric oxide (NO) seems to play an important pathophysiologic role in modulating the systemic changes associated with anaphylaxis. Even if some effects of NO may be protective, animal models of anaphylaxis have shown that the summation effects of NO are deleterious, resulting in hypotension and loss of intravascular volume. There are no studies of NO production during anaphylaxis in humans. OBJECTIVE: To measure the level of exhaled NO during anaphylaxis induced by bee venom cluster immunotherapy in a 34-year-old beekeeper. METHODS: Exhaled NO was measured using a chemiluminescence analyzer at different flow rates, and alveolar NO concentration and airway NO production were calculated. RESULTS: We measured a high level of exhaled NO (78 ppb at 50 mL/s, with increased alveolar concentration and airway production) during anaphylaxis induced by bee venom immunotherapy in this patient. Normal values of exhaled NO were measured in the same patient 1 week later before and after a modified regimen of desensitization. CONCLUSIONS: Nitric oxide production was increased in the respiratory tract during anaphylaxis. Having excluded all the common causes of increased exhaled NO levels, these resultssupport the hypothesis that NO plays an important role in anaphylaxis.

Adult↗

Anaphylaxis: a review of 601 cases.

BACKGROUND: The allergist usually sees patients with anaphylaxis after the event for the purposes of identifying the cause, establishing a prognosis, and preventing further episodes. Knowledge of the characteristics of such patients is essential to achieve these goals. OBJECTIVE: To examine the natural history, clinical manifestations, and factors that affect the patients' adherence to suggested treatment and preventive strategies of anaphylaxis. METHODS: A retrospective medical record review spanning 25 years (1978-2003) and follow-up questionnaires were used to obtain data on 601 patients who presented with anaphylaxis of unknown origin to a private university-affiliated allergy-immunology practice. RESULTS: Patients ranged in age from 1 to 79 years, with a mean age of 37 years. Females comprised 62% of cases. Causes of anaphylaxis were elucidated in 41% of cases. Known causes included foods in 131 patients (22%), medications in 69 cases (11%), and exercise in 31 cases (5%). Two hundred twenty-three patients (37%) were found to be atopic by history confirmed with skin prick testing. The most common manifestation was urticaria and/or angioedema, reported in 87% of patients. Systemic mastocytosis was found in 3 patients. Episodes tended to decline in frequency with time. Adherence to instructions to carry epinephrine can be improved with more effective teaching. CONCLUSIONS: In most cases, the cause of anaphylaxis is undetermined. Women are affected more commonly than men. Systemic mastocytosis should be considered in cases of idiopathic anaphylaxis, and patients with a history of atopy are at an increased risk of developing anaphylaxis. Patients are more reliably carrying epinephrine as a result of changes in physician instructions. Finally, anaphylactic episodes tend to decrease in frequency and severity with time.

Adolescent↗

Anaphylaxis: a 7-year follow-up survey of 46 children.

BACKGROUND: Little is known about the frequency of and the features associated with recurrent anaphylaxis in pediatric populations. During 1994 to 1996, we enrolled 76 children affected by anaphylaxis in a prospective study to analyze their clinical and allergic features. OBJECTIVE: To undertake a follow-up study of these children to ascertain how many experienced a recurrence of anaphylaxis. METHODS: After a mean interval of 7 years, a pediatric allergist conducted a telephone interview of patients who had been enrolled in our 1994-1996 study. RESULTS: A telephone interview was successfully completed in 46 (61%) of the 76 patients who had been enrolled in our 1994-1996 study. Of these 46 patients, 14 (30%) had experienced a recurrence of anaphylaxis. Children with atopic dermatitis either during 1994 to 1996 (64% vs 34%; P = .04) or at the time of the current study (43% vs 16%; P = .03) and those with urticaria-angioedema at the time of the current study (93% vs 31%; P = .0002) were found to be at a significantly higher risk for recurrent anaphylaxis. Furthermore, those children who were sensitive to at least 1 food allergen during 1994 to 1996 were more likely to have experienced a recurrence of anaphylaxis (93% vs 56%; P < .04). CONCLUSIONS: This study suggests that patients may have a greater risk of recurrence of anaphylaxis if they have atopic dermatitis, urticaria-angioedema, or at least 1 positive result of skin prick tests to food allergens.

Adolescent↗

Idiopathic anaphylaxis: a descriptive study of 81 patients in Spain.

BACKGROUND: Few European groups have published data on series of patients with idiopathic anaphylaxis. OBJECTIVE: Our aim was to report on our experience with this entity in Spain. METHODS: We conducted a two-part investigation. The first part was a descriptive cross-sectional study of 81 patients with idiopathic anaphylaxis, diagnosed between January 1990 and December 1995 in the allergy unit of the General Hospital of Albacete in Albacete, Spain. The second prong was a prospective, longitudinal study that evaluated the activity of the condition. RESULTS: Female patients constituted 68% of the study group with idiopathic anaphylaxis; the mean age of the 81 patients was 30.0 +/- 17.3 years. The number of episodes of idiopathic anaphylaxis during the year of greatest frequency varied widely (median, 2; range, 1 to 130). The duration also varied considerably, with a range of 0.03 to 300 months (median, 2 years). Most patients entered the study in remission, and 93% of these patients remained in remission throughout the followup period. Only 9% of the patients had vascular involvement. Our series of patients with idiopathic anaphylaxis had a notable prevalence of atopic diseases (48%), food allergy (20%), and episodes of anaphylaxis with an identifiable cause (15%). In addition, a high frequency (58%) of idiopathic urticaria was noted; the urticaria was acute in 62% of the affected patients. CONCLUSIONS: Our series of patients with idiopathic anaphylaxis is similar to previously published series.

Adolescent↗

Ethanol-induced anaphylaxis following ingestion of overripe rock melon, Cucumis melo.

BACKGROUND: Anaphylactic reactions to ethanol are rare with only seven cases reported in the literature. All previous cases have occurred following ingestion of alcoholic beverages or food to which an alcoholic beverage has been added. To date there are no cases in the literature of ethanol-induced anaphylaxis caused by the accumulation of endogenous ethanol in overripe fruit. METHODS: We report a patient with ethanol-induced anaphylaxis who developed anaphylaxis following ingestion of overripe, but not fresh rock melon (Cucumis melo). The patient is a 24-year-old, previously well woman who experienced five episodes of acute anaphylaxis following ingestion of various alcoholic beverages and, on one occasion, following ingestion of overripe rock melon to which no ethanol was added. Ethanol-induced anaphylaxis was confirmed on blinded challenge; however, challenge with freshly prepared rock melon was negative. The patient declined further challenges. CONCLUSION: Ingestion of overripe fruits may cause anaphylaxis in patients with ethanol-induced anaphylaxis. These patients should therefore, be advised to avoid ingestion of overripe fruits.

Adult↗

Usefulness of UniCAP-Tryptase fluoroimmunoassay in the diagnosis of anaphylaxis.

BACKGROUND: Serum tryptase level measured by RIA is the main in vitro tool to confirm the diagnosis of anaphylaxis. METHODS: Serum tryptase levels were determined by UniCAP-Tryptase fluoroimmunoassay (Pharmacia & Upjohn, Uppsala, Sweden), in 30 consecutive patients who presented at the emergency room with a clinical allergic reaction of less than 6-h duration to assess the value of this method in the diagnosis of anaphylaxis. Anaphylaxis was established by clinical criteria and by immunoallergic study. Baseline tryptase levels were determined 1 month later in 21 patients. The receiver operating curve (ROC) was used to establish the best cutoff point of tryptase levels to confirm the diagnosis of anaphylaxis. RESULTS: Seventeen patients were diagnosed with anaphylaxis. In this group, tryptase levels were higher than in the nonanaphylaxis group, composed mostly of patients with urticaria or angioedema (P<0.001). ROC established the best cutoff of tryptase levels at 8.23 ng/ml with a 94.12% sensitivity and 92.31% specificity, whereas the 13.5 ng/ml cutoff recommended by the manufacturers showed 35.29% sensitivity and 92.31% specificity. The reaction-tryptase/baseline-tryptase ratio was 2.85 in the anaphylaxis group and 1.29 in the nonanaphylaxis group. CONCLUSIONS: Serum tryptase levels of >8.23 ng/ml by UniCAP-Tryptase fluoroimmunoassay identify anaphylaxis in patients with symptoms of less than 6-h duration. The usefulness of this determination is higher if baseline tryptase levels are available.

Adolescent↗

Anaphylaxis: risk factors for recurrence.

BACKGROUND: There are few studies on the incidence or recurrence of anaphylaxis. OBJECTIVE: To examine the incidence of anaphylaxis and risk factors for recurrence. METHODS: A prospective study of 432 patients referred to a community-based specialist practice in the Australian Capital Territory with anaphylaxis, followed by a survey to obtain information on recurrence. RESULTS: Of 432 patients (48% male, 73% atopic, mean 27.4 years, SD 19.5, median 26) with anaphylaxis, 260 patients were seen after their first episode; 172 experienced 584 previous reactions. fifty-four percent of index episodes were treated in hospital. Aetiology was identified in 91.6% patients: food (61%), stinging insects (20.4%) or medication (8.3%). The minimum occurrence and incidence of new cases of anaphylaxis was estimated at 12.6 and 9.9 episodes/100,000 patient-years, respectively. Follow-up data were obtained from 304 patients (674 patient-years). One hundred and thirty experienced further symptoms (45 serious), 35 required hospitalization and 19 administered adrenaline. Accidental ingestion of peanut/tree nut caused the largest number of relapses, but the highest risk of recurrence was associated with sensitivity to wheat and/or exercise. Rates of overall and serious recurrence were 57 and 10 episodes/100 patient-years, respectively. Of those prescribed adrenaline, 3/4 carried it, 2/3 were in date, and only 1/2 patients faced with serious symptoms administered adrenaline. Five patients each developed new triggers for anaphylaxis, or re-presented with significant psychiatric symptoms. CONCLUSION: In any 1 year, 1/12 patients who have suffered anaphylaxis will experience recurrence, and 1/50 will require hospital treatment or use adrenaline. Compliance with carrying and using adrenaline is poor. Occasional patients develop new triggers or suffer psychiatric morbidity.

Adolescent↗

Anaphylaxis caused by the new ant, Pachycondyla chinensis: demonstration of specific IgE and IgE-binding components.

BACKGROUND: There have been no reports dealing with the pathogenic mechanism and IgE-binding components in patients with anaphylaxis caused by a sting from Pachycondyla chinensis. OBJECTIVES: This study was conducted to observe the clinical features of patients with P chinensis -induced anaphylaxis. The roles of specific (s) IgE and sIgG4 antibodies were evaluated, and IgE-binding components were identified. METHODS: Seven patients with P chinensis -induced anaphylaxis and 15 unexposed control subjects were enrolled. P chinensis ants were collected at the patients' homes, and venom was prepared as P chinensis extract. Five patients complained of bee venom-induced anaphylaxis and had positive sIgE levels to yellow jacket venom, wasp venom, or both as well. Serum sIgE and sIgG4 were detected by means of ELISA. To identify IgE-binding components within P chinensis extracts, 12% SDS-PAGE with immunoblot analysis was applied. RESULTS: All patients had positive skin prick test responses to P chinensis antigen and positive sIgE levels. Five (71%) patients had positive sIgG4 levels. Eight IgE-binding components (58, 46, 3l, 29, 27, 25, 22, and 12 kd) were noted, and the component at 12 kd was the most frequently found allergen (85%). IgE ELISA inhibition tests were performed on 2 groups of sera: one from patients with anaphylaxis induced by both P chinensis and bee venom (group A) and the other from patients with anaphylaxis induced by P chinensis venom alone without bee venom allergy (group B). ELISA inhibition tests with serum from group A showed significant inhibitions with addition of P chinensis extract, partial inhibitions with yellow jacket antigen, and minimal inhibitions with wasp or imported fire ant antigens. However, ELISA inhibition tests with serum from group B showed significant inhibitions with P chinensis antigen but no inhibition with wasp, yellow jacket, or imported fire ant antigens. CONCLUSIONS: IgE-mediated reactions contributed to the development of P chinensis -induced anaphylaxis. Eight IgE-binding components and one major allergen (12 kd) were identified. Further studies will be needed to clarify the role of sIgG4 and to identify allergenic relationships with major bee and wasp allergens.

Adult↗

Pathways of anaphylaxis in the mouse.

BACKGROUND: Although anaphylaxis is classically mediated by IgE, FcepsilonRI, mast cells, and histamine, several rodent studies suggest that an alternative pathway involving IgG, FcgammaRIII, macrophages and platelets, and platelet-activating factor (PAF) may be more important in the anaphylactic response to antigen challenge. OBJECTIVES: We sought to determine the relative roles of the classical and alternative pathways of anaphylaxis in a mouse model characterized by mastocytosis and a high level of antigen-specific IgE antibody. METHODS: Wild-type, IgE-deficient, FcepsilonRI-deficient, and mast cell-deficient mice were immunized with goat anti-mouse IgD antibody, which induces mastocytosis and a large IgE and IgG anti-goat IgG response, and then challenged 14 days later with antigen (goat IgG) or rat anti-mouse IgE mAb. Specific vasoactive mediators, cell types, Ig isotypes, or Ig receptors were blocked or eliminated before challenge in some experiments. The severity of anaphylaxis was gauged by changes in body temperature, physical activity, and mortality. RESULTS: Equal doses of antigen or anti-IgE mAb induced similar anaphylactic responses. Anti-IgE mAb-induced anaphylaxis was FcepsilonRI and mast cell dependent and mediated predominantly by histamine. In contrast, neither mast cells nor platelets appeared important for antigen-induced anaphylaxis, which was FcgammaRIII and macrophage dependent and mediated predominantly by PAF. CONCLUSIONS: Antigen-induced anaphylaxis in the mouse proceeds primarily through the IgG, FcgammaRIII, macrophage, and PAF pathway, even in an experimental model that is characterized by strong mast cell and IgE responses. The presence of FcgammaRIII on human macrophages makes it possible that the IgG, FcgammaRIII, macrophage, and PAF pathway also contributes to human anaphylaxis.

Anaphylaxis↗

Why do people die of anaphylaxis? A clinical review.

Anaphylaxis is a source of anxiety for patients and healthcare providers. It is a medical emergency that presents with a broad array of symptoms and signs, many of which can be deceptively similar to other diseases such as myocardial infarction, asthma, or panic attacks. In addition to these diagnostic challenges, anaphylaxis presents management difficulties due to rapid onset and progression, lack of appropriate self-treatment education and implementation by patients, severity of the allergic response, exacerbating medications or concurrent disease, and unpredictability. The most common causes of anaphylaxis are food allergies, stinging insects and immunotherapy (allergy shots) but idiopathic anaphylaxis, latex allergy and drug hypersensitive all contribute to the epidemiology. Reactions to IVP and other dyes are coined anaphylactoid reactions but have identical pathophysiology and treatment, once the mast cell has been degranulated. As many antigens can be the trigger for fatal anaphylaxis, it is useful to examine the features of each etiology individually, highlighting factors common to all fatal anaphylaxis and some specific to certain etiologies. Generally what distinguishes a fatal from non fatal reaction is often just the rapidity to apply correct therapy. Prevention is clearly the key and should identify high-risk patients in an attempt to minimize the likely of a severe reaction. Although fatal anaphylaxis is rare, it is likely underreported.

Anaphylaxis↗

Postmortem diagnosis of acute anaphylaxis by serum tryptase analysis. A case report.

Systemic anaphylaxis is an acute allergic emergency resulting from generalized mast cell degranulation. In the United States, it is estimated that anaphylaxis accounts for about 500 deaths each year. Hymenoptera-sting hypersensitivity is one of the most common causes of systemic anaphylaxis. The authors report a case of a healthy 26-year-old man who developed acute anaphylaxis after a bee sting, could not be resuscitated, and died within 1 hour. At autopsy, performed 14 hours after the event, the only pathologic findings were laryngeal edema and congestion of lung. Postmortem tryptase levels in the blood were obtained and were instrumental in confirming a diagnosis of acute anaphylaxis. This case is reported to discuss the difficulties associated with using traditional histamine levels in making a diagnosis of anaphylaxis and to validate the value of using tryptase levels to document acute anaphylaxis as a cause of death, even when serum is not obtained until many hours after death.

Adult↗

Anaphylaxis.

Anaphylaxis is a severe systemic allergic reaction that can involve multiple systems of the body. Anaphylaxis often is unpredictable, can have a rapid onset, and, if serious enough, can have life-threatening consequences. If an anaphylactic reaction is the result of an antigen antibody response, it is considered anaphylaxis. If the reaction is caused by a nonantibody trigger, it is considered anaphylactoid. Clinically, however, both responses appear the same and require the same management and treatment. With the development of new protein drugs and their use as therapeutic agents, the risk of anaphylaxis will most likely increase. For this reason, the infusion nurse specialist needs to have the knowledge and skills necessary to recognize and respond appropriately when anaphylaxis occurs. This article discusses the history, definition, incidence, risk factors, etiology, pathophysiology, and clinical findings of anaphylaxis. Appropriate prevention, management, and treatment also are discussed, with special attention given to medication-related anaphylaxis.

Anaphylaxis↗

The role of the vagus nerves in the respiratory and circulatory reactions to anaphylaxis in rabbits.

1. Rabbits, previously sensitized to egg albumen, were anaesthetized and then rendered anaphylactic by a further injection of egg albumen; total lung conductance of flow, lung compliance, breathing rate, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Before induction of anaphylaxis, some rabbits were vagotomized, some had their vagi cooled to block differential conduction, and others were paralysed and artificially ventilated to minimize secondary changes in afferent activity from the lungs and in blood gas tensions.2. Lung conductance was reduced by anaphylaxis in spontaneously breathing and in artificially ventilated rabbits, and the effect was lessened by vagal cooling and greatly reduced by vagotomy; the hyperventilation of anaphylaxis took the form of an increase in tidal volume rather than in respiratory frequency during vagal cooling, and all changes in ventilation were abolished by vagotomy. These effects are therefore dependent on the integrity of vagal nervous pathways.3. Lung compliance was reduced by anaphylaxis to a similar degree in all groups of rabbits; all groups showed similar falls in end-tidal CO(2)%. These effects are therefore not dependent on the integrity of vagal conduction.4. Anaphylaxis reduced systemic arterial blood pressure, the response being smaller when the vagi were cooled or cut.5. It is concluded that anaphylaxis has direct actions on the pulmonary vascular bed, the distal airways or the alveoli. However, the changes in breathing, blood pressure and large airway calibre are mainly dependent on vagal reflex activity. By analogy with responses to injections of histamine and phenyl diguanide (Karczewski & Widdicombe, 1969b) it is concluded that anaphylaxis stimulates lung deflation and irritant receptors which mediate much of the reflex responses.

Anaphylaxis↗

Drug-induced anaphylaxis : case/non-case study based on an italian pharmacovigilance database.

OBJECTIVE: To identify the number of cases of anaphylaxis reported in association with different classes of drugs and compare it with other reports contained in the same database. METHODS: The data were obtained from a database containing all of the spontaneous reports of adverse drug reactions (ADRs) coming from the Italian regions of Emilia Romagna, Lombardy and the Veneto, which are the main contributors to the Italian spontaneous surveillance system. The ADRs reported between January 1990 and December 2003 with a causality assessment of certainly, probably or possibly drug related (according to the WHO criteria) were analysed using a case/non-case design. The cases were defined as the reactions already coded by the WHO preferred terms of 'anaphylactic shock' or 'anaphylactoid reaction' (this last term also included anaphylactic reaction) and those with a time of event onset that suggested an allergic reaction and involved at least two of the skin, respiratory, gastrointestinal, CNS or cardiovascular systems; the non-cases were all of the other ADR reports. The frequency of the association between anaphylaxis and the suspected drug in comparison with the frequency of anaphylaxis associated to all of the other drugs was calculated using the ADR reporting odds ratio (ROR) as a measure of disproportionality. RESULTS: Our database contained 744 cases (including 307 cases of anaphylactic shock with 10 deaths) and 27 512 non-cases. The percentage of anaphylaxis cases reported in inpatients was higher than that among outpatients (59.1% vs 40.9%). This distribution is significantly different from that of the other ADR reports that mainly refer to outpatients. After intravenous drug administrations, anaphylactic shock cases were more frequent than anaphylactoid reactions or other ADRs, but more than one-third of these reactions were caused by an oral drug. Blood substitutes and radiology contrast agents had the highest RORs. Among the systemic antibacterial agents, anaphylaxis was disproportionally reported more often for penicillins, quinolones, cephalosporins and glycopeptides, but diclofenac was the only NSAID with a significant ROR. As a category, vaccines had a significantly lower ROR, thus indicating that anaphylaxis is reported proportionally less than other ADRs. CONCLUSIONS: Anaphylaxis is a severe ADR that may also occur with commonly used drugs. It represents 2.7% of all of the ADRs reported in an Italian spontaneous reporting database.

Adverse Drug Reaction Reporting Systems↗

The mechanisms, causes, and treatment of anaphylaxis.

Anaphylaxis is a severe life-threatening systemic reaction that offers many challenges to the clinician. The incidence of anaphylaxis is significant in the general population and an important cause of morbidity and mortality. While the most common causes of anaphylaxis include drugs, foods, and venoms, other important etiologies must be considered. The etiology of anaphylaxis is classically based on IgE mediated hypersensitivity but multiple mechanisms may be involved. The clinical presentation of anaphylaxis may be extremely variable with a broad differential diagnosis which will be outlined. Although the diagnosis of anaphylaxis can many times be based on a careful history and physical examination, there are laboratory and skin tests which may be helpful in establishing a diagnosis in some cases. The cornerstone of treatment of anaphylaxis remains epinephrine. Other supportive therapies will be discussed.

Anaphylaxis↗

[Allergy and hypersensitivity to drugs: anaphylaxis].

Anaphylaxis due to allergic or non-allergic hypersensitivity to drugs is an acute fatal or potentially fatal reaction. The estimate rate of 3.2 cases of drug-associated fatal anaphylaxis per 100.000 inhabitants per year seems to be approximately 10 times greater in hospitalised patients. The most common agents that are responsible for anaphylaxis in hospitalised patients are muscle relaxants, latex, antibiotics, anaesthesia-inducing drugs, plasma expanders followed by local anaesthetics and iodinated radio contrast media, and many others. Antibiotics and non-steroid anti-inflammatory drugs (NSAID) are the common cause of anaphylaxis in non-hospitalised patients. Predictive tests for high-risk patients have not been established. However, several procedures for prevention are proposed. These include preoperative screening to detect sensitisation to anaesthetic drugs and latex, or pre-treatment with antihistamines and corticosteroids to prevent anaphylaxis to iodinated contrast media. Challenge tests are useful for the determination of a safe anaesthetic or NSAID. Unfortunately, the causative agents cannot be identified in all cases of anaphylaxis. Subjects at risk for idiopathic anaphylaxis should have epinephrine available for self-administration.

Anaphylaxis↗

Patterns of anaphylaxis: acute and late phase features of allergic reactions.

Anaphylaxis is usually defined as a multi-system allergic reaction, but includes isolated shock or airway obstruction. Hives do not occur in 20-30% of cases. Gastrointestinal (GI) symptoms are more common with foods. Cardiac anaphylaxis can cause arrhythmias, bradycardia or chest pain with ECG changes. Plasma histamine level correlates with hives and GI symptoms. Serum tryptase is elevated less often in food allergy, and correlates poorly with plasma histamine level. Anaphylaxis occurs in 30/100,000 population/year (mortality 1-2%) and is caused by foods (35%), drugs/ biologicals (25%), insect stings (15%), exercise (5%) or is idiopathic (20%). Onset of anaphylaxis to stings or allergen injections is usually rapid: 70% begin in < 20 minutes and 90% in < 40 minutes. Food/ingestant anaphylaxis may have slower onset or slow progression. Rapid onset is associated with greater severity. Prolonged anaphylaxis can be resistant to epinephrine and i.v. fluids. Biphasic allergic reactions which recur some hours after the early phase of the reaction were reported in 25% of cases of fatal and near-fatal food reactions, and in 23% of drug/biological reactions. But they occurred in only 6% of anaphylaxis of mixed causes and are uncommon with insect stings. Late phase (biphasic) reactions rarely occur without initial hypotension or airway obstruction.

Allergens↗