Management of the Anaphylactic Shock

Management of the Anaphylactic Shock
Emergency Medicine Symposium Hué March 2012 Management of the Anaphylactic Shock Eric Revue1, MD Pr A. Bellou2, MD 1 European Society for Emergency Medicine Head of Emergency Medicine Department Director of Prehospital Emergency Medicine (SMUR) Louis Pasteur ‘s Hospital, Chartres, France Anaphylaxis is an acute, life-threatening systemic reaction with varied mechanisms, clinical presentations, and severity that results from the sudden systemic release of mediators from mast cells and basophils. (B) The more rapidly anaphylaxis develops, the more likely the reaction is to be severe and potentially life-threatening.(C) Prompt recognition of signs and symptoms of anaphylaxis is crucial. Anaphylaxy is the most severe reaction Allergenes Proteiques (hymnopteres, aliments, enzymes, pollens, latex) Polysaccharidiques (dextrans amidon..) Haptenes (medicaments, produits contraste, oxyde ethylene) Majorité medicamenteuse (curares, antibiotiques) 2 President of European Society for Emergency Medicine Head of Emergency Medicine Department Director of Emergency Medicine Training Program University Hospital, Faculty of Medicine, Rennes, France

What is anaphylaxis? An acute systemic allergic reaction
The result of a re-exposure to an antigen that elicits an IgE mediated response Usually caused by a common environmental protein that is not intrinsically harmful Often caused by medications, foods, and insect stings It is a Type I hypersensitivity Classiquement, le terme « anaphylactique» est réservé aux réactions IgE-dépendantes et le terme « anaphylactoïde» aux réactions IgE-indépendantes. Ces deux types de réactions ne peuventpas être différentiés sur le plan clinique. La World Allergy Organization qui regroupe des sociétés savantes et des organisations dédiées à l’amélioration dela prise en charge des maladies allergiques préconise d’utiliser le terme de réaction anaphylactique immunologique (IgE ou non IgE dépendante) ou non immunologique(2). Cette distinction sémantique reposant sur des données physiopathologiques ne peut pas être utilisée en situation de prise en charge enurgence au niveau préhospitalier au d’un service d’urgence. Le terme anaphylaxie est plus simple et correspond bien au processus de prise en charge enurgence où l’urgentiste est en situation de suspicion diagnostique dans laquelle il va proposer un traitement adapté sur un ensemble d’arguments cliniques.

History 1st recorded 2640 BC in hieroglyphics Richet & Portier
bee sting of a pharoah Richet & Portier South Seas Man-o-war coined term anaphylaxis Although the term anaphylaxis was introduced as far back as 1902 by Portier and Richet,1 the definition continues to be contentious. A recent guideline from the Anaphylaxis Working Party of the Australasian Society of Clinical Immunology and Allergy Inc. (ASCIA) defined anaphylaxis as ‘‘a rapidly evolving generalised multi-system allergic reaction characterised by one or more symptoms or signs of respiratory and/or cardiovascular involvement, and involvement of other systems such as the skin and/or gastrointestinal tract’’.2 ASCIA also defined a generalised allergic reaction as ‘‘one or more symptoms or signs of skin and/or gastrointestinal tract involvement without respiratory and/or cardiovascular involvement’’.

IgE Low-molecular-weight medications induce an IgE mediated reaction only after combining with a carrie rprotein to produce a complete multivalent antigen. B70. Penicillin is the most common cause of drug-induced anaphylaxis. C Binds irreversible to FcεRI receptors on mast cells, basophils, and eosinophils Is usually for parasitic infections E heavy chain

REVISED NOMENCLATURE FOR ANAPHYLAXIS
Allergic anaphylaxis Non-allergic anaphylaxis Anaphylaxis results from the action on different targets organs of different mediators liberated by an immunologic mechanism usually IgE –dependant, in response to antigenic stimulation. Most of the anaesthetc agents implicated in anaphylactic reactions are of low molecular weight. Immunologic, non-IgE-mediated anaphylaxis IgE- mediated anaphylaxis Johansson SGO et al JACI 2004,113:832-6

Anaphylaxis J Allergy Clin Immunol 2007;120:506-15
In anaphylactic shock, vascular collapse results when mediators with vasoactive properties are released from basophils and mast cells during allergen challenge (1-3). Of the mediators released, the autacoids, which include histamine, prostaglandins, and leukotrienes, have assumed important etiological roles in contributing to cardiovascular collapse in anaphylactic shock. Histamine may act through H1, H2, and H3 receptors to promote shock during allergen challenge (5, 7-10). H1 receptors mediate coronary vasoconstriction and cardiac depression (5, 11), whereas H2 receptor agonists produce coronary and systemic vasodilation as well as increases in heart rate (HR) and ventricular contractility (11). On the other hand, histamine H3 receptors have recently been identified on presynaptic terminals of sympathetic effector nerves that innervate the heart and systemic vasculature (7, 9). These receptors have been found to inhibit endogenous norepinephrine release from the sympathetic nerves (7). H3 receptor activation would therefore be expected to accentuate the degree of shock observed during antigen challenge since compensatory neural adrenergic stimulation would be blocked. The eicosanoids that encompass the prostaglandins and leukotrienes may also contribute to the cardiovascular collapse observed during allergen challenge (4, 12-14). Cyclooxygenase pathway products, such as prostaglandin (PG)I2, PGE1, and PGA1 cause systemic vasodilation and positive inotropy (14), whereas other products such as thromboxane A2 (TXA2) and PGD2 are vasoconstrictors and cause cardiac systolic dysfunction either by direct or indirect effects (14). Alternatively, the lipoxygenase pathway yields mainly systemic vasoconstrictors of which leukotriene (LT)D4, LTC4, and LTE4 have been purported to cause cardiac depression in many experimental preparations J Allergy Clin Immunol 2007;120:506-15

MEDIATORS The clinic presentation of the anaphylactic shock is explained by huge mediators. Stimulation of H1 and H2 hstamine receptors by histamine released from mast cells and basophils leads to the symptoms observed in ana anaphylactic reaction: cutaneous vasodilatation, increased capillary permeability with extravasation of plasma, arteriolar dilatation, tachycardia, increased myocardial contractility and excitability, decreased auriculoventricular conductivity, and bronchoconstriction. These effectsadded to those, beneficial or harmful, of other mediators such as the newly formed lipid mediators (PDG2, TXA2, leukotrienes)serotonin, NO and calcitonin gene related peptide. Anaphylactic reactions caused by muscle relaxation are due to presence of two clusters of quaternary ammonium ions on the molecule.

Mast Cell Has high affinity for IgE molecules (105 IgE/cell)
Originates in the bone marrow, reside in connective tissues Increases host response to parasitic infections Contain immunological mediators in granules ie. Histamine, ECF-A, HMW-NCF 2 populations that vary in granule content and activity Connective tissue Mucosal

What is happening? Initial exposure sensitizes mast cells.
Antigen specific IgE molecules attach to high affinity Fc receptors on the mast cell surface. Cross linking of IgE molecules on surface causes intracellular signaling pathway Inflammatory mediators are released upon degranulation

Mediators Involved Include histamine, proteases, chemotactic factors, leukotrienes, prostaglandin D, and cytokines Primary: released before degranulation Interleukin 4 used by T cells induces B cell maturation IL-3 and IL-5 released by T and mast cells are chemo attractants for eosinophils Secondary: come from granules

Diagnostic of Anaphylaxis
Anaphylaxis network symposium: J Allergy Clin Immunol 2006 ;117 : 391-7 Definition : severe allergic reaction with sudden onset and risk of death Natural rubber latex–induced anaphylaxisThere are 3 groups at high risk of reaction to latex: health careworkers, children with spina bifida and genitourinary abnormalities,and workerswith occupational exposure to latex. We used the defi nition of anaphylaxis established by the NIAID-FAAN Symposium, which states that anaphylaxis is probable when any of the following criteria are satisfi ed: a) The presence of skin signs or symptoms together with respiratory involvement or signs of organic dysfunction or hypotension, b) the involvement of at least 2 organs or systems after recent exposure to an allergen, or c) signs of organ dysfunction or hypotension after exposure to a known allergen [

Criteria 1 : skin lesions and/or mucosa lesions (urticaria, itching or erythema, lips oedema or tongue-uvula edema). With one or more following signs : Respiratory troubles (dyspnea, bronchospasm, stridor, decreased of peak flow, hypoxia) Systolic BP<90 mmHg) ou organ dysfunction (hypotonia, syncope, incontinence) It can be difficult to differentiate between immune and non immune mast cell–mediated reactions and pharmacologic effects from the variety of medications administered during general anesthesia. In addition,cutaneous manifestations of anaphylaxis are less likely to beapparent when anaphylaxis occurs in this setting. (B) The evaluation of IgE-mediated reactions to medications used during anesthesia can include skin testing to a variety of anesthetic agents. (B) Specifically, thiopental allergy has been documented by skin tests. (B) Neuromuscular blocking agents such as succinylcholine can cause non immunologic histamine release,but there have also been reports of IgE-mediated reactions in some patients.

Criteria 2 : 2 or more signs after exposition to a probable allergen: skin lesions and/or mucosa lesions (urticaria, itching or erythema, lips oedema or tongue-uvula edema). With one or mors following signs : Respiratory troubles (dyspnea, bronchospasm, stridor, decreased of peak flow, hypoxia) Systolic BP<90 mmHg) ou organ dysfunction (hypotonia, syncope, incontinence) Persistant gastrointestinal troubles (abdominal pain, vomiting)

Criteria 3: Decrease of SBP< 90mmHg or more than 30% compared to basal in adults* after exposition to known allergen. *In child decrease of SBP is defined as: SBP < 70 mmHg from 1 month to 1 year, below (70 mmHg + [2 x age]) from 1 to 10 years, <90mmHg from 11 to 17 years. Anaphylactic shock develops in three successive phases: Intitaily, hyperkinetic shock with tachycardia and collapse of peripheral vascular resistance due to precapillary arteriolar vasodilataion Extension of vasodilatation to the postcapillary venous network, leading to a decrease of neous return and cardiac output Hypokinetic shock with a secondary hypovolaemic component resulting from transcapillary plasma extravasation.

Triggers Drugs causing anaphylaxis Antibiotics (especially penicillin)
Anaesthetic agents Aspirin NSAID’S IV Contrast media Opioid analgesics Common causes: Foods Bee and wasp stings Drugs Latex rubber Foods reported as triggers Peanuts 8 Fish Shellfish Eggs Milk Sesame, Pulses etc Others Note:Anaphylaxis may be worse in those on beta blockers Rare Causes: Exercise Semen Vaccines No trigger : 10 % idiopathic anaphylaxis Aspirin and other nonsteroidal anti-inflammatory drugs(NSAIDs), including COX-2–specific inhibitors, have been reported to produce anaphylactic reactions. Aspirin and NSAIDs are the second most common cause of drug-induced anaphylaxis(after antibiotics).244 Anaphylactic reactions to NSAIDs are unrelated to other reactions caused by these drugs, such as respiratory reactions and exacerbations of chronic idiopathic urticaria.245 Although respiratory and urticarial reactions are often referred to as anaphylactic, efforts to detect drug-specific IgE antibodies(through skin testing or in vitro testing) have generally been unsuccessfu lin patients who experience these reactions. In children aged 0 to 4 years, the main foods responsible for anaphylaxis were, in order, cow’s milk, then egg, fruit, and fish (responsible for 81.4% of all episodes of food-induced anaphylaxis).

The Big Eight/Most Common Food Allergens
SHELLFISH FISH COWS MILK EGGS SOYA WHEAT PEANUTS TREE NUTS There is an increase number of anaphylactic reaction caused by food allergens. Food is the most common cause of anaphylaxis in the outpatient setting, and food allergens account for 30% of fatal cases of anaphylaxis. (D) The most commonly implicated foods responsible for food-induced anaphylaxis include peanuts, tree nuts, fish,shellfish, cow’s milk, soy, and egg. In addition, sesame seed has recently been identified as a significant cause of food-induced anaphylaxis. Common themes associated with fatal food anaphylaxis include the following: reactions commonly involve peanuts and tree nuts; cutaneous and respiratory symptoms are frequently observed; victims are typically teenagers and youngadults; patients have a previous history of food allergy and asthma;and there is a failure to administer epinephrine promptly. (C) As isthe case of anaphylaxis following other agents, asthma is a risk factor for more severe food-induced anaphylaxis

International Food Allergen List
Buckwheat Another 20 allergens are recommended Japan 4 of Top 8 *Milk *Egg *Peanuts *Wheat Plus + Buckwheat + Sesame + Molluscs + Sulfites + Gluten + Celery + Mustard + Lupin E.U. Top 8 Plus Sesame Molluscs Sulfites Gluten Canada Top 8 Plus Sulfites Gluten (in place of wheat) Hong Kong Top 7 Plus U.S. TOP “8” Fish Crustacean Shellfish Egg Milk Peanuts Tree-nuts Soy Wheat Gluten ? Sesame Molluscs Sulfites Gluten Australia/NZ Top 8 Plus + Gluten (in place of wheat) + Sulfites Codex Top 7 Plus

INCIDENCE and PREVALENCE
Indicators: - prevalence of all suspected allergic reaction with medical assistance - prevalence of severe reactions - prevalence of severe anaphylaxis complicated by death Results from different ways: registres, allergy network, hospitals, ED, Schools The crude cumulative incidence of anaphylaxis was 0. 9 episodes per 1000 emergency episodes and 0.8 episodes per 1000 people. These distributions of incidence are related to the epidemiology of these triggers. Food allergies (mainly to cow’s milk and hen egg) are most common in the early years of life [26], while drug allergy is more common among adults. The annual incidence of paediatric anaphylaxis was 1:1000 total ED presentations. This compares with an incidence of 2.3:1000 adult ED presentations reported in the local adult study. The higher incidence of anaphylaxis in adults compared to children has been recognised previously. The incidence of anaphylaxis appears to be increasing. The incidence of anaphylaxis presentations to ED in the paediatric population was 1:1000 cases and the incidence of generalised allergic reactions was 9.3:1000. The most common cause of anaphylaxis in children was food, and of generalised allergic reaction was drugs.

Prevalence in Emergency Departments
Gaeta, 2007-Ann Allergy 12 millions allergic reactions over 12 years (1993 à 2004) in US 1% of all ED visits 1 million per year 12,400 anaphylaxis per year in ED In numerous countries authors have reported cases of anaphylactoid reacation. Depending on the country, anaphylactoid reactions represent 9 to 19 % of complications associated with anesthesia.The mortality rate is about 5 to 7 %. In US, Food is the most common cause of anaphylaxis in the outpatient setting, and food allergens account for 30% of fatal cases of anaphylaxis. (D) The most commonly implicated foods responsible for food-induced anaphylaxis include peanuts, tree nuts, fish,. We observed differences in the distribution of the cumulative incidence of anaphylaxis according to age, and these differences were particularly pronounced when the denominator of incidence was the number of emergencies. The peaks in such cases were between 1.6 and 1.7 per 1000 emergencies (0-4 and age groups). Gaeta et al [12] used a national survey to estimate the incidence of acute allergic reactions (including anaphylaxis) in general and short-stay hospitals throughout the United States, and reported the highest incidence (>10.5 cases per 1000 emergencies) in patients aged 20 to 70 years. One possible explanation for the differences between our findings and those of Gaeta et al is the fact that in their case, patient selection was based on IC-9-M codes for acute allergic syndromes, with no further refinement of data, whereas in our case, only patients with anaphylaxis were selected. In the study by Gaeta et al, the rate per 1000 population was also higher than in our study (overall 3.8), with no peak in the 0-4 year group. In our study, the lack of peaks in incidence in the general population older than 4 years and the presence of these peaks in the emergency department population may be related to a lower percentage of emergency department visits by patients aged over 4 years. Such an effect would decrease the denominators of the emergency population and, consequently, increase the cumulative incidence of anaphylaxis in emergency visits

French Allergy Vigilance
Network 2000 : 2831 cases 2004 : 3573 cases 22% increase In France, 500 anaphylactic shock during anesthesia in 2001, 55 % neuromuscular blockers, 22 % latex, 15 % antibiotics. The incidence due to neuromuscular blockers reaction was estimated 1/ 6500. In 1996 the incidence of anaphylactic reactions in France was estimated to be 1/13000 general and local or regional anesthetics, all types of substances included.The muscle relaxants mots often involved in Anaphylaxis in France in were rocuronium, suxamethonium, atracurium and vecuronium. Clin Exp Allergy, 2010

Allergy Network Clinical Aspects
Children: 34% Adults: 66% ED visits: 80.5% Epinephrine: 44.5% Hospitalisation rate : 59.3% Moneret-Vautrin et al Rev Méd Int 2006;120:S70-72

Allergy Network Clinical Aspects
Anaphylactic Shock: 47.6% Severe systemic reactions: 36.7% Laryngeal Angio-Edema: 12.4% Severe asthma: 4.4% Moneret-Vautrin et al Rev Méd Int 2006;120:S70-72

Clinical Signs Shock Myocardial infarction Cardiac arrest
Cardiac anaphylaxis Anaphylactic shock is the most serious manifestation of anaphylaxis.The very severe initial cardiac and/or bronchial signs are not yet explained.The occurrence of specific myocardial injury during the course of anaphylaxis in humans has been substantiated by clinical observations but is still a controversial matter. The hypothesis of a direct myocardial effect of anaphylaxis si supported by numerous experimental studies. Cardiac mast cells have particular biochemical and immunologic characteristics that might give them a privileged role in the mechanism of myocardial injury in anaphylaxis. The development of an arrhythmia, angina pectoris or myocardial infarction could be unrelated but could equally be the result of hypoxemia, decreased mypcardial perfusion pressure or be a consequence of drugs administrated for the treatment of shock.The situation is often worsedened by underlying cardiac pathology or by saturation of the organism by drugs such as beta adrenergic blocking agents

Symptoms Peripheral vasodilation Bronchospasm Cardiac arrhythmias
vascular permeablility (edema) Bronchospasm Cardiac arrhythmias Smooth muscle contractions

Laryngeal Angioedema

Mortality Review: 4 for 20,381 cases of anaphylaxis cared in ED=2 for 10,000 Moneret-Vautrin, 2005-Allergy 0.65 to 2%=1 to 3 for 1 million in Europe Neugut, 2001-Arch Int Med : 20 for 1 million in US The mortality is weak. In Europe, the estimated mortaility is 1 to 3 million in Europe Anaphylaxis during general anesthesia, the intraoperative period, and the postoperative period The incidence of anaphylaxis during anesthesia has been reported to range from 1 in 4000 to 1 in 25,000. Anaphylaxis during anesthesia can present as cardiovascular collapse, airway obstruction, and/or skin manifestation.

Mortality Risk Factors: Delayed adrenalin administration
Beta blokers, AC Inhibitors Asthma, co-morbidity Allergen introduced IV 90% of died patients had dyspnea before then cardiac arrest Drug allergy=Shock is the main symptom The risk factors are increasing the risk of death. Data regarding fatalities associated with anaphylactic reactions are limited. It is estimated, however, that between 500 and 1000 individuals die of anaphylaxis each year, and that the risk of death in those who experience such a reaction approximates 1%. It is clear that the risk for an increased severity of anaphylaxis or death may be related to alterations in the body’s homeostatic mechanisms, as in patients receiving beta blockers, ACE inhibitors, or in the presence of underlying adrenal insufficiency. Beta blocking drugs or the presence of asthma may worsen the airway response to treatment and complicate resuscitative efforts. Moreover, epinephrine administration in the face of beta blocker treatment may lead to unopposed -adrenergic effects and significant hypertension. Preexisting cardiac disease or the rapid intravenous infusion of an allergen may also be responsible for poor outcomes. Importantly, the failure to administer epinephrine immediately after the onset of anaphylactic symptoms has been shown to be an independent risk factor contributing to fatal outcomes. Miller RL. Epidemiology of anaphylaxis. Presented at: Anaphylaxis: Safely Managing Your Patients at Risk for Severe Allergic Reactions. Postgraduate Institute for Medicine; October 8, 1999; Washington, DC. Bocher BS. Anaphylaxis. N Engl J Med 1991:324:1785–1790.

Anaphylaxis and Food Allergy
32 deaths in patients with age between 2 to 32 ans - peannut >90% of reations - history of asthma - majority didn’t receive epinephrine In this slide, you can note thatin a clinical review of anaphylactic fatalities, Bock SA et al. J Allergy Clin Immunol 2001;107:191-3

Uniphasic Anaphylaxis
Treatment Initial Symptoms Uniphasic anaphylaxis resolves within hours either spontaneously or with treatment. Time Antigen Exposure

Biphasic Reaction Treatment Treatment 1 to 38 hours Initial phase
Fig. 1: Schematic representation of a biphasic anaphylactic reaction. The second-phase reaction has been described as occurring between 1 and 8 hours after the initial reaction, but new evidence suggests that this second phase may occur up to 38 hours (mean 10 hours) after the initial reaction. About one third of the second-phase reactions are more severe, one-third are as severe and one-third are less severe. Initial phase Recurrent phase Allergen contact Time (h) Ellis AK, Day JH, Can Med Ass,2003

Meta-analysis 2003 to 2008 : 12 1995 to 2001 : 5 6- Bellou, 2003-Emerg Med J, France 7- Brown, 2004-JACI, Australia 8- Clarck, 2004-JACI, USA 9- Clarck, 2005-JACI, USA 10- Haymore, 2005-JACI, USA 11- De Villiers Smit, 2005-J Emerg Med Hong Kong 12- Luke, 2006-Ann Emerg Med, USA 13- Braganza, 2006-Arch Dis Child Australia 14- Gaeta, 2007-Ann Allergy, USA 15- Melville N, 2008-Emerg Med J, UK 16- De Silva IL, 2008-Allergy, Australia 17- Ross MP, 2008-JACI, USA 1- Schwartz, 1995-Allergy Proc : US 2- Klein, 1995-JACI US 3- Stewart, 1995-Q J Med UK 4- Pastorello, 2001-J Chrom Biomed Sc Appl Italy 5- Brown, 2001-JACI Australia There are few multicentric studies in literature.. Anaphylaxis 2000 results. The limitation are a few multicentric studies with huge variation definition of anaphylaxis. Finally only 17 papers on anaphylaxis care in ED in Literature from 1995 to 2008. The absence of large-scale international studies means that data on anaphylaxis in emergency departments in different geographic areas are still necessary. Anaphylaxis series have been reported at different health care levels [1-9], including emergency departments [2, 10-22], where anaphylactic reactions are generally treated [12]. However, reports on anaphylaxis in these departments are difficult to compare due to important differences in incidence, severity, cause, and management [3,10-22]. International collaboration based on uniform defi nitions and information on the number of emergencies attended, type of health system, distribution of emergency services at different care levels, and local health care resources makes it easier to compare studies.

Type of Allergen Food : 33% Hymenoptera Venom : 28% Drugs : 26%
The type of allergen is food in 33% Penicillin spontaneously degrades to major and minor antigenic determinants, both of which should be included in skin testing for penicillin hypersensitivity. B72. The negative predictive value of penicillin skin testing with both major and minor determinants (for immediate-type reactions) is between 97% and 99%(depending on the reagents used), and the positive predictive value is at least 50%. Three families of the order Hymenoptera can cause anaphylaxis:the bees (honeybees, bumblebees), vespids (yellow jackets,hornets, wasps), and stinging ants (genus Solenopsis). There have been increasing reports of anaphylaxis due to other species ofstinging ants in Asia and Australia. At least 50 fatal reactions to an insect sting occur each year in the United States. Half of these occur in individuals who had no history of a previous reaction to an insect sting. In placebo-controlled trials venom immunotherapy (VIT) was90-98% effective in completely preventing systemic reactions tostings The indications for VIT are a history of a systemicallergic reaction to a sting and a positive diagnostic test for venom-specific IgE. Those with a recent history of anaphylaxis from an insect sting and a positive skin test have a 30% to 70%chance of a systemic reaction to a subsequent sting.273,294,303VIT is not required when the chance of a systemic reaction is<10%, as in large local reactors and children with cutaneous systemic reactions, but still may be considered in this setting.304 Reasons other than differences in the definition of anaphylaxis should thus be sought to explain the considerable differences in incidence between our study and others. Possible reasons are differences in age ranges (children or adults), methods used to select possible cases. We found that the 3 main causes of anaphylaxis were food (28.6%), drugs (28.2%), and unknown causes (27.2%). In most series of anaphylaxis, drugs and food are the main causes of episodes seen in the emergency department. One of the main differences in other series is the higher percentage of Hymenoptera venom anaphylaxis, which ranges from 7.1% to 29.0% [3,10,13,16] depending on the prevalence of Hymenoptera allergy in the catchment areas analyzed.

Epinephrin Administration in ED
15-Ross MP, USA: 19% 17-Melville N, UK: 5% 20000 cases of anaphylaxis the care of anaphylaxis in Ed is not optimum. The use of epinephrin varies from zero to 83 % patients Emerg Med J Oct;25(10):655-8. Paediatric allergic reactions in the emergency department: a review. Melville N, Beattie T. Source Royal Hospital for Sick Children, 10/7 Wellington Street, Edinburgh EH75ED, UK. Abstract BACKGROUND: Allergic diseases are increasing in incidence worldwide and large numbers of children are now affected by allergy. Few studies have examined allergic reactions in children, particularly in the emergency department (ED) setting. OUTCOME MEASURES: Primary--to describe the epidemiology of acute paediatric allergic reactions. Secondary--to describe the treatment and outcome of allergic reactions presenting to a paediatric ED. SETTING: The ED of a paediatric tertiary referral hospital with approximately 29,000 ED attendances annually. METHODS: A retrospective review of allergic reactions presenting to a paediatric ED over a 2-year period. MAIN RESULTS: 237 patients (61% male, median age 46 months) had reactions. 137/100,000 children attend the ED annually. The main identified causative agents were nuts (23%), dairy products (16.5%) and medication (10%). Oral contact was associated with 58.6% of reactions and dermatological symptoms were the most frequent presentation. Only 11(5%) received adrenaline (epinephrine). 46 (19%) were admitted. 55% of all patients received no formal follow-up. CONCLUSIONS: Acute allergic reactions affect boys more than girls and frequently occur at a young age. Food allergies, in particular to nuts, are a major cause of reactions. Allergy represents a frequent presentation to the paediatric ED. There remains a concern about the adequacy of follow-up. The initial drug of choice is epinephrine The following are salient points regarding administration of epinephrine:d The concentration is 1:1000 and the adult dose is 0.2 to 0.5ml (mg). The dose in a child is 0.01 ml (mg)/kg.d The time to highest blood concentration (Cmax), when studied in asymptomatic subjects, is shorter when injectionis given intramuscularly in the vastus lateralis muscle(lateral thigh) than when it is administered either subcutaneously or intramuscularly in the deltoid muscle of the arm.

Epinephrin Self-injected
In literature, we found the is a lack of use of self epinephrin/adrenalin from 0 to 36% routes of administration during anaphylaxis. There areno data indicating that epinephrine is ineffective when administered either subcutaneous or intramuscular inthe deltoid muscle of the arm.d Epinephrine may be administered every 5 to 10 minutesas necessary. If the clinician deems it appropriate, the 5minute interval between injections can be liberalized to promote more frequent administration.d Epinephrine should be administered as soon as the diagnosisof anaphylaxis is suspected.d Although the diagnosis of anaphylaxis usually depends oninvolvement of two organ systems (e.g., skin plus respiratory,skin plus cardiovascular), anaphylaxis may presentas an acute cardiac or respiratory event or with hypotensionas the only manifestation of anaphylaxis.

Allergist Follow-up In literature , we also found a lack of follow up
Follow-up of patients who have experienced anaphylaxis mustbe individualized and based on such factors as clinical scenario and distance from patient’s home to closest emergency facility.At the time of discharge from medical supervision, patients should be provided with autoinjectible epinephrine and instructedin its use. In circumstances where an allergist/immunologist is not already involved, it is strongly recommended that consultation with an allergist/immunologist be obtained.

Hospitalization after ED Care
Revue générale :Moratlity 3 pour cas d’anaphylaxie arrivant dans les SU Moneret-Vautrin, 2005-Allergy : anaphylaxie sévère avec risque vital=1 à 3 pour 10000, mortalité=0.65 à 2%=1 à 3 pour 1 million en Europe Neugut, 2001-Arch Int Med : 1500 à 4000/an soit 20 pour 1 million aux USA

SUMMARY 75 to 85% of anaphylaxis are cared in EDs +++
4 guideline recommendations not fully respected: (1) adrenaline at the acute phase, (2) prescription of self-injected adrenaline, (3) education of patient, (4) follow-up by allergist The majority of patients with anaphylaxis and generalised allergic reactions may be definitively managed in the ED alone, provided that follow up is organised, including allergist referral when indicated, and that all patients are given clear and comprehensive discharge advice. Epidémiologie : Gaeta, 2007-Ann Allergy 12.4 millions de réactions allergiques sur 12 ans (1993 à 2004) au USA 1% de toutes les admissions au SU 1.03 millions d’admission par an 3.8 pour 1000 admissions/an pas de données de mortalité 12400 anaphylaxie par an

Guidelines Anaphylaxis network symposium :
J Allergy Clin Immunol 2006 ;117 : 391-7 Self-injected Adrenaline: cardiovascular or respiratory signs and know allergen Information of patient Allergy follow-up after ED visit Monitoring in ED: 8 to 24 h, hospitalisation for severe or recurrent anaphylaxis, asthmatic patient How to care anaphylactic shock

Guidelines for ED Treatment
Suspicion of severe anaphylaxis ABC Diagnostic (definition) 1e line : Adrenaline + Fluid resuscitation: crystalloïds or saline 0.9%, adult 500 ml to1000 ml ( up to 4000ml), children 20ml/Kg Jasmeet S. Resuscitation 2008;77:

A U T H O R S ’ C O N C L U S I O N S Implications for practice
Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock (Review) Sheikh A, Shehata YA, Brown SGA, Simons FER This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library 2010, Issue 10 A U T H O R S ’ C O N C L U S I O N S Implications for practice We found no relevant evidence for adrenaline use in the treatment of anaphylaxis. We are, therefore, unable to make any new recommendations based on the findings of this review. Guidelines on the management of anaphylaxis need to be more explicit about the basis of their recommendations regarding the use of adrenaline.

A U T H O R S ’ C O N C L U S I O N S Implications for research
Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock (Review) Sheikh A, Shehata YA, Brown SGA, Simons FER This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library 2010, Issue 10 A U T H O R S ’ C O N C L U S I O N S Implications for research Although placebo-controlled trials of adrenaline in anaphylaxis would be unethical, it might be possible to conduct randomized controlled trials comparing two different doses of adrenaline, or two different routes of administration of adrenaline, in addition to other standard-of-care treatments (Simons 2008). If there is any doubt, it is generally better to administer epinephrine. (C) Epinephrine and oxygen are the most importantt herapeutic agents administered in anaphylaxis. Epinephrine is the drug of choice, and the appropriate dose should be administered promptly at the onset of apparent anaphylaxis. (C) Appropriate volume replacement either with colloid or crystalloids and rapid transport to the hospital are essential for patients who are unstable or refractory to initial therapy for anaphylaxis in the office setting. (B)Medical facilities should have an established plan of action to deal with anaphylaxis that is regularly practiced and the appropriate equipment to treat anaphylaxis.

Epinephrine Injection: IM vs. SQ
Intramuscular epinephrine injected into the lateral thigh (vastus lateralis) produces a more rapid rate of rise in blood epinephrine levels than does subcutaneously injected epinephrine injected into the upper arm. There are no outcome data comparing the results of these two administrations in terms of their therapeutic effect. It should also be noted that the area under the curve is essentially equivalent for both of these routes of administration. Recommend that patients maintain two stationary 2-packs of epinephrine, one for home and the other for work or school environment. Prospective, randomized, blinded study in children T-max was 8 ± 2 minutes after injection of epinephrine 0.3 mg from an EpiPen IM in the vastus lateralis vs. 34 ± 14 minutes (range, 5 to 120) after injection of epinephrine 0.01 mg/kg SQ in the deltoid region. Simons FER, Gu X, Simons KJ. Epinephrine absorption in adults: intramuscular versus subcutaneous injection. The Journal of Allergy and Clinical Immunology 2001;108:871–3.

Adrenaline I.M Adrenaline IM: dilution 1/1000
Adult : 500 microgramms (0,5ml) Child > 12 years: 500 microgrammes (0,5ml) Child 6 to 12 years: 300 microgrammes (0,3ml) Child < 6 years: 150 microgrammes (0,15ml) The rapid use of injectableepinephrine has been shown to be effective in the initial management of food-induced anaphylaxis, but subsequent doses may be needed. Travaux récents suggèrent que la voie IM chez enfant efficacité > SC avec doses adrénalines supérieures et délai plus court Jasmeet S. Resuscitation 2008;77:

Self-injected epinephrine
All patients at risk should be instructed as to the proper administration of EpiPen/EpiPen Jr before the need for its use arises. Detailed instructions for self-administration (contained in each auto-injector package) should be carefully reviewed with the patient. In addition, a training device (known as the EpiPen Trainer) that simulates the auto-injection process without actual drug delivery is available. Using the EpiPen Trainer, patients should practice self-administration under the supervision of a physician (or a trained assistant) until an appropriate administration technique and a satisfactory comfort level are assured. To prepare the EpiPen/EpiPen Jr for use, grasp the auto-injector with the hand (forming a fist around the unit) with the black tip facing downward. Immediately before use, remove the gray activation cap with the other hand, being careful not to touch the black tip, where the needle is located, at any time. EpiPen/EpiPen Jr package instructions. Napa, Calif: Dey, L.P., December 2000.

After uncapping the auto-injector, place the black tip near the fleshy outer portion of the thigh. Instruct the patient that it is not necessary to remove any clothing; the EpiPen/EpiPen Jr auto-injector is designed to work effectively through clothing. Remind the patient not to touch the black tip of the auto-injector at any time. EpiPen/EpiPen Jr package instructions. Napa, Calif: Dey, L.P., December 2000.

With a quick motion, swing out and jab firmly into the outer thigh, so that the injector is at a 90 degree angle to the thigh. Hold firmly in the thigh for several seconds. During this time, a spring-activated mechanism is released, and a dose of epinephrine is administered. When practicing with the trainer, a “click” indicates that the device worked properly. Remove the unit and massage the injection site for an additional few seconds. Once administration is complete, the patient should check the black tip of the auto-injector. If the needle is exposed, a dose of epinephrine was injected. If not, the above steps should be repeated. Inform the patient that most of the liquid (90%) stays in the auto-injector after the dose is administered and cannot be reused. To avoid an accidental needle stick, the needle of the fired unit should be bent back against a hard surface. Carefully return the auto-injector to its carrying tube (NEEDLE FIRST) without replacing the gray safety cap. Recap the carrying tube and bring it to the emergency care facility for proper disposal. Patients should be instructed to go immediately to the nearest Emergency Room for further medical attention. Medical personnel should be told that a dose of epinephrine has been given and should dispose of the auto-injector properly. Patients should be reminded to store their EpiPen/EpiPen Jr in a dark place at room temperature; prolonged temperature extremes (refrigeration or car glove box, trunk) should be avoided for optimal functioning of the auto-injector. Patients should check the EpiPen/EpiPen Jr monthly for expiration date and discoloration. If the unit has expired or the drug solution appears brown, the unit should be discarded and replaced immediately. EpiPen/EpiPen Jr package instructions. Napa, Calif: Dey, L.P., December 2000.

Adrenaline I.V Intravenous adrenaline has been associated with fatal cardiac arrythmias and myocardial infarction, these cases have been associated with too rapid injection, undiluted doses, or excessive doses (Fischer, 1995; Pumphrey, 2000; Brown, 2001; Montanaro and Bardana, 2002). To minimise these adverse effects, the use of intravenous adrenaline is now recommended at a dilution of 1:10,000 (Project Team of the Resuscitation council, UK, 2005).

Adrenaline I.V IV: dilution 1/10000 (10 ml with 100 microgrammes/ml adrenaline), routinely used by EPs: Adult: bolus of 50 microgrammes (0.5ml) Child: bolus of 1 microgramme/Kg If repeated administration=perfusion by pump (1 to 4 microgrammes/min) Jasmeet S. Resuscitation 2008;77:

Can epinephrine inhalations be substituted for epinephrine injection in children at risk for systemic anaphylaxis? Simons FE, Gu X, Johnston LM, Simons KJ. Pediatrics Nov;106(5): NO In a study in children, those treated with adrenaline inhalers had blood adrenaline levels no higher than a control group treated with placebos.

Implications for practice
Glucocorticoids for the treatment of anaphylaxis (Review) Choo KJL, Simons FER, Sheikh A This This is a reprint of a Cochrane review, prepared and maintained by The Cochrane Collaboration and published in The Cochrane Library 2010, Issue 10 A U T H O R S ’ C O N C L U S I O N S Implications for practice We found no relevant evidence for the use of glucocorticoids in the treatment of an acute episode of anaphylaxis. We are, therefore, unable to make any new recommendations based on the findings of this review. While we do not necessarily suggest that anaphylaxis guidelines no longer recommend glucocorticoids, these guidelines need to be more explicit about the basis of their recommendations regarding the use of these agents (Alrasbi M, Sheikh A. Comparison of international guidelines for the emergency medical management of anaphylaxis. Allergy 2007; 62:838–41.).

Second line treatment Histamine antagonists
Dexchlorpheniramine=against itching Corticosteroids Hydrocortisone-Methylprednisolone=prevent recurrent anaphylaxis Jasmeet S. Resuscitation 2008;77:

Guidelines for ED Treatment
Specific situations Glucagon : 1-2 mg every 5 min, resistance to adrenaline, patient treaed by β blokers Cardiac arrest : follow current guidelines fluid resuscitation=4 to 8l adrenaline : 1 to 3 mg IV (3min), 3 to 5 mg (3min), 4 to 10 microg/min pump perfusion

Positive Diagnosis in ED
 Medical history to identify allergen  Tryptase - Specific for mast cells degranulation, confirm anaphylactic reaction - Still increased at 6th hour Lieberman PL et al, J Allergy Clin Immunol 2005;115:S

Biologic tests in anaphylaxis
Plasma histamine Serum tryptase 24-hr Urinary histamine metabolite Histamine: a perform mediator contained in cytoplasmic granules of mast cells and basophils. An increase in the concentration of histamine in the plasma is a sign of in vivo histamine release. The peak is immediate and the half –life in the plasma in 15 minutes. Tryptase: a performed enzyme present exclusively in mast celles.An increase of serum tryptase, resulting from the degranulation of mast cells, favours an anaphylactic mechanism. The peak of the tryptase concentration occurs between 30 minutes and 2 hours after the onset of the reaction and its half-life is 90 minutes. Serum tryptase measurements may not be elevated in cases of food-induced anaphylaxis. (C) An obvious increased in the level of serum trptase (> 25 ùg/l is in favour of an anaphylactic mechanism. Determination of urinary methylhistamine concentration is no longer recommended, as it is less sensitive for diagnosis than histamine and tryptase. These assays rquire taking 7.5 ml of blood in a dry tube and 7.5 ml in a EDTA tube as soon as possible after the control of clinical situation, ideally in the hour following the first signs of the reaction. Theses tubes should be carried to the local laboratory within 2 hours. In case of impossibility, they can be stored in a refrigerator at + 4°C, but not for more than 12 hours. If the patient is at risk to die, the blood samples should be obtained before rescuscitation is stopped rather than post mortem. Serum tryptase should be systematic for hymenopters bites. T1 = after emergency treatment start, T2 = 1 to 2 h after T1 et T3 at 24 h in the ward. Put serum at -20°C.

Anaphylactic Shock Bellou A. Shock, 2003

Vasodilatation

Effect of NO Synthase, Histamine and Serotonine Inhibition Pathways
Antihistamines Block H1 and H2 receptors Epinephrine for bronchospasms stimulates the reformation of tight junctions between endothelial cells IV fluids to support blood pressure Desensitization Bellou A. Shock, 2003

New treatments of Anaphylactic Shock Vasopressin?
Vasopressin mediates vaoconstriction via V1 receptor activation on vascular smooth muscle. Anesthesiology, V 106, No 5, May 2007

Management of the Anaphylactic shock

Position: Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure Oxygen. Administer oxygen at high flow rates. Epinephrine. Administer epinephrine to all patients with clinical signs of shock, airway swelling, or definite breathing difficulty Antihistamines. Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). H2 blockers. Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV) Inhaled b-adrenergic agents. Provide inhaled albuterol if bronchospasm is a major feature. If hypotension is present,administer parenteral epinephrine before inhaled albuterol to prevent a possible further decrease in blood pressure.Inhaled ipratropium may be especially useful for treatment of bronchospasm in patients on b-blockers. Position. Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure. c Oxygen. Administer oxygen at high flow rates. c Epinephrine. Administer epinephrine to all patients with clinical signs of shock, airway swelling, or definite breathing difficulty. Administer intravenous epinephrine if anaphylaxis is profound and life-threatening and vascular access is available. If vascular access is not available or if anaphylaxis is not profound and life-threatening, administer epinephrine by intramuscular injection. Subcutaneous administration may be used but absorption and subsequent achievement of maximum plasma concentration may be delayed with shock.8—The IM dose of 0.3 to 0.5 mg (1:1000; 1 mL) may be repeated after 5 to 10 minutes if no clinical improvement.—Intravenous epinephrine (1:10 000; 10 mL) 1 to 5 mL or 0.1 to 0.5 mg over 5 minutes should be used only for profound, immediately life-threatening manifestations and when there are no delays in intravenous access.Epinephrine may be diluted to a 1: solution before infusion. An intravenous infusion (1 mg in 250 mL D5W[4 mg/mL]) at rates of 1 to 4 mg/min may avoid frequent repeat epinephrine injections. 9c Antihistamines. Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). c H2 blockers. Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV).10c Isotonic solutions. Give isotonic crystalloid (normal saline)if hypotension is present and does not respond rapidly to epinephrine. A rapid infusion of 1 to 2 L or even 4 L maybe needed initially. c Inhaled b-adrenergic agents. Provide inhaled albuterol ifbronchospasm is a major feature. If hypotension is present,administer parenteral epinephrine before inhaled albuterol to prevent a possible further decrease in blood pressure.Inhaled ipratropium may be especially useful for treatment of bronchospasm in patients on b-blockers. c Corticosteroids. Infuse high-dose intravenous corticosteroidsslowly or administer intramuscularly after severeattacks, especially for asthmatic patients and those already receiving steroids. The beneficial effects are delayed at least 4 to 6 hours. c Envenomation. Rarely insect envenomation by bees, but not wasps, leaves a venom sac. Immediately scrape away any insect parts at the site of the sting.11 Squeezing is alleged to increase envenomation. Judicious local applicationof ice may also slow antigen absorption. The application of papain (available in meat tenderizers) to the stinger site is a common home remedy that appears to have no therapeutic value.12c Glucagon. For patients unresponsive to epinephrine, especiallythose receiving b-blockers, glucagon may be effective.This agent is short-acting (1 to 2 mg every 5 minutes IM or IV). Nausea, vomiting, and hyperglycemia arecommon side effects. c Observation. Observe closely up to 24 hours. Manypatients do not respond promptly to therapy, and symptomsmay recur in some patients (up to 20%) within 1 to 8 hoursdespite an intervening asymptomatic period.13–15

Management of Anaphylactic Shock
Position: Oxygen. Epinephrine. Antihistamines. H2 blockers. Inhaled b-adrenergic agents. Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV)

Corticosteroids. Infuse high-dose intravenous corticosteroids slowly or administer intramuscularly after severe attacks, especially for asthmatic patients and those already receiving steroids. The beneficial effects are delayed at least 4 to 6 hours Envenomation. Rarely insect envenomation by bees, but not wasps, leaves a venom sac. Immediately scrape away any insect parts at the site of the sting.Squeezing is alleged to increase envenomation. Judicious local application of ice may also slow antigen absorption. The application of papain (available in meat tenderizers) to the stinger site is a common home remedy that appears to have no therapeutic value. Glucagon. For patients unresponsive to epinephrine, especially those receiving b-blockers, glucagon may be effective.This agent is short-acting (1 to 2 mg every 5 minutes IM or IV). Nausea, vomiting, and hyperglycemia are common side effects. Observation. Observe closely up to 24 hours. Many patients do not respond promptly to therapy, and symptoms may recur in some patients (up to 20%) within 1 to 8 hours despite an intervening asymptomatic period phedrine ( /ɨˈfɛdrɪn/ or /ˈɛfɨdriːn/; not to be confused with ephedrone) is a sympathomimetic amine commonly used as a stimulant, appetite suppressant, concentration aid, decongestant, and to treat hypotension associated with anaesthesia. Ephedrine is similar in structure to the (semi-synthetic) derivatives amphetamine and methamphetamine. Chemically, it is an alkaloid derived from various plants in the genus Ephedra (family Ephedraceae). It works mainly by increasing the activity of noradrenaline on adrenergic receptors.[1] It is most usually marketed in the hydrochloride and sulfate forms. In traditional Chinese medicines, the herb má huáng (麻黄, Ephedra sinica) contains ephedrine and pseudoephedrine as its principal active constituents. The same is true of other herbal products containing extracts from some of the other Ephedra species.

Rapid Progression to Lethal Airway Obstruction
Close observation is required during conventional therapy Early, elective intubation is indicated for patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling. If respiratory function deteriorates, perform semi elective (awake, sedated) tracheal intubation without paralytic agents Angioedema. Patients are at high risk for rapid deterioration. Most will present with some degree of labial or facial swelling. Patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling are at particular risk for respiratory compromise Early tracheal intubation. If intubation is delayed, patients can deteriorate over a brief period of time (0.5 to 3 hours),with development of progressive stridor, severe dysphonia oraphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. At this point both tracheal intubation and cricothyrotomy may be difficult or impossible. Rapid Progression to Lethal Airway Obstruction Close observation is required during conventional therapy. Early, elective intubation is indicated for patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling. If respiratory function deteriorates, perform semi elective (awake, sedated) tracheal intubation without paralytic agents. Angioedema. Patients with angioedema pose a particularly worrisome problem because they are at high risk for rapid deterioration. Most will present with some degree of labial orfacial swelling. Patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling are at particular risk for respiratory compromise.Early tracheal intubation. If intubation is delayed, patients can deteriorate over a brief period of time (0.5 to 3 hours),with development of progressive stridor, severe dysphonia oraphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. At this point both tracheal intubation and cricothyrotomy may be difficult or impossible.Attempts at tracheal intubation may only further increase laryngeal edema or compromise the airway with bleeding into the oropharynx and narrow glottic opening. The patient may become agitated as a result of hypoxia and may be uncooperative with oxygen therapy.Paralysis followed by an attempt at tracheal intubation mayprove lethal, because the glottic opening is narrow and difficult to see because of the lingual and oropharyngeal edema and the patient is iatrogenically apneic. If tracheal intubation is not successful, even bag-mask ventilation maybe impossible, because laryngeal edema will prevent air entry and facial edema will prevent creation of an effective seal between the face and bag mask. Pharmacological paralysis at this point may deprive the patient of the sole mechanism for ventilation, ie, spontaneous breathing attempts.

During Cardiac Arrest: Key Interventions and Modifications of BLS/ALS Therapy
Airway, Oxygenation, and Ventilation Death may result from angioedema and upper or lower airway obstruction. Bag-mask ventilation and tracheal intubation may fail. Cricothyrotomy may be difficult or impossible because severe swelling will obliterate landmarks. In desperate circumstances, consider the other airway techniques: Fiber optic tracheal intubation Digital tracheal intubation, in which the fingers are used to guide insertion of a small (#7 mm) tracheal tube Needle cricothyrotomy followed by transtracheal ventilation Cricothyrotomy as described for the patient with massive neck swelling Support of Circulation : rapid volume resuscitation and administration of vasopressors to support blood pressure. Epinephrine is the drug of choice for treatment of both vasodilation/hypotension and cardiac arrest. Rapid volume expansion is an absolute requirement.—When anaphylaxis occurs, it can produce profound vasodilation that significantly increases intravascular capacity. Very large volumes should be administered over very short periods; typically 2 to 4 L of isotonic crystalloid should be given During Arrest: Key Interventions and Modifications of BLS/ALS Therapy Death from anaphylaxis may be associated with profound vasodilation, intravascular collapse, tissue hypoxia, and asystole.No data is available on how cardiac arrest procedures. ; should be modified, but difficulties in achieving adequate volume replacement and ventilation are frequent. Reasonable recommendations can be based on experience with non fatalcases.Airway, Oxygenation, and Ventilation Death may result from angioedema and upper or lower airway obstruction. Bag-mask ventilation and tracheal intubationmay fail. Cricothyrotomy may be difficult or impossiblebecause severe swelling will obliterate landmarks. Inthese desperate circumstances, consider the following airwaytechniques:c Fiberoptic tracheal intubationc Digital tracheal intubation, in which the fingers are used toguide insertion of a small (#7 mm) tracheal tubec Needle cricothyrotomy followed by transtracheal ventilationc Cricothyrotomy as described for the patient with massive neck swelling16 Support of Circulation Support of circulation requires rapid volume resuscitation and administration of vasopressors to support blood pressure.Epinephrine is the drug of choice for treatment of both vasodilation/hypotension and cardiac arrest .c Rapid volume expansion is an absolute requirement.—When anaphylaxis occurs, it can produce profound vasodilation that significantly increases intravascular capacity. Very large volumes should be administered over very short periods; typically 2 to 4 L of isotonic crystalloid should be given. c High-dose epinephrine IV (ie, rapid progression to high dose) should be used without hesitation in patients in full cardiac arrest.—A commonly used sequence: 1 to 3 mg IV (3 minutes),3 to 5 mg IV (3 minutes), then 4 to 10 mg/min. c Antihistamines IV. There is little data about the value of antihistamines in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result. c Steroid therapy. Although steroids should have no effectif given during a cardiac arrest, they may be of value in the post resuscitation period. Asystole/PEA Algorithms. Because the arrest rhythm inanaphylaxis is often PEA or asystole, the ILCOR panelrecommended adding the other steps in the Asystole and PEA Algorithms. These include—Administration of atropine—Transcutaneous pacing c Prolonged CPR. Cardiac arrest associated with anaphylaxis may respond to longer therapy than usual.—In these circumstances the patient is often a young person with a healthy heart and cardiovascular system.Rapid correction of vasodilation and low blood volume is required.—Effective CPR may maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reaction resolve.

During Cardiac Arrest: Key Interventions and Modifications of BLS/ALS Therapy
High-dose epinephrine IV (ie, rapid progression to high dose) should be used without hesitation in patients in full cardiac arrest.—A commonly used sequence: 1 to 3 mg IV (3 minutes),3 to 5 mg IV (3 minutes), then 4 to 10 mg/min. Antihistamines IV. There is little data about the value of antihistamines in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result. Steroid therapy. Although steroids should have no effect if given during a cardiac arrest, they may be of value in the post resuscitation period. Asystole/PEA Algorithms. Because the arrest rhythm in anaphylaxis is often PEA or asystole, the ILCOR panel recommended adding the other steps in the Asystole and PEA Algorithms: Administration of atropine—Transcutaneous pacing Prolonged CPR. Cardiac arrest associated with anaphylaxis may respond to longer therapy than usual.—In these circumstances the patient is often a young person with a healthy heart and cardiovascular system.Rapid correction of vasodilation and low blood volume is required.—Effective CPR may maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reaction resolve

Càm on ! CONCLUSION Develop research in anaphylaxis
EPs : critical role=first line Improve knowledge in Allergy Use Adrenaline even without hypotension Collaboration with allergist is essential Develop research in anaphylaxis Evaluation and management of the patient with a history of episodes of anaphylaxis The history is the most important tool to determine whether a patient has had anaphylaxis and the cause of the episode (C).A thorough differential diagnosis should be considered, and other conditions should be ruled out (C). Laboratory tests can be helpful to confirm a diagnosis of anaphylaxis or rule out other causes. Proper timing of such tests (eg, serum tryptase) is essential (B). In the management of a patient with a previous episode of anaphylaxis,education is necessary. Emphasis on early treatment,specifically the self-administration of epinephrine, is essential. Avoidance management should be individualized, takinginto consideration factors such as age, activity, occupation,hobbies, residential conditions, access tomedicalcare, and the patients’ level of personal anxiety. C96. Even in cases when the allergen is known, avoidance measures may not always be successful. Therefore, patients should be instructed in self-management of anaphylaxis.C97. Venom immunotherapy (VIT) is successful in preventing anaphylaxis in up to 98% of patients who have previously experienced venom-induced anaphylaxis. A98. Pharmacologic prophylaxis should be used in select situations,e.g. to prevent recurrent anaphylactic reactions to radiographic contrast material and fluorescein, as well as to prevent idiopathic anaphylaxis.In these specific situations, prophylaxis with glucocorticosteroids and antihistamines markedly reduces the occurrence of subsequent reactions. C99. Desensitization to medications that are known to have caused anaphylaxis can be effective. The desensitization is temporary, and if the medication is required in the future,the desensitization process must be repeated. C100. Patient education might be the most important preventive strategy. Càm on !

Management of the Anaphylactic Shock

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