World Allergy Organization anaphylaxis guidelines: Summary F. Estelle R. Simons, MD, FRCPC, Ledit R.F. Ardusso, MD, M. Beatrice Bilò, MD, Yehia M. El-Gamal, MD, PhD, Dennis K. Ledford, MD, Johannes Ring, MD, PhD, Mario Sanchez-Borges, MD, Gian Enrico Senna, MD, Aziz Sheikh, MD, FRCGP, FRCP, Bernard Y. Thong, MD  Journal of Allergy and Clinical Immunology  Volume 127, Issue 3, Pages 587-593.e22 (March 2011) DOI: 10.1016/j.jaci.2011.01.038 Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Patient factors that contribute to anaphylaxis. Age-related factors, concomitant diseases, and concurrent medications potentially contribute to severe or fatal anaphylaxis. Cofactors potentially amplify anaphylaxis. Multiple factors and cofactors likely contribute to some anaphylactic episodes. For relevant references, please see the Fig 1 legend published online at www.jacionline.org. Beta-blockers, β-adrenergic blockers; ACE inhibitors, angiotensin-converting enzyme inhibitors. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Anaphylaxis mechanisms and triggers. Anaphylaxis typically occurs through an IgE-dependent immunologic mechanism, most commonly triggered by foods, stinging insect venoms, or medications. Medications can also trigger anaphylaxis through an IgE-independent immunologic mechanism and through direct mast cell stimulation. Radiocontrast media can trigger anaphylaxis through both IgE-dependent and IgE-independent mechanisms. In patients with idiopathic anaphylaxis, the possibility of a novel allergen trigger or of underlying mastocytosis or a clonal mast cell disorder should be considered. For relevant references, please see the Fig 2 legend published online at www.jacionline.org. HMW, High molecular weight; NSAID, nonsteroidal anti-inflammatory drug. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 Clinical criteria for the diagnosis of anaphylaxis. For relevant references describing the clinical criteria of anaphylaxis, please see the Fig 3 legend published online at www.jacionline.org. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 Basic management of anaphylaxis. This figure summarizes the basic initial treatment which is relatively inexpensive to implement and should be possible even in a low resource environment. Steps 4, 5 and 6 should be performed promptly and simultaneously as soon as anaphylaxis is diagnosed. Resuscitation guidelines recommend initiating cardiopulmonary resuscitation with chest compressions only (hands-only) before giving rescue breaths. In adults, chest compressions should be performed at a rate of 100-120/minute and a depth of 5-6 cm. In children, the rate should be at least 100 compressions/minute at a depth of 5 cm (4 cm in infants). If precious minutes are lost early in the treatment of an acute anaphylactic episode, subsequent management can become more difficult. For relevant references, please see the Fig 4 legend published online at www.jacionline.org. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 5 Discharge management and prevention of future anaphylaxis recurrences in the community. Panel 1 describes management at the time of discharge after treatment of an acute anaphylactic episode in a healthcare setting. Panel 2: Anaphylaxis triggers suggested by the history of the acute episode should be confirmed by measurement of allergen-specific IgE levels (sometimes performed before discharge) and by allergen skin tests (generally performed 3-4 weeks after the acute anaphylactic episode; however, for most allergens, this time interval has not been definitively established in prospective studies). Patients with a convincing history of anaphylaxis and negative tests should therefore be retested weeks or months later. Panel 3 summarizes long-term risk reduction through avoidance of known confirmed triggers and where relevant, immunomodulation, for example, medication desensitization according to published protocols, or immunotherapy with appropriate standardized venom to prevent anaphylaxis recurrences from insect (Hymenoptera) stings. For relevant references, please see the Fig 5 legend published online at www.jacionline.org. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 1 Patient factors that contribute to anaphylaxis. Age-related factors, concomitant diseases, and concurrent medications potentially contribute to severe or fatal anaphylaxis. Co-factors potentially amplify anaphylaxis. Multiple factors and co-factors likely contribute to some anaphylactic episodes.2,8-13,31-47,57 Atopic diseases are a risk factor for anaphylaxis triggered by food, exercise, and latex, but not for anaphylaxis triggered by insect stings and medications. Beta-blockers: beta-adrenergic blockers; ACE inhibitors: angiotensin-converting enzyme inhibitors. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 2 Anaphylaxis mechanisms and triggers. Anaphylaxis typically occurs through an IgE-dependent immunologic mechanism, most commonly triggered by foods, stinging insect venoms, or medications. Medications can also trigger anaphylaxis through an IgE-independent immunologic mechanism and through direct mast cell activation. Radiocontrast media can trigger anaphylaxis through both IgE-dependent and IgE-independent mechanisms. Anaphylaxis triggered by seminal fluid or by inhalant allergens is rare, and likely involves some systemic absorption of the allergen. In patients with idiopathic anaphylaxis, the possibility of a novel allergen trigger or of underlying mastocytosis or a clonal mast cell disorder should be considered.2,22-25,31,32,53-87 NSAID, nonsteroidal anti-inflammatory drug; HMW, high molecular weight. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 3 Clinical criteria for the diagnosis of anaphylaxis. The clinical criteria pictured are taken from reference 2. Anaphylaxis with involvement of only one body organ system is described in references 2 and 33. Anaphylaxis in infants and young children is described in reference 34. Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 4 Basic management of anaphylaxis. This figure summarizes the basic initial treatment which is relatively inexpensive to implement and should be possible even in a low resource environment. Steps 4, 5 and 6 should be performed promptly and simultaneously as soon as anaphylaxis is diagnosed. Resuscitation guidelines recommend initiating cardiopulmonary resuscitation with chest compressions only (hands-only) before giving rescue breaths. In adults, chest compressions should be performed at a rate of 100-120/minute and a depth of 5-6 cm. In children, the rate should be at least 100 compressions/minute at a depth of 5 cm (4 cm in infants). If precious minutes are lost early in the treatment of an acute anaphylactic episode, subsequent management can become more difficult.2,22-25,32,93-99 Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 5 Discharge management and prevention of future anaphylaxis recurrences in the community. Panel 1 describes management at the time of discharge after treatment of an acute anaphylactic episode in a healthcare setting. Panel 2: Anaphylaxis triggers suggested by the history of the acute episode should be confirmed by measurement of allergen-specific IgE levels (sometimes performed before discharge) and by allergen skin tests (generally performed 3-4 weeks after the acute anaphylactic episode; however, for most allergens, this time interval has not been definitively established in prospective studies). Patients with a convincing history of anaphylaxis and negative tests should therefore be retested weeks or months later. Panel 3 summarizes long-term risk reduction through avoidance of known confirmed triggers and where relevant, immunomodulation, for example, medication desensitization according to published protocols, or immunotherapy with appropriate standardized venom to prevent anaphylaxis recurrences from insect (Hymenoptera) stings.2,22-25,32,59,68,69,72,73,76,77,87,96,97,99,132-139 Journal of Allergy and Clinical Immunology 2011 127, 587-593.e22DOI: (10.1016/j.jaci.2011.01.038) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions