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GLORIA Module 8: Anaphylaxis

GLORIA Module 8: Anaphylaxis. Updated: June 2011. Sponsored by an unrestricted educational grant from. Global Resources in Allergy (GLORIA™).

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GLORIA Module 8: Anaphylaxis

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  1. GLORIA Module 8:Anaphylaxis Updated: June 2011

  2. Sponsored by an unrestricted educational grant from

  3. Global Resources in Allergy (GLORIA™) Global Resources In Allergy (GLORIA™) is the flagship program of the World Allergy Organization (WAO). Its curriculum educates medical professionals worldwide through regional and national presentations. GLORIA modules are created from established guidelines and recommendations to address different aspects of allergy-related patient care.

  4. World Allergy Organization (WAO) The World Allergy Organization is an international coalition of 89 regional and national allergy and clinical immunology societies.

  5. WAO’s Mission WAO’s mission is to be a global resource and advocate in the field of allergy, advancing excellence in clinical care, education, research and training through a world-wide alliance of allergy and clinical immunology societies

  6. GLORIA Module 8:Anaphylaxis WAO Expert PanelRichard F. Lockey, USAMichael A. Kaliner, USAF. Estelle R. Simons, CanadaCassim Motala, South AfricaBob Lanier, USAAdditional contributor: Aziz Sheikh, UK

  7. Definition of anaphylaxis Anaphylaxis is a severe life-threatening generalized or systemic hypersensitivity reaction. It is commonly, but not always, mediated by an allergic mechanism, usually by IgE. Allergic (immunologic) non-IgE-mediated anaphylaxis also occurs. Non-allergic anaphylactic reactions, formerly called anaphylactoid or pseudo-allergic reactions, may also occur. Johansson SGO et al JACI 2004,113:832-6

  8. Revised nomenclature for anaphylaxis Anaphylaxis Allergic anaphylaxis Non-allergic anaphylaxis IgE- mediated anaphylaxis Immunologic, non-IgE-mediated anaphylaxis Johansson SGO et al JACI 2004,113:832-6

  9. Gell and Coombs classification of hypersensitivity Type I Immediate hypersensitivity Type II Cytotoxic reactions Type III Immune complex reactions Type IV Delayed hypersensitivity Anaphylaxis can occur through Types I, II and III immunopathologic mechanisms Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8

  10. Mechanisms of allergic anaphylaxis …a severe, acute, systemic allergic reaction caused by the rapid, IgE-mediated release of potent mediators such as histamine from tissue mast cells and peripheral blood basophils

  11. Acutely released mediators of anaphylaxis • degranulation of mast cells and basophils causes the release of: - preformed granule-associated substances, eg histamine, tryptase, chymase, carboxypeptidase, and cytokines - newly-generated lipid-derived mediators, eg prostaglandin D2, leukotriene (LT) B4, LTC4, LTD4, LTE4, and platelet activating factor. Kemp SF and Lockey RF. J Allergy Clin Immunol 2002; 110:341-8

  12. Primary symptoms of anaphylaxis • Skin: flushing, itching, urticaria, angioedema • Respiratory: dysphonia, cough, stridor, wheezing, dyspnea, chest tightness, asphyxiation, death • Gastrointestinal: nausea, vomiting, bloating, cramping, diarrhea Cardiovascular: tachycardia, hypotension, dizziness, collapse, death • Other: • feeling of impending doom, • metallic taste

  13. Comments about anaphylaxis signs and symptoms • skin symptoms occur most commonly ( > 90% of patients) • skin, oral, and throat symptoms are often the first ones noted • respiratory symptoms occur in 40% to 70% of patients • gastrointestinal symptoms occur in about 30% of patients • shock occurs in about 10% of patients • signs and symptoms are usually seen within 5 to 30 minutes • the more rapid the onset, the more serious the reaction Lieberman P. In: Middleton’s Allergy: Principles and Practice, 6th edition, Mosby Inc., St. Louis, MO, 2003

  14. Biphasic and protracted anaphylaxis • biphasic anaphylaxis is defined as return of symptoms after resolution of initial symptoms, without subsequent allergen exposure • usually, symptoms return within 1 to 8 hours (sometimes longer) • up to 20% of anaphylactic reactions are biphasic • patients with biphasic anaphylaxis may require more epinephrine to control initial symptoms • in protracted anaphylaxis, symptoms may be continuous for 5-32 hrs Lieberman P. Ann Allergy Asthma Immunol 2005;95:217-26

  15. Biphasic/late-phase reaction Cellular infiltrates: 3 to 6 hours (LPR) Eosinophil CysLTs, GM-CSF, TNF-, IL-1, IL-3, PAF, ECP, MBP Histamine IL-4, IL-6 Allergen Basophil 3 to 6 hours (CysLTs, PAF,IL-5) Histamine,CysLTs,TNF-, IL-4, IL-5, IL-6 Return of Symptoms Monocyte CysLTs CysLTs, TNF-, PAF, IL-1 PGs Proteases Mast cell Lymphocyte IL-4, IL-13, IL-5, IL-3, GM-CSF EPR 15 min (Early-Phase Reaction)

  16. Differential diagnosis of anaphylaxis • vasovagal reactions • flushing • mastocytosis • carcinoid syndrome • hyperventilation syndrome • globus hystericus • hereditary angioedema • other types of shock, eg. cardiogenic, septic • scombroid poisoning Montanaro A and Bardana EJ Jr. J Investig Allergol Clin Immunol 2002;12:2-11

  17. Incidence and prevalence of anaphylaxis • “anaphylaxis in the US: an investigation into its epidemiology" - on the basis of a literature review, more than 1.21% of the population may be affected • independent US Omnibus Studies (2002 and 2003) - 32 million have had 2 or more symptoms - 18 million diagnosed - 11 million have suffered a life-threatening reaction Neugut AI et al. Arch Intern Med 2001;161:15-21 Dey, L.P. Independent omnibus studies. Data on file. 2002-2003

  18. Incidence and prevalence of anaphylaxis (cont.) • 5-year review of 1.15 million persons in Manitoba, Canada • dispensing patterns of epinephrine for out-of-hospital treatment • 0.95% of the general population had epinephrine dispensed • dispensing rates in the general population varied with age - 1.44% for individuals <17 years of age - 0.9% for those 17-64 years of age - 0.32% for those >65 years of age • interpretation: anaphylaxis from all triggers, occurring out of hospital, appears to peak in childhood, and then gradually decline Simons FER et al. J Allergy Clin Immunol 2002;110:647-51

  19. International collaborative study of severe anaphylaxis • Objective • To quantify the risk of anaphylaxis due to drugs and other exposures in hospital patients • Methods • Hospitals in Sweden, Hungary, India and Spain • Incident cases 1992-1995 • Clinical diagnosis using a priori agreed criteria, independent of presumed trigger • Epidemiology 1998;9:141-46

  20. International collaborative study of severe anaphylaxis (cont.) • Main findings • 123/481,752 i.e. risk of 15-20/100,000 admissions • 33% males • Median age ~53 • 79% respiratory symptoms; 70% cardiovascular symptoms; 49% both • Death in 2% of cases • Epidemiology 1998;9:141-46

  21. UK anaphylaxis death register • Objective • To understand the circumstances leading to fatal anaphylaxis • Methods • Running since 1992; ONS mortality data coded for anaphylaxis since 1993 • Detailed information obtained from medical records, medical staff, coroners officers and mast cell serum tryptase • Adrenaline rarely used before cardiac arrest Pumphrey RSH, Clin Exp Aller 2000; J Clin Pathol 2000; Novartis Found Symp 2004

  22. UK anaphylaxis death register (cont.) • Main findings • ~20 recorded deaths/year i.e. ~1:2.8 million • 50% iatrogenic; 25% food and 25% venom • ~50% died from asphyxia (food) and 50% from shock (iatrogenic and venom) • Median time to death: 5 mins if iatrogenic; 15 mins venom; and 30 mins food • Adrenaline rarely used before cardiac arrest Pumphrey RSH, Clin Exp Aller 2000; J Clin Pathol 2000; Novartis Found Symp 2004

  23. Hong Kong ED • Objective • To describe the epidemiology, clinical features and management of anaphylaxis • Methods • Retrospective review of all age patients in one ED, 1999-2003 • Clinical diagnosis of anaphylaxis • Main findings • ~1/2800 attendances for anaphylaxis Smit DV et al. J Emer Med 2005;28:381-88

  24. foods (eg peanut, tree nuts, seafood) medications (eg, β-lactam antibiotics) venoms latex allergen immunotherapy diagnostic allergens exercise (with food or medication co-trigger) hormones animal or human proteins colorants (insect-derived, eg. carmine) enzymes polysaccharides aspirin and NSAIDs (possibly through IgE) Agents that cause anaphylaxis: IgE-dependent triggers Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

  25. Risk of anaphylaxis • estimated risk in US: 1-3% • fatalities per year in the US: • - food-induced: 150 • - antibiotic-induced: 600 • - venom-induced: 50 Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

  26. Food-induced anaphylaxis • many anaphylactic reactions are caused by food - accidental food exposures are common and unpredictable • anaphylaxis from food can occur at any age, but children, teens and young adults are at highest risk • prevalence of peanut allergy has doubled in children <5 years of age in the last 5 years • seafood allergy is reported by 2.3% of the US population, and is more common in adults than in children Sampson HA. J Allergy Clin Immunol 2004;113:805-19 Sicherer SH et al. J Allergy Clin Immunol 2004;114:159-65

  27. Most common food allergies • peanut • tree nut • seafood • fin fish • milk • egg • soy • wheat

  28. Fatal food-induced anaphylaxis • in a retrospective analysis of 32 deaths in patients age 2-33 years - peanut and tree nuts caused >90% of reactions - most patients had a history of asthma - most did not have injectable epinephrine available at the time of their reaction and death Bock SA et al. J Allergy Clin Immunol 2001;107:191-3

  29. Hymenoptera stings • 0.5% to 5% of the US population is allergic to Hymenoptera venom(s) • bees • wasps • yellow jackets • hornets • fire ants • at least 50 deaths per year • incidence rising due to - increased numbers of fire ants and Africanized bees - increased numbers of people engaged in outdoor activities Neugut AI et al. Arch Intern Med 2001;161:15-21

  30. Iatrogenic anaphylaxis • estimated 550,000 serious allergic reactions to drugs/year in US hospitals • most common drug triggers - penicillin (highest number of documented deaths from anaphylaxis) - sulfa drugs - non-steroidal anti-inflammatory drugs - muscle relaxants • most common biologic triggers - anti-sera for snakebite - anti-lymphocyte globulin - vaccines - allergens Neugut AI et al. Arch Intern Med 2001;161:15-21 Lazarou J et al. JAMA 1998;279:1200-5

  31. Latex-induced anaphylaxis • <1% of the US general population • prevalence is highest among healthcare workers • latex gloves, especially if powdered, are a common trigger • repeated exposure leads to higher risk • incidence increased dramatically in the mid-1980s, but has decreased progressively with more use of non-powdered latex gloves and use of non-latex gloves Neugut AI et al. Arch Intern Med 2001;161:15-21

  32. Peri-operative anaphylaxis • neuromuscular blocking drugs (muscle relaxants), eg suxamethonium, rocuronium, alcuronium, atracurium • induction agents, eg thiopentone, propofol, alfathesin • other: including local anesthetics, antibiotics, protamine, • and latex • predisposing factors: atopy, asthma; previous exposure Fisher M. In: Anaphylaxis, John Wiley & Sons Ltd., Chichester, UK, 2004:193-206

  33. Allergen immunotherapy-induced anaphylaxis • fatal reactions are uncommon: 1 per 2,000,000 injections • risk factors for fatality include: - dosing errors - poorly controlled asthma (FEV1 < 70%) - concomitant β-blocker use - lack of proper equipment and trained personnel - inadequate epinephrine treatment Stewart GE and Lockey RF. J Allergy Clin Immunol 1992;90:567-78 Bernstein DI et al, J Allergy Clin Immumol 2004;113:1129-36

  34. Food-dependent exercise-induced anaphylaxis • reported in USA, Thailand and Japan • most commonly occurs in females, and from late teens to mid-30’s • triggered by exercise 2-4 hours after ingesting offending food • foods implicated: wheat, seafood, fruit, milk,celery and fish. • associations: asthma, positive skin prick tests to foods • mechanism: two signals required Aunhachoke K et al. J Med Assoc Thai 2002;85:1014-8 Aihara Y et al. J Allergy Clin Immunol 2001;108:1035-9

  35. Anaphylaxis from immune causes other than IgE • cytotoxic (Type II) - transfusion reactions to cellular elements (IgG, IgM) • immune aggregates (Type III) - intravenous immunoglobulin - Dextran (possibly) Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

  36. Anaphylaxis: non-immunologic causes MULTIMEDIATOR COMPLEMENT ACTIVATION/ACTIVATION OF CONTACT SYSTEM • radiocontrast media • ethylene oxide gas on dialysis tubing (possibly through IgE) • protamine (possibly) • ACE-inhibitor administered during renal dialysis with sulfonated polyacrylonitrile, cuprophane, or polymethylmethacrylate dialysis membranes Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

  37. Anaphylaxis: non-immunologic causes NONSPECIFIC DEGRANULATION OF MAST CELLS AND BASOPHILS • opiates • physical factors: - exercise (no food or medication co-trigger) - temperature (cold, heat) Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8

  38. Idiopathic anaphylaxis • common in adults who are referred to allergists for evaluation of anaphylaxis • uncommon in children • negative skin tests, negative dietary history, no associated diseases eg. mastocytosis • preventive medication: oral corticosteroids, H1 & H2 antihistamines, anti-leukotrienes • deaths rare • may gradually improve over time Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-S523

  39. Most common precipitating causes De Bruyne JA and Lee BW. Allergy Clin Immunol Int: J World Allergy Org 2004;16:137-41

  40. -Adrenergic blockade • by mouth or topically • paradoxical bradycardia, severe hypotension and bronchospasm • can exacerbate disease and impede treatment • selective β-blockers can produce clinically significant adverse respiratory effects even in mild-moderate asthma and COPD; not studied in anaphylaxis Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-523

  41. Diagnosing anaphylaxis • clinical diagnosis based on clinical presentation and exposure history • flushing and tachycardia are invariably present, other cutaneous symptoms (hives, itch) may be absent • anaphylaxis may be difficult to diagnose, especially when patients present with bradycardia (instead of tachycardia, which is usual) • very rarely, patients present only with profound hypotension. The exposure to some inciting event is one key to the diagnosis in this rare circumstance Lieberman PL et al. J Allergy Clin Immunol 2005;115:S483-523

  42. Diagnosing anaphylaxis (cont.) • careful history to identify possible causes • can be confirmed by an elevated serum tryptase level - specific for mast cell degranulation - remains elevated for up to 6 hours - may not be elevated, especially in food allergy • refer to allergist for specific testing Lieberman PL et al, J Allergy Clin Immunol 2005;115:S483-523

  43. Laboratory tests in the diagnosis of anaphylaxis Plasma histamine Serum tryptase 24-hr Urinary histamine metabolite 0 30 60 90 120 150 180 210 240 270 300 330

  44. Problems with laboratory tests • histamine and tryptase levels may not correlate with each other • histamine level was elevated in 42 of 97 patients in the Emergency Department, but only 20 of 97 had an elevated tryptase level • histamine levels also correlated better with symptoms and signs • plasma histamine levels only remain elevated for one hour after symptom onset; therefore, this test is usually not practical Lin RY et al. J Allergy Clin Immunol 2000;106:65-71

  45. Diagnosing anaphylaxis Allergists can identify specific causes by: • complete and accurate medical/allergy history • skin tests/specific IgE levels - foods - insect venoms - drugs (some) • challenge tests: (selected patients, physician-monitored, preferably in hospital) - foods - NSAIDs - exercise Simons FER. J Allergy Clin Immunol 2006;117:367-77

  46. Office management of anaphylaxis: checklist of equipment and drugs required • stethoscope and sphygmomanometer • tourniquets, syringes, needles (including large bore 14-gauge) • injectable epinephrine (adrenaline) 1:1000 • oral airway and endotracheal tubes • oxygen, and equipment to administer it • diphenhydramine (or similar) injectable antihistamine • corticosteroids for IV injection • vasopressor (eg dopamine, noradrenaline) • glucagon • automatic defibrillator

  47. Physician-supervised management of anaphylaxis I. Speed is critical: a) assess airway, breathing, circulation, and mentation b) epinephrine, IM into the muscle of the anterolateral thigh; 1:1000 dilution, 0.3 - 0.5 mL (0.01 mg/kg in children); repeat, every 5-15 minutes as necessary. Kemp S and Lockey R. J Allergy Clin Immunol 2002;110:341-8 Simons FER et al. J Allergy Clin Immunol 1998;101:33-7 Simons FER et al. J Allergy Clin Immunol 2001;108:871-3

  48. Physician-supervised management of anaphylaxis II. Secondary measures: a) place patient in recumbent position and elevate his/her legs b) maintain airway (endotracheal tube or cricothyrotomy) c) oxygen, 6 - 8 liters/minute d) normal saline IV; volume expanders (colloid solution) for severe hypotension Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8

  49. Physician-supervised management of anaphylaxis III. Other measures: a) epinephrine 1:1000, ½ dose (0.1- 0.2 mg) into reaction site diphenhydramine, 50 mg IV or orally (1.25 mg/kg, up to 50 mg dose for children); maximum daily dose: adults 400 mg; children 200 mg b) ranitidine, 50 mg in adults and 12.5 - 50 mg (1 mg/kg) in children, dilute in 5% D/W, total 20 ml, inject slowly IV, over 5 minutes (cimetidine 4 mg/kg OK for adults, dose not established for children) Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8

  50. Physician-supervised management of anaphylaxis • for bronchospasm - nebulized albuterol (salbutamol) 2.5 - 5 mg in 3 ml normal saline • for refractory hypotension - dopamine, 400 mg in 500 ml normal saline IV 2 - 20 μg/kg/min - glucagon, 1- 5 mg (20 - 30 μg/kg, max 1 mg in children), IV over 5 minutes followed with continuous IV infusion 5-15 μg/min - methylprednisolone, 1- 2 mg/kg per 24 hr Kemp SF and Lockey RF. J Allergy Clin Immunol 2002;110:341-8

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