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GLORIA ™ is supported by unrestricted educational grants from

GLORIA ™ is supported by unrestricted educational grants from. GLORIA Module 3 Allergic Emergencies. WAO Expert Panel Authors: Richard F Lockey, USA Connie H Katelaris, Australia Michael Kaliner, USA Contributors: F.Estelle R. Simons, Canada Daniel Vervloet, France. Allergic Emergencies.

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  1. GLORIA™ is supported by unrestricted educational grants from

  2. GLORIA Module 3Allergic Emergencies

  3. WAO Expert PanelAuthors:Richard F Lockey, USAConnie H Katelaris, AustraliaMichael Kaliner, USAContributors:F.Estelle R. Simons, CanadaDaniel Vervloet, France Allergic Emergencies

  4. Allergic Emergencies Section 1: Anaphylaxis Section 2: Upper Airway Oedema Section 3: Severe Asthma Exacerbations

  5. Allergic Emergencies Section 1: Anaphylaxis

  6. Anaphylaxis Lecture Objectives After this lecture, participants will: • Have knowledge of the different mechanisms which cause anaphylaxis and the agents which are most likely to cause it; • Be able to recognize the signs and symptoms of anaphylaxis; • Understand how to treat anaphylaxis.

  7. Definition of Anaphylaxis • Anaphylaxis – a syndrome with varied mechanisms, clinical presentations, and severity. • An acute life-threatening reaction. • Usually mediated by an immunologic mechanism, allergic anaphylaxis, but not always. • Includes non-allergic anaphylaxis (formerly referred to as an anaphylactoid reaction). • Results from the release of mast-basophil mediators. WAO Nomenclature Review Committee JACI2004

  8. Gell and Coombs’ Hypersensitivity (immunopathologic reactions) • Type I Immediate • Type II Cytotoxic • Type III Immune Complex • Type IV Delayed Hypersensitivity • Types I, II and III can result in immunologically-induced or allergic anaphylaxis Kemp and Lockey JACI 2002

  9. Biochemical Mediators and Chemotactic Substances • Degranulation of mast cells and basophils. • Preformed granule-associated substances, e.g., histamine, tryptase, chymase, heparin, histamine-releasing factor, other cytokines. • Newly generated lipid-derived mediators, e.g., prostaglandin D2, leukotriene B4, PAF, LTC4, LTD4, and LTE4. • Eosinophils may play pro-inflammatory role (release of cytotoxic granule-associated proteins) or anti-inflammatory role (e.g., metabolism of vasoactive mediators). Kemp and Lockey JACI 2002

  10. Shock Organs in Anaphylaxis • Guinea pig – bronchial smooth muscle constriction. • Rabbit– fatal pulmonary artery vasoconstriction with right ventricular failure. • Dog – venous system of liver contracts producing hepatic congestion. • Human – shock organs are the cardiovascular system, respiratory tract, skin, and gastrointestinal tract. Laryngeal oedema, respiratory failure, and circulatory collapse are common. • Asthma is an important risk factor for death from anaphylaxis. Kemp and Lockey JACI 2002 Bock, Munoz-Furlong, Sampson JACI 2001

  11. Incidence • Analysis of published studies of most common causes • 3.3 to 4 million Americans at risk. • 1,433 to 1,503 at risk for fatal reaction. Neugut, Ghatak, Miller Arch Int Med 2001 Incidence Based on Epinephrine Rx for Out-of-Hospital Use • From Canada and Wales. • 0.95% of population in Manitoba, Canada. • 0.2 per 1000 in Wales. • Incidence increased in Wales between 1994 & 1999. Simons, Peterson, BlackJACI 2002 Rangaraj, Tuthill, Burr, AlfahamJACI 2002

  12. Incidence of Anaphylaxis to Specific Agents 1 Antibiotics • Most common cause of drug induced anaphylaxis. Latex • Increased incidence last decade. • Population at risk includes multiple mucosal exposure to latex (catheterization & surgery) and healthcare workers. Radiocontrast agents • Introduction of lower osmolarity agents reduced reaction rate Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  13. Incidence of Anaphylaxis to Specific Agents 2 Hymenoptera stings • Incidence ranges from 0.4% to 5% • Estimated fatalities 100 per year in U.S.A. Food • Estimated 2% of US population has food allergies with up to 100 deaths per year • Shellfish most common in adults; peanuts in children Lieberman In Allergy: Principles and Practice Mosby, 2003

  14. Incidence of Anaphylaxis to Specific Agents 3 Perioperative anaphylaxis • Incidence ranges from 1 in 4500 to 1 in 2500 cases of general anaesthesia • Mortality rate can be as high as 3.4% • Most common agents responsible are muscle relaxants, which account for 50% to 75% of reactions. Lieberman In Allergy: Principles and Practice Mosby, 2003

  15. Incidence of Anaphylaxis to Specific Agents 4 Non Steroidal Anti-Inflammatory Drugs (NSAIDs) • Incidence varies depending on whether asthmatic subjects are included • NSAIDs probably second most common offending drug next to antibiotics. Lieberman In Allergy: Principles and Practice Mosby, 2003

  16. Incidence of Anaphylaxis to Specific Agents 5 Antisera • Heterologous antisera to treat snake bites (4.6% to 10%) • Immunosuppression, incidence for anti-lymphocyte globulin as high as 2% Idiopathic • Estimated to be between 20,592 and 47,024 cases in USA – deaths rare Lieberman in Allergy: Principles and Practice Mosby 2003

  17. Allergen Immunotherapy • Incidence of systemic reaction from 0.8% to 46.7% depending on the dose of allergen and schedule used. • Deaths occur at a rate of 1 per 2,000,000 injections. Stewart and Lockey JACI 1992 Kemp et al In: Allergens and Allergen Immunotherapy Marcel Dekker, 2004

  18. Diffuse erythema Diffuse pruritus Diffuse urticaria Angioedema Bronchospasm Laryngeal edema Hyperperistalsis Hypotension Cardiac arrhythmias Nausea Vomiting Lightheadedness Headache Feeling of impending doom Unconsciousness Flushing Signs and Symptoms of Anaphylaxis Kemp and Lockey JACI 2002

  19. Differential Diagnostic Considerations in Anaphylaxis • Vasovagal reactions • Idiopathic flushing • Mastocytosis • Carcinoid syndrome • Anxiety-induced hyperventilation • Globus hystericus • Serum sickness • C-1 esterase inhibitor deficiency • Shock-associated with myocardial infarction, blood loss, septicemia • Scombroid poisoning Montanaro and Bardana JACI 2002

  20. Comments About Signs and Symptoms of Anaphylaxis • Urticaria or angioedema and flush most common ( > 90%). • Cutaneous manifestations may be delayed or absent • Next most common manifestations are respiratory (40% to 60%). • Next are dizziness, unconsciousness (30% to 35%). • Gastrointestinal symptoms (20% to 30%). • More rapid onset, more likely serious. • Signs and symptoms within 5 to 30 minutes, but may not develop for hours. Lieberman In Allergy: Principles and Practice Mosby, 2003

  21. Foods (peanut, tree nuts, and crustaceans) Milk, egg and fish also important, especially in children Medications (antibiotics) Venoms Latex Allergen vaccines Hormones Animal or human proteins Diagnostic allergens Muscle relaxants Colorants (insect-derived, such as carmine) Enzymes Polysaccharides Aspirin and other non-steroidal anti-inflammatory drugs (probably) Exercise (possibly, in food and medication-dependent events) Agents that Cause Anaphylaxis 1Anaphylactic (IgE-Dependent) Kemp Immunol Allergy Clin N Am 2001

  22. Agents that Cause Anaphylaxis 2 (Allergic but not IgE Mediated) Immune aggregates (Type II) • Intravenous immunoglobulin • Dextran (possibly) Cytotoxic (Type III) • Transfusion reactions to cellular elements (IgG, IgM) Kemp Immunol Allergy Clin N Am 2001

  23. Agents that Cause Anaphylaxis 3 (Non-allergic or IgE-independent) Multimediator complement activation/activation of contact system: • Radiocontrast media • Ethylene oxide gas on dialysis tubing • Protamine (possibly) • ACE-inhibitor administered during renal dialysis with sulfonated polyacrylonitrile, cuprophane, or polymethylmethacrylate dialysis membranes Kemp Immunol Allergy Clin N Am 2001

  24. Agents that Cause Anaphylaxis 4(Non-allergic or IgE Independent) Nonspecific degranulation of mast cells and basophils • Opiates • Idiopathic • Physical factors: • Exercise • Temperature (cold, heat) Kemp Immunol Allergy Clin N Am 2001

  25. -Adrenergic Blockade • By mouth or topically. • Paradoxical bradycardia, profound hypotension, and severe bronchospasm. • Can exacerbate disease and may impede treatment. • Selective β-blockers do not produce clinically significant adverse respiratory effects in mild-moderate asthma (including COPD). Not studied in anaphylaxis. Toogood CMAJ 1987 Kivity and Yarchovsky JACI 1990 Salpeter, Ormiston, Salpeter Annals Int Med 2002

  26. Recurrent and Persistent Anaphylaxis • Recurrent or biphasic anaphylaxis occurs 8 to 12 hours in up to 20%. • Subjects with biphasic do not differ clinically but more epinephrine may be necessary for initial symptoms. • Persistent anaphylaxis may last from 5 to 32 hours. Lee and Greenes Pediatrics, 2000 Kemp and deShazo In: Allergens and Allergen Immunotherapy to Treat Allergic Diseases. Marcel Dekker, 2004

  27. Physician-Supervised Management of Anaphylaxis 1 I. Immediate Intervention a) Assessment of airway, breathing, circulation, and mentation. b) Administer EPI, 1:1000 dilution, 0.3 - 0.5 ml (0.01 mg/kg in children, max 0.3 mg dosage) IM, to control SX and BP. Repeat, as necessary. Kemp and Lockey JACI 2002 Simons et al JACI 1998 Simons, Gu, Simons JACI 2001

  28. Physician-Supervised Management of Anaphylaxis 2 I. Immediate Intervention continued c) IM into the anterolateral thigh (vastus lateralis) produces higher & more rapid peak plasma level versus SQ & IM in arm. Therefore, with moderate, severe, or progressive ANA, EPI IM into anterolateral thigh. Alternatively, an EPI autoinjector given through clothing in same manner. Repeat, as necessary. Kemp and Lockey JACI 2002 Simons et al JACI 1998 Simons, Gu, Simons JACI 2001

  29. Physician-Supervised Management of Anaphylaxis 3 I. Immediate Intervention - continued d) Aqueous EPI 1:1000, 0.1- 0.3ml in 10ml NS (1:100,000 to 1:33,000 dilution), IV over several minutes prn. e) For potentially moribund subjects, tubercular syringe, EPI 1:1000, 0.1 ml, insert into vein (IV), aspirate 0.9 ml of blood (1:10,000 dilution). Give as necessary for response. Kemp and Lockey JACI 2002

  30. Physician-Supervised Management of Anaphylaxis 4 II. General measures a) Place in recumbent position and elevate lower extremities. b) Maintain airway (endotracheal tube or cricothyrotomy). c) O2, 6 - 8 liters/minute. d) NS, IV. If severe hypotension, give volume expanders (colloid solution). e) Venous tourniquet above reaction site. Question if decreases absorption of allergen. Kemp and Lockey JACI 2002

  31. Physician-Supervised Management of Anaphylaxis 4 III. Specific Measures that Depend on Clinical Scenario a) Aqueous EPI 1:1,000, ½ dose (0.1- 0.2 mg) at reaction site. b) Diphenhydramine, 50 mg or more in divided doses orally or IV, maximum daily dose 200 mg (5 mg/kg) for children and 400 mg for adults. c) Ranitidine, 50 mg in adults and 12.5 - 50 mg (1 mg/kg) in children, dilute in 5% G/W, total 20 ml, inject IV, over 5 minutes. (Cimetidine 4 mg/kg OK for adults, not established for pediatrics). Kemp and Lockey JACI 2002

  32. Physician-Supervised Management of Anaphylaxis 5 III. Specific Measures that Depend on Clinical Scenario d) Bronchospasm, nebulized albuterol 2.5 - 5 mg in 3 ml NS or levalbuterol 0.63 - 1.25 mg as needed. e) Aminophylline, 5mg/kg over 30 min IV may be helpful. Adjust dose based on age, medications, disease, current use. f) Refractory hypotension, give dopamine, 400 mg in 500 ml G/W IV 2 - 20 μg/kg/min more or less. Kemp and Lockey JACI 2002

  33. Physician-Supervised Management of Anaphylaxis 6 III. Specific Measures that Depend on Clinical Scenario g) Glucagon, 1- 5 mg (20 - 30 μg/kg [max 1 mg] in children), administered IV over 5 minutes followed with IV infusion 5-15 μg/min. h) Methylprednisolone, 1- 2 mg/kg per 24 hr; prevents prolonged reactions and relapses. Kemp and Lockey JACI 2002

  34. Vasodepressor (Vaso-Vagal) Definition • Non-allergic reaction characterized by slow pulse nausea, pallor, sweating, clammy skin, and/or hypotension. Kemp and Lockey JACI 2002

  35. Vasodepressor (Vaso-Vagal) Management a) Place patient in supine position with elevated lower extremities. b) For severe vasodepressor reaction ONLY (i.e., bradycardia, nausea, pallor, sweating, cool clammy skin, hypotension), atropine 0.3 - 0.5 mg (0.02 mg/kg) SQ every 10 minutes (max 2 mg/adult and 1 mg/child). c) If hypotension persists, give IV fluids. Kemp and Lockey JACI 2002

  36. Measures to Reduce the Incidence of Drug- Induced Anaphylaxis and Anaphylactic Deaths 1 General Measures • Obtain thorough history for drug allergy. • Avoid drugs with immunological or biochemical cross-reactivity with any agents to which the patient is sensitive. • Administer drugs orally rather than parenterally when possible. • Check all drugs for proper labeling • Keep patients in clinic for 20 to 30 minutes after injections. Lieberman In: Allergy: Principles and Practice Mosby, 2003

  37. Measures to Reduce the Incidence of Anaphylaxis and Anaphylactic Deaths 2 Measures for Patients at Risk • Avoid causative factor/s. • Have patient wear and carry warning identification. • Teach self-injection of epinephrine and caution patient to keep epinephrine kit with them. • Discontinue -adrenergic blocking agents, ACE inhibitors (controversial), monoamine oxidase inhibitors, and tricyclic antidepressants, where possible. Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  38. Measures to Reduce the Incidence of Anaphylaxis and Anaphylactic Deaths 3 Measures for Patients at Risk • Use preventive techniques when patient is required to undergo a procedure or take an agent which places them at risk. Such techniques include: Pretreatment Provocative challenge Desensitization Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  39. Summary Prognosis FactorPoorGood Dose of antigen (allergen) Large Small Onset of symptoms Early Late Initiation of treatment Late Early Route of exposure Parenteral Oral* β-adrenergic blocker use Yes No Presence of underlying disease Yes No * True for drugs, not foods

  40. Allergic Emergencies Section 2: Upper Airway Oedema

  41. Upper Airway Oedema Lecture Objectives • To understand the causes of angioedema; • To review the spectrum and management of hereditary angioedema; • To review Angiotensin Converting Enzyme (ACE) inhibitor related angioedema.

  42. Outline of Lecture • Clinical description • Classification • Examples of life-threatening oedema: • Hereditary angioedema • Acquired oedema • Angiotensin enzyme inhibitor-induced oedema • Clinical description • Pathophysiology • Management

  43. Angioedema • First described by Quincke in 1882 • Well-demarcated non-pitting oedema • Caused by same pathological factors that cause urticaria • Reaction occurs deeper in dermis and subcutaneous tissues • Face, tongue, lips, eyelids most commonly affected • May cause life-threatening respiratory distress if larynx involved

  44. Classification of Angioedema 1 Hereditary • Type 1: C1 esterase inhibitor deficiency • Type 2: functional abnormality of C1 esterase inhibitor Acquired • Idiopathic • IgE-mediated • Non-IgE-mediated • Systemic disease • Physical causes • Other

  45. Classification of Angioedema 2 IgE-mediated • Drugs • Foods • Stings • Infections (eg viral, helminthic) Non-IgE-mediated • Cyclooxygenase inhibition (ASA and other NSAIDS) • Angiotensin converting enzyme inhibition

  46. Systemic diseases Systemic lupus erythematosis Hypereosinophilia Lymphoma: abnormal antibodies activate complement system Classification of Angioedema 3

  47. Physical causes Cold Cholinergic Solar Vibratory Other Some contact reactions Autoantibodies to C1-esterase inhibitor Unopposed complement activation Classification of Angioedema 4

  48. Incidence • Chronic idiopathic urticaria/angioedema occurs in 0.1% population • 65% remit within 3 years 85% remit within 5 years 95% remit within 10 years • Angioedema occurs most commonly with urticaria (40% cases) • May occur in isolation (10% cases)

  49. Hereditary Angioedema (HAE) • 1888 - family described by William Osler • 1963 - Donaldson and Evans described the biochemical defect responsible - absence of C1 inhibitor

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