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GLORIA Module 3: Allergic Emergencies

GLORIA Module 3: Allergic Emergencies. Updated: June 2011. Global Resources in Allergy (GLORIA™).

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GLORIA Module 3: Allergic Emergencies

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  1. GLORIA Module 3:Allergic Emergencies Updated: June 2011

  2. 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.

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

  4. 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 WAO’s Mission

  5. GLORIA Module 3:Allergic Emergencies

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

  7. Allergic Emergencies Section 1: Anaphylaxis

  8. 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. Anaphylaxis lecture objectives

  9. 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. Definition of anaphylaxis WAO Nomenclature Review Committee JACI 2004

  10. 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 Gell and Coombs’ Hypersensitivity (immunopathologic reactions) Kemp and Lockey JACI 2002

  11. 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). Biochemical mediators and chemotactic substances Kemp and Lockey JACI 2002

  12. 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. Shock organs in anaphylaxis Kemp and Lockey JACI 2002 Bock, Munoz-Furlong, Sampson JACI 2001

  13. 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. 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. Neugut, Ghatak, Miller Arch Int Med 2001 Simons, Peterson, Black JACI 2002 Rangaraj, Tuthill, Burr, Alfaham JACI 2002

  14. 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 Incidence of anaphylaxis to specific agents 1 Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  15. 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 Incidence of anaphylaxis to specific agents 2 Lieberman In Allergy: Principles and Practice Mosby, 2003

  16. 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. Incidence of anaphylaxis to specific agents 3 Lieberman In Allergy: Principles and Practice Mosby, 2003

  17. 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 Incidence of anaphylaxis to specific agents 4 Lieberman In Allergy: Principles and Practice Mosby, 2003

  18. 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 Incidence of anaphylaxis to specific agents 5 Lieberman in Allergy: Principles and Practice Mosby 2003

  19. 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. Allergen immunotherapy Stewart and Lockey JACI 1992 Kemp et al In: Allergens and Allergen Immunotherapy, Marcel Dekker, 2004

  20. 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

  21. 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 Differential diagnostic considerations in anaphylaxis Montanaro and Bardana JACI 2002

  22. 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 Comments about signs and symptoms of anaphylaxis Lieberman In Allergy: Principles and Practice Mosby, 2003

  23. 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

  24. Immune aggregates (Type II) Intravenous immunoglobulin Dextran (possibly) Cytotoxic (Type III) Transfusion reactions to cellular elements (IgG, IgM) Agents that cause anaphylaxis 2 (allergic but not IgE mediated) Kemp Immunol Allergy Clin N Am 2001

  25. 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 Agents that cause anaphylaxis 3 (non-allergic or IgE-independent) Kemp Immunol Allergy Clin N Am 2001

  26. Nonspecific degranulation of mast cells and basophils Opiates Idiopathic Physical factors: Exercise Temperature (cold, heat) Agents that cause anaphylaxis 4(non-allergic or IgE independent) Kemp Immunol Allergy Clin N Am 2001

  27. 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 -Adrenergic blockade Toogood CMAJ 1987 Kivity and Yarchovsky JACI 1990 Salpeter, Ormiston, Salpeter Annals Int Med 2002

  28. 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. Recurrent and persistent anaphylaxis Lee and Greenes Pediatrics, 2000 Kemp and deShazo In: Allergens and Allergen Immunotherapy to Treat Allergic Diseases. Marcel Dekker, 2004

  29. 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. Physician-supervised management of anaphylaxis 1 Kemp and Lockey JACI 2002 Simons et al JACI 1998 Simons, Gu, Simons JACI 2001

  30. 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. Physician-supervised management of anaphylaxis 2 Kemp and Lockey JACI 2002 Simons et al JACI 1998 Simons, Gu, Simons JACI 2001

  31. 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. Physician-supervised management of anaphylaxis 3 Kemp and Lockey JACI 2002

  32. 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. Physician-supervised management of anaphylaxis 4 Kemp and Lockey JACI 2002

  33. 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). Physician-supervised management of anaphylaxis 4 Kemp and Lockey JACI 2002

  34. 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. Refractory hypotension, give dopamine, 400 mg in 500 ml G/W IV 2 - 20 μg/kg/min more or less. Physician-supervised management of anaphylaxis 5 Kemp and Lockey JACI 2002

  35. 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. Physician-supervised management of anaphylaxis 6 Kemp and Lockey JACI 2002

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

  37. 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 Vasodepressor (Vaso-Vagal) Kemp and Lockey JACI 2002

  38. 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 Measures to reduce the incidence of drug- induced anaphylaxis and anaphylactic deaths 1 Lieberman In: Allergy: Principles and Practice Mosby, 2003

  39. 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. Measures to reduce the incidence of anaphylaxis and anaphylactic deaths 2 Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  40. 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 Measures to reduce the incidence of anaphylaxis and anaphylactic deaths 3 Lieberman In: Allergy: Principles and Practice. Mosby, 2003

  41. 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 Summary

  42. Allergic Emergencies Section 2: Upper Airway Oedema

  43. To understand the causes of angioedema; To review the spectrum and management of hereditary angioedema; To review Angiotensin Converting Enzyme (ACE) inhibitor related angioedema. Upper airway oedema lecture objectives

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

  45. 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 Angioedema

  46. 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 Classification of angioedema 1

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

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

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