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World Allergy Organization
WAO's mission: To be a global resource and advocate in the field of allergy, advancing excellence in clinical care through education, research and training as a world-wide alliance of allergy and clinical immunology societies.

World Allergy Congress 2007 Symposium

Anaphylaxis: Causes and Treatment


Ruby Pawankar
Nippon Medical School
Tokyo, Japan

Ruby Pawankar, MD, PhD is with the Department of Otolaryngology at Nippon Medical School in Tokyo, she is guest professor at Kyung Hee University School of Medicine in Seoul, Korea, and she has been guest professor, Division of Allergy, Department of Pediatrics, at Showa University School of Medicine in Tokyo.

Prof. Dr. Pawankar is on the Board of Directors of the World Allergy Organization (WAO), Executive Committee of the WHO Rhinitis Guidelines Initiative (ARIA) and Chair of the ARIA Asia-Pacific Affiliate. She has been the Vice Chair of the Rhinitis Committee of the American Academy of Allergy Asthma & Immunology, and has held several key positions in the organization of international congresses including the International Symposium on Asthma & Allergic Rhinitis (ISBAAR), 10th Biennial Congress of the Transpacific Allergy & Immunology Society and 9th Asian Research Symposium in Rhinology.

Abstract

Anaphylaxis is a severe systemic allergic reaction involving the release of mediators from mast cells, basophils and recruited inflammatory cells, that can involve multiple systems of the body, is often sudden and can have life-threatening consequences. Anaphylaxis manifests as a number of signs and symptoms, alone or in combination, occurring from within minutes to up to a few hours after exposure to a provoking agent. Severe initial symptoms develop rapidly, reaching a peak within 3-30 minutes, with occasionally a quiescent phase lasting for 1–8 hours before the onset of a second reaction (a biphasic response). Protracted anaphylaxis may occur, with symptoms persisting for days. The initial manifestation of anaphylaxis may be loss of consciousness, and the symptoms and signs may be isolated to one organ or involve multiple organs, gastro-intestinal, oral, respiratory, cutaneous, cardiovascular, ocular, and/ or genito-urinary. A variety of causes can contribute to the development of anaphylaxis, including foods such as peanuts, tree nuts, shell fish, milk, eggs, fruits and seeds; a severe allergy to pollen that has crossreactivity with certain foods; food-associated, exercise-induced anaphylaxis; antibiotics and drugs such as muscle relaxants; hymenoptera venoms; latex and foreign proteins; whole blood or its products, including serum or plasma; radiocontrast media; low-molecular weight chemicals; narcotics; modulators of arachidonic acid metabolism; sulfiting agents, and idiopathic causes.

The emergency treatment of anaphylaxis comprises:

  1. ensuring and establishing a patent airway,
  2. assessing the adequacy of ventilation, providing the patient with sufficient oxygen, and treating bronchospasm as necessary, and
  3. eliminating the continued exposure to the causative agent.

Assessing the adequacy of perfusion and use of a vasopressor (such as dopamine) may be necessary. Epinephrine is the drug of choice for anaphylaxis and should be given early in the course of the reaction, 0.3-0.5 mg of a 1:1000 w/v solution IM every 10-20 minutes or as necessary for adults, and 0.01- 0.3 mg/kg IM every 5-30 minutes as necessary for children. Antihistamines are helpful once the patient stabilizes. Although diphenhydramine may be administered IV, IM, or orally, cimetidine (up to 300 mg every 6 - 8 hours orally or slowly IV) offers the benefit of reducing both histamine-induced cardiac arrhythmias (mediated via H2 receptors), and anaphylaxis-associated vasodilation (mediated by H1 and H2 receptors). Corticosteroids are not effective for acute anaphylaxis but may prevent relapses or protracted anaphylaxis.

To prevent further episodes it is crucial to identify the causative agent/s by obtaining a comprehensive history and performing relevant tests, including allergen skin tests and measurement of allergen-specific IgE in the serum. Risk reduction strategies include avoidance of specific triggers, relevant specific preventive treatment, training of at-risk individuals in the use of self-injectable epinephrine and an anaphylaxis emergency action plan. Anaphylaxis education should be provided for patients, their families, caregivers, health care professionals, and the general public.

References

  1. Johansson SGO et al JACI 2004,113:832-6
  2. Lieberman P. Ann Allergy Asthma Immunol 2005;95:217-26
  3. Kemp SF and Lockey RF, J Allergy Clin Immunol 2002;110:341-8
  4. Sampson HA. J Allergy Clin Immunol 2004;113:805-19
  5. Simons FE J Allergy Clin Immunol. 2006 Feb;117(2):367-77
  6. Freeman TM, N Eng J Med 2004;351:1978-84

Slide presentation

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