Allergy

The Allergy Report

Volume 1

Overview of Allergic Diseases:Diagnosis, Management, and Barriers to Care Introduction Background Prevention Diagnostic Testing Management of Allergic DiseasesEnvironmental Control Pharmacologic Therapy Allergen Immunotherapy Patient Education

Recommendations for Policy and Interventions Volume 2

Diseases of the Atopic DiathesisIntroduction Rhinitis Asthma Atopic Dermatitis Associated Disease: Rhinosinusitis Associated Disease: Chronic or Recurrent Otitis Media Volume 3

Conditions That May Have an Allergic ComponentIntroduction Conjunctivitis Urticaria and Angioedema Contact Dermatitis Drug Reactions Food Reactions Insect Sting Reactions Latex Reactions Anaphylactic and Anaphylactoid Reactions

Copyright 2000. The American Academy of Allergy, Asthma & Immunology, Inc. All rights reserved. The material contained in this publication is the exclusive property of the American Academy of Allergy, Asthma & Immunology, Inc. (AAAAI) and, as to copyrighted works of others which are contained herein, such other copyright owners. This work is protected under U.S. copyright law and other international treaties and conventions. Except as stated herein, none of the material contained in this publication may be copied, reproduced, distributed, republished, downloaded, displayed, posted or transmitted in any form or by any means, including, but not limited to, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of AAAAI or, as to copyrighted material of others, the copyright owner. Any inquiries regarding such permission should be directed to: Ms. Amy Stone American Academy of Allergy, Asthma & Immunology, Inc. 555 East Wells Street, Suite 1100 Milwaukee, WI 53202-3823 Phone: (414) 272-6071 Fax: (414) 272-6070 Certain material in this publication is taken or derived from NIH Publication Nos. 974051 (Guidelines for Diagnosis and Management of Asthma) (July 1997) and 97-4053 (Practical Guide for Diagnosis and Management of Asthma) (October, 1997) of the U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung and Blood Institute. AAAAI gratefully acknowledges the assistance of the Academic Services Consortium, University of Rochester, in the preparation of this publication. Permission is granted to display, copy, distribute and download the materials in this publication for personal, non-commercial use only provided that such materials are not altered or modified and AAAAIs copyright notice is displayed thereon. DISCLAIMER: This publication and the material and information contained herein have been produced for informational purposes as a service to members and the general public and are provided as is, without warranty of any kind, either express or implied, including, without limitation, implied warranties of merchantability and fitness for a particular purpose. AAAAI shall not be liable for direct, indirect, special, incidental or consequential damages related to the users decision to use this publication or any material or information contained herein.

CONTENTSIntroduction ..................................................... 11 Conjunctivitis .................................................... 19The Allergic Response in the Eye (Allergic Conjunctivitis)............. 19 Classification of Allergic Conjunctivitis............ Seasonal Allergic Conjunctivitis.................... Perennial Allergic Conjunctivitis............... Atopic Keratoconjunctivitis ........................... Vernal Conjunctivitis ...................................... Giant Papillary Conjunctivitis .................... Contact Allergy................................................... Classification of Nonallergic Conjunctivitis .... Bacterial Conjunctivitis .................................. Viral Conjunctivitis.......................................... Chlamydial Conjunctivitis .............................. Diagnosing the Patient with Allergic Conjunctivitis ........................... Medical History .................................................. Ocular Examination......................................... Diagnostic Testing ............................................. Skin Testing.................................................. Differential Diagnosis (chart) ..................... 20 20 20 20 21 21 22 22 22 23 23 23 24 24 25 25 26

Managing the Patient with Allergic Conjunctivitis .......................... 28 Nonpharmacologic Management............... 28 Pharmacologic Therapy ................................ 28 Antihistamines ........................................... 28 Topical Vasoconstrictors ........................... 28 Mast Cell Stabilizers ................................ 29 Nonsteroid Anti-inflammatory Medications.................... 29 Corticosteroids ........................................... 29 Allergen Immunotherapy ............................ 29 Tips for Administering Eyedrops................ 31 Specialist Referral ........................................ 31 Opthalmic Preparations (chart)................... 32 References .............................................................. 33

Urticaria and Angioedema........................ 35Urticaria ................................................................... 35 Angioedema ........................................................... 36 Pathology of Urticaria and Angioedema .... 36 Classification .......................................................... 37 Chronic Urticaria ............................................. 37 Physical Urticaria and Angioedema .......... 37 Cold-induced Urticaria............................. 38 Heat-induced Urticaria............................. 39 Cholinergic Urticaria ............................... 39 Exercise-induced Anaphylaxis .............. 40 Dermographism (or dermatographism). 40 Delayed Pressure-induced Urticaria ... 41 Solar-induced Urticaria .......................... 41 Aquagenic Urticaria ................................. 41 Urticaria with Vasculitis .............................. 41 Heredity Angioedema .................................. 42 Acquired C1 -esterase Inhibitor Deficiency. 42 Diagnosing the Patient with Urticaria and Angioedema ..........................43 Medical History ................................................ 43 Physical Examination .................................. 44 Diagnostic Testing .......................................... 44 Considerations for the Differential Diagnosis of Urticaria and Angioedema 46 Erythema Multiforme............................... 46 Bullous Pemphigoid ................................ 46 Dermatitis Herpetiformis ........................ 46 Urticaria Pigmentosa ............................... 46 Managing the Patient with Urticaria and Angioedema......................... 46 Nonpharmacologic Management................ 46 Avoidance.................................................... 46

Palliative Measures .................................... 46 Pharmacologic Management ..................... 47 Antihistamines .......................................... 47 Corticosteroids ............................................ 47 Special Considerations for Managing Urticaria and Angioedema . 48 Papular Urticaria ....................................... 48 Cold-induced Urticaria............................. 48 Cholinergic Urticaria .............................. 48 Dermographism ........................................ 48 Delayed Pressure-induced Urticaria ... 48 Specialist Referral ........................................ 48 Features of common types of urticaria (chart)........................... 49 References .............................................................. 50

Contact Dermatitis ....................................... 51Mechanisms ............................................................ 51 Allergic contact dermatitis involves .......... 51 Irritant Contact Dermatitis .......................... 52 Diagnosing the Patient with Contact Dermatitis............. 53 Medical History ............................................... 53 Common Causes (chart) ......................... 54 Physical Examination .................................... 55 Most reported cases of contact dermatitis occur on the hands 55 Eruptions may be broadly classified as acute or chronic . 56 Urticaria reactions (wheal-and-flare responses)...... 57 Differentiating Allergic and Irritant Contact Dermatitis ............ 58 Irritant Contact Dermatitis.....................58 Allergic Contact Dermatitis .................. 58 Clinical Features ....................................... 59 Photosensitivity reactions are a type of contact dermatitis .. 60 Diagnostic Testing ...........................................61 Patch Testing ............................................... 61

Managing the Patient with Contact Dermatitis........................... 63 Nonpharmacologic Management................ 63 Pharmacologic Management ..................... 63 Acute Eruptions ........................................ 63 Chronic or Subacute Dermatitis .......... 64 Severe and Chronic Dermatitis ............64 Special Considerations................................... 65 Specialist Referral .......................................... 66 Topical corticosteroids (chart).................... 67 References .............................................................. 68

Drug Reactions ............................................. 69Classification of Allergic Drug Reactions ..70 IgE-mediated Reactions .............................. 70 Cytotoxic/Cytolytic Reactions...................... 71 Immune Complex Reactions ....................... 71 T-cell-mediated Reactions ...........................72 Other Reactions ............................................... 72 Delayed Dermatologic Reactions ........ 72 Drug-induced Fever ................................. 73 Hepatic Hypersensitivity Reactions ...... 73 Pulmonary Hypersensitivity Reactions.. 73 Aseptic Meningitis from Drugs ............ 74 Nonimmunologic Drug Reactions ....... 74 Multiple Drug Allergy Syndrome ......... 74 Diagnosing Drug Allergy .................................... 75 Medical History ................................................ 75 Factors to consider .................................. 75 Concurrent disease and therapy may influence risk......... 75 Diagnostic Testing .......................................... 76 Skin Testing.................................................. 76 Managing the Patient with Drug Allergy ....... 77

Treatment of Severe Immediate or Accelerated Reactions .. 77 Treatment of Late Reactions ....................... 77 Treating Through........................................... 77 Premedication (radiocontrast media) .... 78 Desensitization for IgE-mediated Reactions............ 79 Desensitization for Non-IgE-mediated Reactions ....... 79 Specialist Referral ........................................ 79 Specific Considerations for Managing Drug Allergy Reactions...... 80 Penicillin and Other Beta-lactam Antibiotics.....80 Insulin Reactions ............................................. 81 Sulfonamides ................................................... 82 Local Anesthetic Agents ................................. 82 Radiocontrast Media .................................... 82 Aspirin and NSAIDs ........................................ 82 Avian-based Vaccines..................................... 83 References .............................................................. 85

Food Reactions ............................................. 87Mechanisms of Food Reactions ........................ 88 IgE-mediated Food Allergy Reactions........ 89 The Oral Allergy Syndrome ......................... 90 Non-IgE-mediated Food Hypersensitivity.. 91 Food-induced Enterocolitis..................... 91 Food-induced Proctocolitis..................... 91 Food-induced Enteropathy .................... 91 Celiac Disease............................................. 92 Allergic Eosinophilic Gastroenteritis .. 92 Food Intolerance .......................................93 Diagnosing the Patient with Food Allergy .... 93 Medical History ................................................ 93 Diet diaries may be useful ....................94 Physical Examination .................................. 95 Diagnostic Testing ...........................................95 Elimination Diets....................................... 95 Skin and In Vitro Testing.......................... 99

Double Blind, Placebo-Controlled Food Challenge (DBPCFC) ..................... 100 Managing the Patient with Food Allergy .......... 101 Nonpharmacologic Management................ 101 Pharmacologic Management ...................... 102 Epinephrine................................................... 102 Other treatments ...................................... 102 General Considerations for Treating Food Allergy ............... 103 Treating the Patient with a Suspected Food Allergy ................................................. 103 Treating Children with Food Allergy .. 103 Specialist Referral ........................................... 104 Patient Education ............................................ 104 References .............................................................. 105

Insect Sting Reactions ................................. 107Reactions to Stinging Insects ........................... 108 Immediate Local Reaction........................... 108 Large Local Reaction....................................... 108 Anaphylaxis...................................................... 109 Signs and Symptoms of Anaphylaxis..... 109 Toxic Reaction ................................................. 110 Unusual (Delayed) Reactions ..................... 110 Diagnosing the Patient with Insect Sting Allergy................... 111 Medical History and Insect Identification .................... 111 Identifying stinging insects (Hymenoptera) (chart)........ 112 Diagnostic Testing .......................................... 113 Managing the Patient with Insect Sting Allergy ........................ 113 Nonpharmacologic Management................ 113 Pharmacologic Management ...................... 114 Immediate Local Reactions ..................... 114

Oral Corticosteroids ................................ 114 Epinephrine................................................... 115 Venom Immunotherapy............................ 117 Specialist Referral ....................................... 118 References .............................................................. 119

Latex Reactions .......................................... 121Allergic Responses to Latex .......................... 122 Types of Allergic Responses to Latex ....... 122 Diagnosing the Patient with Latex Allergy ... 123 Medical History ............................................ 123 Physical Examination .................................. 124 Allergic Reactions ................................ 124 Nonallergic Reactions .......................... 125 Diagnostic Testing .......................................... 125 Managing the Patient with Latex Allergy....... 126 Avoidance ........................................................ 126 Avoiding natural latex products ......... 126 Additional avoidance measures for extremely allergic patients... 127 Sources of latex exposure (chart)....... 129 Latex products and safe alternatives (chart)........... 130 References .............................................................. 131

Anaphylactic and Anaphylactoid Reactions............... 133Anaphylactic Reactions...................................... 133 Possible Causes of Anaphylactic Reactions...................... 133 Risk Factors for Anaphylaxis...................... 134 Anaphylactoid Reactions ................................... 135 Possible Causes of Anaphylactoid Reactions....................... 135

Diagnosing Anaphylactic/Anaphylactoid Reactions........................ 136 Medical History ............................................ 136 Signs and Symptoms of Anaphylactic/ Anaphylactoid Reactions...................... 136 Physical Examination .................................. 138 Diagnostic Testing .......................................... 138 Specialist Referral ....................................... 139 Managing the Patient........................................... 140 Managing Acute Events .............................. 140 General considerations for treating an acute event........... 140 Hospitalize the patient who is unresponsive to initial Therapy ... 141 Preventing Events ........................................... 143 Patient Education is Essential. .................. 143 Suggestions for reducing risk .................... 144 Special Considerations ...................................... 145 The Pregnant Patient ................................... 145 Reactions in the Operating Room .......... 145 Refractory Cases Due to Beta-adrenergic Blocking Agents ....... 146 Exercise-induced Reactions ....................... 146 Idiopathic Reactions ................................... 147 References .............................................................. 148

Resource Organizations .............................. 149 Glossary.............................................................. 151

The Allergy ReportIntroduction

T

o improve the health and well being of allergy sufferers, the American Academy of Allergy, Asthma, and Immunology (AAAAI) in partnership with the National Institute of Allergy and Infectious Diseases (NIAID) and 20 other medical associations, advocacy groups, and government agencies, has undertaken a comprehensive initiative Allergic Disorders: Promoting Best Practice. The goal of this initiative is to ensure that a broad spectrum of healthcare providers learns about, understands, and implements clinical and best practice information for diagnosing and managing patients with allergic diseases. The Allergy Report represents the outcome of a first step of the initiative: development of an evidence-based, practical and easy-toaccess guide to allergic disorders to help family practice physicians, internists, pediatricians, nurse practitioners, school nurses, and others who manage or interact with patients with allergies. The Allergy Report provides guidance on the clinical management of allergic disorders, examines the barriers to effective care, and addresses future research needs for allergy mechanisms and clinical approaches to treatment. The Report is organized into three volumes. This Volume provides information on conditions in which there may be an allergic component, including: conjunctivitis, urticaria and angioedema, contact dermatitis, drug reactions, food reactions, insect sting reactions, latex reactions, and anaphylactic/anaphylactoid reactions. Volume 1 provides an overview of the allergic process, the principles in common to the diagnosis and management of all allergic diseases, and discusses potential interventions for improving care for patients with allergic disorders. Volume 2 focuses on the diseases of atopic diathesis (rhinitis, asthma, allergic dermatitis) and includes sections on two commonly associated diseases: rhinosinusitis and recurrent or chronic otitis media.

Introduction i

Overview of Sections of Volume 3: Conditions That May Have an Allergic Component ConjunctivitisConjunctivitis refers to a group of ocular disorders that result in inflammation of the conjunctiva. Conjunctivitis is the most common form of allergic eye disease with symptoms that can occur seasonally or perennially, depending on the allergens. Discussion includes differentiating allergic from nonallergic conjunctivitis, classification of other ocular conditions, and a protocol for management based on the severity of symptoms.

Urticaria and AngioedemaUrticaria and angioedema represent the same increase in vascular leakage (permeability) observed within minutes following injection of histamine. Urticaria, which occurs in the dermis, is characterized by pruritic and erythematous elevations (i.e., rash), and is usually associated with itching. Angioedema occurs in the deeper cutaneous layers, those containing fewer mast cells and sensory nerve endings. As a result, while angioedema is associated with swelling, the skin may appear normal, and the patient usually complains of pain or burning rather than itching. Angioedema most often involves the face, tongue, extremities, or genitalia whereas urticaria can occur virtually anywhere on the body. Considerations for diagnosis and management are given.

Contact DermatitisContact dermatitis refers to a broad range of reactions resulting from the direct contact of an exogenous agent with the surface of the skin. It is the most common occupational disease and one of the most commonly acquired skin diseases in adults. Contact dermatitis comprises up to 40% of all occupational illnesses reported in the U.S. It accounts for about 90% of all occupational skin diseases. Discussion includes how to differentiate allergic contact dermatitis from irritant contact dermatitis, some common causes of contact dermatitis (including jobs with increased risk for developing the condition), and recommendations for diagnosis and treatment.

Introduction ii

Drug ReactionsDrug reactions can potentially result from any medication or biologic agent, and it is estimated that up to 10% of all adverse drug reactions are due to allergic responses. This section describes the different types of drug reactions that can occur, factors to consider in differential diagnosis, general principles of management, and recommendations for managing allergic reactions to specific drugs.

Food ReactionsFood reactions represent a group of disorders, some of which are characterized by immunologic responses to specific food proteins. The prevalence is greatest in the first few years of life and is higher in children with atopic disease. Approximately 35% of children with moderate to severe atopic dermatitis also have food allergy. This section describes the different types of food-related reactions, the common clinical manifestations of food allergy, techniques for diagnosing food allergy (including discussion of the role of elimination diets, food challenges), and considerations for management.

Insect Sting ReactionsInsect sting reactions should always be considered serious as the venom of the stinging insects (Hymenoptera) may cause anaphylaxis. This is in contrast to biting insects (e.g., mosquitoes, gnats) which can cause local allergy symptoms (e.g., swelling) but rarely are associated with severe systemic reactions. Clinical manifestations of insect stings, from mild to severe, are described along with recommendations for treatment and for prevention.

Latex ReactionsLatex reactions can be caused by an allergic response to the proteins in natural latex rubber or to the additives used in processing latex. The prevalence of latex allergy is increasing, and it is an important concern for both healthcare professionals and patients. This section describes the different types of allergic responses to latex, persons at increased risk for latex allergy, and provides suggestions for diagnosis and medical management. Sources of latex exposure, latex precautions, and tips for avoidance are included.

Introduction iii

Anaphylactic and Anaphylactoid ReactionsAnaphylaxis is a rapid, immune-mediated, systemic reaction to allergens to which the patient has been previously exposed. It has many etiologies. Anaphylactoid reactions look like anaphylaxis, but are not immune mediated. Anaphylaxis is the most severe form of allergic reaction and should always be considered a medical emergency. The reaction occurs rapidly, often dramatically, and is usually unanticipated. This section describes the anaphylactic reaction, its potential causes, differentiation from anaphylactoid reactions, management, and prevention.

Comment on TerminologyThe Allergy Report represents the collaboration and team effort of 22 organizations (see page vii). Eight drafts of the document were developed, reviewed, and revised by some or all of the Task Force before the final sign-off and endorsement. Several terms had different definitions and/or interpretations by members of different groups. As a result, it was necessary for the Task Force to reach consensus on the following: Allergy: In most of The Allergy Report, the term: Allergen refers to substances that can induce IgE antibody responses. Allergy refers to IgE antibody responses to allergens. Allergic disease is the resulting clinical manifestations generated

by IgE antibody responses. Allergens include generally harmless materials such as: Pollens Cockroaches Mold spores Animal danders House dust mites Penicillin and other drugs Foods Latex Insect venoms

In several places in The Report, the terms allergy and allergic disease are more broadly encompassing and include altered immunologic reactivity that may be either IgE-mediated or non-IgE-mediated. The reader should note that this broader definition is used selectively.

Introduction iv

Examples of this can be seen in the following sections in this volume: Drug Reactions and Food Reactions describe clinical responses that are both IgE-mediated and non-IgE-mediated. Contact Dermatitis describes specific, non-IgE-mediated immune cell

reactions (i.e., T-cell responses to contact antigens). Another term that is frequently confused with allergy is atopy. Atopy refers to the genetic tendency to develop the classical allergic diseases, namely, allergic rhinitis, asthma, and atopic dermatitis. Atopy is typically associated with a genetically determined capacity to mount IgE responses to common allergens, especially inhaled allergens and food allergens. Recently, it has been shown that IgE responses to latex are more frequent in atopic families, and thus, latex allergy may be considered an atopic disease. In contrast, IgE responses to insect venom and drugs are not more common in atopic families. Hence, these disorders are considered allergic, but not atopic, diseases. Specialist: The Allergy Report identifies many clinical situations in which referral to a specialist is warranted. Specialists may include: Allergy/immunology specialists Dermatologists Infectious disease specialists Ophthalmologists Otolaryngologists Otolaryngologic allergy specialists Pulmonologists

In many cases, the type of specialist varies with the provider network and the geography/community. For example, the Asthma section (Volume 2) uses the term asthma specialist in the same manner used by the National Asthma Education and Prevention Program1 to refer to a fellowship-trained allergist or pulmonologist or, occasionally, other physicians with experience in asthma management developed through additional training and experience. Similar complexities exist in

1

Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma: Clinical Practice Guidelines. NIH Publication No. 97-4051, page 10.Introduction v

identifying specialists for management of such diseases as atopic dermatitis, rhinosinusitis, otitis media, conjunctivitis, urticaria and angioedema, and contact dermatitis. Therefore, consultation or comanagement is recommended, as appropriate, with the type of specialist determined by the referring healthcare provider and taking into account the patients health insurance coverage and the healthcare resources available in the community. Allergies are the sixth leading cause of chronic disease in the United States, costing the healthcare system over $18 billion annually. Each year more than 50 million Americans suffer from allergic disease, and these numbers are increasing. On a daily basis, allergies cause time lost from work, school, and leisure activities and decrease productivity at work, in school, and at home; but they dont have to! Learning what triggers allergies and understanding how to treat the diseases may make the difference between a chronic debilitating illness and a productive, healthy lifestyle. To help healthcare professionals bridge the gap between current knowledge and practice, The Allergy Report presents basic recommendations for the diagnosis and management of allergic diseases. It is the hope of the Task Force responsible for developing The Allergy Report, and those who have reviewed it, that this initiative will improve healthcare and productivity for patients with allergic diseases.

AcknowledgementsThe Task Force acknowledges the support of Schering/Key, which provided an unrestricted educational grant for development, publication, and distribution of The Allergy Report.

Introduction vi

ChairsHarold S. Nelson, M.D., FAAAAI American Academy of Allergy, Asthma and Immunology National Jewish Medical and Research Center Denver, CO Gary S. Rachelefsky, M.D., FAAAAI American Academy of Allergy, Asthma and Immunology Allergy Research Foundation, Inc. University of California at Los Angeles Los Angeles, CA

Task Force MembersJohn Bernick, M.D., Ph.D. American College of Occupational and Environmental Medicine A. Wesley Burks, M.D. American Academy of Pediatrics Don Cui, PA-C, C.M.C.M. American Academy of Physicians Assistants Mark Dykewicz, M.D., F.A.C.P . American College of Physicians/ American Society of Internal Medicine Ivor Emanuel, M.D. American Academy of Otolaryngic Allergy John Georgitis, M.D., F.C.C.P . American College of Chest Physicians Peter Gergen, M.D. Agency for Health Care Policy and Research James Hadley, M.D., F.A.C.S. American Academy of Otolaryngology/ Head and Neck Surgery Sharon Hipkins, R.N., M.S.N. Asthma and Allergy Foundation of America Joel Karlin, M.D. American Medical Association Monica Kraft, M.D. American Thoracic Society Barry Lampl, D.O. American Osteopathic College of Allergy and Immunology Doris Luckenbill, R.N., M.S., C.R.N.P . National Association of School Nurses Bryan Martin, D.O. American Osteopathic College of Allergy and Immunology

Introduction vii

Anne Muoz-Furlong The Food Allergy Network Donna Nativio, Ph.D., C.R.N.P ., F.A.A.N. American College of Nurse Practitioners Marshall Plaut, M.D. National Institute of Allergy and Infectious Diseases, National Institutes of Health Stephen Redd, M.D. Centers for Disease Control and Prevention

Daniel Rotrosen, M.D. National Institute of Allergy and Infectious Diseases, National Institutes of Health Nancy Sander Allergy and Asthma Network Mothers of Asthmatics, Inc. William Storms, M.D. American College of Allergy, Asthma and Immunology Karen Tietze, Pharm.D. American Pharmaceutical Association Barbara Yawn, M.D. Specialist in Family Medicine

Outside ReviewersThe panel of content experts who reviewed the draft document included: Leonard Bielory, M.D., FAAAAI; S. Allan Bock, M.D., FAAAAI; William W Busse, M.D., FAAAAI; Harold M. Friedman, M.D.,FAAAAI; . Mitchell Friedlaender, M.D., FAAAAI; Anthony Gaspari, M.D.; David B. K. Golden, M.D., FAAAAI; Michael A. Kaliner, M.D., FAAAAI; Michael A. LeNoir, M.D.; Mark T. O'Hollaren, M.D., FAAAAI; Harold C. Pillsbury, III, M.D.; Thomas E. Platts-Mills, M.D., Ph.D., FAAAAI; Hugh Sampson, M.D., FAAAAI; Gail Shapiro, M.D., FAAAAI; F. Estelle R. Simons, M.D., FAAAAI; David Skoner, M.D.; Stuart Stoloff, M.D.; Abba Terr, M.D., FAAAAI; John Warner, M.D.; Jill Warner, Ph.D.; Robert Zeiger, M.D., Ph.D., FAAAAI.

Introduction viii

Conjunctivitis Conjunctivitis: o Refers to a group of ocular disorders that result

in inflammation of the conjunctiva.o May be of allergic or nonallergic origin. The eye is a common target of allergic inflammatory

The conjunctiva is the most immunologically active tissue of the external eye. Conjunctivitis may be allergic or nonallergic.

disorders because of its:o Marked vascularity. o Sensitivity of conjunctival vessels. o Direct contact with the environment.

Ocular allergy diseases include: Seasonal allergic conjunctivitis Perennial allergic conjunctivitis Atopic keratoconjunctivitis Vernal conjunctivitis Contact allergy Giant papillary conjunctivitis (hypothesized

Allergic conjunctivitis is the most common form of allergic eye disease. It may be seasonal or

allergic origin)

perennial, depending on the cause.

The Allergic Response in the Eye (Allergic Conjunctivitis) In response to various stimuli, the conjunctiva

undergoes a variety of morphological changes. o The type of response depends upon the nature of the stimulus. Seasonal and perennial allergic conjunctivitis are examples of immunological diseases initiated by an IgE-mediated reaction. o Airborne allergens (e.g., pollen, animal dander) dissolve in tear film, traverse the conjunctiva, and are processed to allergenic peptides that bind to IgE receptors on conjunctival mast cells.

Seasonal allergic conjunctivitis is the most common type of allergic conjunctivitis.

Conjunctivitis

1

o As in other tissues, the degranulation of mast cells

The allergic response in the eye is usually associated with other allergic disorders, most commonly allergic rhinitis. Treating associated

releases an array of inflammatory mediators ultimately resulting in the ocular allergic response. The ocular allergic response exhibits both early-phase and late-phase reactions similar to allergic reactions in other tissues (see Volume 1: Background, page 4). The allergic response in the eye is usually associated with other allergic disorders, most commonly allergic rhinitis.

Classification of Allergic ConjunctivitisSeasonal Allergic Conjunctivitis The most common form of allergic conjunctivitis. Usually associated with allergic rhinitis. Signs and symptoms may include: o Bilateral ocular and periocular pruritus o Tearing o Burning and stinging o Pinkish or milky conjunctiva Symptoms are usually bilateral. Symptoms may persist throughout the allergy season

allergic rhinitis may improve allergic conjunctivitis.

Seasonal allergic conjunctivitis is rarely observed in the absence of allergic rhinitis.

but are subject to exacerbations and remissions.

Perennial Allergic ConjunctivitisThe symptoms of perennial allergic conjunctivitis are usually not as intense as the symptoms of seasonal allergic conjunctivitis.(see Volume 1: Background, Common Allergens, page 12) Reflects sensitivity to allergens that are present throughout the entire year. Less prevalent than seasonal allergic conjunctivitis. Symptoms are usually milder than those of seasonal allergic conjunctivitis.

Atopic Keratoconjunctivitis Associated with atopic dermatitis of the eyelid and face. Signs and symptoms may include: o Redness o Pruritus o Burning o Tearing

2

Conjunctivitis

o Stringy, ropy discharge o Papillary hypertrophy of lower and upper tarsal

conjunctivae. o Corneal vascularization, ulceration and scarring, cataract, and punctate epithelial keratitis may occur but are not common. Age of onset is usually the late teens and early 20s. Patients often have a history of allergy, particularly allergic rhinitis and/or asthma.

Atopic keratoconjunctivitis is usually associated with atopic dermatitis affecting the face. Most often occurs in

Vernal Conjunctivitis Typically a childhood disease. Observed more often in males than in females. Commonly occurs during the spring and summer. Most patients have a personal history of atopic disease,

late adolescence and early adulthood. History of allergy, particularly allergic rhinitis and/or asthma, is common.

though vernal conjunctivitis is not IgE-mediated. Patient presents with chronic, bilateral inflammation of the conjunctivae. Other signs and symptoms may include: o Intense itching (patients vigorously rub their eyes) o Photophobia o Blurred vision o Blepharospasm o Stringy, ropy discharge o Giant papillae on the palpebral conjunctiva (cobblestoning) o Trantas dots (small white dots at the limbal conjunctiva, eosinophils) Patients often have a history of allergy, particularly allergic rhinitis and/or asthma. If untreated, corneal scarring can occur, leading to vision loss.

Vernal conjunctivitis usually occurs in children, most commonly in boys. Patient usually has a

history of allergy, particularly allergic rhinitis and/or asthma.

Vernal conjunctivitis can lead to corneal scarring with loss of vision, if not treated.

Giant Papillary Conjunctivitis Associated with contact lens use. Hypothesized to be an allergic reaction involving proteins

that adhere to the intraocular surfaces of contact lenses, ocular protheses, sutures, and cyanoacrylate adhesives.

Giant papillary conjunctivitis is associated with using contact lenses.Conjunctivitis

3

Signs and symptoms may include: o Mild pruritus o Occasional slight blurring of vision o Mild hyperemia o Abnormal thickening of the conjunctiva o Small strands of mucus o Macropapillae and giant papillae on the

upper tarsal conjunctiva o Opacification of the conjunctiva

Contact AllergyContact allergies affecting the eye are being observed more frequently due to increasing use of topical medications and contact lens solutions. Contact allergy of the eyelids may be caused by cosmetics applied to the hair, face, hands, or fingernails through inadvertent spreading. Preservatives in ophthalmic preparations associated with contact allergy: Benzalkonium chloride Thimerosal (merthiolate) Chlorobutanol Chlorhexidene Phenylmercuric nitrate Results from repeated exposure to various sensitizing

agents, such as ophthalmic medications, cosmetics, and preservatives in solutions (e.g., thimerosal). May involve the skin of the eyelid as well as the conjunctiva. Signs and symptoms may include: o Severe itching o Burning o Photophobia o Vasodilation and chemosis of the conjunctiva o Fine epithelial punctate keratitis o Occasionally, corneal opacity

Classification of Nonallergic Conjunctivitis Conjunctivitis of a nonallergic nature is often due

to infection: o Bacterial o Viral Determination of etiology is important.

Bacterial Conjunctivitis Characterized by: o Velvety, beefy-red conjunctiva o Serous, mucoid, or mucopurulent discharge Ocular pruritus is usually absent.

and acetate4Conjunctivitis

Patients often complain of: o Unilateral or bilateral burning o Stinging o Foreign body sensation o Morning crustiness of the eyelids, causing difficulty

in eye opening Not seasonal Often preceded by, or associated with, infections of the upper respiratory tract, especially in children.

Viral Conjunctivitis Characterized by a watery discharge. Follicular hypertrophy and preauricular lymphadenopathy

Bacterial conjunctivitis is often preceded by, or associated with, upper respiratory infections, especially in children.

may be present upon ocular examination. Patients often complain of: o Unilateral or bilateral burning o Stinging o Foreign body sensation

Chlamydial Conjunctivitis Includes trachoma and inclusion conjunctivitis of adults

and newborns. Patient presents with: o Mucopurulent discharge lasting for more than 2 weeks. o Conjunctival follicles (not usually present in newborns).

Diagnosing the Patient with Allergic Conjunctivitis Many factors should be considered, including: o Age o Patient and family histories o Presenting clinical signs and symptoms It is important to remember that the presence and

The hallmark symptom of allergic ocular disorders is itching.

intensity of various symptoms can vary greatly.

Conjunctivitis

5

Medical History A complete medical and ocular history is essential.

Loss in visual acuity and eye pain may indicate conditions threatening to the patients vision (e.g., keratitis, uveitis, glaucoma).

Consider: o Patient and family history of allergic disease. Particularly, the presence of allergic rhinitis. o Onset of symptoms: Seasonal Perennial o Specific exposures to: Allergens Irritants (particularly, occupational irritants) Cosmetics and/or perfumes Topical or systemic medications with the potential to cause ocular inflammation o Exposure to other persons with conjunctivitis. o A recent respiratory infection. o Recent trauma to the eye. o Use of contact lenses. o Use of ocular medications. Characteristic symptoms: o Itching o Stinging o Tearing o Burning o Redness o Ocular discharge o Irritation

Ocular Examination Note unilateral or bilateral presence of clinical signs. o Clinical signs most often occur bilaterally in allergic

conjunctivitis. Corneal involvement is rare, but scarring may occur in severe cases. Look for ocular discharge. o Allergic conjunctivitis is associated with a stringy or ropy discharge. Evaluate conjunctivae for edema and appearance. o Periorbital edema is most often observed in severe cases, usually involving the lower lids. Evaluation of conjunctival scrapings for cellular contents is a useful diagnostic tool for determining the basis of ocular inflammation.6Conjunctivitis

o Eosinophils suggest allergic conjunctivitis.

The absence of eosinophils does not rule out an allergic etiology. Eosinophils may not be present in the upper layers of the conjunctiva. o Mast cells are often observed in patients with vernal keratoconjunctivitis. o Neutrophils usually indicate an infectious etiology, usually bacterial. o Mononuclear cells and lymphocytes are observed with viral infection.

Characteristic appearance of allergic conjunctivitis.Reprinted from Wiley L, Arffa R, Fireman P Allergic . Immunologic Ocular Diseases. In: Fireman P Slavin R (eds). , Atlas of Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 192. By permission of the publisher Mosby.

Diagnostic TestingThe general principles of diagnostic testing are included in Volume 1: Diagnostic Testing, page 31. Specific tests used for diagnosing conjunctivitis are included here.

Skin Testing Usually not required for seasonal allergic conjunctivitis

unless immunotherapy is contemplated. Limited testing may be helpful when there are conjunctival symptoms without any previous seasonal history. Can assist in confirming the diagnosis of, and directing environmental control measures for, perennial allergic conjunctivitis. Contact testing can be useful for patients with eyelid involvement. Referral to an allergy/immunology specialist for consultation and/or comanagement is recommended.Conjunctivitis

7

8

Conjunctivitis

Differential diagnosis of conjunctival inflammatory disorders:Type of Conjunctivitis Vernal Atopic KeratoGiant Papillary Contact Bacterial Viral Chlamydial

Allergic

SignsLymphocyte Lymphocyte Lymphocyte Lymphocyte PolymorphoEosinophil Eosinophil Eosinophil nuclear cell Monocyte Lymphocyte

Predominant cell type

Mast cell Eosinophil

Chemosis ++ Stringy mucoid + + ++ Stringy mucoid Clear white ++ ++ +

+

Polymorphonuclear cell Monocyte Lymphocyte ++

+

Lymph node

Cobble stoning

Discharge

Clear mucoid

++ Clear mucoid ++ Mucopurulent Mucopurulent

Eyelid involvement

Symptoms++ + + ++ ++ + + + +

Pruritus

+

Gritty sensation

Seasonal variation

+

+ = present; = not present; = may or may not be present

Reproduced with permission from Gotto A, Current Practice of Medicine. Vol 2. Philadelphia: Current Medicine; 1999: 4.

When is it allergy? Ocular itching is a key distinguishing feature. o Differentiate from burning, scratchy, or sandy

eyes. Ocular discharge is mucoid, watery, or stringy. o Purulent and/or morning matting is common with infection. Lid involvement is usually associated with atopic or contact dermatitis. o Occasionally seen with seborrhea or rosacea. o Commonly associated with staphylococcal colonization. Patient has history of other allergic diseases: o Atopic dermatitis o Allergic rhinitis o Asthma

Ocular pruritus suggests allergy.

Symptoms suggesting nonallergic origin: Burning, scratchy,

sandy eyes Dandruff Rosacea

Masqueraders of ocular allergy: Infectious conjunctivitis (bacterial, viral,

chlamydial) Dry eye Blepharoconjunctivitis (inflammation of lid margin) Trauma Foreign substance Drug-related, toxic, or chemical reaction Neoplasm Nasolacrimal duct obstruction Uveitis Episcleritis or scleritis

Conjunctivitis

9

Managing the Patient with Allergic ConjunctivitisNonpharmacologic ManagementFour general principles of allergy management1. Avoid factors that cause symptoms. 2. Use appropriate medications. 3. Evaluate for immunotherapy. 4. Educate and follow-up. Avoiding the offending allergen(s) is critical. In some cases, physical removal of the antigens from

the eye by irrigation with a saline solution or artificial tears may provide temporary relief of symptoms. Cold compresses may provide symptomatic relief.

Pharmacologic TherapyAntihistamines Can be administered orally or topically to relieve

Symptomatic relief may be provided by: Cold compresses. Irrigation with saline

solution or artificial tears.

Topical antihistamines provide rapid relief of acute ocular symptoms, particularly itching.

itching. Topical antihistamines provide rapid onset of relief for acute ocular symptoms, particularly ocular itching. Oral antihistamines often only partially relieve allergic ocular symptoms, but may be preferred by some patients. o Nonsedating antihistamines are preferred. o Sedating antihistamines are associated with drowsiness and may cause dryness of mucous membranes.

Topical Vasoconstrictors Topical decongestants do not treat the underlying

pathophysiology of ocular allergy, but can: o Decrease eye redness. o Relieve ocular itching. Indicated for the treatment of mild to moderate allergic conjunctivitis. Are often combined with antihistamines. Common side effects may include: o Transient stinging or burning on instillation o Decreased accommodation o Blurred vision

10

Conjunctivitis

Mast Cell Stabilizers Indicated for the relief of mild to moderate ocular

allergy. Most effective when administered prophylactically. o Some patients report an improvement of symptoms within 24 to 48 hours after initiating therapy with cromolyn. The most common side effect is transient burning or stinging upon administration. May be used in conjunction with a systemic antihistamine to treat more difficult cases of ocular allergy.

Nonsteroid Anti-inflammatory Medications Effective in relieving ocular itching associated with

seasonal allergic conjunctivitis.

Corticosteroids Use of topical corticosteroids is indicated for severe

cases of ocular allergy. o Patients should be closely monitored for: Cataracts Glaucoma Superinfections of the cornea and conjunctivae (i.e., herpes). o Treatment with topical corticosteroids should be initiated and monitored by an ophthalmologist. Rarely, a short course (e.g., 5 to 7 days) of oral corticosteroids may be necessary for acute exacerbations of severe ocular symptoms.

Allergen Immunotherapy May be effective in reducing the symptoms of seasonal

and perennial allergic conjunctivitis. Should be reserved for patients with: o Severe disease o Significant associated rhinitis Referral to an allergy/immunology specialist for consultation and/or comanagement is recommended.

Conjunctivitis

11

General management of allergic conjunctivitis by symptom severity:Mild Symptoms Avoidance

Moderate Symptoms Avoidance

Severe Symptoms Avoidance

measures Cold compresses and artificial tears Oral nonsedating antihistamine

measures Cold compresses and artificial tears Oral nonsedating antihistamine Topical antihistamine/ decongestant combination OR Topical antihistamine With or without: Topical mast cell stabilizer OR Topical NSAID Consider allergen immunotherapy

measures Cold compresses and artificial tears Oral nonsedating antihistamine Topical corticosteroid (with ophthalmologist consultation) Allergen immunotherapy

12

Conjunctivitis

Tips for administering eye drops: Lie down. Steady hand by resting it on face. Eyes open method: o Approach eye from side or top. o Keep eye open, and pull down lower lid,

forming a pouch. o Place drop into the pouch. o Look up to prevent blinking and draining of medicine. Eyes closed method: o Close eye. o Place drop on inside corner of eyelid. o Open eye slowly for drop to fall in. o Look up to prevent blinking and draining of medicine. When administering multiple eye medications, wait 5 to 15 minutes before delivering second medication to same eye in order to prevent dilution. Eye drop medical devices are available. Avoid contaminating eye dispenser from contact with eye, eyelid, eyelashes, or finger.

Specialist Referral Referral to an allergy/immunology specialist for

consultation and/or comanagement is recommended for patients having: o To undergo immunotherapy. o Skin testing for diagnosis. o Eye symptoms that do not resolve with treatment and that may be secondary to other allergic conditions (e.g., atopic dermatitis, contact dermatitis). Referral to an ophthalmologist for consultation and/or comanagement is recommended for patients having: o To use topical corticosteroids. o Severe symptoms of questionable allergic origin. o Difficult-to-control vernal conjunctivitis. o Difficult-to-control giant papillary conjunctivitis.Conjunctivitis

13

Ophthalmic preparations for allergic conjunctivitis*:Antihistamines Emedastine difumarate, 0.05% (Emadine) Levocabastine hydrochloride, 0.05% (Livostin) Antihistamine-vasoconstrictor combinations Pheniramine, 0.3%-naphazoline, 0.025% (Naphcon-A, Opcon-A, Occuhist) Antazoline, 0.5%-naphazoline, 0.05% (Vasocon-A) Mast cell stabilizers Cromolyn sodium, 4% (Crolom) Lodoxamide tromethamine, 0.1% (Alomide) Nedocromil, 2% (Alocril) Cromolyn sodium, 4% (Opticrom) Pemirolast, 0.1% (Alamast) Antihistamine/mast cell stabilizers Ketotifen fumarate, 0.025% (Zaditor) Olopatadine hydrochloride, 0.1% (Patanol) Azelastine, 0.05% (Optivar) Nonsteroid anti-inflammatory medications Ketorolac tromethamine, 0.5% (Acular) Diclofenac sodium, 0.1% (Voltaren)

Corticosteroids Dexamethasone, 0.1% Dexamethasone sodium phosphate, 0.05% Fluorometholone, 0.1%, 0.25% Fluorometholone acetate, 0.1% Loteprednol etabanate, 0.2% (Alrex) Medrysone, 1% Prednisolone acetate, 0.12%, 0.125%, 1% Prednisolone sodium phosphate, 0.125%, 1%*

This list is not all-inclusive; consult package inserts for full prescribing information.

14

Conjunctivitis

ReferencesAbelson MB, Schaefer K. Conjunctivitis of allergic origin: immunologic mechanisms and current approaches to therapy. Surv Ophthalmol 1993; 38: S115-132. Bielory L. Allergic and immunologic disorders of the eye. In: Middleton E, Reed CE, Ellis EF, et al (eds). Allergy Principles and Practice, 5th ed. St. Louis:Mosby, 1998: 1148-1161. Foster CS. The pathophysiology of ocular allergy: current thinking. Allergy 1995; 50: S6-9. Friedlander MH. A review of the causes and treatment of bacterial and allergic conjunctivitis. Clin Therap 1995; 17: 800-810. Friedlander MH. Conjunctivitis of allergic origin: clinical presentation and differential diagnosis. Surv Ophthalmol 1993; 38: S105-114. Friedlander MH. Management of ocular allergy. Ann Allergy Asthma Immunol 1995; 75: 212-222. Hingorani M, Lightman S. Therapeutic options in ocular allergic disease. Drugs 1995; 50: 208-221. Jackson WB. Differentiating conjunctivitis of diverse origins. Surv Ophthalmol 1993; 38: S91-104. Lieberman PL, Blaiss MS. Allergic diseases of the eye and ear. In: Patterson R, Grammer LC, Greenberger PA (eds). Allergic Diseases - Diagnosis and Management, 5th ed. Philadelphia: Lippincott-Raven, 1997: 223-251. Titi MJ. A critical look at ocular allergy drugs. Am Fam Physician 1996; 53: 2637-2646.

Conjunctivitis

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16

Urticaria and AngioedemaUrticariaUrticaria is characterized by the appearance of pruritic, erythematous, cutaneous elevations that blanch with pressure, indicating the presence of dilated blood vessels and edema in the dermis. In its simplest form, urticaria is the same wheal-andflare reaction observed within minutes after histamine is injected into the skin. Urticaria may occur virtually anywhere on the body and is usually associated with itching. o Individual lesions usually resolve within 24 hrs. Acute urticaria is a self-limited disorder that usually lasts for a few days. o Commonly caused by an allergic reaction to a food or drug. o May be associated with a viral illness in children. Chronic urticaria lasts longer than 6 weeks. o 50% of chronic urticaria patients continue to have symptoms beyond 6 months. o 20% have problems for 10 years or more. o The cause is usually not identified.

Acute urticaria is very common, affecting 10% to 20% of the population at some time in their lives. Acute urticaria usually

lasts for a few days. Chronic urticaria lasts longer than 6 weeks.

Acute urticaria.Photo provided by Anthony Gaspari, M.D., University of Rochester.

Urticaria and Angioedema

17

AngioedemaAngioedema is similar to urticaria but occurs in deeper skin layers. The area with Angioedema is caused by the same, or similar edematous process as urticaria, but angioedema extends into the deep dermis and/or subcutaneous tissue. Angioedema occurs in deeper skin layers which contain fewer mast cells and sensory nerve endings. Angioedema often involves the face, tongue, extremities, or genitalia. An area with angioedema shows swelling, but the skin may appear normal. o Lesions have little or no associated pruritus, and the swelling may be painful or burning in nature. o Swellings do not usually occur in dependent areas, are asymmetrically distributed, and are transient.(A) (B)

angioedema shows swelling, but the skin may appear normal.

Urticaria and angioedema often occur together. Types of urticaria and angioedema: Acute Chronic Physicalo Cold-induced o Heat-induced o Cholinergic o Exercise-induced

(anaphylaxis) o Dermographism (dermatographism) o Delayed pressureinduced o Solar-induced o Aquagenic Urticaria with vasculitis Hereditary angioedema Acquired C1-esterase inhibitor deficiency

Facial angioedema following allergen exposure (A) and resolution after treatment (B).Reprinted from Tharp M, Levine M, Fireman P Urticaria and angioedema. . In: Fireman P Slavin R (eds). Atlas of Allergies. 2nd ed. London: , Mosby-Wolfe; 1996: 250. By permission of the publisher Mosby.

Pathology of Urticaria and Angioedema Urticaria and angioedema are associated with the

release of various vasoactive mediators from activated cells or enzymatic pathways. o Histamine is the major mediator of these reactions. o The key mechanism of histamine release is the classic combination of an antigen with IgE antibody on the surface of mast cells and basophils. (See Volume 1: Background, page 5.)

18


o The major responses to histamine (and the other

mediators): Itching Vasodilation (erythema) Increased vascular permeability An axon reflex (increasing the extent of the reaction) Urticaria can be induced through allergen exposure by any route. o Allergic reactions to foods and drugs are common causes of acute urticaria. o In the majority of chronic urticaria cases, an inciting agent is not identified.

Urticaria can be induced through allergen exposure by any route. Allergic reactions to foods

ClassificationChronic Urticaria Lesions appear quickly and usually disappear in less

and drugs are common causes of acute urticaria.

than 24 hours. Characterized by a non-necrotizing perivascular mononuclear cell infiltrate with an accumulation of mast cells. Most cases are idiopathic (i.e., etiological factor unidentified): o An autoimmune origin is suspected. o IgG anti-IgE receptor antibodies are implicated as a potential cause. o Not associated with atopy.

Idiopathic urticaria is the most common chronic form of the disease. The lesions of chronic urticaria appear quickly and usually disappear within 24 hours.

Physical Urticaria and Angioedema Some types of urticaria or angioedema can be

reproducibly induced by: o Environmental factors (such as changes in temperature) o Direct stimulation of the skin by: Pressure Stroking Vibration Light Physical urticarias, except the delayed forms, typically last only 1 to 2 hours.

Most physical urticarias last only 1 to 2 hours. Delayed physical

urticarias can last longer.Urticaria and Angioedema

19

Cold-induced Urticaria Cold-induced urticaria is caused by a rapid change in temperature, not by the absolute temperature. Follows exposure to a rapid change in ambient

Fatalities by drowning have been reported secondary to coldinduced hypotension. Patients should be

warned that swimming alone, or in cold water, is dangerous.

temperature. o It is the rapid change in temperature, not the absolute temperature, that induces the response. Response is characterized by rapid onset of: o Pruritus o Erythema o Edema (swelling) Swelling is usually confined to portions of the body in contact with the cold stimulus. o Swelling of the tongue and pharynx is less common. o Laryngeal edema and abdominal complaints are rare. Total body exposure, such as while swimming, may cause massive mediator release, resulting in hypotension. Symptoms may be maximal after the exposed area is warmed. Symptoms may occur while outside on cold, windy days, and while holding cold objects. Reported with diseases characterized by abnormal immunoglobulins with cold-dependent properties: o Cryoglobulinemia o Cold agglutinin disease o Cryofibrinogenemia o Paroxysmal cold hemoglobinuria Most cases are idiopathic.

Positive ice cube test, demonstrating cold urticaria. 20Photo provided by Anthony Gaspari, M.D., University of Rochester.Urticaria and Angioedema

Heat-induced Urticaria May be localized or generalized (cholinergic). May occur alone or with other forms of physical allergy

(e.g., combined cold-induced urticaria, local heatinduced urticaria). o Pathogenesis of local heat-induced urticaria is unknown.

Cholinergic Urticaria Characterized by pruritus and small punctate wheals

surrounded by a prominent erythematous flare associated with: o Exercise o Hot showers o Sweating o Anxiety Lesions may affect the entire body except for the palms, soles, and axilla. Often remits within several years, but can last for more than 20 or 30 years.

Characteristic lesions of cholinergic urticaria.Reprinted from Tharp M, Levine M, Fireman P Urticaria and . angioedema. In: Fireman P Slavin R (eds). Atlas of Allergies. , 2nd ed. London: Mosby-Wolfe; 1996: 260. By permission of the publisher Mosby.


21

Exercise-induced Anaphylaxis Exercise-induced anaphylaxis should be considered a MEDICAL EMERGENCY. Patients should (see Anaphylaxis, page 128). Caused by exercise. Characterized by hives, lesions larger than the small punctate lesions characteristic of cholinergic urticaria, and at times, angioedema. o May be associated with fatigue, diffuse warmth, and/or wheezing. o May be associated with hypotension and collapse. Food ingestion within 3 to 4 hours of excerise has been associated with increased risk. o Reactions may be IgE-mediated, related to a specific food, or may be a nonspecific effect of ingestion. Role of aspirin or NSAIDs in aggravating exerciseinduced anaphylaxis is unclear. Exercise should be discontinued at the onset of symptoms. Patients should avoid exercise during the postprandial period.

discontinue exercise at the first sign of symptoms. Patients need to avoid exercise during the postprandial period. Patients should not exercise alone.

Dermographism (or dermatographism) Gentle stroking of the skin provokes local pruritus,

erythema, and swelling within 5 to 15 minutes. Affects 2% to 5% of the population. Commonly seen in patients with chronic urticaria.

Dermatographism seen after light stroking of the skin.Reprinted from Tharp M, Levine M, Fireman P Urticaria and angioedema. . In: Fireman P Slavin R (eds). Atlas of , Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 260. By permission of the publisher Mosby.

22


Delayed Pressure-induced Urticaria Manifestations occur 4 to 6 hours after pressure

has been applied. Commonly seen in patients with chronic urticaria. Symptoms may occur on: o Skin covered by tight clothing. o Hands after activity such as hammering. o Feet after walking. o Buttocks after prolonged sitting.

Solar-induced Urticaria A rare disorder in which exposure to sun light

(at specific wavelengths) causes urticaria within 1 to 3 minutes.

Aquagenic Urticaria A rare form of urticaria with small wheals

(indistinguishable from those of cholinergic urticaria) after contact with water, regardless of its temperature. May occur with cholinergic urticaria. Histamine release into the circulation has been documented upon challenge with water.

Aquagenic urticaria is a rare form of urticaria that occurs after contact with water, regardless of its temperature. The lesions of urticaria with vasculitis may occur with: Serum sickness Systemic lupus

Urticaria with Vasculitis Lesions: o Usually last longer than 24 hours. o Are more prominent on lower extremeties. o Have a purpuric component. o Leave a stippling of hemosiderin pigment. o Are associated with constitutional symptoms,

including: Arthralgia/arthritis Gastrointestinal complaints Low grade fever Respiratory complaints

erythematosus (SLE) Viral infections (including hepatitis B and hepatitis C) Lyme disease


23

May occur with: o Serum sickness o Systemic lupus erythematosus (SLE) o Viral infections (including hepatitis B and hepatitis C) o Lyme disease Biopsy of lesions shows necrotizing vasculitis involving

small venules (hypersensitivity angiitis). o Immunofluorescent studies demonstrate deposition of immunoglobulins and complement.

Hereditary AngioedemaEpisodes of hereditary angioedema may be associated with abdominal complaints which may lead to unnecessary surgery. Comanagement with Onset usually occurs in adolescence and early

an allergy/immunology specialist is recommended.

adulthood. Not associated with urticaria. o Not part of differential diagnosis of urticaria. Not pruritic. Episodes may be associated with abdominal complaints. o May lead to unnecessary surgical procedures. Acute episodes may be caused by trauma (e.g., accidents, dental work, surgery), but often no causal factor is identified. Comanagement with an allergy/immunology specialist is recommended.

Acquired C1 -esterase Inhibitor DeficiencyPatients with acquired C1-esterase inhibitor deficiency may have a similar presentation as hereditary angioedema, but this disease is not inherited. In adults, may be associated with lymphoma or other

malignancies. Due to decreased levels of C1-esterase inhibitor activity. Patients may have a similar presentation as hereditary angioedema, but this disease is not inherited.

24


Diagnosing the Patient with Urticaria and AngioedemaMedical History The history is critical. Consider: o Drug reactions o Reactions to foods o Inhalation, ingestion of, or contact with antigens o Infections (e.g., bacterial, fungal, viral, helminthic) o Insect bites (e.g., papular urticaria) o Collagen vascular diseases:

Urticaria may be associated with: Systemic lupus

Cutaneous vasculitis Serum sickness Systemic lupus erythematosus o Exacerbation by aspirin, NSAIDS, or food additives o Environmental or physical factors, including: Cold Heat Pressure Sun/UV Water o Malignancy (e.g., lymphoma, Hodgkins disease) o Systemic mastocytosis o Thyroid disease

erythematosus Serum sickness Cutaneous vasculitis Lymphoma Hodgkins disease Thyroid disease

Recent viral upper respiratory tract infections, especially in children, are the most common cause of urticaria caused by infections.

Urticaria is rarely the sole sign of an underlying disease.

Typical lesions of urticaria.Reprinted from Tharp M, Levine M, Fireman P Urticaria and . angioedema. In: Fireman P Slavin R (eds). Atlas of Allergies. , 2nd ed. London: Mosby-Wolfe; 1996: 250. By permission of the publisher Mosby.Urticaria and Angioedema

25

The lesions of urticaria: o Appear suddenly. o Are usually pruritic. o Rarely lasts longer than 24 hours (for individual

lesions). o May continue to recur for indefinite periods.

When diagnosing urticaria, the history is critical in terms of exposure to: Anything ingested (e.g., foods, medications, nutritional supplements) should be considered a potential cause of urticaria or angioedema. Is it urticaria? Did the lesions Foods Drugs Contact allergens Viral illness in children Insect bites Environmental and physical factors

Physical Examination A thorough physical examination is necessary to

appear suddenly? Are the lesions pruritic? Do individual lesions tend to resolve within 24 hours? Have lesions recurred over indefinite periods of time?

exclude diseases that are commonly associated with skin manifestations.

Diagnostic TestingThe general principles of diagnostic testing are included in Volume 1: Diagnostic Testing page 31. Specific tests used for diagnosing urticaria and angioedema are included here. Clues in the medical history and physical examination may suggest a need for further testing. o Selective laboratory testing should be based on the history and physical examination. Blood counts are usually normal. Consider infections (e.g., hepatitis, mononucleosis).

26


Diagnostic testing for patients with urticaria and angioedema:For patients with suspected: Vasculitis with arthralgia Consider: CBC with differential Erythrocyte

sedimentation rate Blood urea nitrogen (BUN) Creatinine Urinalysis Possibly, antinuclear antibody titer (ANA) Physical-induced urticaria or angioedema Cold-induced urticaria Challenge testing to

document a reaction Testing for

cryoglobulinemia and cold agglutinins Food-induced uticaria Skin testing or in vitro

testing for suspect foods, THEN CONSIDER provocation tests with the specific foods Chronic urticaria in which the individual lesions: Commonly remain in the same location for longer than 24 hours. Have a pigmented or purpuric component. Are painful. 4 mm punch biopsy


27

Considerations for the Differential Diagnosis of Urticaria and AngioedemaErythema Multiforme Presentation can range from urticarial lesions to overt

bullous lesions. Compared to urticarial lesions, the lesions of erythema multiforme typically: o Last longer. o Are peripherally distributed, except in severe cases.

Bullous Pemphigoid Is an autoimmune bullous eruption.

Dermatitis Herpetiformis Is an autoimmune vesiculobullous disorder. Lesions: o Are markedly pruritic. o Usually appear on elbows, knees, buttocks,

shoulders, sacral area.

Urticaria Pigmentosa A cutaneous disorder of mast cell hyperplasia. Characterized by Dariers sign. o Individual lesions develop a wheal when the overlying

skin is stroked.

It may be difficult to identify and eliminate factors causing chronic urticaria. Four general princples of allergy management1. Avoid factors that cause symptoms. 2. Use appropriate medications. 3. Evaluate for immunotheropy. 4. Educate and follow-up28Urticaria and Angioedema

Managing the Patient with Urticaria and AngioedemaNonpharmacologic ManagementAvoidance Minimize (ideally, avoid) exposure to causal factors as

demonstrated by history or challenge. Causal factors: o Increase the underlying inflammation (e.g., allergens, viral respiratory infections). o Provoke symptoms (e.g., exercise, cold air). Minimize (ideally, avoid) modulating factors (e.g., stress, exertion, alcohol). Patients with chronic urticaria usually should avoid ACE inhibitors, aspirin, and NSAIDs.

Palliative Measures A tepid shower or oatmeal bath may temporarily relieve

pruritus.

Pharmacologic ManagementThe most effective treatment for acute attacks of either urticaria or angioedema is epinephrine (see Anaphylaxis, page 122).

Antihistamines Oral H1-antihistamines are the treatment of choice for

the management of urticaria and angioedema. Nonsedating antihistamines are preferred. Clarinex (desloratadine) is indicated for chronic idiopathic urticaria. For chronic urticaria, antihistamines can usually: Reduce the pruritus. Minimize lesions. Allow patients to be reasonably comfortable and to function normally. Adding other medications to the H1-antihistamines may be useful for some patients: H2-antihistamines Tricyclic antidepressants (doxepin) Leukotriene pathway modifiers Further clinical studies are necessary to assess the role of leukotriene modifiers in therapy. If the patient is unresponsive to conventional antihistamines, consider referral to an allergy/immunology or dermatology specialist for evaluation and/or comanagement.

Oral H1-antihistamines are the treatment of choice for managing urticaria and angioedema. Nonsedating

antihistamines are preferred.

Newer H1-antihistamines Nonsedating: Fexofenadine Loratadine

Less-sedating: Cetirizine(see Volume 1: Pharmacologic Therapy, page 51)

Corticosteroids If the combination of H1-antihistamines,

H2-antihistamines, and leukotriene pathway modifiers are not enough to control chronic urticaria, addition of an oral corticosteroid is indicated. An alternate-day regimen is effective in most patients, with the corticosteroid being slowly withdrawn. Continue medications which have been helpful, concomitant with the corticosteroid. Start tapering the corticosteroid dose as soon as the urticaria is under control: Usually within 3 weeks. Can be variable. Referral to an allergy/immunology or dermatology specialist for evaluation or comanagement is recommended.Urticaria and Angioedema

29

Special Considerations for Managing Urticaria and AngioedemaPapular Urticaria Use local cold compresses. Apply calamine lotion and/or topical corticosteroids.

Cold-induced Urticaria Cyproheptadine is reported to be useful. Nonsedating antihistamines may be used if sedation

is a problem.

Cholinergic Urticaria Hydroxyzine is reported to be useful. Nonsedating antihistamines may be used if sedation

is a problem.

Dermographism Patients should wear loosely fitting clothing.

Delayed Pressure-induced Urticaria Antihistamines may have little effect. NSAIDs may help. Patients with severe disease often require

corticosteroids. Direct therapy toward chronic urticaria if the pressureinduced urticaria is associated with chronic disease.

Specialist Referral Referral to an allergy/immunology specialist and/or

dermatologist for evaluation, consultation, comanagement, or additional patient education is recommended when the patient: o Fails to respond to treatment. o Has complications. o Requires hospitalization. o Needs oral corticosteroid therapy. Referral to an allergy/immunology specialist for evaluation, consultation, or comanagement is recommended for: o Anaphylaxis (see Anaphylaxis, page 115) o Assistance with diagnostic testing of possible allergic factors.30Urticaria and Angioedema

Features of common types of urticaria:Type of Urticaria Chronic idiopathic Principal Clinical Features Profuse or sparse generalized, pink or pale edematous papules or wheals, often annular with itching. Itchy, linear wheals with a surrounding bright-red flare at sites of scratching or rubbing. Itchy pale or red swelling at sites of contact with cold air, cold surfaces, or fluids. Associated Angioedema Diagnostic Test Special Considerations

+/

Symptomatic dermatographism

_

Light stroking of skin causes an immediate wheal with itching. In most cases, 10 min application of ice produces wheal within 5 min after removal of ice. Application of pressure perpendicular to skin produces persistent red swelling after a latent period of 1 to 4 hr. 30 to 120 sec irradiation by a 2.5 kW solar simulator (290690 nm) produces wheals within 30 min. Exercise or a hot shower elicits eruption.

Wear loosefitting clothing.

Cold

+/

Delayed Pressure

Large painful or itchy red swelling at sites of pressure (soles, palms, or waist), lasting 24 hr.

+

NSAIDs may help in mild to moderate cases; corticosteroids may be required.

Solar

Itchy pale or red swelling at site of exposure to ultraviolet or visible light.

+/

Cholinergic

Itchy, monomorphic pale or pink wheals on trunk, neck, and limbs, and classic pencil-erasersized wheals.

+/

Use hydroxyzine if other antihistamines are not effective.

+ = Associated with angioedema. +/ = May or may not be associated with angioedema. = Not associated with angioedema.


31

ReferencesBeltrani VS. Urticaria and angioedema. Dermatol Clinics 1996; 14: 171-198. Black AK, Greaves MW. Urticaria and angioedema. In: Kay AB (ed). Allergy and Allergic Diseases. Blackwell Science Ltd. (Vol 2). Malden, 1997: 1586-1607. Champion RH, Roberts SO, Carpenter RG, Roger JH. Urticaria and angioedema. A review of 554 patients. Br J Dermatol 1969; 81: 588-597. Charlesworth EN. Urticaria and angioedema: a clinical spectrum. Ann Allergy Asthma Immunol 1996; 76: 484-496. Cooper KD. Urticaria and angioedema: diagnosis and evaluation. Clin Rev Allergy 1991; 25: 166-176. Gannon T. Dermatologic emergencies: when early recognition can be lifesaving. Postgrad Med 96: 67-82. Ghosh S, Kanwar AJ, Kaur S. Urticaria in children. Ped Dermatol 1993; 10: 107-110. Greaves M, Lawlor F. Angioedema: manifestations and management. J Am Acad Dermatol 1991; 25: 155-165. Greaves MW. Chronic urticaria. N Engl J Med 1995; 332: 1767-1772. Huston DP Bressler RB. Urticaria and , angioedema. Med Clin N America 1992; 76: 805-840. Joint task force on practice parameters. Exercise-induced anaphylaxis. J Allergy Clin Immun. 1998; 101: S523-524. Juhlin L, Landor M. Drug therapy for chronic urticaria. Clin Rev Allergy 1992; 10: 349-369. Kaplan AP Urticaria and angioedema. . In: Kaplan AP (ed). Allergy, 2nd ed. Philadelphia: Harcourt Brace, 1997: 573-592. Kaplan AP Urticaria and angioedema. In: . Middleton E, Reed CE, Ellis EF, et al (eds). Allergy Principles and Practice, 5th ed. St. Louis: Mosby-Year Book, 1998: 1104-1122. Lehach JG, Rosenstreich DL. Clinical aspects of chronic urticaria. Clin Rev Allergy 1992; 10: 281-301. Leung DYM, Diaz LA, DeLeo V, Soter NA. Allergic and immunologic skin disorders. J Am Med Assoc 1997; 278: 1914-1923. Mahmood T. Urticaria. Am Fam Physician 1995; 51: 811-816. Ormerod AD. Urticaria: recognition, causes, and treatment. Drugs 1994; 48: 717-730. Soter NA. Acute and chronic urticaria and angioedema. J Am Acad Dermatol 1991; 25: 146-154. Tharp MD. Chronic urticaria: pathophysiology and treatment approaches. J Allergy Clin Immunol 1996; 98: S325-330. Wade JP Liang MH, Sheffer AL. Exercise, induced anaphylaxis: epidemiologic observations. Prog Clin Biolog Res 1989; 297: 175-182.

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Contact Dermatitis Contact dermatitis refers to a broad range of

reactions resulting from direct contact of an exogenous agent with the surface of the skin.o The agent can be an allergen or an irritant.

Once the inflammatory process has started,

the pathologies of both types of reactions are similar. Microscopic and clinical findings are

Contact dermatitis is the most common occupational disease and one of the most commonly acquired skin diseases in adults. 30% to 40% of all

often identical. All age groups are affected. Precipitating factors may be found in any

occupational illness. 90% of occupational skin disease.

workplace, home, school, or play area.o Of the more than 6 million chemicals in the

environment, about 3,000 are known contact allergens.o Under certain specific circumstances, almost any

chemical can cause contact dermatitis.

Irritant responses account for 80% of contact dermatitis reactions. Allergic responses account for 20%. Of the more than 6 million chemicals in the environment, about 3,000 are known contact allergens.

Allergic contact dermatitis on the hand due to silvadene cream.Photo provided by Anthony Gaspari, M.D., University of Rochester.

MechanismsAllergic contact dermatitis involves: Allergic response against hapten-self complex which is

recognized by the immune system as foreign. Immunologic memory and specificity. o T-cell-mediated inflammatory response to a chemically reactive hapten (i.e., the allergen). Hapten reacts with protein to form antigen.Contact Dermatitis

33

Irritant Contact Dermatitis Is not defined by a single clinical entity. Represents a clinical spectrum based on the: o Type of injury. o Dermatologic reaction to injury. Reaction involves mediator released by nonspecifically

activated T cells. o The stimulus comes into direct contact with the keratinocytes of the epidermis. o Does not involve haptens. o The inflammation is concentration dependent. o Many allergenic and nonallergenic substances can be irritants at high concentrations. o The reaction causes direct tissue injury.Classification Allergic contact dermatitis % of Reactions 20% Causative Agent Allergen Mechanism Inflammatory

Irritant contact dermatitis

80%

Irritant

process resulting from T-cellmediated response to chemically reactive hapten. Antigen recognized by immune system is likely to be hapten-self complex. Direct tissue damage by an irritant. Concentration dependent toxic reaction.

34

Contact Dermatitis

Diagnosing the Patient with Contact Dermatitis Diagnosis is usually based on: o History o Distribution of the eruption o Diagnostic testing Early diagnosis and treatment are essential to: o Minimize disruption to everyday activities. o Prevent long-term skin sensitivity.

Medical History When diagnosing contact dermatitis, consider: o Age o Current and previous occupations o Hobbies, leisure activities o Use of cosmetics and skincare products o Application of cosmetics and skincare products to

When diagnosing contact dermatitis, ask the patient about: Hobbies Sports activities Gardening Home improvement

other people (e.g. cosmetologist) o Medications (topical and systemic) o Personal and family history of allergy o History of eczema and other atopic manifestations o Details of other skin conditions o Weather conditions (e.g., cold, wind, low humidity) Unless the cause is immediately obvious, identify all substances the patient applies topically, including: o Moisturizers o Shaving creams o Cosmetics o Shampoos o Skin creams o Soaps o Perfumes o Powders o Sunscreens o Medications o Hair dyes

projects Use of chemicals at work Painting Specific contact with: o Adhesives o Resins o Lubricating oils

Contact Dermatitis

35

Common causes of allergic contact dermatitis:Substance SourcesPoison ivy, poison oak, mango Philodendron, hydrangea, chrysanthemum, tulip bulbs Metal alloys, hairpins, earrings, zippers, door handles, silverwork, hair dyes and bleaches, insecticides, fungicides Cement, leather, household cleaners, bleaches Cosmetics, fabrics, cigarettes, newsprint and newspaper, preservatives, cardboard, plywood, rubber cement, shoes Dyes, fungicides*

Common causes of irritant contact dermatitis: Soaps Detergents Cleaners Alkalis (e.g., bleach) Benzocaine Antimicrobials Formalin Latex

Rhus (urushiol) Other plant-derived saps Nickel sulfate*

Potassium dichromate* Formaldehyde*

Ethylenediamine* Mercaptobenzothiazole Thiuram*

Rubber products Fungicides, insecticides, rubber products Hair dyes, fur dyes, chemicals used in photographic work

Paraphenylenediamine*

*

Included in the screening tray for standard diagnostic testing.

Allergic contact dermatitis over temporal area secondary to nickel present in eyeglass frame.Photo provided by Anthony Gaspari, M.D., University of Rochester.

36

Contact Dermatitis

Jobs with increased risks for developing allergic contact dermatitis:Occupation Hairdressers Builders and plasterers Electronic assembly workers Healthcare workers Substance(s) Perm solutions, tints Chromate in cement and plaster Epoxy resins and hardeners

Mechanics and machinists Oils Antimicrobials, formalin, latex, benzocaine

Occupational allergic contact dermatitis to paraphenylenediamine (black/ brown hair dye) in hairdresser.Photo provided by Anthony Gaspari, M.D., University of Rochester.

Physical ExaminationMost reported cases of contact dermatitis occur on the hands. However, contact dermatitis can occur on any mucous

membrane or skin surface. Allergic or irritant contact eruptions may have an atypical appearance if superimposed on a pre-existing dermatosis. The eyelids, neck, and genitalia are among the most readily sensitized areas. o The palms, soles, and scalp are more resistant.

Contact Dermatitis

37

The hands are the most common sites of contact dermatitis. Causative agents may be

Causative agents (i.e., allergens, irritants) may be

transferred to secondary body sites by the hands. o Nail polish allergy may present as eyelid, rather than finger, dermatitis.

transferred to secondary body sites by the hands.

Secondary site of contact dermatitis on the eyelids due to contact with nail polish on the patients hands.Photo provided by Anthony Gaspari, M.D., University of Rochester.

Eruptions may be broadly classified as acute or chronic. However, no sharp delineation exists. The acute phase is marked by: o Multiple, severe vesicles or bullae filled with clear

fluid. When vesicles rupture, oozing, eroded skin emerges (eczema). o Edema o Erythema o Secondary infection with gram positive bacteria frequently occurs. The subacute phase progresses with: o Increased erythema o Decreased edema o Papules replacing vesicles Chronic lesions show: o Minimal redness and swelling. o More pronounced scaling, hyperkeratosis, and lichenification of affected skin.

38

Contact Dermatitis

Characteristics of contact dermatitis lesions:Acute Lesions Multiple,

Subacute Lesions

Chronic Lesions Less erythma Less edema Increased

Increased erythema severe vesicles or bullae filled Decreased with clear fluid edema Edema Papules Erythema Secondary infection with gram positive bacteria is common

scaling Hyperkeratosis Lichenification

Urticaria reactions (wheal-and-flare responses) are now recognized as an important subtype of allergic contact reactions. The reported incidence of contact urticaria has

increased rapidly in the last few years. Many new cases are caused by natural rubber latex proteins. Latex allergy may also cause hand and glove contact dermatitis. (see Latex Reactions, page 103)

Positive scratch test to latexPhoto provided by Anthony Gaspari, M.D., University of Rochester.

Contact Dermatitis

39

Differentiating Allergic and Irritant Contact DermatitisIt may be difficult to differentiate allergen and irritant eruptions, especially after they become chronic. Irritant contact dermatitis usually develops gradually, after repeated exposures. Causes a variety of However, they may present very different inflammatory

responses.

Irritant Contact Dermatitis Develops gradually in most instances, after repeated

symptoms other than pruritus (e.g., pain, stinging, burning).

exposures. The cutaneous response: o Can cause a variety of symptoms other than pruritus, such as: Pain Smarting Stinging Burning Abnormal sensations (without shmulus) o Has sharply demarcated redness with: Heat Tenderness Swelling o May have apparent necrosis in severe cases. Severe acute reactions caused by potent irritants, such as acids, often resemble burns. The patient usually can identify the contactant (i.e., the contacted substance) because eruptions develop rapidly.Acute bullous contact dermatitis to rhus (allergic) complicated by self-treatment with bleach (irritant).Photo provided by Anthony Gaspari, M.D., University of Rochester.

Allergic contact dermatitis often flares 24 to 48 hours after allergen exposure. Most patients complain

Allergic Contact Dermatitis Cutaneous reactions: o Often flare 24 to 48 hours after exposure to allergen. o Pruritus is a common complaint. Repeated exposures to allergens to which the patient is

of pruritus.40Contact Dermatitis

sensitive, or exposures to irritants (e.g., in the workplace), can obscure the pattern of response.

Clinical features of allergic and irritant contact dermatitis:Clinical Feature Reaction delay after contact Sharp demarcation Time for clinical resolution after removal of agent Allergic Many hours to 5 to 6 days May occur Many days Irritant Usually within 48 hours Often typical Frequently diminished after 96 hours

The severity of both allergic and irritant reactions is

determined by the: o Chemical nature of the contactant o Concentration o Duration of exposure o Site of exposure o Hydration of the skin o Degree of occlusion o Local trauma

Repeated exposures, multiple exposures, or mixed exposures (i.e., to allergens and irritants) can obscure the pattern of response, making diagnosis difficult.

The distribution of the eruption often provides the best clue to the cause of contact reactions. In most cases, the reaction is localized and most

pronounced at the point of maximum contact. Contactants carried as dust or aerosols often affect the ears, eyelids, face, neck, and other exposed areas. Liquid contactants often leave a characteristic drip or smear pattern on exposed skin. Cosmetics, skin care products, and topically applied Allergic contact dermatitis to medications often polysporin ointment around cause reactions in surgical incision. the areas of Photo provided by Anthony Gaspari, application. M.D., University of Rochester.

A widespread eruption can develop when: Irritation is severe. Allergic reactions

are strong. Antigen exposure is systemic.

A detailed diary of day-to-day activities may be helpful to identify patterns of exposure to allergens and irritants.Contact Dermatitis

41

Most contact dermatitis reactions are localized and most pronounced at the point of maximum contact. Severe reactions may cause a widespread eruption: Severe irritation Strong allergic reactions Systemic antigen

Work-related exposure is most often seen on the hands. Indirect contact with clothing or animal fur containing

the contactant may also cause eruptions. Systemic administration of medications previously used topically, and to which the patient is sensitized, may elicit a generalized eruption. Cross-contamination can occur. An allergen applied to a certain area may cause dermatitis at a distant site by inadvertent spreading (e.g., nail polish causing secondary dermatitis on face).

exposure

The pattern of the lesions often provides the best clue to the cause of contact reactions.

Left: Pruritic vesicles arranged linearly are characteristic of poison ivy dermatitis. Right: Poison ivy (rhus).Reprinted from Slavin R. Allergic contact dermatitis. In: Fireman P Slavin R (eds). Atlas of Allergies. 2nd ed. London: , Mosby-Wolfe; 1996: 220. By permission of the publisher Mosby.

Photosensitivity reactions are a type of contact dermatitis. Systemic photosensitivity reactions: o Usually involve systemic drug exposure. o Are expressed symmetrically on sun-exposed skin. Contact photosensitivity reactions: o Involve topical contact with a photosensitizer. o Are expressed only on skin exposed to both the

photosensitizer and ultraviolet light.

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Contact Dermatitis

Phototoxic reactions: o Often resemble bad sunburn, BUT peak at 48 hours

Masqueraders of contact dermatitis: Atopic dermatitis Dyshidrotic eczema Psoriasis Fungal infections Seborrheic dermatitis Xerosis

rather than 12 to 24 hours as in sunburn. o The skin is usually tender and erythematous. o Severe phototoxic reactions can produce bullae. Photoallergens tend to prod

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