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					              Anaphylaxis

               Scot A. Laurie, MD
       Dallas Allergy and Asthma Center
           Clinical Assistant Professor,
       Division of Allergy & Immunology
University of Texas Southwestern Medical Center
       Historical Background

• Discovered by Portier and Richet in 1902
  – While attempting to immunize dogs to the
    venom of a sea anemone, they unknowingly
    sensitized the dogs
     • Dogs unexpectedly reacted to a previously
      nonlethal dose
       – Coined the term “anaphylaxie”, meaning without, or
         against, protection
                   DEFINITIONS
• Anaphylaxis
   – Systemic, immediate hypersensitivity reaction caused by IgE-
     mediated release of histamine and other mediators from mast
     cells and basophils
   – Clinical syndrome with multi-organ symptoms
       •   cutaneous
       •   respiratory
       •   cardiovascular
       •   gastrointestinal


• Anaphylactoid

   – Identical symptoms as anaphylaxis
   – Non-IgE-mediated mechanism
                  EPIDEMIOLOGY
• Hospitalization for Anaphylaxis
  – 13 yr retrospective review of anaphylactic shock from a hospital
    in Denmark
      • incidence of 3.2 cases per 100,000 inhabitants per year
      • mortality rate of these 20 cases was 5%
          – Sørensen H et al. Allergy 1989;44:288.
• ER Visits for Anaphylaxis
  – Klein individually reviewed all 19,122 ER records during a 4
    month period from St. Mary’s Hospital in Rochester, MN
  – Incidence of anaphylaxis was 17 per 19,122 emergency visits or
    0.09%
  – Only 4/17 had ICD-9 codes for anaphylaxis
      • most were simply classified as having an “allergic reaction”
          – Klein J, Yocum M. J Allergy Clin Immunol 1995;95:637-
            8.
     Epidemiology of Anaphylaxis
• Retrospective review of          • Anaphylaxis occurrence
    1255 cases of                      rate 30/100,000 person
    “anaphylaxis” identified           years
    in Olmsted County from         •   Suspect allergen found
    1983-1987                          68%
•   133 residents met              •   Allergy consultation in
    criteria for anaphylaxis           only 52%
    and had 154 reactions
    • 116 single episode
                                   •   1 patient died
                                       • 0.65% fatality rate
    • 13 had 2 episodes
    • 4 had 3 episodes



           Yocum MW et al. J Allergy Clin Immunol 1999;104:452-6.
Yocum MW et al. J Allergy Clin Immunol 1999;104:452-6.
    Anaphylaxis: Risk factors
                          • Gender
• Age                       – Males
     – More common in          • Hymenoptera
       adults
                            – Females
•   Atopy
                               • Latex
     – Foods
                               • Muscle relaxant
     – Exercise                • Idiopathic
     – Latex
     – RCM
     – Idiopathic
•   Exposure route
     – Oral less likely
Mediators of Anaphylaxis
  MEDIATOR        PHYSIOLOGIC              CLINICAL EFFECT
                    EFFECT
   Histamine       Smooth muscle                    Flush
                     contraction            Urticaria/angioedema
                 Vascular permeability            Wheezing
                   Vasodilatation               Hypotension

    PGD2        Peripheral Vasodilation           Flushing
               Coronary vasoconstriction       Bronchospasm
                 Bronchoconstriction            Hypotension


 LTC4/D4/E4         Smooth muscle              Bronchospasm
                     contraction               ?Hypotension
                Vascular permeability
                  Mucus production
   Tryptase       Inactivates bradykinin         Unknown
                Activates angiotensin I
“SHOCK” ORGANS IN
ANAPHYLAXIS
   • Skin
   • Respiratory tract
   • Cardiovascular
     system
   • Gastrointestinal
     tract
CUTANEOUS SYMPTOMS
   • Pruritus
     – initially palms, soles, groin, and axilla
   • Urticaria & Angioedema
     – most common finding
     – usually resolves within 24 hours
     – angioedema may persist for 2-3 days
   • Warmth
   • Flushing
   • Erythema
 RESPIRATORY SYMPTOMS
• Lower respiratory symptoms
  – Dyspnea, wheezing, and chest tightness
• Upper respiratory symptoms
  – Nasal congestion, sneezing, rhinorrhea
  – Laryngeal edema
        – often begin with a sensation of a “lump in the
          throat”
        – may progress to:
             dysphonia
             hoarseness
             drooling due to inability to swallow secretions
             stridor
             asphyxia
GASTROINTESTINAL
SYMPTOMS

    • Abdominal cramping
    • Nausea
    • Vomiting
    • Diarrhea
CARDIOVASCULAR
                           • Signs
 • Symptoms                  – Arrhythmias
   –   lightheadedness          • premature atrial
                                    contractions
   –   tachycardia              •   atrial fibrillation
   –   bradycardia              •   bundle branch block
   –   hypotension              •   peaked P waves and
                                    right axis deviation
   –   vascular collapse
                                •   ventricular premature
                                    contractions
                                •   ventricular fibrillation
                                •   asystole
                                •   myocardial infarction
FREQUENCY OF ANAPHYLACTIC
SYMPTOMS
    Signs & Symptoms                 Kemp et al.            Ditto et al.
                               266 cases of anaphylaxis   335 cases of IA
  Urticaria, Angioedema                 90%                   100%
    Dyspnea, Wheezing                   60%                    39%
  Dizziness, Pre-syncope,               29%                    23%
         Syncope
     Gastrointestinal                   26%                    22%
   Upper airway edema                   24%                    63%
       Hypotension                      20%                    23%
          Rhinitis                      16%                    ND
 Conjunctivitis, Periorbital            12%                    ND
          edema
   BIPHASIC & PROTRACTED
   ANAPHYLAXIS
• Stark & Sullivan • Douglas et al.
  – Prospective study of 25          – Biphasic anaphylaxis in only
    patients with anaphylaxis at       5% of 44 inpatients
    PMH                                  • Douglas D et al. J Allergy Clin
  – 5 (20%) had " biphasic                 Immunol 1994;93:977-85.
    anaphylaxis"
  – 6 had "protracted
                                   • Both Studies
    anaphylaxis"                     – Glucocorticoid therapy did not
                                       prevent either recurrent or
  – Risk Factors
                                       prolonged anaphylaxis
      • oral agent
                                     – Patients without hypotension
      • anaphylaxis began > 30
          minutes after exposure       or laryngeal edema did not
                                       have biphasic reactions
      •   Stark B, Sullivan T. J
          Allergy Clin Immunol
          1986;78:76-83.
Fatal Anaphylaxis




    Pumphrey RSH Clin Exp Allergy 2000:30:1144-50.
Timing of Epinephrine in Fatal
Anaphylaxis




    Pumphrey RSH Clin Exp Allergy 2000:30:1144-50.
Self-injectable Epinephrine Use
in Fatal Anaphylaxis




     Pumphrey RSH Clin Exp Allergy 2000:30:1144-50.
        Differential Diagnosis of
     Anaphylaxis and Anaphylactoid
               Reactions
•   Vasodepressor reactions
•   Flush syndromes- carcinoid
•   “Restaurant syndromes”- scombroidosis
•   Excessive endogenous production of histamine-
    mastocytosis
•   Nonorganic disease- panic disorder, vocal cord
    disorder, undifferentiated somatoform
    anaphylaxis
•   Chronic idiopathic urticaria/angioedema
 EVALUATION OF PATIENTS
 WITH ANAPHYLAXIS
• Working definition of anaphylaxis
  – Either
     • Airway obstruction such as laryngeal, pharyngeal,
       or glossal edema or severe bronchospasm
  – Or
     • Documented hypotension or syncope
  – Plus
     • Symptoms of generalized mediator release
        – urticaria, angioedema, pruritus, or flushing

• Review ER records for objective findings
DETERMINING THE ETIOLOGY OF
ANAPHYLAXIS
  • Detailed History
    – Time of day
    – Relationship to exercise, meals, and
      medications
    – Prescribed medications
       • different formulations or lots of medications
    – Non-prescribed ingestants
       • vitamins, health food supplements, laxatives,
         and suppositories
       • specific ingredients of meals
       • within 4 hours of episode(s)
    – Women
       • menses or intercourse
SPECIFIC IgE in ANAPHYLAXIS
• Skin testing                          • RAST testing
  – Accuracy > RAST
                                          – Without risk
  – Risk of fatal reactions
  – Allergens                             – Limited applicability
      • medications, anesthetics,           due to
          venoms, foods, insulin,            • lower accuracy
          latex
      •   heterologous sera,                 • Few allergens available
          vaccines, and other foreign            – venoms, foods, latex,
          proteins                                 and the major
  – Specificity fairly good                        determinant of
  – Sensitivity of many tests is ?                 penicillin
  – Some drugs can cause
    direct histamine release
            – opiates, RCM , some
              muscle relaxants
 FOOD SKIN TESTING IN
 ANAPHYLAXIS
• Stricker et al
   – Panel of 79 antigens
   – Identified 7 food-induced anaphylaxis of 102 patients with IA
       • Stricker W et al. J Allergy Clin Immunol 1986;77:516-519.
• Patients frequently unaware of foods that caused
  reactions
   – Food allergic patients failed to identify causative food in 67%
     of positive DBPCFC
      • Atkins F. J Allergy Clin Immunol 1985;75:348-355.
   – Most all patients with fatal food-induced anaphylaxis
     unknowingly ingested their fatal food
• Skin testing with fresh foods
   – Commercial food extracts may lack antigenic epitopes
MEDIATOR MEASUREMENT IN
ANAPHYLAXIS
     MAST CELL          BODY FLUID      COMMENTS
     MEDIATOR
      Histamine         Plasma, Urine   In circulation breifly
                                        False positives in urine
      Histamine          24 hr Urine    Cumbersome
  metabolites (MIAA)                    More specific and sensitive
                                        than histamine
                                        measurements
  Tryptase (G5 & B12)      Serum        B12-measured tryptase
                                        commercially available
                                        Measures total tryptase
     9 ,11ß-PGF2        24 hr Urine    Available from Mayo Labs
TRYPTASE
• Neutral protease in secretory granules of mast
    cells
•   Specific for mast cells
    • very minimal amounts in basophils
• -tryptase
    • predominant form of tryptase in circulation in both
      normals and mastocytosis patients
• b-tryptase
    • released from secretory granules with systemic mast
      cell activation
TRYPTASE MEASUREMENTS
 • Total tryptase
   • measured with mAb B12
   • measures both  & b-tryptase
   • normal values < 15 ng/ml
      • increases detectable earlier than G5 assay
   • available through commercial labs
 • b-tryptase
   • measured with mAb G5
   • normal values < 1 ng/ml
      • undetectable within 30 minutes
      • peaks in 1-2 hours
   • available through Dr. Schwartz’s lab at
     MCV
CLASSIFICATION OF
ANAPHYLAXIS

  • IgE Mediated
  • Complement/Immune Complex
    Activation
  • Direct Histamine Release
  • Unknown Mechanisms
     IgE MEDIATED
     ANAPHYLAXIS
• Antibiotics                        • Therapeutics
   – Penicillin, Cephalosporins,        – Allergen extracts
     Sulfamethoxazole
                                        – Vaccines - including
• Proteins                                fillers (gelatin)
   – Venoms, Heterologous sera,         – Intraoperative agents
     Latex, Seminal fluid                    • Thiopental, Muscle
   – Hormones: ACTH, Insulin, PTH,             relaxants,
          GnRH                                 ?Protamine, Fentanyl
   – Enzymes: Chymopapain,              – Chemotherapeutics,
     Streptokinase                        Ethylene oxide gas,
• Foods                                   Psyllium
   – Peanut, Tree nuts,                 – Local anesthetics,
     Crustaceans, Fish, Seeds,            ?Corticosteroids,
     Spices                               ?NSAID’s
   – Milk, Egg, Soy, Many others
    LOCAL ANESTHETIC
    ALLERGY
• Allergy rare and anaphylaxis extremely rare
     – allergy to parabens also rare
•   Non-cross-reacting local anesthetic groups
     – defined based on patch testing for contact
       dermatitis
     – unclear if any relevance to anaphylaxis
•   Skin testing & incremental challenge
     – validated method
     – recommended for evaluation of possible allergy
IMMUNE COMPLEX/COMPLEMENT
ACTIVATION
  • ? Radiocontrast Media
  • Blood/Blood products
    – Plasma, Serum, cryoprecipitate
    – IgE mediated anaphylaxis
       • passive sensitization
       • IgE anti-IgA in IgA deficient patients
       • FVIII
  • Hemodialysis membranes
  • IVIG
   THE MYTH OF SEAFOOD ALLERGY &
   RCM REACTIONS
• Despite the common belief that
 individuals with seafood allergy have a
 higher risk of RCM reactions, there is no
 data to support this and it has no
 theoretical basis
  – Shellfish allergic patients are allergic to
    muscle proteins, not iodide
  – RCM reactions are not caused by iodide
  – Low-ionic RCM have a lower incidence of
    anaphylactoid reactions despite containing
    more iodide per particle than traditional RCM
DIRECT HISTAMINE
RELEASE
 • Hypertonic Solutions
   – RCM, Mannitol
 • Plasma Expanders
   – Dextran, Hydroxyethyl starch
 • Drugs
   – Opiates, Vancomycin, Curare,
     Fluoroscein
Anaphylaxis with Unknown
Mechanism

  • Exercise Induced Anaphylaxis
  • Idiopathic Anaphylaxis
  • Progesterone Anaphylaxis
ACUTE TREATMENT OF
ANAPHYLAXIS
• Early recognition and treatment
    – delays in therapy are associated with fatalities
• Assessing the nature and severity of the
    reaction
•   Brief history
    – identify allergen if possible
        • initiate steps to reduce further absorption
    – medications (especially b-blockers)
• General Therapy
    – supplemental oxygen, IVF, vital signs, cardiac
      monitoring
• Goals of therapy
    – ABC’s
              EPINEPHRINE
• First-line drug of                    • Subcutaneous
                                          administration
  choice in anaphylaxis                    – dose: 0.3 to 0.5 mg of a
• Mechanisms of action                       1:1,000 dilution prn q 10-
   – agonist                               15 min
       • increase BP by peripheral         – IV epinephrine for
         vasoconstriction                    cardiovascular collapse
   – b-agonist
       • reverse bronchoconstriction    • Side effects
       • positive ionotropic and           – severe hypertension,
         chronotropic activity               arrhythmias, myocardial
       • increases cyclic AMP levels         ischemia and infarction
           – inhibit further mediator   • DO NOT WITHHOLD
              release from mast cells     EPINEPHRINE BECAUSE OF
              and basophils               CARDIAC HISTORY
Epinephrine Absorption: SQ vs. IM




      Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
Epinephrine Subcutaneous            Epinephrine Intramuscular




    Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
Epinephrine Subcutaneous            Epinephrine Intramuscular




     Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
Outdated EpiPens




 Simons FER et al. J Allergy Clin Immunol 1998;101:33-7.
Simons FER et al. J Allergy Clin Immunol 2000;105:1025-30.
Use of EpiPen in Children with
Anaphylaxis
• Retrospective survey of children with
    anaphylaxis who attended an allergy clinic in
    North Adelaide Australia
•   45 episodes of anaphylaxis
    • EpiPen given            13 (29%)
    • EpiPen not given        32 (71%)
• Hospitalization for anaphylaxis
    • EpiPen given            2 (14%) p< .05
    • EpiPen not given        15 (47%)

           Gold MS, Sainsbury R. J Allergy Clin Immunol 2000;106:171-6.
ANTIHISTAMINES IN ANAPHYLAXIS
  • Not a substitute for epinephrine
  • H1-antagonists
    – useful for cutaneous symptoms
  • H2-antagonists
    – somewhat controversial
    – combination of H1 and H2 antagonists was
      required for optimal prevention of hypotension in
      studies of histamine infusions
    – overall evidence favors the addition of H2-
      antagonists
       • especially in the presence of hypotension
     b -BLOCKED
•
     ANAPHYLAXIS
    Beta blockade                   • May be especially refractory
    – increase release of
      mediators
                                      to therapy
    – enhance the responsiveness    • Treatment
      of pulmonary,
      cardiovascular, and              – high doses of
      cutaneous systems to               isoproterenol or
      mediators                          dopamine
    – paradoxical responses to         – atropine
      epinephrine
        • bronchoconstriction and      – glucagon
          bradycardia                      • increases c-AMP
            – unopposed -                     independent of b-
              adrenergic and                   receptor
              reflex vagotonic             •   nausea and vomiting
              effects                          common
    PREVENTION OF ANAPHYLAXIS

• Referral to BC/BE allergist
   – Determine an etiology
      • skin testing
      • challenges
      • desensitization.
   – Educate the patient on avoidance
      • proper use and indications of injectable epinephrine
      • when to seek medical attention
      • obtain a Medic-Alert® bracelet
   – Develop a management plan
      • prevent and reduce further anaphylactic episodes
• Select an alternative drug if on b-blocker
  ACUTE DESENSITIZATION
• Indications
  – Patients allergic to an essential therapeutic agent
  – Systemic reactions to venoms (optional)
• Technique
  – Escalating doses of antigen administered over a brief period
  – Oral route preferred when possible
• Desensitization procedures are dangerous
• Mechanism of desensitization
  – Unknown
  – Desensitized state is antigen specific
     • not due to tachyphylaxis to mediators, mast cell
       depletion, or unresponsiveness to any IgE signal
CASE REPORT
• LB is a 62 yo WM who presented with
    recurrent syncopal episodes. These episodes
    were associated with pruritus, urticaria,
    lightheadedness, and syncope with urinary &
    fecal incontinence and occurred after playing
    basketball or ping-pong. However, he has
    performed more vigorous exercise without
    reactions.     An echocardiogram, Holter
    monitor and head CT were all normal.
•   Physical examination was unremarkable
 EXERCISE-INDUCED
 ANAPHYLAXIS
• Classification
  – Food dependent EIA
     • Specific food dependent EIA
        – occurs only if exercise after eating specific food(s)
        – implicated foods
             shellfish, wheat, celery, tomato, apple, grapes,
              litchi, hazlenut, chestnut, peanut, milk, rice,
              potato
     • Non-specific food dependent EIA
        – occurs if exercising after eating any food
  – Food independent EIA
    POSSIBLE MECHANISMS OF EIA
• Subthreshold amount of mast cell associated IgE cross-
    linking
      – Endogenous opioid stimulus can trigger primed mast
        cells to degranulate
           – Increases in codeine skin test reactivity after exercise
           – Increased wheal response to compound 48/80 in
             individuals with food-dependent EIA, but only after
             challenges with specific foods and exercise.
     – Gastrin can stimulate mediator release from mast
       cells
•   Abnormal responses of the autonomic nervous system
     – Increases in parasympathetic responses
     – Decreases in sympathetic activity
   CLINICAL FEATURES OF EIA
• 7% of anaphylaxis due to        • Exercise triggers
  EIA                                – Tennis, warmups, dancing,
• Symptoms & signs of EIA              soccer, basketball, running
  similar to other forms of          – vaginal delivery
  anaphylaxis                     • Predisposing factors
   – premonitory symptoms            – personal or family history of
        • generalized warmth,          atopy
          pruritus                       • familial EIA has been
        • urticaria are usually            reported
          10-15 mm in                – aspirin ingestion prior to
          diameter                     exercise may trigger 30%
        • angioedema of face,        – exercising in warm or humid
          palms, and soles             weather
   – reactions occur while           – menses
      exercising or shortly
      thereafter
   – duration of 0.5 to 4
      hours
  THERAPY OF EIA
• Acute treatment
  – epinephrine
     • available while exercising
• Prevention
  – exercise with a partner
  – limiting or discontinuing exercise at the first sign of prodromal
    symptoms
  – avoid NSAID’s
  – avoiding foods for 4-5 hours prior to exercise
  – antihistamines - unable to totally prevent attacks
  – oral disodium cromoglycate
  – “exercise desensitization”
      Natural History of EIA
• 279 EIA patients completed mailed survey
• Clinical course
  –   Attacks/yr decreased from 14.5 to 8.3
  –   47% decrease in attacks
  –   46% same
  –   7% increased
• Food Associated EIA
  – 37% patients
  – Shellfish, alcohol, tomato most common triggers
• Avoidance behaviors
  – Avoid exercise in extreme hot/cold or allergy season
  – Avoid eating before exercise
      Shadick NA et al. J Allergy Clin Immunol 1999;104:123-7.
Case Report
• CW is a 14 yo WF with a history of large
 local reactions to “bees”. 3 weeks prior to
 evaluation she was bit in the forehead by
 an ant and within 5 minutes developed
 facial urticaria, chest tightness, and throat
 tightness which improved with H1 & H2
 antagonists administered by her father a
 cardiologist.
  – Prick testing to imported fire ants was positive
      IMPORTED FIRE ANTS
• IFA most common cause of anaphylaxis to
    stinging insects in this area
•   Imported fire ant species
    – Solenopsis richteri
       • introduced from Uruguay or Argentina accidentally into
         the USA through the port of Mobile, Alabama in 1918
       • localized to northeastern Mississippi and northwestern
         Alabama
    – Solenopsis invicta
       • Brazilian species introduced later between 1933-1941
          Fire Ant Anaphylaxis
• 0.6% to 2% of patients requiring medical treatment for stings
• Texas has the 2nd highest number of IFA sting fatalities
• Diagnosis
   – anaphylaxis history after sting with development of a pustule
   – fire ant-specific IgE by skin tests
       • 25% of nonallergic individuals in endemic areas have IFA
         specific IgE
• Immunotherapy
   – Indicated for patients with systemic reactions, especially
     anaphylaxis
   – IFA whole body immunotherapy efficacy
       • field re-stings
            – 2.1% risk of anaphylaxis
       • intentional sting challenge
            – 0/30 reactions
       • Optimal duration of immunotherapy unknown
            CASE REPORT
• 34 yo BF with recurrent episodes of pruritus,
    urticaria, angioedema, chest tightness, and syncope.
    One episode required ER treatment and hypotension
    was documented. All episodes occurred shortly after
    sexual intercourse. She was seen initially by a
    neurologist who thought she was having
    hypoglycemic attacks and recommended eating prior
    to intercourse which did not help. She also had an
    ETT performed and the cardiologist thought she
    “was crazy”.
•   Skin testing with her partners semen at 1:1,000
    dilution was markedly positive while her partner was
    skin test negative
•   Condom use was recommended and prevented the
    attacks
HUMAN SEMINAL PLASMA ANAPHYLAXIS
• First reported by Specken in 1958
• Pathogenesis
   – Halpern et al. (1967)
      • Evaluated a woman with anaphylaxis occurring 15-30
        minutes after coitus
      • Scratch tests were positive to
          – husband’s whole sperm & seminal fluid devoid of
            spermatozoa
          – donor seminal fluid devoid of spermatozoa
      • Scratch tests negative to
          – husband’s serum
          – semen from rabbit, guinea-pig, horse and bull
      • Passive transfer (Prausnitz-Küstner reaction)
          – positive in 5 female controls as well as in monkeys
      • Chromatography and electrophoresis of seminal fluid
        identified basic protein fractions that were the most
        antigenic
 HUMAN SEMINAL PLASMA
 ANAPHYLAXIS
• Antigens
 – Isolated to seminal plasma
    • reactions can occur with vasectomized partners
    • only one case reported of a women reactive to spermatozoa
      and HSP
    • canine sperm can also induce anaphylaxis due to bestiality
 – Antigenic fraction of seminal fluid
    • MW of 20,000 to 30,000 daltons
    • heat stable
    • prostatic origin
    • prostate specific antigen (PSA) may be a major allergen
   THERAPY OF HSP ANAPHYLAXIS

• Condoms                           • Immunotherapy
   – universally successful           – extracts of antigenic
   – may induce remission if            fractions of HSP most
     used for prolonged periods         successful
                                          • Immunologic changes
• Prophylactic                              variable
  antihistamines                               – decrease in IgE
   – may control local HSP                     – progressive rise in
     reactions                                   IgG
   – ineffective for systemic         – rapid desensitization
     reactions
                                          • parenteral and local
• Pregnancy                                 (intravaginal)
   – successful impregnation          – long term success
     may be achieved using                • up to 8 years after
     artificial insemination with           immunotherapy
     isolated spermatozoa                 • maintaining sexual
                                            activity 2-3 times per
                                            week
          Idiopathic Anaphylaxis
• Diagnosis of exclusion
    – Careful evaluation for known causes should be performed
• Mechanism is unknown
• Patients present with the same constellation of
    symptoms as others with anaphylaxis
•   Treatment approach is the same
    – Preventative therapy with qd or qod prednisone may be required
• Patients require education and support as part of their
    disease management
                CONCLUSIONS

• Anaphylaxis is the most dramatic and potentially
    fatal manifestation of immediate hypersensitivity
•   Majority of reactions are due to medications, insect
    stings, radiocontrast media and food, however many
    are idiopathic
•   Most anaphylactic reactions respond to aggressive
    therapy, but fatalities still occur, especially if
    treatment is delayed
•   Epinephrine is still underutilized in many patients
•   Almost all cases of anaphylaxis should be referred to
    an allergist

				
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