Causes of anaphylaxis.ppt

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					ANAPHYLAXIS
       Causes of anaphylaxis
• Immunologic mechanisms
    IgE-mediated
         - drugs
         - foods
         - hymenoptera (stinging insects)
         - latex
    Non-IgE mediated
         - anaphylotoxins-mediated e.g.
               mismatched blood
       Causes of anaphylaxis
• Direct activation of mast cells
     - opiates, tubocurare, dextran,
     radiocontrast dyes
• Mediators of arachidonic acid metabolism
     - Aspirin (ASA)
     - Nonsteroidal anti-inflammatory drugs
     (NSAIDs)
• Mechanism unknown
     - Sulphites
         Causes of anaphylaxis
•   Exercise-induced
•   food-dependent, exercise-induced
•   cold-induced
•   idiopathic
         Risk of anaphylaxis
• Yocum etal. (Rochester Epidemiology
  Project) 1983-1987:
     incidence: 21/100,000 patient-years
• food allergy 36%, medications 17%,
     insect sting 15%
 Frequency of symptoms in
       Anaphylaxis
Urticaria/angioedema   88%
Upper airway edema     56%
Dyspnea or wheeze      47%
Flush                  46%
Dizziness,             33%
hypotension, syncope
Gastrointestinal sx    30%
Rhinitis               16%
              Anaphylaxis
• Onset of symptoms of anaphylaxis: usually
  in 5 to 30 minutes; can be hours later
• A more prolonged latent period has been
  thought to be associated with a more benign
  course.
• Mortality: due to respiratory events (70%),
  cardiovascular events (24%)
     Prevention of anaphylaxis
• Avoid the responsible allergen (e.g. food,
  drug, latex, etc.).
• Keep an adrenaline kit (e.g. Epipen) and
  Benadryl on hand at all times.
• Medic Alert bracelets should be worn.
• Venom immunotherapy is highly effective
  in protecting insect-allergic individuals.
     Treatment of anaphylaxis
• EPINEPHRINE (1:1000) SC or IM
     - 0.01 mg/kg (maximal dose 0.3-0.5 ml)
     - administer in a proximal extremity
     - may repeat every 10-15 min, p.r.n.
• EPINEPHRINE intravenously (IV)
     - used for anaphylactic shock not
  responding to therapy
     - monitor for cardiac arrhythmias
• EPINEPHRINE via endotracheal tube
     Treatment of anaphylaxis
• Place patient in Trendelenburg position.
• Establish and maintain airway.
• Give oxygen via nasal cannula as needed.
• Place a tourniquet above the reaction site
  (insect sting or injection site).
• Epinephrine (1:1000) 0.1-0.3 ml at the site
  of antigen injection
• Start IV with normal saline.
     Treatment of anaphylaxis
• Benadryl (diphenhydramine)
     - H1 antagonist

• Tagamet (cimetidine)
     - H2 antagonist

• Corticosteroid therapy: hydrocortisone IV
  or prednisone po
     Treatment of anaphylaxis
• Biphasic courses in some cases of
  anaphylaxis:
      - Recurrence of symptoms: 1-8 hrs later
      - In those with severe anaphylaxis,
  observe for 6 hours or longer.
      - In milder cases, treat with prednisone;
  Benadryl every 4 to 6 hours; advise to
  return immediately for recurrent symptoms
   Treatment of Anaphylaxis in
      Beta Blocked Patients
• Give epinephrine initially.
• If patient does not respond to epinephrine
  and other usual therapy:
      - Isoproterenol (a pure beta-agonist)
      1 mg in 500 ml D5W starting at
      0.1 mcg/kg/min
      - Glucagon 1 mg IV over 2 minutes
Fatal Food-induced Anaphylaxis
SERIES     YUNGINGER SAMPSON
           (n=7)       (n=6)
Ages       16-43 years 2-16 years

Atopy                    All asthmatics

Locale     1/7 at home   1/6 at home

Allergen   Peanut- 4     Peanut- 3
           Tree nut- 1   Tree nut- 2
           Seafood- 2    Egg- 1
         Use of epinephrine in
            Food Allergy
• Epinephrine should be used immediately
  after accidental ingestion of foods that have
  caused anaphylactic reactions in the past.
• An individual who is allergic to peanut,
  nuts**, shellfish, and fish should
  immediately take epinephrine if they
  consume one of these foods.
• A mild allergic reaction to other foods (e.g.
  minor hives,vomiting) may be treated with
  an antihistamine
  Exercise-induced anaphylaxis
• Exercise induces warmth, pruritus, urticaria.
• Hypotension and upper airway obstruction
  may follow.
• Some types: associated with food allergies
  (e.g. celery, nuts, shellfish, wheat)
• In other patients, anaphylaxis may occur
  after eating any meal (mechanism has not
  been identified)
     Cold-induced anaphylaxis
• Cold exposure leads to urticaria.
• Drastic lowering of the whole body
  temperature (e.g. swimming in a cold lake):
  hypotensive event in addition to urticaria
• mechanism: unknown
DRUG ALLERGY
          DRUG ALLERGY
• Adverse drug reactions
      - majority of iatrogenic illnesses
      - 1% to 15% of drug courses
• Non-immunologic (90-95%): side effects,
  toxic reactions, drug interactions, secondary
  or indirect effects (eg. bacterial overgrowth)
  pseudoallergic drug rx (e.g. opiate
  reactions, ASA/NSAID reactions)
• Immunologic (5-10%)
        Drugs as immunogens
• Complete antigens
     - insulin, ACTH, PTH
     - enzymes: chymopapain, streptokinase
     - foreign antisera e.g. tetanus antitoxin
• Incomplete antigens
     - drugs with MW < 1000
     - drugs acting as haptens bind to
  macromolecules (e.g. proteins,
  polysaccharides, cell membranes)
     Factors that influence the
    development of drug allergy
• Route of administration:
     - parenteral route more likely than oral
  route to cause sensitization and anaphylaxis
     - inhalational route: respiratory or
  conjunctival manifestations only
     - topical: high incidence of sensitization
• Scheduling of administration:
            -intermittent courses: predispose to
  sensitization
     Factors that influence the
    development of drug allergy
• Nature of the drug:
     - 80% of allergic drug reactions due to:
          - penicillin
          - cephalosporins
          - sulphonamides (sulpha drugs)
          - ASA/NSAIDs
    Gell and Coombs reactions
• Type 1: Immediate Hypersensitivity
            - IgE-mediated
            - occurs within minutes to 4-6
  hours of drug exposure
• Type 2: Cytotoxic reactions
            - antibody-drug interaction on the
  cell surface results in destruction of the cell
            eg. hemolytic anemia due to
  penicillin, quinidine, quinine,cephalosporins
    Gell and Coombs reactions
• Type 3: Serum sickness
      - fever, rash (urticaria, angioedema,
  palpable purpura), lymphadenopathy,
  splenomegaly, arthralgias
      - onset: 2 days up to 4 weeks
      - penicillin commonest cause
• Type 4: Delayed type hypersensitivity
      - sensitized to drug, the vehicle, or
  preservative (e.g. PABA, parabens,
  thimerosal)
          Penicillin Allergy
• beta lactam antibiotic
• Type 1 reactions: 2% of penicillin courses
• Penicillin metabolites:
     - 95%: benzylpenicilloyl moiety (the
  “major determinant”)
     - 5%: benzyl penicillin G, penilloates,
  penicilloates (the “minor determinants”)
           Penicillin Allergy
• Skin tests: Penicillin G, Prepen (benzyl-
  penicilloyl-polylysine): false negative rate
  of up to 7%

• Resolution of penicillin allergy
     - 50% lose penicillin allergy in 5 yr
     - 80-90% lose penicillin allergy in 10 yr
        Cephalosporin allergy
• beta-lactam ring and amide side chain
  similar to penicillin
• degree of cross-reactivity in those with
  penicillin allergy: 5% to 16%
• skin testing with penicillin determinants
  detects most but not all patients with
  cephalsporin allergy
          “Ampicillin rash”
• non-immunologic rash
• maculopapular, non-pruritic rash
• onsets 3 to 8 days into the antibiotic course
• incidence: 5% to 9% of ampicillin or
  amoxicillin courses; 69% to 100% in those
  with infectious mononucleosis or acute
  lymphocytic leukemia
• must be distinguished from hives secondary
  to ampicillin or amoxicillin
 Sulphonamide hypersensitivity
• sulpha drugs more antigenic than beta
  lactam antibiotics
• common reactions: drug eruptions (e.g.
  maculopapular or morbilliform rashes,
  erythema multiforme, etc.)
                        Type 1 reactions:
  urticaria, anaphylaxis, etc.
• no reliable skin tests for sulpha drugs
• re-exposure: may cause exfoliative
  dermatitis, Stevens-Johnson syndrome
   ASA and NSAID sensitivity
• Pseudoallergic reactions
     - urticaria/angioedema
     - asthma
     - anaphylactoid reaction
• prevalence: 0.2% general population
                  8-19% asthmatics
                  30-40% polyps & sinusitis
• ASA quatrad: Asthma, Sinuitis, ASA
  sensitivity, nasal Polyps (ASAP syndrome)
    ASA & NSAID sensitivity
• ASA sensitivity: cross-reactive with all
  NSAIDs that inhibit cyclo-oxygenase
     ASA & NSAID sensitivity
• no skin test or in vitro test to detect ASA or
  NSAID sensitivity
• to prove or disprove ASA sensitivity: oral
  challenge to ASA (in hospital setting)
• ASA desensitization: highly successful
  with ASA-induced asthma; less successful
  with ASA-induced urticaria
           Allergy skin testing
• Skin tests to detect IgE-mediated drug
  reactions is limited to:
     Complete antigens
           - insulin, ACTH, PTH
           - chymopapain, streptokinase
           - foreign antisera
     Incomplete antigens (drugs acting as
     haptens)           - penicillins
                        - local anesthetics
                        - general anesthetics
   Management of drug allergy
• Identify most likely drugs (based on
  history).
• Perform allergy skin tests (if available).
• Avoidance of identified drug or suspected
  drug(s) is essential.
• Avoid potential cross-reacting drugs (e.g.
  avoid cephalosporins in penicillin-allergic
  individuals).
   Management of drug allergy
• A Medic-Alert bracelet is recommended.
• Use alternative medications, if at all
  possible.
• Desensitize to implicated drug, if this drug
  is deemed essential.
  Desensitization to medications
• Basic approach: administer gradually
  increasing doses of the drug over a period
  of hours to days, typically beginning with
  one ten-thousandth of a conventional dose

				
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