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					Allergy and Drug
       Reactions
      Michelle Gros, MD FRCPC

            December 2, 2009
Patients with Allergies
 Risk of allergic drug reaction: 1-3% for most drugs

 ~5% of adults in U.S. may be allergic to 1 or more drugs

 Pts often refer to adverse drug effects as allergy

 ~15% of adults in U.S. believe they are allergic to
  specific medication
Adverse Drug Reactions - Predictable
 Account for ~80% of ADRs
 Often dose-dependent (overdosage)
 Related to known pharmacologic actions of drug
 Inadvertent route (eg. lidocaine induced seizures or
  cardiovascular collapse)
 Side effects
   Most common ADRs
   Undesirable pharmacologic actions of drugs
   Occurs at usual prescribed dosages
Drug Interactions
 Represent predictable ADRs

 Dose-dependent

 Independent of allergy

 IV fentanyl after IV benzos in unstable patient – may
  cause hypotension
Unpredictable ADRs


 Usually dose-independent

 Usually not related to drug’s pharmacologic actions

 Related to immunologic response
Criteria to help distinguish allergic
reaction from other ADRs

1) Allergic reactions occur only in a small percentage of
   patients receiving the drug

2) Clinical manifestations DO NOT resemble known
   pharmacologic actions

3) Drugs administered for several weeks without
   complications - rarely responsible for drug allergy

4) Time between exposure and manifestations
Hypersensitivity Responses (Allergy)

 Gell and Coombs first described classification

 Immune pathway functions as a protective mechanism

 Can react inappropriately to produce hypersensitivity or
  allergic response

 4 basic types
Type 1 Reactions
 Anaphylactic or immediate-type hypersensitivity
  reactions

 Ag binding to IgE Abs on mast cells and basophils

 Physiologically active mediators released

 Eg. Anaphylaxis, allergic rhinitis
Type 1 Reactions
Type 2 Reactions


 Antibody-dependent cell-mediated cytotoxic
  hypersensitivity
 Mediated by IgG or IgM Abs directed against Ags on
  surface of foreign cells
 Ags may be either:
  1) integral cell membrane components
    eg. A or B blood group Ags in ABO incompatibility

  2) Haptens that absorb to cell surface – stimulating
     production of antihapten Abs
     eg. Autoimmune hemolytic anemia
Type 2 Reactions


 Cell damage produced by:
   1) Direct cell lysis after complete complement
      cascade activation
   2) Increased phagocytosis by macrophages
   3) Killer T-cell lymphocytes producing Ab-
      dependent cell-mediated cytotoxic effects

   Eg. ABO-incompatible transfusion reactions
     drug-induced immune hemolytic anemia
     heparin-induced thrombocytopenia
Type 2 Reactions
Type 3 Reactions
 Immune complex reactions
 Circulating soluble Ags and Abs bind to form insoluble
  complexes – deposit in microvasculature
 Complement is activated
 Neutrophils are localized to site of complement deposition to
  produce tissue damage


 Eg. serum sickness after snake bite
      immune complex vascular injury
      protamine-mediated pulmonary vasoconstriction
Type 3 Reactions
Type 4 Reactions
 Delayed hypersensitivity reactions

 Result from sensitized lymphocytes interacting with
  specific antigens

 Produces lymphokine synthesis, lymphocyte
  proliferation, generation of cytotoxic T cells, attracts
  macrophages and other inflammatory cells

 Cytotoxic T cells kill target cells that bear Ags identical
  with those that triggered the reaction
Type 4 Reactions
 Manifest in 18-24 hours
 Peak at 40-80 hours
 Disappear in 72-96 hours


 Examples:
     Tissue rejection
     Graft-vs-host reactions
     Contact dermatitis (eg. poison ivy)
     Tuberculin immunity
Type 4 Reactions
Immunologic Mechanisms of Drug
Allergy

 Different immunologic responses to an antigen can
  occur

 Eg. Penicillin
     Anaphylaxis (Type 1)
     Hemolytic anemia (Type 2)
     Serum sickness (Type 3)
     Contact dermatitis (Type 4)
Intraoperative Allergic Reactions
 1 in 5000 – 25,000 anesthetics

 3.4% mortality rate

 >90% of allergic reactions evoked by anesthetic drugs
  occur within 5 mins of administration

 Anaphylaxis is most feared, with circulatory collapse,
  reflecting vasodilation and decreased venous return
Anaphylaxis
 1st used by Portier and Richet

 “ana” – against

 “prophylaxis” – protection

 To describe profound shock and resulting death in dogs
  immediately after a 2nd challenge with a foreign antigen

 Mediated by antibodies
Anaphylactoid
 Non-immunologic reactions

 Term rarely used now

 Cannot be distinguished from immune-mediated
  reactions clinically
Anaphylactic Reactions
 Ag binding to IgE Abs – initiates anaphylaxis

 Prior exposure needed to produce sensitization (or substance
  of similar structure)

 Allergic history often unknown to patient

 Re-exposure – Ag bridges IgE Abs on surfaces of mast cells and
  basophils

 Causes release of stored mediators – histamine, tryptase,
  chemotactic factors
Anaphylactic Reactions
 Arachidonic acid metabolites (leukotrienes and
  prostaglandins), kinins and cytokines – synthesized
  and released


 Released mediators produce a symptom complex of:
   Bronchospasm and upper airway edema (resp
    system)
   Vasodilation and increased capillary permeability
    (CVS)
   Urticaria (cutaneous)
Chemical Mediators of Anaphylaxis -
Histamine

 Stimulates H1, H2, H3 receptors

 H1 activation:
   Releases NO from vascular endothelium
   Increases capillary permeability
   Controls airway and vascular smooth muscle

 H2 activation:
   Gastric secretion
   Inhibits mast cell activation
   Contributes to vasodilation
Peptide Mediators of Anaphylaxis –
Arachidonic Acid Metabolites

 Leukotrienes and prostaglandins

 Leukotrienes
     Slow-reacting
     Bronchospasm
     Increased capillary permeability
     Vasodilation
     Coronary vasoconstriction
     Myocardial depression
Peptide Mediators of Anaphylaxis –
Arachidonic Acid Metabolites

 Leukotrienes and prostaglandins

 Prostaglandins
     Vasodilation
     Bronchospasm
     Pulmonary hypertension
     Increased capillary permeability
Peptide Mediators of Anaphylaxis –
Kinins

 Synthesized in mast cells and basophils

 Produce vasodilation, increased capillary permeability,
  and bronchospasm

 Stimulate endothelium to release prostacyclin and nitric
  oxide
Peptide Mediators of Anaphylaxis –
Platelet-Activating Factor

 Unstored lipid

 Synthesized in activated human mast cells

 Extremely potent

 Aggregates and activates human platelets to release
  inflammatory products

 Causes intense wheal and flare, smooth muscle
  contraction and increased capillary permeability
Mediators of Anaphylaxis
Anaphylaxis - Epidemiology
 1 in 10-20,000 anesthetics

 Exact incidence underestimated 2° under-reporting

 Morbidity remains unknown

 France – 3% of anesthesia-related deaths involve
  anaphylaxis

 10% anaphylactic rxns in UK are fatal
Anaphylaxis - Epidemiology
 France
   NMBA’s most common agent
   Followed by latex and antibiotics

 Norway
   NMBA’s most common
   Latex in very few cases
   No causal agent in ⅓ of cases

 Spain
   Antibiotics, then NMBA’s
Anaphylaxis - Epidemiology
 Patient characteristics:
   NMBA’s and latex – female patients

   Antibiotics – smoking (increased Abx use for URTI’s?)

   Hx of atopy, asthma, certain food allergies – latex

   Pts with asthma or on β-blockers – more severe reactions,
    may be refractory to treatment
Which drugs or agents?
 NMBA’s
 Latex
 Antibiotics


 Usually shortly after induction
 May occur anytime
 Dyes, hypnotics, local anesthetics, opioids, colloids,
  aprotinin, protamine, chlorhexidine, contrast agents
AGENTS IMPLICATED IN ALLERGIC REACTIONS DURING ANESTHESIA
Anesthetic Agents
Induction agents (cremophor-solubilized drugs, barbiturates, etomidate, propofol)
Local anesthetics (para-aminobenzoic ester agents)
Muscle relaxants (succinylcholine, gallamine, pancuronium, d-tubocurarine, metocurine,
atracurium, vecuronium, mivacurium, doxacurium, rocuronium)
Opioids (meperidine, morphine, fentanyl)
Other Agents
Antibiotics (cephalosporins, penicilli n, sulfonamides, vancomycin)
Aprotinin
Blood products (whole blood, packed cells, fresh frozen plasma, platelets,
cryoprecipitate, fibrin glue, gamma globulin)
Bone cement
Chymopapain
Corticosteroids
Cyclosporin
Drug additives (preservatives)
Furosemide
Insulin
Mannitol
Methylmethacrylate
Nonsteroidal anti-inflammatory drugs
Protamine
Radiocontrast dye
Latex (natural rubber)
Streptokinase
Vascular graft material
Vitamin K
Colloid volume expanders (dextrans, protein fractions, albumin, hydroxyethyl startch)
NMBA’s


 Frequently involved

 50-70% of periop anaphylaxis

 According to different reports in Europe

 Limited data available in US and Canada

 NO epidemiologic study of causative agents in US or
  Canada
NMBA’s


 ALL NMBA’s may elicit anaphylaxis

 Not uncommon in pts w/o any known previous exposure to
  any NMBA

 Source of sensitizing agent unknown

 Quaternary ammonium ions are suggested to be allergenic
  determinants

 Commonly used chemicals (toothpastes, detergents,
  shampoos, cough medicines) share these determinants

 Also – can have uneventful previous exposure – does not
  preclude risk of anaphylaxis with subsequent drug exposure
NMBA’s


 Sensitivity of skin tests 95%

 Reproducibility excellent

 Cross-reactivity between NMBA’s common (~60-70%) –
  must investigate all NMBA’s to identify safe alternatives

 Cross-reactivity also shown between succinylcholine and
  NMBA’s

 Arbitrary contraindication to ALL NMBA’s cannot be
  accepted
NMBA’s


 Increased incidence of anaphylaxis with rocuronium in
  France and Norway

 Norwegian Medicine Agency – published alert reserving
  its use for urgent intubations only
NMBA’s


 Apparent increased incidence of anaphylaxis to
  rocuronium might be due to:
   1)   Reflection of usage and market share
   2)   Biased reporting of adverse effects of new drugs
   3)   Statistical issues
   4)   Genotypic difference


 This issue requires further study
Latex
 1st case reported in 1979 – contact urticaria

 1989 – 1st reports of intra-op anaphylaxis

 Increased risk:
   1)   Health care workers
   2)   Many urologic procedures
   3)   Allergy to bananas, avocados, kiwis (latex-fruit
        syndrome)
Latex
 •    Brown et al reported in anesthesiologists:
      24% incidence of contact dermatitis
      12.5% incidence of latex-specific IgE positivity
      Of this group – 10% clinically asymptomatic,
         although IgE positive

        ? Early stages of sensitization
        ? Avoidance of latex may prevent progression to
         symptomatic disease

                             Anesthesiology 89:292, 1998.
Latex
 •   Usually 30-60 minutes after start of surgery

 •   IV and mucous membrane exposure – associated with
     faster onset and more severe symptoms
Latex
 •   Pediatric hospital in France including OR and periop
     care areas

 •   Latex-free policy has been adopted

 •   No allergic reaction to latex has been reported in
     25,000 anesthetized children or in healthcare workers
Antibiotics
 Primarily penicillins and cephalosporins – 70%

 Share a β-lactam ring

 May occur at 1st exposure
Antibiotics
 Specificity with skin testing 97-99%, sensitivity 50%

 Cross-reactivity low – 10% (attributed to common β-
  lactam ring)

 Recent meta-analysis:
   Pts allergic to penicillin or amoxicillin
   Higher incidence of rxn to 1st generation cephalosporins,
    but not to later generations
Hypnotics
 Thiopental or propofol – rarely reported

 Etomidate or ketamine – extremely rare
Opioids
 Very rare

 Morphine induces histamine release

 Cross-reactivity uncommon between fentanyl,
  remifentanil, sufentanil
Local Anesthetics
 Very uncommon
 Most due to metabolic product of esters – PABA
 Therefore, cross-reactivity among all LA agents in ester
  group
 Allergic rxns to amide LA agents remain anecdotal
 Preservatives (metabisulfite, parabens) may elicit rxn
 Cross-reactivity rarely seen in amide group
 ABSENT between esters and amides
Colloids
 Rare

 Gelatins (0.35%) vs. hydroxyethyl-starch (0.06%)
Aprotinin
 Risk ~ 2.8% in re-exposed pts

 Some fibrin glue products still contain aprotinin
NSAIDS
 Inhibition of PGE2 pathway – excessive leukotriene
  synthesis and subsequent mediator release – urticaria or
  bronchospasm

 IgE-mediated reactions also

 Fatal anaphylaxis described after oral NSAIDS
Antiseptics
 Increased reactions to chlorhexidine recently

 Contact dermatitis to life-threatening anaphylaxis

 Occurred when used for urological and gyne procedures

 Also insertion of central lines and epidurals

 Allow to dry completely before beginning invasive
  procedure
Recognition of Anaphylaxis During Regional and
              General Anesthesia
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How To Diagnose Periop Anaphylaxis?

 Clinical History:
   Initial diagnosis is presumptive, yet essential
   Usually occurs within minutes, even 1 minute after
    induction
   May progress within minutes to become life-threatening
   Primarily linked to IV agents
   Most common initial clinical features – pulselessness,
    desaturation, severe bronchospasm
   Resp signs enhanced in pts with underlying resp disease
Anaphylaxis
 Enigma of anaphylaxis lies in:

   1)   Unpredictability of happening
   2)   Severity of attack
   3)   Lack of prior allergic history
How To Diagnose Periop Anaphylaxis?

 Clinical History:

     4-step grading scale by Ring and Messmer
     Grades 1 and 2 – usually NOT life-threatening
     Grades 3 and 4 – emergency situations
     Grading scale used to guide treatment with epi
Predictive Criteria of Anaphylaxis
Severity

1) The more rapidly anaphylaxis occurs after allergen
   exposure – more likely to be severe

2) Cutaneous signs may be absent in rapidly progressive
   anaphylaxis (may only appear after normalization of
   BP)

3) Bradycardia – as a result of Bezold-Jarisch reflex
Bezold-Jarisch Reflex
 Cardioinhibitory reflex

 Origin in sensory receptors of left ventricle

 Transmitted by unmyelinated vagal C fibres

 Paradoxical bradycardia occurring during extreme
  hypovolemia

 Occurs in up to 10% of pts with anaphylaxis
Bezold-Jarisch Reflex
 Bradycardia may be life-protecting adaptive mechanism

 Allows ventricles to fill before contracting again,
  despite massive hypovolemia

 Atropine to tx bradycardia – potential for circulatory
  arrest

 Treat with large volume expansion and epi
 What biochemical tests?


 Histamine:

   Preformed inflammatory mediator

   Contained in granules of mast cells and basophils

   Early increase in allergic or nonallergic rxns

   Absence of increased histamine – does not preclude allergic rxn
What biochemical tests?


 Histamine:

   Plasma ½-life very short (15-20 mins)

   Blood samples should be drawn within 30 minutes after
    grade 1 or 2 reaction

   May be increased to 2 hours after grade 3 or 4 reactions
What biochemical tests?


 Tryptase:

   Mast cell neutral serine protease
   Preformed enzyme
   Peaks 15-60 minutes after rxn
   ½-life ~ 2 hours
   Blood samples should be drawn 15-60 minutes after grade 1
    or 2 rxn, 30-120 minutes after grade 3 or 4 rxn
   Absence of increase does not preclude diagnosis
What biochemical tests?


 Tryptase:

   Nonallergic rxn (eg. histamine release) – histamine may be
    increased and tryptase normal

   Some recommend histamine and tryptase, others only
    tryptase
Skin Tests
 Gold standard

 Exposes mast cells of skin to suspected allergen
Why to perform skin tests?
 Premedication (H1 +/- H2 receptor antagonists, steroids)
  has not proven to be preventative

 Identify culprit agent

 Prove pathophysiologic mechanism of rxn (allergic vs.
  nonallergic)

 Suggest safe alternative drug for future
When to perform skin tests?
 4-6 week delay after reaction

 To avoid false negative test because of mast cell
  depletion
How to perform skin tests?
 According to clinical history

 All drugs injected just before reaction AND latex must
  be tested

 Read tests after 15-20 minutes

 Prick tests, followed by intradermal tests
Diagnosis
 Should link clinical history with biochemical tests and
  skin tests
 Severe clinical history + increased tryptase + skin test
  positivity to suspected agent
   Confirms diagnosis
   Agent should be avoided

 Not a severe clinical history +/- increased histamine +
  normal tryptase + neg skin test
   Non-allergic reaction (histamine release with drugs such as
    mivacurium, vancomycin)
   Agent used with caution
Treatment
 Titrated to desired effect with careful monitoring

 Severe reactions need aggressive therapy

 May be protracted with persistent hypotension,
  pulmonary HTN, lower resp obstruction, or laryngeal
  obstruction

 May persist 5-32 hours despite vigorous therapy

 All pts should be admitted to ICU for monitoring –
  manifestations may recur after successful treatment
Treatment – Initial Therapy
1) Stop offending agent

2) Maintain airway and 100% O2
   •   Profound V/Q abnormalities can occur
   •   Follow ABG’s

3) D/C all anesthetic drugs
   •   Inhalational agents NOT bronchodilators of choice,
       especially during hypotension
Treatment – Initial Therapy
4) Volume Expansion

  •   Hypovolemia rapidly follows
  •   Significant changes in vascular permeability
  •   Up to 50% transfer of intravascular fluid into interstitial
      space within 10 minutes
  •   Fluid therapy early
  •   Start with 2-4 L of crystalloid or colloid
  •   Additional 25-50 mL/kg may be necessary
Treatment – Initial Therapy
4) Volume Expansion

  •    If refractory hypotension after volume expansion and
       epi:
       Need additional hemodynamic monitoring
       TEE – rapid assessment of intraventricular volume
           and ventricular function
       Colloids have not proven to be more effective than
           crystalloids
Treatment – Initial Therapy
5) Epinephrine
  •   Drug of choice

  •   α-adrenergic effects – vasoconstrict to reverse
      hypotension

  •   β2-receptor stimulation – bronchodilates and inhibits
      mediator release by increasing cAMP in mast cells and
      basophils

  •   Route and dose depend on patient’s condition
Treatment – Initial Therapy
5) Epinephrine

  •   Poor outcomes associated with either late or absent
      administration of epi, or inadequate dosing

  •   Rapid intervention and careful titration

  •   Pts under GA – altered responses

  •   Pts under spinal or epidural – partially
      sympathectomized – may need even larger doses
Treatment – Initial Therapy
5) Epinephrine

  •   Clinical severity scale by Ring and Messmer

  •   Grades 1 -4
Treatment – Initial Therapy
5) Epinephrine

  •   Never injected during grade 1 reactions
  •   Titrated boluses 10-20 μg for grade 2
  •   Titrated boluses 100-200 μg for grade 3
  •   High dose epi for grade 4 (1-3 mg over 3 mins)
  •   Pts with laryngeal edema without hypotension –
      subcutaneous epi
  •   Epi should not be given IV to pts with Normal BP
Secondary Treatment - Antihistamines

 H1 receptors mediate many of adverse effects

 Diphenhydramine 0.5-1 mg/kg

 Antihistamines DO NOT inhibit anaphylactic reactions or
  histamine release

 Compete with histamine at receptor sites

 Indications for H2 receptor antagonists remain unclear
Secondary Treatment -
Catecholamines

 Epi infusions for persistent hypotension

 5-10 μg/min

 Norepi for refractory hypotension secondary to
  decreased SVR (5-10 μg/min)
Secondary Treatment - Aminophylline

 Nonspecific phosphodiesterase inhibitor

 Bronchodilates

 Decreases histamine release by increasing cAMP

 Increases R and L ventricular contractility

 Decreases PVR

 Loading dose of 5-6 mg/kg IV over 20 mins, followed by
  infusion of 0.5-0.9 mg/kg/hr
Secondary Treatment - Steroids
 Anti-inflammatory effects
 Require 12-24 hours to work
 Unproven
 Exact dose and preparation unclear
 Recommend:
   0.25-1 g IV hydrocortisone – for IgE mediated rxns
   1-2 g methylprednisolone – for rxns believed to be
    complement mediated (eg. protamine rxn)

 May be important for late phase reactions that occur 12-24
  hours after
Secondary Treatment - Bicarb
 Acidosis develops quickly

 Decreases effectiveness of epi

 0.5 – 1 mEq/kg and follow ABG’s
Alternative Therapy - Vasopressin
 May get desensitization of adrenergic receptors

 Vasopressin as alternative

 Vasoconstrictive effects at V1 receptors

 Vasopressin decreases nitric oxide 2nd messenger – cGMP
Airway Evaluation
 Laryngeal edema may occur
   Suggested by facial edema


 Leave intubated until edema subsides



 Air leak useful



 Consider direct laryngoscopy
Non-IgE mediated reactions
 Other immunologic and nonimmunologic mechanisms

 Release many of same mediators

 Independent of IgE

 Clinical syndrome identical with anaphylaxis
Non-IgE mediated reactions -
Complement

 C3a and C5a – anaphylatoxins

 Release histamine from mast cells and basophils

 Contract smooth muscle

 Increase capillary permeability

 Cause interleukin synthesis
Non-IgE mediated reactions –
Complement – C5a

 Causes leukocyte aggregation and activation

 Aggregated leukocytes embolize to organs
   Microvascular occlusion
   Liberation of inflammatory products

 Involved in:
     Transfusion reactions
     Protamine reactions
     ARDS
     Septic shock
Nonimmunologic Histamine Release

 Many agents involved

 Dose-dependent

 Mechanisms not well understood

 Selective mast cell and not basophil activation

 Antihistamine pretreatment
   Does not inhibit histamine release
   Competes with histamine at receptor
   May attenuate decrease in SVR
Drugs Capable of Nonimmunologic
Histamine Release

 Antibiotics (vancomycin)

 Hyperosmotic agents

 Muscle relaxants (atracurium, mivacurium)

 Opioids (morphine, meperidine, codeine)

 thiobarbiturates
Should I give a test dose of IV
antibiotic?
Should I give a test dose of IV
antibiotic?

 No

 Predictive testing would require serial challenges with
  increasing doses

 Starting with a minuscule dose

 Allowing at least 30 minutes between each dose

 This approach is impossible within the constraints of an
  operating list
Should I avoid cephalosporins in a patient who
gives a history suggestive of penicillin allergy?
  Should I avoid cephalosporins in a patient who
  gives a history suggestive of penicillin allergy?


 Most patients with a history of penicillin-related rash – not
  allergic to cephalosporins

 However, many suitable alternatives to cephalosporins

 If convincing history of anaphylaxis – avoid 1st generation
  cephalosporins
Should I use crystalloid or colloid in
the immediate management?
Should I use crystalloid or colloid in
the immediate management?

 No evidence that one is better than the other

 If colloid given before clinical signs of anaphylaxis:
   Should be discontinued
   Replaced with crystalloid or colloid of different class
Should I give an H2-blocking drug as
part of immediate management?
Should I give an H2-blocking drug as
part of immediate management?

 No evidence to support the use of H2-blocking drugs in
  this situation
What should I say to a patient who wishes to
be screened for anesthetic allergy
preoperativley?
What should I say to a patient who wishes to
be screened for anesthetic allergy
preoperativley?

 If no history of previous anesthetic anaphylaxis –
  preoperative screening is of no value

 Sensitivity and specificity of skin tests and blood tests is
  relatively low

 If pretest probability is very low (no positive history) –
  neither a neg. or pos. test is likely to be predictive of
  outcome
Should I avoid propofol in patients who are
allergic to eggs, soya, or nuts?
Should I avoid propofol in patients who are
allergic to eggs, soya, or nuts?

 No published evidence

 Propofol contains purified egg phosphatide and soya-
  bean oil

 Likely that manufacturing process removes or denatures
  proteins responsible for egg and soya allergy
Patient with previous anaphylaxis during anesthetic
presents for emergency surgery without being
tested

 Latex-free environment

 Inhalational agents likely safe (unless MH)

 View previous records if possible
   Avoid all drugs given prior to anaphylaxis (except
    inhalationals)
   Avoid all NMBA’s if pt received NMBA (cross reactivity)
Patient with previous anaphylaxis during anesthetic
presents for emergency surgery without being
tested


 Previous records not available:
     Avoid all NMBA’s if possible (risk vs. benefit)
     Amide LA agents likely safe for regional or local
     Avoid chlorhexidine (allergy to proviodine less common)
     Avoid histamine-releasing drugs eg. Morphine
     No evidence for pretreatment with hydrocortisone or
      histamine-blocking drugs
Summary
• 4 types of hypersensitivities
• 3 involve antibodies
• Anaphylaxis mediated by IgE
• Anaphylactoid is Ab independent
Anaphylaxis
• Bronchospasm

• Vasodilation, increased capillary permeability

• Urticaria

• Profound CV collapse
Mediators
• Histamine

• Leukotrienes and prostaglandins

• Kinins

• Platelet-activating factor

• complement
Management
• ABCs

• Volume expansion

• Epinephrine



• Antihistamines, steroids, infusions
Common Drugs Involved
• Muscle relaxants

• Antibiotics

• Latex

• Blood products

• Colloids
References
1) Barash P. Clinical Anesthesia, 5th ed. Ch 49. 200?

2) Miller R. Miller’s Anesthesia, 6th ed. Ch 27. 2005.

3) Dewachter, Mouton-Faivre, Emala: Anaphylaxis and
   Anesthesia: Controversies and New Insights.
   Anesthesiology 3(5): 1141-1150, 2009.

4) Harper, Dixon, et al: Guidelines: Suspected
   Anaphylactic Reactions Associated with Anaesthesia.
   Anaesthesia 64: 199-211, 2009.

				
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