Anaphylaxis

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Anaphylaxis

• Prepared by Dr. Akram Saadeh
• Discussed by Dr. A. Alfaqih

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• 62 yr old Mrs Young was stung by a bee from a
  hive in her back garden.
• Harvesting the honey had left her with several
  stings during the course of summer.
• Several min. after the recent sting she
  complained of an itching sensation in her hands,
  feet and groin with cramping abd. Pain .

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• Shortly afterwards she felt faint and acutely
  short of breath.
• Moments later she collapsed and lost
  consciousness.
• Her husband ,a Dr , noticed that her breathing
  was rapid and wheezy and that she had swollen
  eyelids and lips.
• She was pale and had patchy erythema across her
  neck and arms.

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• Her apex beat could be felt but her radial pulse
  was weak.
• Her husband immediately administered 0.5 ml of
  1/1000 adrenaline im 10 mg of chlorpheniramine
  iv 10 mg of H.C.
• She regained consciousness and her RR dropped.
• By the following day she had recovered completely.

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• Mrs Young had no hx of adverse reactions to bee
  venom ,foods or AB.
• No Hx of allergic disorders.

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• Dx Anaphylaxis
• Desensitisation therapy.

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• What mech. Are involved in anaphylaxis?
• What are the clinical features and management of
  acute anaphylaxis?
• How may such sensitivity be detected, and what
  can be done to desensitise pt?

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• What mech. Are involved in anaphylaxis?
• What are the clinical features and management of
  acute anaphylaxis?
• How may such sensitivity be detected, and what
  can be done to desensitise pt?

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• What mech. Are involved in anaphylaxis?

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• Traditionally the term anaphylaxis has been used
  to describe a systemic clinical syndrome caused
  by IgE mediated degranulation of mast cells and
  basophils.
• Susceptible individuals exposed to a sensitizing
  antigen producing specific IgE antibodies which
  bind to high affinity IgE receptors found on mast
  cells and basophils.
• The receptor binds the Fc portion of the antibody
  leaving the Fab binding sitesavailable to
  interact with antigen.

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• The avidity of this Fc binding reactionis high
  and therefore the dissociation of IgE from the
  receptors is slow, with a long half life.
• On subsequent exposure, the antigen is bound by
  the IgE receptor complexes, which causes receptor
  mediated activiation of the cells with release of
  performed and denovo synthesized mediators.
• Degranulation is rapid and is completed within 30
  minutes.
• These mediators, released on a large scale, are
  responsible for the clinical manifestations of
  anaphylaxis.

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• The IgE mediated mechanism of mast cell
  degranulation has been implicated in the
  pathogenesis of anaphylaxis triggered by a
  variety of agents. These include antibiotics
  like penecillins, cephalosporins, food like milk,
  nuts, shell fish, foreign proteins eg. Insulin
  Bee venom, latix and pharmacologic agents as
  streptokinase and vaccines.
• The patient may or may not have a history of
  atopy indeed natural allergin exposure in atopics
  is a rare cause of anaphylaxis.

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• Mast cell degranulation can occur by IgE
  independent pathways.
• Prior exposure is not a pre-requisite as specific
  IgE antibodies are not involved.
• Three putative mechanisms of anaphylactoid
  reactions are given below

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• Blood, blood products and immunoglobulins can
  cause an anaphylactoid reaction. The suggested
  mechanism is the formation of immune complexes
  with subsequent complement activation and
  production of C3a and C5a. Both of these
  components are capable of degranulating mast
  cells directly. In addition both components
  increase vasopermiability and may induce
  hypotention. Mellitin a major component of venom
  is able to activate the alternative pathway of
  complement and also produce an anphylactoid
  reaction through anaphylatoxin.

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1. Certain therapeutic and diagnostic agents as
   opiates ACTH, muscle relaxants and cotrast media
   are also capable of directly causing mast cell
   degranulation and anaphylaxis
2. 5-10 of asthmatic subjects produce a reaction to
   NSAIDs such as aspirin or indocin. Symptoms
   commonly include bronchospasm, rhinorrhea and
   vascular collapse, the ability of these agents to
   cause anaphylaxis appears to correlate with their
   effectivness in inhibiting prostaglandin
   synthesis. The mechanism of this sensitivity is
   unknown but may involve mast cell degranulation
   in some patients.

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• What are the clinical features and management of
  acute anaphylaxis?

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• There is a great variation in the timing and
  nature of anaphylactic symptoms.
• The onset is usually within seconds or minutes of
  exposure although delays of an hour have been
  reported.
• The following are common presentations which may
  occur singly or in comination

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1. Cutaneuous erythema, pruritis of hands, feet and
   abdomen, urticaria, angiodema.
2. Repiratory laryngeal edema, bronchoconstriction,
   rhinorrhea.
3. Cardiovascular hypotention, arrhythmias,
   tachycardia, vascular collapse.
4. GI cramping abdominal pain, nausea, vomiting,
   diarrhea.

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• The majority of cases of anaphylactic reactions
  are not fatal. It has been estimated that 1-2
  of courses of penicillin are complicated by
  systemic reactions but only 10 of these are
  serious.
• In the USA some 400-800 people die per year from
  penicillin anaphylaxis with a similar figure for
  contrast media.
• 70 of deaths result from respiratory
  complications.
• 25 resulting from CVS dysfunction.

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Treatment

• Recovery position
• O2
• Adrenaline
• This has the effect of raising BP relaxing
  bronchial smooth muscle and preventing further
  mediator release.
• IV antihistamine vasodilation, cardiac
  arrhythmias and bronchospasm.
• Corticosteroids reduce any late phase response.

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• How may such sensitivity be detected, and what
  can be done to desensitise pt?

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• The first step is to obtain a thorough history of
  previous adverse reactions.
• The timing and nature of such reactions should be
  noted.
• Skin prick testing with insect venom is a fast
  and sensitive method of detecting anti-venom IgE.
• Radioallergosorbent tests can detect venom
  specific IgE, but are positive in only 80 of
  those with significant reactions to venom skin
  prick tests.

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• Immunotherapy is best reserved for those with
  life threatening systemic reactions to insect
  venom.
• The patient is given increasing SC dosages and is
  then given a monthly maintenance dose of 100
  microgram.
• The clinical protection rate is in the order of
  98 for both adults and children.

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Thank You