ANAPHYLAXIS
Dr P K Maharana,
K I M S. Bhubaneswar, India
Anaphylaxis
 It is an acute multi-system severe
type I hypersensitivity reaction
characterized cardiovascular collapse,
bronchospasm & skin changes i.e. urticaria,
itching, redness etc.
 The clinical presentation of anaphylaxis &
Anaphylactoid reactions are same.
 The term comes from the Greek words νά anaἀ
(against) and φύλαξις phylaxis (protection),
Epidemiology
 The incidence is 0.4 cases per million & is
increasing.
 In USA, in 1980 it was 21 per 1,00,000
population, in 1990 it was 50 per 1,00,000
population.
 It is more common in young female.
 In young it mostly food related where as in
adults it because of a previous medication
or sting bite.
Anaphylactic shock
 Anaphylactic shock is anaphylaxis associated
with systemic vasodilation which results in
low blood pressure .
Types
It is of two types.
1. True Anaphylaxis or Classical (IgE
mediated)
2. Pseudo Anaphylaxis/ Anaphylactoid
Reaction (non IgE mediated)
True Anaphylaxis
 Pathophysiology: - Here the Pt has an previous
exposure to an allergen, when he is re exposed to
the same allergen again because of new a
challenge an IgE mediated antigen- antibody
reaction takes place and mediator chemical
substances are released from the Mast cells &
Basophiles, which act on the skin and mucous
membrane to produce severe vasodilatations
leading to cardiovascular collapse, bronchospasm,
urticaria, itching, edema etc.
The Mediators are:
 On re-exposure, the antigen binds to the
antibody, and the receptors are activated.
Clinical manifestations result from release of
immune response mediators such as
“histamine, leukotrienes, tryptase, and
prostaglandins.”
Pathologic
Process
Sign or Symptom Mediator
Responsible
Vasodilatations Urticaria,
angioedema,
laryngeal oedema.
Histamine (H1)
leukotrienes,
prostaglandins
Vascular
permeability
Flushing,
headache
Histamine(H2)
&H1 + do
Smooth-muscle
contraction
Wheezing,
gastrointestinal
cramps, diarrhea
Histamine( H1)
+ do
Congestion Rhinorrhea,
bronchorrhea
H2 + do
Pseudo anaphylaxis/ Anaphylactoid
reaction
 It is not IgE mediated. There is no
sensitization by previous exposure, here the
substances directly acting on the mast cells
liberate histamine, i.e. Morphine
Causes:
 Drugs – Penicillin, Cephalosporin, NSAID, Local
Anesthetics ,ACE inhibitors.
 IV Contrasts- ( 1-3% of patients who receive
hyperosmolar & 0.5% with LMW
IV contrast experience a reaction.)
 Hymenoptera stings-
 Food Allergy. - Includes peanuts, tree nuts, soy,
legumes, fish and shellfish, milk, and eggs.
 Latex allergy –when we use gloves or other
latex products.
Signs & symptoms
 The most common areas affected include:
Skin (80% to 90%),
 Respiratory (70%),
 Gastrointestinal (30% to 45%),
 Heart and vasculature (10% to 45%),
 Central nervous system (10% to 15%)
 These symptoms usually develop over
minutes to hours.
Clinical symptoms
 Skin- generalized hives, itchiness, flushing
 Respiratory- Wheeze, Strider
 CVS- hypotension, coronary artery spasm,
myocardial infarction arrhythmia.
 GI- Colic pain, diarrhea, vomiting
 CNS- loss of consciousness, bladder
bowel involvement, muscular
weakness
Urticaria
Skin Reactions
Urticarial Rash
Urticaria
Erythematous Patches
Anaphylactoid purpura
Erythematous Rashes on Lower Limb
Evaluation of severity
 Based on the examination the degree of severity of the anaphylaxis
should be evaluated and the most threatening symptom of
anaphylaxis identified. The most life-threatening symptom of
anaphylaxis should be treated with priority.
 This may lead to 6 possible scenarios:
 1.Cardiac or circulatory arrest (anaphylaxis grade IV)
 2.Predominant cardiac and circulatory reaction (anaphylaxis grade
II/III)
 3.Predominant obstruction of upper airways (anaphylaxis grade
II/III)
 4.Predominant obstruction of lower airways (anaphylaxis grade II/III)
 5.Predominant gastrointestinal involvement (anaphylaxis grade II)
 6. Systemic generalized skin manifestations and subjective
symptoms (anaphylaxis grade I).
TREATMENT OF ANAPHYLAXIS
It is an medical emergency.
The main stay of treatments are as follows:-
Stop further administration of the drug.
1. Adrenaline( EPINEPHRINE)
2. IV fluids
3. Maintenance of Air way
4. Oxygen therapy
5. Use of Antihistaminic & Steroids.
6. Bronchodilators
7. IPPV if respiratory failure & Others
Adrenaline
 It is the mainstay of treatment in Anaphylaxis.
 Dose- 1mcg/kg body wt. as bolus IV as
diluted solution, repeated up to 1mg .
 Never give undiluted adrenaline IV,
Can be given intramuscular /
subcutaneous/ intraoseous/ intratracheal.
Intravenous epinephrine continuous infusion
and indications
 Patients who do not respond to several IM
injections of epinephrine and aggressive fluid
resuscitation .
 A simple method for quickly preparing a solution of
1 mcg/mL for adults and adolescents is to add the entire
10 mL contents of a 0.1mg/mL (1:10,000) prefilled
"cardiac" epinephrine syringe (1 mg) to a 1000 mL (1
liter) bag of normal saline, the resultant solution of
1mcg/mL .
 Infants and children – The dose for IV infusion is 0.1 to
1 mcg/kg/minute with use of an infusion pump. The
dose can be increased after 3-5minutes interval.
Intramuscular Adrenaline
 For patients of any age is
0.01 mg/kg (maximum dose of 0.5 mg) per
single dose, injected IM into the mid-outer
thigh (vastus lateralis muscle).
 IM epinephrine may be repeated at 5- to 15-minute
intervals if there is no response or an inadequate
response or even sooner if clinically indicated.
Fluids.
 Both crystalloids and colloids are
administered very fast to make up the
volume deficit.
 It may be up to 2Lts or 25%of the blood
volume.
 Children 20ml/kg over 15-20 minutes period,
repeat if needed up to 1ooml/kg may be
required.
 If colloids is offending agent it should not be
administered.
Glucagon for patients taking beta-blockers 
 Beta-blocker therapy, alone or in combination with
angiotensin-converting enzyme inhibitors, has been
shown to be refractory to epinephrine, in such cases
glucagon can be administered because it has inotropic
and chronotropic effects that are not mediated through
beta-receptors .
 Adult dosing is 1 to 5 mg slow IV bolus over five
minutes. May be followed by an infusion of 5 to
15 mcg/minute titrated to effect.
 Pediatric dosing is 20 to 30 mcg/kg (maximum 1 mg)
slow IV bolus over five minutes. May be followed by
an infusion of 5 to 15 mcg/minutetitrated to effect (ie, not
weight-based).
 Rapid administration of glucagon can induce vomiting.
H1 antihistamines
 Relieve itch and hives.
 These medications do not relieve upper or lower airway
obstruction, hypotension or shock, and in standard
doses, do not inhibit mediator release from mast cells
and basophils.
 Only first-generation H1 antihistamines
are available in parenteral formulations,
and rapid IV administration may increase
hypotension.(Diphenhydramine & Avil).
Diphenhydramine HCL/Avil
 For 25 to 50 mg can be administered IV over
five minutes, which may be repeated up to a
maximum daily dose of 400 mg per 24 hours.
 ●For children weighing less than 50
kg, diphenhydramine 1 mg/kg (maximum 50
mg) can be administered IV over five
minutes, which may be repeated up to a
maximum daily dose of 5 mg/kg or 200 mg
per 24 hours.
Avil 22.75mg/ml Injection
 An alkylamine derivative is a histamine H1-receptor
antagonist with anticholinergic and moderate sedative
effects.
 It is used for treating allergic conditions like Pruritus,
urticaria or hay fever ,allergic conjunctivitis and also as
an over-the-counter sleeping pill similar to other sedating
antihistamines.
 Contraindications: Pregnancy, below 5years, glaucoma,
Prostatic Hypertrophy, on MAO inhibitors, with Alcohol.
 Dose: IV/IM/SC ( 0,25mg/kg).
Pharmacodynamic properties
 Antihistamines, including chlorphenamine, used in the treatment of
allergy act by competing with histamine for H1-receptor sites on cells
and tissues.
 Chlorphenamine also has anticholinergic activity.
 The mechanism by which chlorphenamine exerts its anti-emetic,
anti- motion sickness and anti-vertigo effects is not precisely known
but may be related to its central actions.
 Further, most antihistamines, including chlorphenamine, cross the
blood-brain barrier and probably produce sedation largely by
occupying H1-receptors in the brain.
Glucocorticosteroids
 Due to their slow onset of action, glucocorticosteroids play a minor
role in the acute phase of anaphylaxis treatment .
 There are no systematic clinical trials regarding this indication.
 However, glucocorticosteroids are effective in the treatment of
asthma and against protracted or biphasic anaphylactic reactions.
 An unspecific membrane stabilizing effect within the first 10–30
minutes of application of high dose glucocorticosteroids (500–1,000
mg) independent of the potency of the glucocorticosteroids has
been postulated in review article.
 When there is no intravenous catheter, glucocorticosteroids may be
applied rectally, especially in small children (e.g. prednisolone
suppositories) or orally.
Steroids( Glucocorticosteroids)
 Corticosteroid-( hydrocortisone
hemesuccinate) 100-1000mg, Methyl
Prednisolone -30mg/ kg body wt.
The prophylactic use of these substances
are of doubtful value.
Bronchodilators
 For the treatment of bronchospasm not responsive to epinephrine,
inhaled bronchodilators (eg, albuterol, salbutamol) should be
administered by mouthpiece (or facemask for those whose age or
condition requires) and nebulizer/compressor, as needed.
 Aminophyline - as infusion if there is bronchospasm (250mg in
500ml 5% dextrose).
 Bronchodilators are adjunctive treatment to epinephrine
because they do not prevent or relieve mucosal edema in the
upper airway or shock, for which the alpha-1-adrenergic effects
of epinephrine are required
Oxygen Therapy
 To improve saturation.
 Ventilatory support
Anaphylaxis - FOLLOW UP
1. Patients not admitted to the hospital
should be observed for several hours,
because late “biphasic” reactions can begin
as late as 24 hours after the initial
anaphylaxis.
2. Should be treated with steroids during the
acute treatment, and they should be given a
short course of oral corticosteroids to finish at
home.
Cont-
 Must be discharged with autoinjectable
epinephrine (this will provide temporary relief
so the patient will have time to seek medical
assistance).
 Pt must know to seek medical help if
symptoms reappears.
Complications
 Pulmonary edema, pulmonary hemorrhage,
and pneumothorax
 Laryngeal edema with or without airway
obstruction
 Myocardial ischemia and infarction
 Death may result from asphyxiation from
upper airway obstruction or profound
shock or both.
REFRACTORY ANAPHYLAXIS
 Anaphylactic shock displays features of both distributive
(vasodilatory) and hypovolemic shock.
 Further Management – Shifting to ICU & Treat Shock as per
protocol.( Fluid & Vasopressors)
"Norepinephrine, vasopressin, Dopamine and other vasopressors have
been used with success in patients in anaphylaxis with refractory
hypotension“.
Methylene blue 
 — Vasoplegia (profound vasodilation) may
be present in some cases of refractory
anaphylaxis.
 A few case reports and other publications
support the use of methylene blue, an
inhibitor of nitric oxide synthase and
guanylate cyclase, in severe anaphylaxis,
mostly in perioperative settings
Dose of Methylene Blue
 The efficacy and ideal dose of methylene blue is unknown, but
a single bolus of 1 to 2 mg/kg given over 20 to 60 minutes has
been used in cardiac surgery.
 Improvement of vasoplegia (eg, increased systemic vascular
resistance, reduced vasopressor dose) has been observed within
one to two hours in the setting of cardiac surgery, but few data are
available about anaphylaxis.
 This drug should not be given to patients with pulmonary
hypertension, underlying glucose-6-phosphate dehydrogenase
deficiency, or acute lung injury.
 We also advise caution regarding potential drug interactions with
serotonergic agents.
 .
Extracorporeal membrane oxygenation 
 Patients suffering from refractory anaphylaxis have been
resuscitated with extracorporeal membrane oxygenation (ECMO) or
operative cardiopulmonary bypass.
 ECMO is becoming increasingly available in emergency
departments and should be considered in patients unresponsive to
complete resuscitative efforts in institutions with experience in this
technology.
 The decision to initiate ECMO should be considered early in
patients unresponsive to traditional resuscitative measures, before
irreversible ischemic acidosis develops.
Prognosis
 Excellent, provided the trigger can be
avoided.
Establishment of IV line
Intraoseous Needle Placement
Intraoseous
Intraoseous
t

Anaphylaxis

  • 1.
    ANAPHYLAXIS Dr P KMaharana, K I M S. Bhubaneswar, India
  • 2.
    Anaphylaxis  It isan acute multi-system severe type I hypersensitivity reaction characterized cardiovascular collapse, bronchospasm & skin changes i.e. urticaria, itching, redness etc.  The clinical presentation of anaphylaxis & Anaphylactoid reactions are same.  The term comes from the Greek words νά anaἀ (against) and φύλαξις phylaxis (protection),
  • 3.
    Epidemiology  The incidenceis 0.4 cases per million & is increasing.  In USA, in 1980 it was 21 per 1,00,000 population, in 1990 it was 50 per 1,00,000 population.  It is more common in young female.  In young it mostly food related where as in adults it because of a previous medication or sting bite.
  • 4.
    Anaphylactic shock  Anaphylacticshock is anaphylaxis associated with systemic vasodilation which results in low blood pressure .
  • 5.
    Types It is oftwo types. 1. True Anaphylaxis or Classical (IgE mediated) 2. Pseudo Anaphylaxis/ Anaphylactoid Reaction (non IgE mediated)
  • 6.
    True Anaphylaxis  Pathophysiology:- Here the Pt has an previous exposure to an allergen, when he is re exposed to the same allergen again because of new a challenge an IgE mediated antigen- antibody reaction takes place and mediator chemical substances are released from the Mast cells & Basophiles, which act on the skin and mucous membrane to produce severe vasodilatations leading to cardiovascular collapse, bronchospasm, urticaria, itching, edema etc.
  • 7.
    The Mediators are: On re-exposure, the antigen binds to the antibody, and the receptors are activated. Clinical manifestations result from release of immune response mediators such as “histamine, leukotrienes, tryptase, and prostaglandins.”
  • 8.
    Pathologic Process Sign or SymptomMediator Responsible Vasodilatations Urticaria, angioedema, laryngeal oedema. Histamine (H1) leukotrienes, prostaglandins Vascular permeability Flushing, headache Histamine(H2) &H1 + do Smooth-muscle contraction Wheezing, gastrointestinal cramps, diarrhea Histamine( H1) + do Congestion Rhinorrhea, bronchorrhea H2 + do
  • 9.
    Pseudo anaphylaxis/ Anaphylactoid reaction It is not IgE mediated. There is no sensitization by previous exposure, here the substances directly acting on the mast cells liberate histamine, i.e. Morphine
  • 10.
    Causes:  Drugs –Penicillin, Cephalosporin, NSAID, Local Anesthetics ,ACE inhibitors.  IV Contrasts- ( 1-3% of patients who receive hyperosmolar & 0.5% with LMW IV contrast experience a reaction.)  Hymenoptera stings-  Food Allergy. - Includes peanuts, tree nuts, soy, legumes, fish and shellfish, milk, and eggs.  Latex allergy –when we use gloves or other latex products.
  • 11.
    Signs & symptoms The most common areas affected include: Skin (80% to 90%),  Respiratory (70%),  Gastrointestinal (30% to 45%),  Heart and vasculature (10% to 45%),  Central nervous system (10% to 15%)  These symptoms usually develop over minutes to hours.
  • 12.
    Clinical symptoms  Skin-generalized hives, itchiness, flushing  Respiratory- Wheeze, Strider  CVS- hypotension, coronary artery spasm, myocardial infarction arrhythmia.  GI- Colic pain, diarrhea, vomiting  CNS- loss of consciousness, bladder bowel involvement, muscular weakness
  • 13.
  • 14.
  • 15.
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
    Evaluation of severity Based on the examination the degree of severity of the anaphylaxis should be evaluated and the most threatening symptom of anaphylaxis identified. The most life-threatening symptom of anaphylaxis should be treated with priority.  This may lead to 6 possible scenarios:  1.Cardiac or circulatory arrest (anaphylaxis grade IV)  2.Predominant cardiac and circulatory reaction (anaphylaxis grade II/III)  3.Predominant obstruction of upper airways (anaphylaxis grade II/III)  4.Predominant obstruction of lower airways (anaphylaxis grade II/III)  5.Predominant gastrointestinal involvement (anaphylaxis grade II)  6. Systemic generalized skin manifestations and subjective symptoms (anaphylaxis grade I).
  • 21.
    TREATMENT OF ANAPHYLAXIS Itis an medical emergency. The main stay of treatments are as follows:- Stop further administration of the drug. 1. Adrenaline( EPINEPHRINE) 2. IV fluids 3. Maintenance of Air way 4. Oxygen therapy 5. Use of Antihistaminic & Steroids. 6. Bronchodilators 7. IPPV if respiratory failure & Others
  • 22.
    Adrenaline  It isthe mainstay of treatment in Anaphylaxis.  Dose- 1mcg/kg body wt. as bolus IV as diluted solution, repeated up to 1mg .  Never give undiluted adrenaline IV, Can be given intramuscular / subcutaneous/ intraoseous/ intratracheal.
  • 23.
    Intravenous epinephrine continuousinfusion and indications  Patients who do not respond to several IM injections of epinephrine and aggressive fluid resuscitation .  A simple method for quickly preparing a solution of 1 mcg/mL for adults and adolescents is to add the entire 10 mL contents of a 0.1mg/mL (1:10,000) prefilled "cardiac" epinephrine syringe (1 mg) to a 1000 mL (1 liter) bag of normal saline, the resultant solution of 1mcg/mL .  Infants and children – The dose for IV infusion is 0.1 to 1 mcg/kg/minute with use of an infusion pump. The dose can be increased after 3-5minutes interval.
  • 24.
    Intramuscular Adrenaline  Forpatients of any age is 0.01 mg/kg (maximum dose of 0.5 mg) per single dose, injected IM into the mid-outer thigh (vastus lateralis muscle).  IM epinephrine may be repeated at 5- to 15-minute intervals if there is no response or an inadequate response or even sooner if clinically indicated.
  • 25.
    Fluids.  Both crystalloidsand colloids are administered very fast to make up the volume deficit.  It may be up to 2Lts or 25%of the blood volume.  Children 20ml/kg over 15-20 minutes period, repeat if needed up to 1ooml/kg may be required.  If colloids is offending agent it should not be administered.
  • 26.
    Glucagon for patientstaking beta-blockers   Beta-blocker therapy, alone or in combination with angiotensin-converting enzyme inhibitors, has been shown to be refractory to epinephrine, in such cases glucagon can be administered because it has inotropic and chronotropic effects that are not mediated through beta-receptors .  Adult dosing is 1 to 5 mg slow IV bolus over five minutes. May be followed by an infusion of 5 to 15 mcg/minute titrated to effect.  Pediatric dosing is 20 to 30 mcg/kg (maximum 1 mg) slow IV bolus over five minutes. May be followed by an infusion of 5 to 15 mcg/minutetitrated to effect (ie, not weight-based).  Rapid administration of glucagon can induce vomiting.
  • 27.
    H1 antihistamines  Relieveitch and hives.  These medications do not relieve upper or lower airway obstruction, hypotension or shock, and in standard doses, do not inhibit mediator release from mast cells and basophils.  Only first-generation H1 antihistamines are available in parenteral formulations, and rapid IV administration may increase hypotension.(Diphenhydramine & Avil).
  • 28.
    Diphenhydramine HCL/Avil  For25 to 50 mg can be administered IV over five minutes, which may be repeated up to a maximum daily dose of 400 mg per 24 hours.  ●For children weighing less than 50 kg, diphenhydramine 1 mg/kg (maximum 50 mg) can be administered IV over five minutes, which may be repeated up to a maximum daily dose of 5 mg/kg or 200 mg per 24 hours.
  • 29.
    Avil 22.75mg/ml Injection An alkylamine derivative is a histamine H1-receptor antagonist with anticholinergic and moderate sedative effects.  It is used for treating allergic conditions like Pruritus, urticaria or hay fever ,allergic conjunctivitis and also as an over-the-counter sleeping pill similar to other sedating antihistamines.  Contraindications: Pregnancy, below 5years, glaucoma, Prostatic Hypertrophy, on MAO inhibitors, with Alcohol.  Dose: IV/IM/SC ( 0,25mg/kg).
  • 30.
    Pharmacodynamic properties  Antihistamines,including chlorphenamine, used in the treatment of allergy act by competing with histamine for H1-receptor sites on cells and tissues.  Chlorphenamine also has anticholinergic activity.  The mechanism by which chlorphenamine exerts its anti-emetic, anti- motion sickness and anti-vertigo effects is not precisely known but may be related to its central actions.  Further, most antihistamines, including chlorphenamine, cross the blood-brain barrier and probably produce sedation largely by occupying H1-receptors in the brain.
  • 31.
    Glucocorticosteroids  Due totheir slow onset of action, glucocorticosteroids play a minor role in the acute phase of anaphylaxis treatment .  There are no systematic clinical trials regarding this indication.  However, glucocorticosteroids are effective in the treatment of asthma and against protracted or biphasic anaphylactic reactions.  An unspecific membrane stabilizing effect within the first 10–30 minutes of application of high dose glucocorticosteroids (500–1,000 mg) independent of the potency of the glucocorticosteroids has been postulated in review article.  When there is no intravenous catheter, glucocorticosteroids may be applied rectally, especially in small children (e.g. prednisolone suppositories) or orally.
  • 32.
    Steroids( Glucocorticosteroids)  Corticosteroid-(hydrocortisone hemesuccinate) 100-1000mg, Methyl Prednisolone -30mg/ kg body wt. The prophylactic use of these substances are of doubtful value.
  • 33.
    Bronchodilators  For thetreatment of bronchospasm not responsive to epinephrine, inhaled bronchodilators (eg, albuterol, salbutamol) should be administered by mouthpiece (or facemask for those whose age or condition requires) and nebulizer/compressor, as needed.  Aminophyline - as infusion if there is bronchospasm (250mg in 500ml 5% dextrose).  Bronchodilators are adjunctive treatment to epinephrine because they do not prevent or relieve mucosal edema in the upper airway or shock, for which the alpha-1-adrenergic effects of epinephrine are required
  • 34.
    Oxygen Therapy  Toimprove saturation.  Ventilatory support
  • 35.
    Anaphylaxis - FOLLOWUP 1. Patients not admitted to the hospital should be observed for several hours, because late “biphasic” reactions can begin as late as 24 hours after the initial anaphylaxis. 2. Should be treated with steroids during the acute treatment, and they should be given a short course of oral corticosteroids to finish at home.
  • 36.
    Cont-  Must bedischarged with autoinjectable epinephrine (this will provide temporary relief so the patient will have time to seek medical assistance).  Pt must know to seek medical help if symptoms reappears.
  • 37.
    Complications  Pulmonary edema,pulmonary hemorrhage, and pneumothorax  Laryngeal edema with or without airway obstruction  Myocardial ischemia and infarction  Death may result from asphyxiation from upper airway obstruction or profound shock or both.
  • 38.
    REFRACTORY ANAPHYLAXIS  Anaphylacticshock displays features of both distributive (vasodilatory) and hypovolemic shock.  Further Management – Shifting to ICU & Treat Shock as per protocol.( Fluid & Vasopressors) "Norepinephrine, vasopressin, Dopamine and other vasopressors have been used with success in patients in anaphylaxis with refractory hypotension“.
  • 39.
    Methylene blue   —Vasoplegia (profound vasodilation) may be present in some cases of refractory anaphylaxis.  A few case reports and other publications support the use of methylene blue, an inhibitor of nitric oxide synthase and guanylate cyclase, in severe anaphylaxis, mostly in perioperative settings
  • 40.
    Dose of MethyleneBlue  The efficacy and ideal dose of methylene blue is unknown, but a single bolus of 1 to 2 mg/kg given over 20 to 60 minutes has been used in cardiac surgery.  Improvement of vasoplegia (eg, increased systemic vascular resistance, reduced vasopressor dose) has been observed within one to two hours in the setting of cardiac surgery, but few data are available about anaphylaxis.  This drug should not be given to patients with pulmonary hypertension, underlying glucose-6-phosphate dehydrogenase deficiency, or acute lung injury.  We also advise caution regarding potential drug interactions with serotonergic agents.  .
  • 41.
    Extracorporeal membrane oxygenation  Patients suffering from refractory anaphylaxis have been resuscitated with extracorporeal membrane oxygenation (ECMO) or operative cardiopulmonary bypass.  ECMO is becoming increasingly available in emergency departments and should be considered in patients unresponsive to complete resuscitative efforts in institutions with experience in this technology.  The decision to initiate ECMO should be considered early in patients unresponsive to traditional resuscitative measures, before irreversible ischemic acidosis develops.
  • 42.
    Prognosis  Excellent, providedthe trigger can be avoided.
  • 43.
  • 44.
  • 45.
  • 46.
  • 47.

Editor's Notes

  • #24 may not be adequately perfusing muscle tissues, as most commonly occurs in individuals presenting with profound hypotension or symptoms and signs suggestive of impending shock (dizziness, incontinence of urine and/or stool).
  • #25 The dose should be drawn up using a 1 mL syringe using the 1 mg/mL formulation of epinephrine.
  • #27 Therefore, protection of the airway, for example, by placement in the lateral recumbent position, is important in drowsy or obtunded patients.
  • #30 Avil Injection below 5yrs contraindicated, Slow IV. Do not drive after Avil Injection or Operate achines.
  • #41 Methylene blue and other vital dyes are also rarely the cause of perioperative anaphylaxis
  • #46 n comparison with child and infant peripheral IV access, central lines, or umbilical lines, IO access is safer, is associated with fewer complications, can be implemented with less delay, and requires less skill and practice on the part of practitioners who may use the techniques only rarely.