Anaphylaxis

Diagnosis & Management

1. ANAPHYLAXIS
Dr P K Maharana,
K I M S. Bhubaneswar, India

2. 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 ana
ἀ
(against) and φύλαξις phylaxis (protection),

3. 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.

4. Anaphylactic shock
Anaphylactic shock is anaphylaxis associated
with systemic vasodilation which results in
low blood pressure .

5. Types
It is of two 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. Pathophysiology of Anaphylaxis
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

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. Urticaria

14. Skin Reactions

15. Urticarial Rash

16. Urticaria

17. Erythematous Patches

18. Anaphylactoid purpura

19. Erythematous Rashes on Lower Limb

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
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

22. 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.

23. 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.

24. 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.

25. 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.

26. 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.

27. 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).

28. 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.

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 H
1
-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 H
1
-receptors in the brain.

31. 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.

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 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

34. Oxygen Therapy
To improve saturation.
Ventilatory support

35. 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.

36. 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.

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
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“.

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 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.
.

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, provided the trigger can be
avoided.

43. Establishment of IV line

44. Intraoseous Needle Placement

45. Intraoseous

46. Intraoseous

47. t