Final anaphylactic reactions and anaphylactic shock

ANAPHYLACTIC REACTIONS
AND ANAPHYLACTIC
SHOCK IN ANAESTHESIA
PRESENTER- DR NANDINI
DESHPANDE
GUIDE- DR ASHESH SHAH

Discovery of Anaphylaxis
In a few seconds it was extremely ill;
breathing became distressful and panting;
it could scarcely drag itself along, lay on its
side, was seized with diarrhea, vomited blood
and died in twenty five minutes.
Charles Richet 1902

Instead of inducing tolerance ( prophylaxis),
Richet’s experiments in dogs injected with
sea anemone toxin resulted in lethal
responses to doses previously tolerated.
He coined the word ‘Ana’ (without) ‘phylaxis
(protection). He won the Nobel prize for this
work.

Definition of anaphylaxis and
associated reactions
• Anaphylaxis is defined as an acute
allergic reaction resulting in
widespread allergic symptoms
which involves two or more organ
systems, and is potentially life-
threatening, often resulting from
an IgE-mediated mechanism.
• Anaphylactoid reaction – term
falling into disuse but meant to
describe anaphylaxis without IgE
involvement ie ;a non-allergic
mechanism.

Contd:
• Anaphylaxis is a severe, systemic allergic reaction
with multisystem involvement, including the skin,
airway, vascular system, and GI .
• Severe cases may result in complete obstruction of the
airway, cardiovascular collapse, and death.
• Anaphylactic shock is a severe, potentially life-
threatening allergic reaction leading to sudden
cardiovascular collapse. It can occur within seconds or
minutes of exposure to allergen.
• It is an emergency situation and requires prompt
recognition and rapid treatment.

Anaphylactic
reaction
• It is an immune- mediated
reaction.
• IgE antibody plays an
important role .
• The allergen[antigen]
reacts with the IgE
antibody and the complex
causes degranulation of
the mast cells and hence
release of histamine and
other mediators.
Anaphylactoid
reaction
• It is a non- immune
mediated reaction.
• No relation with IgE
antibody.
• The allergen[antigen]
causes direct release of
histamine and other
mediators from the
mast cell and does not
cause degranulation.

Anaphylaxis is highly likely when any
ONE of the following 3 criteria is
fulfilled:
1. Acute onset of an illness (minutes to several hours)
with involvement of the skin, mucosal tissue, or both (eg,
generalized hives, pruritus or flushing, swollen lips-
tongue-uvula)
AND AT LEAST ONE OF THE FOLLOWING
•A. Respiratory compromise (eg, dyspnea, wheeze-
bronchospasm, reduced PEFR in older children and
adults, stridor, hypoxemia)

B. Reduced BP* or associated symptoms of end-organ
dysfunction (eg, hypotension, collapse, syncope,
incontinence) .
2. Two or more of the following that occur
rapidly after exposure to a likely allergen for
that patient (minutes to several hours):
A. Involvement of the skin-mucosal tissue (eg,
generalized hives, itching, flushing, swollen
lips-tongue-uvula) .
B. Respiratory compromise (eg, dyspnea,
wheeze- bronchospasm, stridor, reduced
PEFR in older children and adults,
hypoxemia)

C. Reduced BP or associated symptoms (eg,
hypotonia, collapse, syncope, incontinence).
D. Persistent gastrointestinal symptoms
(eg, crampy abdominal pain, vomiting).
3. Reduced BP after exposure to a known
allergen for that patient (minutes to several
hours):
A] Infants and children: low systolic BP[age-specific]
or greater than 30 % decrease in systolic BP.
B] Adults: systolic BP of less than 90 mmHg or
greater than 30% decrease in systolic BP from the
person ‘s baseline BP.

Intra –operative anaphylactic
reactions
• Understanding peri-operative anaphylaxis is
important because of the potential for morbidity
and mortality.
• The risk of peri-operative anaphylaxis is
reported as between 1:3,500 and 1:20,000 with
the mortality rate of 4% and an additional 2%
surviving with severe brain damage.
• More than 90% of the allergic reactions evoked
by Intravenous drugs occur within the 5 minutes
of administration.

Role of an Anaesthesiologist
Thorough pre-operative evaluation of
FOOD,SPECIFIC DRUG ALLERGIES.
Detailed description regarding previous
anaphylactic reaction and the treatment
given for it should be mentioned in the PAC
CHART.
Ask specifically about episode of anaphylaxis
due to general anaesthetic drugs or during
regional anaesthesia.

Contd:
 If the patient is found to be allergic to specific drugs,
it should be conveyed to the surgeon as well as the OT
staff regarding the allergic reaction so that everyone
is cautious in preventing any untoward event during
surgery and anaesthesia.
 Mention in the PAC and intraoperative chart in
CAPITAL LETTERS regarding it so that it is helpful for
documentation and in future medical and surgical
treatments.
 Pre-operative testing for allergies should be
conducted.

 The anaesthetist should always take a written
informed consent of the patient regarding allergic
reactions that can occur due to regional as well as
general anaesthetic drugs.
 It is not a hard and fast rule that a person who was
not allergic to a drug before won ‘t develop
anaphylaxis for the first time during surgery and
anaesthesia. Hence, anaesthetist should always be
alert.
 Prompt recognition and rapid treatment should be
ensued if anaphylactic reaction or shock develops
perioperatively.

All the emergency drugs like epinephrine,
corticosteroids, antihistaminics, ionotrops,
volume expanders, B- agonists should be
available in the operation theatre.
The surgeon and anaesthetist should have an
co-ordination during an intra-operative
untoward event.
Use of epinephrine within few minutes of the
reaction is LIFE- SAVING.

Contd:
 Non-pharmacological agents- pollen grains, dust,
animal dander, mushrooms, bee-stings, sea-
food, scorpion bites, poisonous plants etc.
 Pharmacological agents-
1. Antibiotics- penicillins, cephalosporins,
fluoroquinolones, vancomycin, sulfonamides, B-
lactams like clavulanic acid- there is incidence of
cross sensitivity among allergic reactions
between penicillins and cephalosporins. Hence,
peri-operatively always do and AST[ANTIBIOTIC
SENSITIVITY TESTING] using a test dose of the
antibiotic to be used during surgery.

2. NSAID’S- aspirin, diclofenac, ibuprofen, paracetamol
etc. A person allergic to one drug can develop
anaphylaxis to another drug due to cross- sensitivity
among the drugs of the same group and same
mechanism of action on COX enzymes.
3.IV contrast agents used during radiological studies,
dyes like methylene blue dyes, gadolinium contrast
etc.
4. Drugs like Insulin, Protamine, Aprotonin
5. Bone cement used during orthopaedic surgeries –
PMMA ie; polymethyl- metha acrylate.
6.IV fluids ie: colloids like hexa-ethyl starch, gelofusin,
dextran, albumin

Anaesthetic drugs causing
anaphylaxis
Muscle relaxants- they account for approximately
50-60% of anaesthetic allergic reactions. Also ,
there is frequent cross- sensitization between the
drugs mainly due to quaternary and tertiary
ammonium ions.
1.Benzyl isoquinolinium compounds[MORE LIKELY]- D-
tubocurarine , metocurine, atracurium ,
mivacurium.
2. Aminosteroid compounds[LESS LIKELY]-
pancuronium, vecuronium, rocuronium.

contd:
Induction drugs- they account for 5% of
anaphylactic events that occur perioperatively.
1. Thiopentone- more commonly due to release of
histamine .
2. Propofol- more commonly due to its contents
like egg lecithin, soyabean emulsion. Hence, in
patients having allergy to egg and soya ,
propofol should be avoided.
3. Allergic reactions to etomidate, ketamine and
midazolam are very rare.

• Local anaesthetics- They account for less than 2
% of allergic reactions.
1. Ester-type: [ MORE LIKELY]: cocaine, tetracaine,
benzocaine etc. These are rarely used now a-
days as compared to amides.
2. Amide type:[LESS LIKELY]: Lignocaine,
bupivacaine, ropivacaine.
Esters cause more allergic reactions than amides
because they get metabolised to para-
aminobenzoic acid which is a highly antigenic
compound. Preservatives used in LA like
methylparaben, propylparaben and
metabisulfite also cause anaphyalctic reactions.

• Opioids - They cause less than 3 % of
anaphylactic reactions.
1. Morphine, codeine, meperidine: they
directly cause release of histamine from
mast cells and basophils.
2. Fentanyl: less likely to cause an allergy.
Hence, more safer than the above
mentioned drugs even in patients allergic
to the other opioids.

Mechanism of anaphylaxis:
It is a Type І hypersensitivity reaction.
The antigen [ allergen i.e; IV drug as far as we are concerned]
when injected binds to the Fc receptor of the IgE antibody .
The IgE antibody is present on the mast cells and basophils . It
causes bridging of the two IgE antibodies and is a calcium-
dependent and an energy- dependent process.
Ultimately, this process results in degranulation of the mast
cells and basophils and further causes release of various
chemical mediators responsible for the classical signs of
anaphylaxis

Chemical mediators of anaphylaxis
Mediators Physiological effects
Histamine Increased capillary permeability
Peripheral vasodilation
Bronchoconstriction
Utricaria
Leukotrienes Increased capillary permeability
Bronchoconstriction
Negative ionotropy
Coronary artery vasoconstriction
Prostaglandins Bronchoconstriction
Eosinophil chemotactic factor Attraction of eosinophils
Platelet - activating factor Platelet aggregation
Release of vasoactive amines

CLINICAL MANIFESTATIONS OF
ANAPHYLAXIS
• SKIN- urticaria, angioedema, pruritus, erythema
• RESPIRATORY- rhinitis, conjunctivitis, cough,
dyspnea, wheeze, stridor, voice change
• GI – throat swelling or tightness, dysphagia,
vomiting, diarrhea, cramps
• CVS – hypotension, dizziness, syncope, cyanosis,
secondary myocardial infarction
• CNS –hypoxic seizures

CLINICAL MANIFESTATIONS OF ALLERGY
• Vasodilation – erythema, nasal congestion,
hypotension.
• Increased vascular permeability – urticaria,
hypotension.
• Smooth muscle spasm – asthma, intestinal
cramps, diarrhea.
• Mucus secretion – allergic rhinitis, asthma.
• Nerve stimulation-itch, sneeze.

URTICARIA
• Raised central white or red wheals
• Surrounding erythema or flare, with itch or burning
• Histamine mediated
• Varies in shape & size – circular, gyrate, linear,
isolated or coalescent
• Well demarcated, blanch with pressure
• Predisposition to warm areas, pressure sites
• Lasts hours, max 24 - 48

ANGIOEDEMA
• Diffuse skin colored subcutaneous swelling
• Pathology similar to urticaria except it occurs in
deeper subcutaneous tissues
• Not itchy or painful, unless in confined site
• Can be histamine, bradykinin etc mediated
• Can last hours or days
• Not very responsive to antihistaminics
• Often found in 40% of urticaria cases

Laryngospasm & Bronchospasm
• These are two common symptoms that occur
during anaphylaxis and which are the most
important areas of concern to an anaesthetist.
• Both the symptoms lead to airway closure,
airflow obstruction, further airway oedema, air
hunger, desaturation, cyanosis , stridor [
laryngospasm] , wheezing [ bronchospasm],
silent chest in severe untreatable cases and
death due to hypoxia if not treated in time.

• Laryngospasm is defined as sudden glottic
closure resulting from a reflex constriction of
the laryngeal muscles.
• Bronchospasm is defined as sudden
constriction of muscles in the walls of the
bronchioles.
• These are two emergency conditions which
require immediate treatment to save the life
of the patient.

Recognition of anaphylaxis during
regional and general anaesthesia
Systems Symptoms Signs
Respiratory Dyspnoea
Chest discomfort
Coughing
Wheezing
Sneezing
Laryngeal oedema
Decreased pulmonary
compliance
Fulminant pulmonary
oedema
Acute respiratory
failure

Systems Symptoms Signs
Cardiovascular Dizziness
Malaise
Retrosternal
oppression
Disorientation
Diaphoresis
Loss of consciousness
Hypotension
Tachycardia
Dysrhythmias
Decreased systemic
vascular resistance
Cardiac arrest
Pulmonary
hypertension
Cutaneous Itching
Burning
Tingling
Urticaria [hives]
Flushing
Periorbital oedema
Perioral oedema

Differential diagnosis of anaphylaxis
during anaesthesia
Drug overdose and interactions
Cardiac/vascular drug effects
Asthma
Arrythmias
Myocardial infarction
Pulmonary oedema
Pericardial tamponade
Pulmonary embolism
Venous embolism
Sepsis
Malignant hyperthermia

Difficulty in diagnosis
• Recognition of an allergic reaction that
occurs during anaesthesia may be
compromised by inability of the patient to
communicate early symptoms such as
pruritis.
• Covering of the patient by surgical drapes
may obscure recognition of cutaneous signs.
• Consequently, cardiovascular collapse may be
the first detectable signal of the event.

Investigations:
 Immunologic and biochemical evidence of anaphylaxis
is provided by an increased plasma tryptase
concentration within 1-2 hours of the suspected event.
• Tryptase, a neutral protease stored in the mast cells is
liberated in the systemic circulation during immune-
mediated but not non- immune- mediated reactions.
Hence, it can be used to differentiated between
anaphylactic and anaphylactoid reactions.
• It’s presence verifies that mast cell activation and
mediator release have occurred , and thus it serves to
distinguish immunologic from chemical reactions.

Plasma histamine concentration- it returns to
baseline within 30-60 minutes of an
anaphylactic reaction.
• Hence, plasma histamine concentration must be
measured immediately after the treatment of
anaphylaxis to capture the change in the plasma
histamine concentration.
Skin prick or intradermal test- most sensitive
and preferred method of testing .
• A positive response to skin prick in the form of
wheal and flare response confirms the presence
of specific IgE antibodies.

• Skin testing should not be performed within 6
weeks of an anaphylactic reaction because mast
cell and basophil mediator depletion may lead
to a false- negative result.
• A preservative- free solution of the suspected
antigen should be used for testing so as to avoid
the risk of inducing any systemic reaction and it
should be performed only by trained personnel
with appropriate resuscitation equipment
available.
• In- vitro immunoassays for allergen – specific IgE
are commercially available for some drugs.

Treatment during anaesthesia
 PRIMARY TREATMENT:
1. General measures:
• Inform the surgeon
• Request immediate assistance
• Stop administration of all drugs, colloids, blood
products
• Maintain airway with 100% oxygen
• Elevate the legs, if practical

2. Epinephrine administration:
• Titrate the dose according to symptom, severity and
clinical response.
• Epinephrine used S/C in the dose of 0.3mg-0.5 mg if
the patient is not in a state of shock.
• In case of shock , S/C injection is not helpful due to
decreased tissue perfusion . Hence, IV INJECTION IS
GIVEN. Adults- 10 mcg to 1mg by bolus IV , repeat
every 1-2 min as needed.
• IV infusion starting at 0.05-1 mcg/kg/min
• Children- 1-10 mcg/kg by bolus, repeat every 1-2 min
as needed.
• EPINEPHRINE is life – saving drug in anaphylactic
reactions and shock.

Effects of EPINEPHRINE
• Increases BP, reverses peripheral vasodilation (
alpha-adrenergic activity)
• Reduces urticaria and angioedema by
vasoconstriction (alpha- adrenergic activity)
• Bronchodilation – relaxes bronchial smooth
muscle (beta-2 adrenergic activity)
• Increases cardiac contractility – force and
volume, increasing heart rate & BP (beta-1
adrenergic activity)
• Prevents further mast cell degranulation (beta-1
adrenergic activity)

Side Effects of EPINEPHRINE
• Tachycardia , tremors, dizziness, headache,
anxiety, fear
• Hypertension and intracranial bleed
• Myocardial ischemia, infarction, arrythmias.

Epinephrine Auto-injectors
• Epipen
– Epipen Jr. (0.15 mg)
– Epipen (0.30 mg)
– One dose: auto-injection
• Twinject
– Twinject 0.15
– Twinject 0.30
– Two doses: first is an auto-
injection, second dose is
manual

3. Fluid therapy:
• Crystalloid : Normal saline 10-25 ml/kg over 20
min, more as needed.
• Colloid: 10ml/kg over 20 min, more as needed.
4. Anaphylaxis resistant to epinephrine:
• Glucagon:1-5 mg bolus followed by 1-2.5
mg/hr IV infusion
• Norepinephrine:0.05-0.1 mcg/kg/min IV
infusion
• Vasopressin: 2-10 units IV bolus followed by
0.01-0.1 unit/min IV infusion

SECONDARY TREATMENT:
1. Bronchodilator:
• B-2 Agonists for symptomatic treatment of bronchospasm
2. Antihistamines :
• H1 antagonist: diphenhydramine 0.5-1 mg/kg IV
• H2 antagonist: ranitidine 50 mg IV
3. Corticosteroids:
• Adults – Hydrocortisone 250 mg IV or methylprednisolone
2mg/kg IV
• Children – Hydrocortisone 50-100 mg IV or
methylprednisolone 2mg/kg IV
4. Aftercare:
• Patient may experience relapse, admit for observation
• Obtain blood samples for diagnostic testing
• Arrange allergy testing at 6-8 wk postoperatively

Management of specific symptoms
• Bronchospasm-
 Inhaled bronchodilators eg: salbutamol .IV if unresponsive
to inhaled.
 Oxygen
 Intubation and ventilation if needed
• Laryngeal oedema-
 Racemic epinephrine via nebulizer
 Intubation or cricothyrotomy or tracheostomy
 Post –operatively electively ventilate the patient till the
oedema subsides as there is post operative risk of airway
obstruction due to it. Once, the patient stabilizes ,
extubation can be done.

• Hypotension:
• Trendelenberg position
• Volume expansion with crystalloid
• Vasopressors eg: dopamine, norepinephrine,
metaraminol, vasopressin
• Glucagon especially if on beta-blocker

Take home message
• Careful history and recognition during
preoperative check ups.
• Avoid the use of offending agent[ allergen].
• Rapid recognition and prompt treatment of
anaphylactic reaction and shock .
• Epinephrine or epipens autoinjectors are life-
saving.
• Manage airway, breathing and circulation
during anaphylaxis.
• Be ready to follow BLS and ALS protocol if
cardiopulmonary arrest develops.

Final anaphylactic reactions and anaphylactic shock

Final anaphylactic reactions and anaphylactic shock

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Final anaphylactic reactions and anaphylactic shock