Transcript anaphylaxis powerpoint

Allergic Reactions & Anaphylaxis
Barry Barkinsky
EMS-I, Paramedic
Sections
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Path physiology
Assessment findings in anaphylaxis
Management
Basement findings in Allergic
Reaction
Management
Patient Education
overview
https://www.youtube.com/watch?v=G9DVfmbt4s
Incidence
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In USA - 400 to 800 deaths/year
Parenterally administered penicillin accounts for
100 to 500 deaths per year
Hymenoptera stings account for 40 to 100 deaths
per year
Risk factors: beta-blockers, adrenal
insufficiency
Why do they die?
Causes of Deaths
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Laryngeal edema and acute bronchospasm with
respiratory failure account for >70%
Circulatory collapse accounts for 25%
Other <5% - ?brain ?MI
bronchospasm
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Bronchospasm is a sudden
constriction of the muscles in the
walls of the bronchioles. It is caused
by the release (degranulation) of
substances from mast cells or
basophils under the influence of
anaphylatoxins.
Laryngeal edema
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The acute laryngeal edema seen
here that killed the patient was
due to an anaphylactic reaction
to penicillin. Such an allergy is
a form of type I
hypersensitivity reaction in
which there is preformed IgE
antibody on mast cells that
quickly reacts with an antigen.
The mast cells release histamine
and other mediators that lead
to the edema.
Allergic Reaction
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é Physiologic response to antigens
– Oversensitive response = allergic
– Occurs after sensitization to antigen
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Antigen binds with Antibody
– Less severe result in inflammatory response
– Type I reaction involves antibodies attached to mast
cells or basophils = most severe form
Define some terms
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Antigen: any
substance capable
of inducing an
immune response
– Most antigens are
proteins
– Following exposure
to an antigen the
body releases
antibodies
Define some terms
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Antibodies
– Substances produced by B
lymphocytes in response to the
presence of a foreign antigen
that will combine with and
control or destroy the antigen,
thus preventing infection
Define some terms
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Mast cells
– Specialized cell of
the immune system
which contains
chemicals that assist
in the immune
response
Systemic mastocytosis
Define some terms
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Sensitized
– The initial exposure to an antigen that
results in an immune response
Allergic Reaction - definition
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An exaggerated response by the
immune system to a foreign
substance
Allergic Reaction
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é Physiologic response to antigens
– Oversensitive response = allergic
– Occurs after sensitization to antigen
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Antibody binds with Antigen
– Less severe result in inflammatory response
– Type I reaction involves antibodies attached to mast
cells or basophils = most severe form
Primary response
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Initial response to an antigen – on
time exposure
several day response by immune
system
Generalized antibodies IgG, IgM are
released
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Secondary response
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Specialized antibodies with memory
now created
Specific to the antigen
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The speed of the reaction is a good
predictor of the severity of the
reaction
Anaphylaxis
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Systemic reaction of multiple organ systems to
antigen-induced IgE-mediated immunulogic
mediator release in previously sensitized
individual
IgE mediated reactions
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IgE-mediated hypersensitive
reactions (allergic rhinitis, asthma,
atopic dermatitis)
Type 1 - immediate (or atopic, or
anaphylactic)
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Symptoms vary from mild irritation to sudden
death from anaphylactic shock
– Allergic asthma
– Allergic conjunctivitis
– Allergic rhinitis ("hay fever")
– Anaphylaxis
– Angioedema
– Urticaria (hives)
– Eosinophilia
– Penicillin
– Cephalosporin
Allergic Reaction
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Antigen
– Induces antibody formation
– Examples
» Drugs (antibiotics)
» Foods (nuts, shellfish)
» Insect venoms
» Animal serum
» Incompatible blood types
Allergic reaction / Anaphylaxis
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Antigens enter body by:
– Injection
– Ingestion
– Inhalation
– Absorption
Mast Cells and the Allergic Response
Mast Cells and the Allergic Response
Mitigating factors?
• Route of administration
• And???????????????
• IMMUNITY
immunity
Pathophysiology- IMMUNITY
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Immune Response
–Exposure to antigen produces primary
response with general antibodies
–Immune system develops antigen-specific
antibodies and memory – secondary response
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Natural and acquired Immunity
Induced Active Immunity
Active and Passive Immunity
The immune system
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Natural immunity - OEM
• Acquired immunity
– Naturally acquired immunity
Natural immunity
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Also called: innate immunity
Genetically predetermined
Not related to previous exposures
Everyone has “some” natural
immunities
Naturally Acquired immunity
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Results from exposure to antigens
Is enhanced by continued exposures
Is believed to be lifelong in duration
Induced active immunity
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Also called artificially acquired
immunity
Designed to protect from a future
exposure to an antigen
Achieved through vaccination
Provides relative protection
Creates antibodies
Induced passive immunity
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Same as induced active immunity but
includes injection of antibodies
Tetanus is an induced passive immunity
example
Duration is largely unknown and is
estimated. Sometimes can be titered
HOW LONG IS
Induced immunity is
good for?
•Until its not
Anaphylaxis Path physiology
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Antigen enters body (primary response)
Antibodies produced
Attach to surface of mast or basophil cells
Mast cells become sensitized
Anaphylaxis Path physiology
behind the scenes
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Mast cells
– Specialized cell which contains chemicals that assist in
the immune response
– In all subcutaneous/submucosal tissues,
– Including conjunctiva, upper/lower respiratory tracts,
and gut
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Basophils
– white blood cell which participates in allergic
response
– Circulate in blood
Anaphylaxis Pathophysiology
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Antigen reenters body (secondary response)
Attaches to antibodies on mast or basophil cells
Mast cell degranulates, releases
–Histamine
– Leukotrienes
– Slow reacting substance of anaphylaxis (SRS-A)
– Eosinophil chemotactic factor (ECF)
Histamine
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Product of mast cells and basophils
that causes:
–Vasodilatation
–Capillary permeability - angioedema
–Bronchoconstriction
–Contraction of the gut
Histamine in detail
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Three histamine
receptor types:
– H1
– H2
– H3
Histamine
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Acts on H1 receptors to cause
– Smooth muscle contraction
– Increased vascular permeability
– Prostaglandin generation (mediators)
Histamine
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Acts on H2 receptors to cause
–* Increased vascular permeability
– Gastric acid secretion
– Stimulation of suppressor lymphocytes
– Decreased PMN enzyme release
–* Release of more histamine from mast cells
and basophils
Histamine
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Acts on H3 receptors to cause
– Inhibition of central, peripheral nervous
system neurotransmitter release
– Inhibition of further histamine formation,
release
Vasodilatation
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Decreased peripheral vascular resistance
CAUSES
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Hypotension
Tachycardia
Peripheral Hypoperfusion
Increased Capillary Permeability
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Tissue edema, urticaria (hives), itching
Laryngeal edema
– Airway obstruction
– Respiratory distress
– Stridor
– Angioedema
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Fluid leakage from vascular space
– Hypovolemic shock
Anaphylaxis Path physiology
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Antigen reenters body (secondary response)
Attaches to antibodies on mast or basophil cells
Mast cell degranulates, releases
– Histamine
–Leukotrienes
– Slow reacting substance of anaphylaxis (SRS-A)
– Eosinophil chemotactic factor (ECF)
Leukotrienes
Potent bronchoconstrictors, é vascular
permeability & possibly coronary
vasoconstriction
– Slower onset than histamine
– Effects last longer than histamine
Anaphylaxis Path physiology
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Antigen reenters body (secondary response)
Attaches to antibodies on mast or basophil cells
Mast cell degranulates, releases
– Histamine
– Leukotrienes
–Slow reacting substance of
anaphylaxis (SRS-A)
– Eosinophil chemotactic factor (ECF)
SRS-A
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Potent bronchoconstrictor and
inflammatory agent released by mast
cells; an important mediator of
allergic bronchial asthma.
Anaphylaxis Path physiology
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Antigen reenters body (secondary response)
Attaches to antibodies on mast or basophil cells
Mast cell degranulates, releases
– Histamine
– Leukotrienes
– Slow reacting substance of anaphylaxis (SRS-A)
–Eosinophil chemotactic factor
(ECF)
ECF
– Eosinophil chemotactic factor (ECF)
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A substrate released from mast cells
and basophils during anaphylaxis
which attracts eosinophils . A
tetrapeptide mediator of Immediate
Hypersensitivity .
Eosinophil
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One of the five different types of white blood cell (WBC) belonging to
the subgroup of WBCs called Polymorphonuclear Leukocytes .
Characterized by large red (i.e. eosinophilic) cytoplasmic granules.
Eosinophil function is incompletely understood. They are prominent
at sites of allergic reactions and with parasitic larvae infections (
helminths ). Eosinophil secretory products inactivate many of the
chemical mediators of inflammation and destroy cancer cells. This
phenomenon is most obvious with mast cell-derived mediators. Mast
cells produce a chemotactic factor for eosinophils.
Produced in the bone marrow, eosinophils then migrate to tissues
throughout the body. When a foreign substance enters the body,
lymphocytes and neutrophils release certain substances to attract
eosinophils which release toxic substances to kill the invader.
In plain English
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When a foreign substance enters the
body, lymphocytes and neutrophils
release certain substances to attract
eosinophils which release toxic
substances to kill the invader.
Urticaria
Angioedema
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Swelling in mouth or throat
Less often the sheer amount of
swelling means that so much fluid
has moved out of your blood
circulation that your blood pressure
drops dangerously
Angioedema
Smooth Muscle Spasm
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Bronchospasm
– Respiratory distress
– “Tight Chest”
– Wheezing
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GI Tract Spasm
– Nausea, vomiting
– Cramping, diarrhea
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Bladder Spasm
– Urinary urgency
– Urinary incontinence
Classification
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Mild allergic reaction
Moderate allergic reaction
Severe allergic reaction
(anaphylaxis)
Mild Allergic Reaction
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Characteristics
– Urticaria (hives), itchy
– Erythema (redness)
– Rhinitis
– Conjunctivitis
– Mild bronchoconstriction
– Usually localized (look on abdomen, chest, back)
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No SOB or hypotension/hypoperfusion
Often self-treated at home
Erythema
Pruritus
urticaria
wheals
Conjunctivitis
Moderate Allergic Reaction
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Characteristics
– Mild signs/symptoms with any of
following:
» Dyspnea, possibly with wheezes
» Angioneurotic edema
» Systemic, not localized
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No
hypotension/hypoperfusion
Severe Allergic Reaction
(Anaphylaxis)
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Characteristics
– Mild and/or moderate signs/symptoms plus
– Shock / hypoperfusion
Clinical Manifestation
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Dependent on:
– Degree of hypersensitivity
– Quantity, route, rate of antigen exposure
– Pattern of mediator release
– Target organ sensitivity and responsiveness
Assessment findings in anaphylaxis
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Focused History and Physical Exam
– Focused History
»Sample and OPQRST history
»Rapid onset usually 30-60 seconds following exposure
»Speed of reaction is indicative of severity
»Previous allergies and reactions
Assessment findings in anaphylaxis
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Physical Exam
Presence of severe respiratory
difficulty / hypotension is key to
differentiating anaphylaxis from
allergic reaction
Clinical Manifestation
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Severity varies from mild to fatal
Most reactions are respiratory, dermatologic
Less severe early findings may progress to lifethreatening over a short time
Initial signs/symptoms do NOT necessarily
correlate with severity, progression, duration of
response
Generally, quicker symptoms = more severe
reactions
Clinical Manifestation
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First manifestations involve skin
– Warmth and tingling of the face, mouth, upper
chest, palms and/or soles, or site of exposure
– Erythema
– Pruritus is universal feature, erythema
– May be accompanied by generalized flushing,
urticaria, nonpruritic angioedema
Erythema
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Erythema exsudativum multiform
majus presents with typical or atypical
targets mainly localized on the limbs
and hemorrhagic erosions of at least
one mucosal site. The skin detachment
is below 10% of the body surface area.
Clinical Manifestation
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May progress to involvement of respiratory
system
– cough
– chest tightness
– dyspnea
– wheezing
– throat tightness
– dysphagia
– hoarseness
Clinical Manifestation
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Other Signs and Symptoms
– lightheadedness or syncope caused by
hypotension or dysrhythmia
– nasal congestion and sneezing
– ocular itching and tearing
– cramping abdominal pain with nausea,vomiting, or
diarrhea
– bowel or bladder incontinence
– decreased level of consciousness
Clinical Manifestation
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Physical Exam findings may include
– urticaria, angioedema, rhinitis, conjunctivitis
– tachypnea, tachycardia, hypotension
– laryngeal stridor, hypersalivation, hoarseness,
angioedema
Insect Sting Hypersensitivity
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Hymenoptera - yellow jackets, honeybees,
hornets, wasps, bumble bees
90%: Local hives, Pruritus
10%: Massive local reaction, including
swelling beyond two joints of extremity
1%: Systemic reaction
10%: have worse reaction on second sting
28%: have recurrent systemic reaction
Management
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Treatment depends upon severity of
reaction and signs/symptoms of its
presentation
Management
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Optimal management requires
– High index of suspicion (suspect, treat within minutes)
– Early diagnosis
– Pharmaceutical intervention
– Observation
– Disposition
Management of Anaphylaxis
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Scene safety
–Consider the Possibility of Trauma
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Protect the Airway
•Use Airway Adjuncts with care
•Intubate early in severe cases to prevent total occlusion of the
airway
•Be prepared to place a surgical airway
Management of Anaphylaxis
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Support breathing
– High flow oxygen or assisted ventilation if
indicated
– Establish IV access
– Patient may be volume depleted due to “third
spacing” of fluid
– Administer crystalloid solution at appropriate
rate. Place a second IV if indicated
Patient Self-Management
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Benadryl 50 mg p.o.
At any sign of anaphylaxis, self-administer IM
epinephrine (Epi-Pen®, Ana-Kit®)
If short of breath or wheezing, use aerosolized
epinephrine (Primatene Mist, Medihaler-Epi)
Mild Allergic Reaction
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Often self-treated at home
Diphenhydramine 25 - 50mg IV or deep IM
– IV is acceptable FOR LAST RESORT – HEROIC
MEASURES
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If stinger present, flick it away with credit card or
fingernail
May consider (if available and indicated):
– cimetidine or ranitidine
– prednisone
– inhaled beta-agonists
Moderate Allergic Reaction
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High flow oxygen
IV NS
–Titrated to systolic BP 90 mm Hg
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ECG monitor
Beta agonists
– Nebulized albuterol, isoetharine, terbutaline
– IM terbutaline or epinephrine 1:1000 or IV aminophylline if severe
bronchoconstriction
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Diphenhydramine 25-50 mg IM or IV
Methylprednisolone 125 mg IV
Transport
Anaphylaxis
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Airway and Breathing
– High concentration oxygen
– Ventilations, ETT, alternative airway prn
– Consider inhaled beta agonists
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Circulation
– Large bore IV NS X 2
– Quickly titrate fluids to perfusion with bolus therapy
– ECG monitor
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Treat as pre-arrest patient
Anaphylaxis
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FOR FAILURE TO RESPOND TO PREVIOUS
Epinephrine 0.5 - 1.0 mg 1:10,000 IV prn
– Hypotension unresponsive to fluids and epinephrine è
consider dopamine ~10 mcg/kg/min
– Bronconstriction unresponsive to Epi è consider
aminophylline
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Diphenhydramine 50 mg IV
Methylprednisolone 125 mg IV
Rapid transport
Disposition
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Regardless of response to therapy, all
patients with systemic features must be
observed for 6 to 8 hours
Latex Allergies
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Due to a growing number of persons
experiencing latex allergies, EMS
providers should be prepared to
treat patients with such allergies
– Have latex free equipment
– Use the patient’s latex free supplies
QUESTIONS?
Case Presentation #1
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You are dispatched to an electronics manufacturing
plant to see a 28-year-old woman. The woman believes
she is having an allergic reaction. Security officers will
meet you at the front gate and escort you to the patient.
What specific information would you like
at this point?
Case Presentation #1
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You find this patient in an office area sitting at her desk.
From a distance, you notice she is awake and speaking
clearly. She does not appear to have any breathing
difficulty. She states she had just returned from lunch
and began to feel hot and light headed. Her friend
pointed out that the patient’s arms and neck are very
red, and that her face appears “puffy”.
Case Presentation #1
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The patient states she is allergic to peanuts but has not
eaten any. She went to a health food café where she had
grilled chicken and steamed vegetables. She has no
other past history and takes no medications. Her last
allergic rx was similar to this. Vitals are: BP-116/70;
Pulse-100; RR-20; Lung sounds-clear and equal. No
difficulty swallowing, redness to her arms, chest, neck
and face.
Would you like to perform any other procedures/exams/testing
or obtain other history before treating?
Case Presentation #1
So, what is your complete treatment plan for
this patient?
Case Presentation #2
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39 year-old male found at home in respiratory arrest
with a bradycardic carotid pulse. His wife states he was
helping a friend paint when he was apparently stung by
a bee. He walked into the house, saying “I don’t feel
good,” and collapsed.
Case Presentation #2
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PMH: depression, gastritis, seasonal allergies
Medications: Ritalin, Zantac, Prozac, Claritin
No known drug allergies
No prior reactions to hymenoptera
What therapies would you like to begin for this man?
Case Presentation #2
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You have done the following:
– intubated orotracheally
– administered intravenous epinephrine, 0.5 mg &
Diphenhydramine 50 mg
– started 2 large-bore IVs of NS and given 500 cc fluid
At this point, the patient no longer has a pulse
Case Presentation #2
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You begin CPR and give the following:
– Dopamine drip at 10 mcg/kg/min
– Epinephrine, 1:10,000, 1 mg IV q 3-5 min
You now note the following:
– ECG: Idioventricular rhythm
– Lung Sounds: difficult to hear
– Obvious facial edema
Can you think of any ideas for further treatment?