Allergic Reactions & Anaphylaxis Barry Barkinsky EMS-I, Paramedic.
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Transcript of Allergic Reactions & Anaphylaxis Barry Barkinsky EMS-I, Paramedic.
Allergic Reactions & Anaphylaxis
Barry BarkinskyEMS-I, Paramedic
Sections
Path physiology Assessment findings in anaphylaxis Management Basement findings in Allergic
Reaction Management Patient Education
overview
https://www.youtube.com/watch?v=G9D-Vfmbt4s
Incidence 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 Laryngeal edema and acute bronchospasm with
respiratory failure account for >70% Circulatory collapse accounts for 25% Other <5% - ?brain ?MI
bronchospasm
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 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
é Physiologic response to antigens– Oversensitive response = allergic– Occurs after sensitization to antigen
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 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
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
Mast cells– Specialized cell of
the immune system which contains chemicals that assist in the immune response
Systemic mastocytosis
Define some terms
Sensitized– The initial exposure to an antigen that
results in an immune response
Allergic Reaction - definition
An exaggerated response by the immune system to a foreign substance
Allergic Reaction
é Physiologic response to antigens– Oversensitive response = allergic– Occurs after sensitization to antigen
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
Initial response to an antigen – on 1st time exposure
several day response by immune system
Generalized antibodies IgG, IgM are released
Secondary response
Specialized antibodies with memory now created
Specific to the antigen
The speed of the reaction is a good predictor of the severity of the reaction
Anaphylaxis Systemic reaction of multiple organ systems to
antigen-induced IgE-mediated immunulogic mediator release in previously sensitized individual
IgE mediated reactions
IgE-mediated hypersensitive reactions (allergic rhinitis, asthma, atopic dermatitis)
Type 1 - immediate (or atopic, or anaphylactic)
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
Antigen– Induces antibody formation– Examples
»Drugs (antibiotics)»Foods (nuts, shellfish)» Insect venoms»Animal serum» Incompatible blood types
Allergic reaction / Anaphylaxis
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
Immune Response–Exposure to antigen produces primary response with general antibodies
–Immune system develops antigen-specific antibodies and memory – secondary response
Natural and acquired ImmunityInduced Active ImmunityActive and Passive Immunity
The immune system
Natural immunity - OEM Acquired immunity– Naturally acquired immunity
Natural immunity
Also called: innate immunity Genetically predetermined Not related to previous exposures Everyone has “some” natural
immunities
Naturally Acquired immunity
Results from exposure to antigens Is enhanced by continued exposures Is believed to be lifelong in duration
Induced active immunity
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
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
Antigen enters body (primary response) Antibodies produced Attach to surface of mast or basophil cells Mast cells become sensitized
Anaphylaxis Path physiologybehind the scenes
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 Basophils
– white blood cell which participates in allergic response
– Circulate in blood
Anaphylaxis Pathophysiology
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
Product of mast cells and basophils that causes:–Vasodilatation–Capillary permeability - angioedema–Bronchoconstriction–Contraction of the gut
Histamine in detail Three histamine
receptor types:– H1– H2– H3
Histamine Acts on H1 receptors to cause
– Smooth muscle contraction– Increased vascular permeability– Prostaglandin generation (mediators)
Histamine 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 Acts on H3 receptors to cause
– Inhibition of central, peripheral nervous system neurotransmitter release
– Inhibition of further histamine formation, release
Vasodilatation
Decreased peripheral vascular resistance
CAUSES Hypotension Tachycardia Peripheral Hypoperfusion
Increased Capillary Permeability
Tissue edema, urticaria (hives), itching Laryngeal edema
– Airway obstruction– Respiratory distress– Stridor– Angioedema
Fluid leakage from vascular space– Hypovolemic shock
Anaphylaxis Path physiology
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
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
Potent bronchoconstrictor and inflammatory agent released by mast cells; an important mediator of allergic bronchial asthma.
Anaphylaxis Path physiology
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) A substrate released from mast cells
and basophils during anaphylaxis which attracts eosinophils . A tetrapeptide mediator of Immediate Hypersensitivity .
Eosinophil 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
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
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
Bronchospasm– Respiratory distress– “Tight Chest” – Wheezing
GI Tract Spasm– Nausea, vomiting– Cramping, diarrhea
Bladder Spasm– Urinary urgency– Urinary incontinence
Classification
Mild allergic reaction Moderate allergic reaction Severe allergic reaction
(anaphylaxis)
Mild Allergic Reaction Characteristics
– Urticaria (hives), itchy– Erythema (redness)– Rhinitis– Conjunctivitis– Mild bronchoconstriction– Usually localized (look on abdomen, chest, back)
No SOB or hypotension/hypoperfusion Often self-treated at home
Erythema
Pruritus
urticaria
wheals
Conjunctivitis
Moderate Allergic Reaction
Characteristics– Mild signs/symptoms with any of
following:» Dyspnea, possibly with wheezes» Angioneurotic edema» Systemic, not localized
No hypotension/hypoperfusion
Severe Allergic Reaction (Anaphylaxis)
Characteristics– Mild and/or moderate signs/symptoms plus– Shock / hypoperfusion
Clinical Manifestation
Dependent on:– Degree of hypersensitivity– Quantity, route, rate of antigen exposure– Pattern of mediator release– Target organ sensitivity and responsiveness
Assessment findings in anaphylaxis
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
Physical Exam Presence of severe respiratory
difficulty / hypotension is key to differentiating anaphylaxis from allergic reaction
Clinical Manifestation
Severity varies from mild to fatal Most reactions are respiratory, dermatologic Less severe early findings may progress to life-
threatening 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
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
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 May progress to involvement of respiratory
system– cough– chest tightness– dyspnea– wheezing– throat tightness– dysphagia– hoarseness
Clinical Manifestation 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 Physical Exam findings may include
– urticaria, angioedema, rhinitis, conjunctivitis– tachypnea, tachycardia, hypotension– laryngeal stridor, hypersalivation, hoarseness,
angioedema
Insect Sting Hypersensitivity
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
Treatment depends upon severity of reaction and signs/symptoms of its presentation
Management
Optimal management requires– High index of suspicion (suspect, treat within minutes)– Early diagnosis– Pharmaceutical intervention– Observation– Disposition
Management of Anaphylaxis
Scene safety–Consider the Possibility of Trauma• 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
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 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 Often self-treated at home Diphenhydramine 25 - 50mg IV or deep IM
– IV is acceptable FOR LAST RESORT – HEROIC MEASURES
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 High flow oxygen IV NS
–Titrated to systolic BP 90 mm Hg ECG monitor Beta agonists
– Nebulized albuterol, isoetharine, terbutaline
– IM terbutaline or epinephrine 1:1000 or IV aminophylline if severe bronchoconstriction
Diphenhydramine 25-50 mg IM or IV Methylprednisolone 125 mg IV Transport
Anaphylaxis
Airway and Breathing– High concentration oxygen– Ventilations, ETT, alternative airway prn– Consider inhaled beta agonists
Circulation– Large bore IV NS X 2 – Quickly titrate fluids to perfusion with bolus therapy– ECG monitor
Treat as pre-arrest patient
Anaphylaxis
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
Diphenhydramine 50 mg IV Methylprednisolone 125 mg IV Rapid transport
Disposition Regardless of response to therapy, all
patients with systemic features must be observed for 6 to 8 hours
Latex Allergies
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
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 likeat this point?
Case Presentation #1
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 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
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
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
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
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?