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?