Anaphylaxis

Introduction

Mast cell release

histamine and other mediators

Immediate hypersensitivit

y

Antibodies directed

against cell or tissue

antigens

Antibody-mediated

Antibody-antigen complex

deposit in blood vessels

immune complex diseases

Reactions of T

lymphocytes

T cell-mediated diseases

Terminology

• IgE-based antibody Responses are common physiologically in parasitic infections.

• Atopic individual Genetic in an individual which is predisposition to suffer from allergies. They produce IgE responses against a number of non-parasitic antigens that induce either no antibody response or antibody response of a different isotype.

Terminology

Beta-blockers (beta-adrenergic blocking antagonist) are drugs that treat several conditions:• Hypertension • Angina • Some abnormal heart rhythms• Myocardial infarction• Anxiety• Migraine• Glaucoma

Objectives

1. What is anaphylaxis? 2. Etiology3. Pathophysiology4. Signs and symptoms 5. Risk factors.6. Complications7. Diagnosis8. Treatment and management9. Prevention10. First aid for Anaphylactic patients.

Anaphylaxis

O Ana (without), phylaxis (protection).

O A serious acute allergic reaction that cause systemic effects and may cause death. (Type I Hypersensitivity)

O Allergen must be systemically absorbed (Ingestion or injection) to cause Anaphylaxis

Etiology

34%

37%

20%

7%

2%

Causes of anaphylaxis in a study of 266 patients (Data from Kemp et al)

Food

Idiopathic

Drugs

Exercise

Latex, hormons, insect bites

EtiologyFOOD Venoms Common

DrugsLatex

Nuts Wasps Beta-Lactam antibiotics

such as penicillin

seafood Bees Acetylsalicylic acid

Dairy Products

Yellow-jackets Trimethoprim-

sulfamethoxazole

Egg Hornets Vancomycin

wheat -------------- NSAIDs

Not

ass

ocia

ted

with

dea

th

Pathophysiology• First exposure Activation of TH2 cell → Stimulate IgE switiching

Allergen

TH2 Cell

B Cell

Pathophysiology• First exposure IgE production

IgE secreting B cell IgE

Mediators

Pathophysiology• First exposure IgE bind to mast cell

Mast cell

FcɛRIIgE

Allergen

Second exposure Antigen recognition

Second exposure Activation of mast cell to release

histamine and other mediators

Pathophysiology

Mediators

Vascoactive aminase & lipid

Immediate hypersensitivity reaction (minutes)

Cytokines

Late phase reaction (6-24 hours)

SummaryThese reaction can affect single tissue or organ (Eczema, asthma and hay fever) - Or multiple ones (anaphylaxis) depending on the

re-exposure of allergen.

Note: This process normally mediated by IgG or immune complex

Result

Mediators Downstream activation of phospholipase A2

Inflammatory cytokine

Releasing• Histamine• Tryptase,• Carboxypeptidas

e A• Proteoglycans(Early Phase)

• Prostaglandins,• Leukotrienes• platelet-

activating factor(Early Phase)

• TNF alpha• IL-13• (Act as late

phase)

OutcomeStimuli Outcome

Histamine Vasodilation, increases vascular permeability, heart rate, cardiac contraction, and glandular secretion.

Prostaglandin D2 Bronchoconstrictor, pulmonary and coronaryvasoconstrictor, and peripheral vasodilator

Leukotrienes Bronchoconstriction, increase vascular permeability, and promote airway remodeling

Platelet-activating factor

Bronchoconstrictor and increases vascular permeability.

TNF- alpha Activate neutrophils, recruits other effector cells, and enhances chemokine synthesis

Signs & Symptoms

Itching flushing

hives (urticaria) swelling

Skin

Signs & Symptoms

Itching tearing

redness swelling around the eyes

Eyes

Signs & Symptoms

Sneezing runny nose nasal congestion

swelling of the tongue metallic taste

Nose & mouth

Signs & Symptoms

Difficulty breathing coughing chest tightness

wheezing or other sounds increased mucus production throat swelling or itching

change in voice or a sensation of choking

Lungs and throat

Signs & Symptoms

Dizziness weakness

fainting rapid, slow, or irregular heart rate

low blood pressure

Heart and circulation

Signs & Symptoms

Nausea vomiting

cramps diarrhea

Digestive system

Signs & Symptoms

Anxiety confusion

sense of impending doom

Nervous system

Skin

flushing

urticariadiffuse erythema

Cardiovascular

Hypotension

tachycardiacardiovascular collapse

Respiratory

cough

wheezing

bronchospasm

Several systems

Rhinitis

hoarseness

stridor

angioedema

Anaphylaxis

-Often, signs begin within 60

minutes of exposure

-The faster the onset of symptoms,

the more severe the reaction

Summary

Risk factor

• History of anaphylaxis, atopy, or asthma. (Some not)

• Food allergy

• Repeated latex exposure

• β-blocker use may limit the effectiveness of epinephrine, resulting in protracted anaphylaxis and severe hypotension

Complications

• Hypoxemia and end-organ damage due to hypoxia

• Shock

• Cardiac arrest

• Death

Diagnosis

Diagnosis

Diagnosis based on:

• Clinical presentation:Involvement of any two or more body systems is observed

• History of exposure to a possible triggers laboratory tests.

Diagnostic test• ECG to eliminate other causes of chest pain.

• Radiographs for chest and neck considering an alternate diagnosis of epiglottitis or other acute respiratory condition

Diagnostic test• Serum tryptase released along with histamine can be

measureable.

• Serum electrolytes • CBC• Clotting studies

• Prick test

exclude electrolyte disturbances or bleeding that is causing hypovolemia

Treatment and management

•Aim:

1. Full resolution of all associated symptoms.

2. Saving the patient's life in serious reactions

3. Prevention of further anaphylactic reactions.

Treatment and management

First line- therapy

Second-line therapy counteract persistent bronchospasm

treat hypotension

Epinephrine H1 Diphenhydramine O2 Administration

Trendeleburg position

Supplemental O2

H2 Cimetidine and ranitidine

Albuterol IV adminstration

IV fluids Corticosteriods Methylprednisolone

Glucagon for patient taking Beta blockers

Treatment and management

1- Epinephrine 2- Antihistamine 3- O2 4- Albuterol

to relieve breathing symptoms

to help compensate for restricted

breathing

to reduce inflammation of

your air passages and improve

breathing

- ANTAGONIST increase BP and Bradycardia to counter shock

- Inhibit further mast cell degranulation

Treatment and management

Epinephrine Action speed When is it used?

Dose

Intramuscular Has rapid onset action

Severe, Anterolateral of the middle thigh

6< 0.15 mL6-12 0.3mL12< 0,5 mL

Intravenous Has rapid onset action

Severe, should be carefully monitored

Slow intravenous injection

Prevention• Allergen avoidance is the best preventive measure.

1- Diet 2-Physical activity

3- Carry auto-injector

4-Environment

5-Medication

6-Immunization*Education is recommended about how to deal with this disease.

First aid

• Aim:

1. limiting allergic response.

2. decreasing the severity of the symptoms.

First aid

Place patient in Trendelenburg position. Establish and maintain airway.

Give oxygen via nasal cannula as needed.

Place a tourniquet above the reaction site.

Epinephrine at the site of antigen injection. Start IV to rise BP.

Refernces • Abbas: Basic immunology• BNF – 2013• Clincalkey.com• Kumar and Clarks Clinical Medicine• MDCONSULT.COM• AUSTRALIAN RESUSCITATION COUNCIL • http://www.resus.org.au/policy/guidelines/section_9/

anaphylaxis_first_aid_management.htm

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