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Overview of Anaphylaxis. General principles
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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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