Overview of Anaphylaxis

866 views
784 views

Published on

Overview of anaphylaxis. General principles

Published in: Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
866
On SlideShare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
43
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide
  • which histamines are produced following exposure to the allergen
  • Allergn:type of antigen that produces an abnormally vigorous immune response in which the immune system fights off a perceived threat that would otherwise be harmless to the body.
  • Downstream activation of phospholipase A2, followed by cyclooxygenases and lipoxygenases, produces arachidonic acid metabolites, including prostaglandins, leukotrienes, and platelet-activating factor.
  • Rhinitis: irritation and inflammation of the mucous membrane inside the nose. hoarseness:disorders of the voice: an impairment in the ability to produce voice sounds using the vocal organs Stridor:high-pitched musical sound resulting from turbulent air flow in the upper airway. Stridor is a physical sign which is caused by a narrowed or obstructed airway. Angioedema: rapid swellin(edema) of the dermis, subcutaneous tissue,[1] mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis.Hypotension due to vascular dilationAirway obstruction due to laryngeal edema
  • (e.g., some combination of cutaneous, respiratory, GI, or cardiovascular systems)
  • - Large volumes of intravenous fluids may be required due to marked peripheral vasodilationAlbuterol:  is indicated for bronchospasm refractory to epinephrineDiphenhydramine: Life-threatening instances of anaphylaxis must be managed using other methods (eg, subcutaneous or intravenous epinephrine)H2 antagonists are indicated for persistent anaphylaxisCorticosteroids are indicated for the prevention of prolonged or recurrent symptomsGlucagon is indicated for epinephrine-resistant anaphylaxis in patients taking β-blockers
  • Diet:Identify food allergies and avoid the causative foodIn case of accidental exposure, seek medical attention immediatelyPhysical activity:In cases of exercise-induced anaphylaxis, stop exercising as soon as symptoms occurAvoid exercise for 4 to 6 hours after eatingSexual behavior:Rare cases of anaphylaxis from semen have been reportedCondoms should be used to avoid contact with semen if this is a cause of anaphylaxis. Patients who are latex-sensitive should avoid condoms made of latexEnvironment:Avoid areas where Hymenoptera species are presentWear protective clothing such as long-sleeved shirts, pants, socks, shoes, and hats when exposure cannot be avoided, and avoid wearing bright colors when going outsideLatex-induced anaphylaxis should be identified, and all contact with latex products should be avoidedMedication history:Patients at risk for anaphylaxis should not take β-blockers, ACE inhibitors, angiotensin II receptor blockers, or tricyclic antidepressants. All of these interfere with drug treatment or the body's ability to respond to anaphylaxisImmunization:Desensitization may be possible with some known allergensOther:Avoid known family allergens; some are known to have a genetic basis, although this is a rare occurrence
  • Overview of Anaphylaxis

    1. 1. Anaphylaxis
    2. 2. Introduction Immediate hypersensitivit y Antibodymediated immune complex diseases T cell-mediated diseases Mast cell release histamine and other mediators Antibodies directed against cell or tissue antigens Antibodyantigen complex deposit in blood vessels Reactions of T lymphocytes
    3. 3. 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.
    4. 4. Terminology Beta-blockers (beta-adrenergic blocking antagonist) are drugs that treat several conditions: • Hypertension • Angina • Some abnormal heart rhythms • Myocardial infarction • Anxiety • Migraine • Glaucoma
    5. 5. Objectives 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. What is anaphylaxis? Etiology Pathophysiology Signs and symptoms Risk factors. Complications Diagnosis Treatment and management Prevention First aid for Anaphylactic patients.
    6. 6. 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
    7. 7. Etiology Causes of anaphylaxis in a study of 266 patients (Data from Kemp et al) Food 2% 7% Idiopathic 34% 20% 37% Drugs Exercise Latex, hormons, insect bites
    8. 8. Etiology Venoms Common Drugs Nuts Wasps Beta-Lactam antibiotics such as penicillin seafood Bees Acetylsalicylic acid Dairy Products Yellow-jackets Trimethoprim sulfamethoxaz ole Egg Hornets Vancomycin wheat -------------- NSAIDs Latex Not associated with death FOOD
    9. 9. Pathophysiology • First exposure  Activation of TH2 cell → Stimulate IgE switiching Allergen TH2 Cell B Cell
    10. 10. Pathophysiology • First exposure  IgE production IgE secreting B cell IgE
    11. 11. Pathophysiology •Second exposure Second exposure First exposure  Antigen recognition IgE bind to mast cell   Activation of mast cell to release   histamine and other mediators Allergen Mast cell Mediators FcɛRI IgE
    12. 12. Pathophysiology Mediators Vascoactive aminase & lipid Cytokines Immediate hypersensitivity reaction (minutes) Late phase reaction (6-24 hours)
    13. 13. Summary These 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
    14. 14. Result Mediators Downstream activation of phospholipase A2 Inflammatory cytokine Releasing • Histamine • Tryptase, • Carboxypeptidas eA • Proteoglycans (Early Phase) • Prostaglandins, • Leukotrienes • plateletactivating factor (Early Phase) • TNF alpha • IL-13 • (Act as late phase)
    15. 15. Outcome Stimuli 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 Bronchoconstrictor and increases vascular factor permeability. TNF- alpha Activate neutrophils, recruits other effector cells, and enhances chemokine synthesis
    16. 16. Signs & Symptoms Skin Itching flushing hives (urticaria) swelling
    17. 17. Signs & Symptoms Eyes Itching tearing redness swelling around the eyes
    18. 18. Signs & Symptoms Nose & mouth Sneezing runny nose swelling of the tongue nasal congestion metallic taste
    19. 19. Signs & Symptoms Lungs and throat Difficulty breathing coughing chest tightness wheezing or other sounds increased mucus production throat swelling or itching change in voice or a sensation of choking
    20. 20. Signs & Symptoms Heart and circulation Dizziness weakness rapid, slow, or irregular heart rate fainting low blood pressure
    21. 21. Signs & Symptoms Digestive system Nausea vomiting cramps diarrhea
    22. 22. Signs & Symptoms Nervous system Anxiety confusion sense of impending doom
    23. 23. Hypotension Summary Respiratory Cardiovascular cardiovascular collapse cough tachycardia broncho spasm wheezing Rhinitis flushing Anaphylaxis angioed ema Skin diffuse erythema Several systems urticaria stridor hoarseness
    24. 24. 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
    25. 25. Complications • Hypoxemia and end-organ damage due to hypoxia • Shock • Cardiac arrest • Death
    26. 26. Diagnosis
    27. 27. 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.
    28. 28. 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
    29. 29. 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
    30. 30. 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.
    31. 31. Treatment and management First linetherapy Second-line therapy counteract treat hypotension persistent bronchospasm Epinephrine H1 Diphenhydramine O2 Trendeleburg Administration position Supplemental H2 Cimetidine and O2 ranitidine Albuterol IV adminstration IV fluids Methylprednis olone Glucagon for patient taking Beta blockers Corticosteriods
    32. 32. Treatment and management 1- Epinephrine - ANTAGONIST increase BP and Bradycardia to counter shock - Inhibit further mast cell degranulation 2- Antihistamine 3to reduce inflammation of your air passages and improve breathing O2 to help compensate for restricted breathing 4- Albuterol to relieve breathing symptoms
    33. 33. 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 mL 6-12 0.3mL 12< 0,5 mL Intravenous Has rapid onset action Severe, should be carefully monitored Slow intravenous injection
    34. 34. 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.
    35. 35. First aid • Aim: 1. limiting allergic response. 2. decreasing the severity of the symptoms.
    36. 36. 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.
    37. 37. 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/anaphyl axis_first_aid_management.htm

    ×