Anaphylaxis PDF

Anaphylaxis Anaphylaxis L: Anaphylaxis Critical ANAPHYLAXIS anaphylaxis Anaphylaxis D...

Anaphylaxis Anaphylaxis L: Anaphylaxis Critical ANAPHYLAXIS anaphylaxis Anaphylaxis Definition Anaphylaxis refers to the characteristic and often life-threatening clinical manifestation of the immunoglobulin E (IgE) mediated- immediate hypersensitivity reaction. Pathophysiology  In type 1 hypersensitivity: - B lymphocytes are stimulated by a definite allergen to produce IgE antibodies - that bind to receptors on the surface of tissue mast cells and blood basophils, - now, mast cells and basophils coated by Ig E antibodies are sensitized cells.  Later: - exposure to the same allergen cross –links the bound IgE on the sensitized cells, - resulting in mast cell and basophil cell degranulation with release of histamine, tryptase, prostaglandins and leukotrienes. - The principal effects of these mediators are vasodilatation, capillary leak and smooth muscle contraction. - These effects can develop from minutes to 30% decrease in SBP b. Reduced BP c. Reduced BP or associated symptoms b. Adults: or associated symptoms of end-organ d. Persistent GI symptoms SBP of 30% decrease from that person's >>baseline Low SBP for children is defined as:  significant cardiac, respiratory or gastrointestinal symptoms (mild to moderate, moderate >>>and severe cases, grade 2, 3, 4) to avoid laryngeal oedema, respiratory failure and death.  If the patient is diagnosed before and carry Epinephrine Autoinjector (EpiPen), it should be administered as soon as anaphylaxis is highly likely. The patient should administer himself no more than 2 doses.  Call for help OR Hospitalization with attention focused on airway, breathing, circulation >>>and adequacy of mentation. The lips, tongue and oral pharynx are assessed for angioedema. The patient is asked to speak to assess the glottic swelling.  Placement of the patient in the supine position with the lower extremities elevated >>>unless there is prominent upper airway obstruction prompting the patient to be upright. If the patient is vomiting, placement of the patient semi recumbent with lower >>>extremities elevated is preferred.  supplemental oxygen at high flow rate providing at least 70% and up to 100% oxygen  Two large -bore IV catheters should be immediately inserted, in normotensive adults, isotonic saline should be infused at a rate of 125mL/hour to >>>maintain venous access. Fluid resuscitation is mandatory for patients with hypotension not responding promptly to >>>epinephrine. Adults should receive 1-2 liters of normal saline within minutes. Volumes up to 7 liters may >>>be required.  Continuous electronic monitoring of cardiopulmonary status, including BP, heart rate, >>>respiratory rate, oxygen saturation by pulse oximetry  Intubation should be performed if stridor or respiratory distress due to upper airway >>>compromise is present. Rarely, emergency cricothyroidotomy may be required. Page 6  Critical ANAPHYLAXIS Epinephrine - No absolute contraindication to epinephrine in anaphylaxis - Epinephrine IM injection: The recommended dose: for patients of any age is 0.01mg/kg, maximum dose of: 0.5mg per single dose, Injected IM into: the mid-outer thigh i.e. Vastus lateralis muscle. The dose should be drawn up using a 1 mL syringe for the 1 mg/mL formulation of epinephrine. >IM epinephrine may be repeated at 5-to -15-minute intervals if there is no response or >inadequate response or even sooner if clinically indicated. - IV bolus epinephrine: 50 to 100 mcg over 10 minutes is associated with significant dose error and cardiovascular complications and should be avoided as possible. - IV epinephrine infusion: is preferred if patients: have not responded to IM injections and are refractory to IM epinephrine and volume resuscitation. Start infusion by: 0.1mcg/kg /minute, infusion could be increased every 2-3minutes by 0.05mcg /kg/minute until BP and perfusion improves. Rarely exceed 1mcg /kg /minute. - Mechanism of action of epinephrine in anaphylaxis and anaphylactic shock:  Alpha -1-adrenergic agonist effect: increase vasoconstriction and decrease mucosal oedema  Beta -1-adrenergic agonist effect: Inotropic and chronotropic  Beta -2- adrenergic agonist effect: Increase bronchodilatation and decrease release of inflammatory mediators from mast cells and basophils. - Side effects of epinephrine: Mild transient frequent include anxiety, restlessness, headache, dizziness, palpitation, tremor and pallor Rarely: ventricular arrhythmia, angina, Myocardial infarction, pulmonary oedema, increased BP and intracranial hemorrhage Antihistamines H1 blockers as Diphenhydramine 25-50 mg IV over 5 minutes can be repeated /4-6 hours or cetirizine 10 mg IV over 5 minutes H2 blockers as Ranitidine 50mg IV or Famotidine 20mg IV over two minutes Page 7 Critical ANAPHYLAXIS Inhaled Bronchodilators As albuterol or salbutamol by nebulizer for bronchospasm Glucagon For patient taking home beta-blocker: 1-2mg IV/ IM over 5 minutes, can be repeated or followed by infusion 5-15mcg /minutes Corticosteroids Is given mainly to prevent 2nd phase reaction that could occur in some cases. Methylprednisolone 1-2mg/kg /day for up to 4 days oral or IV Corticosteroids suppress the production of prostaglandins, and leukotrienes, inhibits inflammatory cell recruitment and migration, causes vasoconstriction that reduces cell and fluid leakage from vasculature. Leukotriene receptor antagonist e.g. the use of Montelukast in aspirin induced asthma. Omalizumab Monoclonal antibody to IgE  In refractory anaphylaxis: - Other vasopressors as Dopamine or Vasopressin - Methylene blue: an inhibitor of nitric oxide synthesis - Extracorporeal membrane oxygenator (ECMO) Page 8 Critical ANAPHYLAXIS PROPHYLACTIC TREATMENT  Patient education to avoid exposure to allergen and carry pre-loaded EpiPen syringes or desensitization if exposure to allergen is unavoidable as insect stings.  Desensitization: Indicated in IgE-mediated hypersensitivity A course of SC injections of increasing doses of the allergen extract. Sublingual grass pollen extract tablets are used in hay fever MECHANISM OF ACTION OF DESENSITIZATION: 1- IgG blocking antibodies: During repeated exposure to desensitizing allergen, IgG class antibodies develop; these compete with IgE for allergen binding and prevent IgE-allergen complexes binding to mast cells receptors. 2- Regulation: Repeated exposure to desensitizing allergen induces regulatory T cells that act to suppress immune response. This end in damping migration, infiltration and inflammation. 3- Immune deviation: A shift away from Th2 to Th1 producing CD4 cells results in the generation of cytokines as IFN-y that are inhibitory to IgE production. Page 9