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![Initial management
Yes
• Assess airway, breathing,
circulation, mentation
• Inject epinephrine(IM)*
• Supine position
• IV access, oxygen, monitoring
No
Initial assessment supports
potential anaphylaxis?
Consider other diagnosis
*0.01ml/kg Epinephrine1:1000[IM]](https://image.slidesharecdn.com/anaphylaxis-220724091816-2cb8b810/85/Anaphylaxis-pptx-12-320.jpg)
![Good clinical
response?
Yes
No
Recumbent position with elevation
lower extremity • Establish airway,
O2 • Repeat epinephrine injection if
indicated
• IV fluids1 if hypotensive
Consider inhaled bronchodilators2 if
wheezing
• H1 and H2 antihistamines3
• Corticosteroids4
• Observation
• Autoinjectible
epinephrine
1NS or RL-30 mL/kg in 1st hr
2 Nebulised Albuterol- (0.83 mg/mL [3 mL]) via mask with O2
3cetrizine-0.25 mg/kg up to 10 mg PO, Ranitidine-1 mg/kg up to 50 mg IV
4methylprednisolone- 1-2 mg/kg up to 125 mg IV](https://image.slidesharecdn.com/anaphylaxis-220724091816-2cb8b810/85/Anaphylaxis-pptx-13-320.jpg)
Anaphylaxis.pptx
- 1.
- 2. Anaphylaxis Anaphylaxis is aserious allergic reaction that is rapid in onset and manifests as under and may cause death. ❖ Cutaneous : urticaria, angioedema, flushing ❖ Respiratory : bronchospasm, laryngeal edema ❖ Cardiovascular : hypotension, dysrhythmias, myocardial ischemia ❖ Gastrointestinal: nausea, colicky abdominal pain, vomiting, diarrhea Mediated by biological substances released from mast cells and basophils. 2
- 3. Anaphylaxis - Etymology ❖Ancient Greek ➢ aná - intensifier ➢ phúlaxis - protection (by antibodies) Become extremely sensitive to harmless allergens to cause anaphylaxis Antibodies that normally protect our body from microbes 3 Multi-systemic symptoms of Anaphylaxis Allergen
- 5. Pathophysiology of Anaphylaxis BCell Immediate hypersensitivity reaction (minutes after repeat exposure to allergen) Allergen(e.g. pollen) Allergen Exposure IgE-secreting B cell IgE B cell Dendritic Cell Production of IgE TH2 Cell Naive T Cell Dendritic cell IgE Cytokines Activation of mast cell; release of mediators Binding of IgE to FCƐRI on mast cells Late phase reaction (2- 24 hours after repeat exposure to allergen) Vasoactive amines, lipid mediators Binding of IgE to FCƐRI on mast cells Mediators B Cell Activation of TH2 cells and IgE class switching in B cell
- 6. ❖IgE-Dependent ❖Mechanism: IgE mediatedreaction ➢ Allergens ■ Food : peanuts, dairy, meat, spices,fish ■ Medications : β-lactam antibiotics, ibuprofen ■ Biologic agents : ● monoclonal antibodies: infliximab, omalizumab ● allergens : challenge tests, specific immunotherapy ■ Natural rubber latex ■ Vaccines ■ Inhalants (rare) : horse or hamster dander, grass pollen Anaphylaxis Immune Mechanisms & Triggers 6
- 7. ❖ Immunological mechnisms(IgE-Independent) • Radio contrast media • NSAIDs • Dextrans(HMW Iron) • Biological agents ❖ NonImmunological mechnisms (Direct mast cell activation) • Physical factors- exercise, cold, heat, sunlight • Ethanol • Opiods ❖ Idiopathic Anaphylaxis • Previously unrecognised allergen • Mastocytosis/clonal mast cell disorder
- 8. Exercise induced anaphylaxis (EIAn) oSymptoms occur after physical activity. o In one third of cases food, drugs (especially NSAID) & change in temp, can be identified. o When symptoms develop after food ingestion, the condition is referred as food-dependent exercise induced anaphylaxis (FDEIAn). o Fasting before exercise is of utmost importance when no precise food has been correlated with the clinical manifestations.
- 9. Risk Factors forAnaphylaxis ❖ Concomitant Diseases ➢ Asthma, Allergic rhinitis and Eczema ➢ Mastocytosis ➢ Depression, cognitive dysfunction, substance misuse ❖ Drugs ➢ β-Adrenergic blockers; Angiotensin-converting enzyme (ACE) inhibitors ➢ Sedatives, antidepressants, narcotics, recreational drugs ➢ Alcohol may lower patient’s ability to recognize triggers and symptoms 9
- 10. ❖ Cofactors thatAmplify Anaphylaxis ➢ Exercise: may be food dependent or food independent; ➢ NSAIDs ➢ Acute infection ➢ Emotional stress ➢ Disruption of routine—for example, travel, jet lag ➢ Premenstrual status in women and girls
- 11. Anaphylactic preparedness Algorithm Managementof Anaphylaxis 1. Manpower(trained in prompt assessment and management of anaphylaxis) 2. Equipments:- (oxygen, suction, larygoscope, ambu bag, mask, endotracheal tube, IV canulas) 3. Drugs 4. Fluids 5. Communication
- 12. Initial management Yes • Assessairway, breathing, circulation, mentation • Inject epinephrine(IM)* • Supine position • IV access, oxygen, monitoring No Initial assessment supports potential anaphylaxis? Consider other diagnosis *0.01ml/kg Epinephrine1:1000[IM]
- 13. Good clinical response? Yes No Recumbent positionwith elevation lower extremity • Establish airway, O2 • Repeat epinephrine injection if indicated • IV fluids1 if hypotensive Consider inhaled bronchodilators2 if wheezing • H1 and H2 antihistamines3 • Corticosteroids4 • Observation • Autoinjectible epinephrine 1NS or RL-30 mL/kg in 1st hr 2 Nebulised Albuterol- (0.83 mg/mL [3 mL]) via mask with O2 3cetrizine-0.25 mg/kg up to 10 mg PO, Ranitidine-1 mg/kg up to 50 mg IV 4methylprednisolone- 1-2 mg/kg up to 125 mg IV
- 14. Poor clinical response • Epinephrineintravenous infusion* • Other intravenous vasopressors • Consider glucagon Cardiopulmonary arrest during anaphylaxis: • CPR and ACLS measures • Consider: High-dose epinephrine Rapid volume expansion Atropine for asystole or pulseless electrical activity • Transport to ICU *0.01 mL/kg/dose of 1:10,000 IV
- 15. POSTEMERGENCY MANAGEMENT Antihistamine-Cetirizine (5-10mg qd) or loratadine (5-10 mg qd) for 3 days Corticosteroids(Optional): Oral prednisone (1 mg/kg up to 75 mg) daily for 3 days Preventive treatment • Prescription for epinephrine autoinjector(Epipen) and antihistamine • Written plan outlining patient emergency management • Follow-up evaluation to determine/confirm
- 16.