Transcript Anaphylaxis
Anaphylaxis Dr Greg Emery Anaphylaxis Anaphylaxis is an exaggerated response to a substance to which an individual has become previously sensitised. Histamine, serotonin and other vasoactive substances are released from mast cells and basophils in response to an IgE mediated reaction Anaphylactoid reactions are clinically indistinguishable but are not mediated by IgE Mortality estimated to be between 3-6% Anaphylaxis during Anaesthesia Diagnostic Card Absence of tachycardia or cutaneous signs does not exclude anaphylaxis Grade 1 Generalised mucocutaneous signs: Erythema, Urticaria+/- Angioedema Grade 2 Moderately severe - Multi-organ manifestations including: Mucocutaneous signs Hypotension, Tachycardia Evidence of Bronchospasm, cough, difficult ventilation Grade 3 Severe-Life Threatening and requiring immediate and specific treatment: Cardiovascular collapse Bradycardia or Tachycardia, Arrhythmias Bronchospasm Cutaneous signs may be absent, or present only after correction of hypotension Grade 4 Cardiopulmonary Arrest PRESENTING SIGNS AND SYMPTOMS Skin and Mucosa Hives, flushing, erythema, urticaria, Swelling head and neck or peripheries Airway Compromise Dyspnoea, wheeze, stridor, difficulty inflating lungs Hypotension Cardiac Arrest POSSIBLE CAUSES Direct Histamine Release Venous Obstruction Head Down Position C1-esterase deficiency (Angioedema only) Mastocytosis Cold induced anaphylaxis Direct Histamine Release Acid aspiration Exacerbation of asthma Intubation; Oesophageal intubation Foreign Body Difficult airway Visceral traction Mastocytosis Consider: Auto PEEP (disconnect from ventilator) Tension pneumothorax (decompress) Direct Histamine Release Visceral Traction Vasodilation by drugs Central Neural Blockade Drug Overdose Vasovagal Hypovolemia Mastocytosis Cold induced anaphylaxis Myocardial Ischaemia/Infarction Electrolyte Abnormality Sepsis Blood Loss Tension Pneumothorax Cardiac Tamponade Pulmonary Embolism Mastocytosis ANZAAG-ANZCA Anaphylaxis Management Guidelines Version 1.1 June 2013 Perioperative Anaphylaxis 60% IgE mediated Australia 1:10,000 to 20,000 anaesthetics UK 1:5,000 to 10,000 France 1:13,000 Norway 1:6,000 Perioperative Anaphylaxis Common causative drugs (France 2005-2007) Neuromuscular blocking drugs 48% Latex 20% Antibiotics 18% Hypnotics 1% Plasma substitutes (eg Gelofusine) 2% Opioids 2% Others: chlorhexidine, protamine None to inhaled anaesthetics Anaphylaxis to NMB drugs Western Australia (2002-2011) BJA doi:10.1093/bja/aes506 80 patients with life threatening anaphylaxis 81% female Agents Rocuronium 56% Suxamethonium 21% Vecuronium 12% Atracurium 10% Mivacurium 3% Pancuronium/Cisatracurium 0% Anaphylaxis to NMB drugs Auckland NZ 2006-2012 (Anesthesiology 2015; 122:39-45) 21 patients with anaphylaxis to NMBD Incidence per use: Suxamethonium 1:2,080 Rocuronium 1:2,499 Atracurium 1:22,451 In Auckland, the rate of anaphylaxis to suxamethonium and rocuronium is 10-fold higher than to atracurium Anaphylaxis to Neuromuscular Blockers Neuromuscular blocking drugs (NMBD) account for ~60% of anaesthetic anaphylactic reactions in Australasia and Europe (11% USA) Cross reactivity is common amongst NMBD esp suxamethonium and rocuronium In contrast to penicillins & cephalosporins, patients with NMBD anaphylaxis often have no history of previous exposure. Pholcodine Pholcodine is an opioid contained in some cough suppressants which contains a quaternary ammonium group. Readily available in Australia, France, England and Norway. Not available in Sweden or USA Norway vs Sweden – much higher incidence of Rocuronium/Suxamethonium allergy in Norway 2007 withdrawn from Norway market with significant drop in NMBD IgE Anaphylaxis during Anaesthesia Refractory Management Ensure possible triggers removed Chlorhexidine including impregnated CVCs Colloid stop if running at time of reaction Latex none in theatre Consider other diagnoses See ‘Diagnostic Card’ in Anaphylaxis Box Monitoring Consider Insert Arterial line and CVC Consider TOE/TTE to assess filling Request more help if required Consider calling arrest code Noradrenaline infusion 0.1mcg/kg/min Resistant Hypotension Continue Adrenaline and IV fluid bolus 50 ml/kg Metaraminol infusion if noradrenaline not available Vasopressin bolus 1-2 units (0.03units/kg) then infusion 2 units per hour Glucagon 1-5mg over 5 min (βblocker reversal) (Child 20-30mcg/kg to max 1mg) Consider cardiac bypass where available Resistant Bronchospasm Salbutamol IV bolus 100-200mcg +/- Salbutamol infusion 5-25mcg/min (Child 5mcg/kg/min for 1 hour then run infusion at 1-2mcg/kg/min) Consider: Auto PEEP (disconnect from ventilator) Tension pneumothorax (decompress) Pregnancy Lateral tilt Caesarean section if arrest or peri-arrest Once stable refer to ‘Post Crisis Management’ ANZAAG-ANZCA Anaphylaxis Management Guidelines Version 1.1 June 2013 Anaphylaxis during Anaesthesia Post Crisis Management Once Situation is Stabilised Consider Steroids Dexamethasone 0.1-0.4 mg/kg Hydrocortisone 2-4 mg/kg Consider ORAL Antihistamines Consider Oral 2nd Generation Antihistamines when patient able to take oral medications Parenteral Antihistamines NOT RECOMMENDED Consider: Proceed/Cancel/Postpone Surgery Postoperative ICU/HDU monitoring Tryptase at 1 hour, 4 hours and > 24 hours – Investigations Tryptase unstable in whole blood: send promptly to laboratory for processing Use Plain, serum or EDTA tube ABG as required Electrolytes, FBE, Coagulation Screen Monitor closely for 6 hours Observations Consider 24 hours ICU/HDU if moderate to severe (up to 20% incidence of biphasic reactions) Anaphylaxis may last up to 32 hours despite aggressive treatment Letter with Patient: Reaction Description + Agents Used Refer Patient for Testing and Allergy Assessment For a referral form & to locate your nearest testing centre go to www.anzaag.com ANZAAG-ANZCA Anaphylaxis Management Guidelines Version 1.1 June 2013 Tryptase Enzyme released from activated mast cells Detected in serum 30mins-8hrs after anaphylaxis, best 1-4hrs Can be used in post mortem if patient died between 1&6hrs after onset and PM within 3 days Tryptase Intradermal Skin Testing Iodine/SeafoodAllergy ‘Iodine allergy’ is a frequently used term and usually refers to reactions with iodinated radiological contrast media or possibly a contact allergy to povidone-iodine. There is little evidence to support iodine as the cause of allergic reactions. Reactions to iodine containing substances are due to other parts of the molecule. Seafood is a rich source of natural iodine Seafood allergy is not caused by the iodine contained in fish, crustaceans or molluscs. Therefore contrast media and povidone-iodine are not contraindicated in patients with seafood allergy. Latex Allergy Health care workers Hairdressers Food-service workers Police officers Patients with atopic background Children with spina bifida or genito-urinary abnormalities who have undergone numerous surgical procedures Some fruits contain cross reacting proteins Banana, avocado, kiwi fruit, peaches, mangos, passionfruit, plums, strawberry and tomato. Propofol & Egg Allergy Propofol currently in lipid vehicle (soy bean oil, egg lecithin, glycerol) Anaphylaxis 1:60,000 Egg lecithin is a purified egg yolk component Ovalbumin (main egg protein) found in egg white 25 pts with documented egg allergy had negative skin testing with propofol Current evidence suggests egg allergic patients are not more likely to develop anaphylaxis with propofol Anaphylaxis Dr Greg Emery