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ANAPHYLAXIS Immunological & non-immunological mechanisms combine to create a clinical presentation known as anaphylaxis A life-threatening histamine & vasoactive mediated systemic event A severe hypersensitivity reaction resulting in cardiovascular &/or respiratory compromise SKIN; Urticaria or generalised acute pruritis RESPIRATORY; airway spasm, oedema, feeling of pharyngeal constriction CARDIOVASCULAR; shock GASTROINTESTINAL; cramps & diarrhoea Histamine actions Relaxes vascular smooth muscle Increased capillary permeability Constricts bronchial smooth muscle Life is threatened Cardiovascular collapse Bronchospasm Laryngeal oedema Anaphylactic reactions can be observed as the development of flush or pallor, urticaria, angioedema, hypotension, tachycardia, & bronchospasm esp. in asthmatics. Reaction occurs usually within a few minutes of IV drug administration, or longer in administrated via other routes. May be followed by abdo cramps, diarrhoea & abnormal coagulation. Causes Stings, food, antibiotics, contrast media, thrombolytics, non-steroid antiinflammatory drugs, anaesthetic agents FACTORS THAT INFLUENCE MORTALITY; asthma, pre-existing hypovolaemia, heart failure, coronary artery disease predispose the patient to increased levels of severity & potentially fatal complications. Drugs may blunt response to adrenaline (beta blockers) Severe anaphylaxis is an important cause of PEA – pulseless electrical activity = cardiac arrest in presence of ECG complexes but no palpable pulse, thought to deteriorate to asystolic arrest due to hypovolaemia & hypoxia. Severity Varies from trivial erythema or urticaria to full blown cardiovascular collapse and asphyxia Mortality is influenced by: Asthma Pre-existing hypovolaemia Heart failure Coronary artery disease ECG findings in patient collapse associated with severe anaphylaxis PEA; cardiac arrest in the presence of ECG complexes but no palpable pulse and is thought to deteriorate to asystolic arrest due to hypovolaemia and hypoxia Immediate management Remove trigger Position supine High flow oxygen Management ADRENALINE; constricts vascular beds, reducing hypotension & capillary leak & dilates bronchial smooth muscle. Most important drug in anaphylaxis management – but remember does increase heart rate,, myocardial irritability & inotropy (force of muscle contraction) – therefore predisposing the myocardium to potentially serious arrhythmias & increased myocardial oxygen requirements predisposing to ischemia. Life threatening shock = IV admin / IM route in majority of situations FLUID THERAPY; rapid fluid replacement therapy required to replace fluid losses from circulation – isotonic saline is an acceptable alternative to colloidal fluids ANTIHISTAMINES; at best second line treatment evidence supporting use is weak and may cause further hypotension. (block the receptor action of histamine therefore may contribute to reducing vascular actions. 2 types of antihistamines; H1 blockers – i.e. promethazine & H2 blockers – i.e. ranitidine.) H1 blockers are most important in obtunding the cardiovascular effects of histamine (H2 blocker may be useful in cardiovascular collapse that responds poorly to adrenaline, fluid & H1) H1 blocking antihistamines are rarely life saving in severe anaphylaxis but should be routinely used in combination with other treatments. CORTICOSTERIODS; slow acting- uncertain benefit in acute phase. Administration must not delayed more life saving therapy (adrenaline & fluids) a parenteral dose may be given in cases of suspected anaphylaxis once initial resus and stablisation is complete. Management is matched to the severity of presentation Adrenaline - Fluid therapy - Antihistamines Corticosteroids If the patient is shocked and exhibiting signs of angioedema or bronchospasm >> ADRENALINE: - 0.3-0.5ml of 1:1000 IM, repeat q5min if no improvement Fluid: - rapid infusion of 1000mls isotonic fluid Management relates to severity of symptoms Repeat IM adrenaline after 5 minutes if there is no improvement in hypotension, airway swelling or bronchospasm IV 0.5-1ml of 1:10,000, increase dose as required IV adrenaline is indicated if the situation cardiac arrest Management relates to severity of symptoms Degree of cardiovascular collapse; pulse & blood pressure Development of swelling of upper airway; stridor & ability to articulate Degree of brochoconstriction; wheeze & ability to ventilate Fluid administration is guided by response to adrenaline and persisting hypotension continued adrenaline suggests additional fluid requirements 1-3 litres is commonly needed, if more is required consider CVP monitoring Additional considerations Nebulised salbutamol 5mg IV fluids: secure access & titrate infusion to maintain blood pressure Hydrocortisone 200mg IV stat Consider nebulised adrenaline 1mg if angioedema persists or worsens Contact ICU if patient not responding to interventions Cardiac arrest Consider giving escalating doses of IV adrenaline if still in cardiac arrest >5 minutes Fluid resuscitation 2 L rapidly Continue CPR for longer than usual New Zealand Resuscitation Council; Whakahauora Aotearoa, August 2011