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Emergency lectures - Anaphylatic shock

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  • Data regarding fatalities associated with anaphylactic reactions are limited. It is estimated, however, that between 500 and 1000 individuals die of anaphylaxis each year, and that the risk of death in those who experience such a reaction approximates 1%. It is clear that the risk for an increased severity of anaphylaxis or death may be related to alterations in the body’s homeostatic mechanisms, as in patients receiving beta blockers, ACE inhibitors, or in the presence of underlying adrenal insufficiency. Beta blocking drugs or the presence of asthma may worsen the airway response to treatment and complicate resuscitative efforts. Moreover, epinephrine administration in the face of beta blocker treatment may lead to unopposed  -adrenergic effects and significant hypertension. Preexisting cardiac disease or the rapid intravenous infusion of an allergen may also be responsible for poor outcomes. Importantly, the failure to administer epinephrine immediately after the onset of anaphylactic symptoms has been shown to be an independent risk factor contributing to fatal outcomes. Miller RL. Epidemiology of anaphylaxis. Presented at: Anaphylaxis: Safely Managing Your Patients at Risk for Severe Allergic Reactions. Postgraduate Institute for Medicine; October 8, 1999; Washington, DC. Bocher BS. Anaphylaxis. N Engl J Med 1991:324:1785–1790.
  • Uniphasic anaphylaxis resolves within hours either spontaneously or with treatment.
  • Intramuscular epinephrine injected into the lateral thigh (vastus lateralis) produces a more rapid rate of rise in blood epinephrine levels than does subcutaneously injected epinephrine injected into the upper arm. There are no outcome data comparing the results of these two administrations in terms of their therapeutic effect. It should also be noted that the area under the curve is essentially equivalent for both of these routes of administration. Recommend that patients maintain two stationary 2-packs of epinephrine, one for home and the other for work or school environment.
  • All patients at risk should be instructed as to the proper administration of EpiPen  /EpiPen  Jr before the need for its use arises. Detailed instructions for self-administration (contained in each auto-injector package) should be carefully reviewed with the patient. In addition, a training device (known as the EpiPen  Trainer) that simulates the auto-injection process without actual drug delivery is available. Using the EpiPen  Trainer, patients should practice self-administration under the supervision of a physician (or a trained assistant) until an appropriate administration technique and a satisfactory comfort level are assured. To prepare the EpiPen  /EpiPen  Jr for use, grasp the auto-injector with the hand (forming a fist around the unit) with the black tip facing downward. Immediately before use, remove the gray activation cap with the other hand, being careful not to touch the black tip, where the needle is located, at any time. EpiPen  /EpiPen  Jr package instructions. Napa, Calif: Dey, L.P., December 2000.
  • After uncapping the auto-injector, place the black tip near the fleshy outer portion of the thigh. Instruct the patient that it is not necessary to remove any clothing; the EpiPen  /EpiPen  Jr auto-injector is designed to work effectively through clothing. Remind the patient not to touch the black tip of the auto-injector at any time. EpiPen  /EpiPen  Jr package instructions. Napa, Calif: Dey, L.P., December 2000.
  • With a quick motion, swing out and jab firmly into the outer thigh, so that the injector is at a 90 degree angle to the thigh. Hold firmly in the thigh for several seconds. During this time, a spring-activated mechanism is released, and a dose of epinephrine is administered. When practicing with the trainer, a “click” indicates that the device worked properly. Remove the unit and massage the injection site for an additional few seconds. Once administration is complete, the patient should check the black tip of the auto-injector. If the needle is exposed, a dose of epinephrine was injected. If not, the above steps should be repeated. Inform the patient that most of the liquid (90%) stays in the auto-injector after the dose is administered and cannot be reused. To avoid an accidental needle stick, the needle of the fired unit should be bent back against a hard surface. Carefully return the auto-injector to its carrying tube (NEEDLE FIRST) without replacing the gray safety cap. Recap the carrying tube and bring it to the emergency care facility for proper disposal. Patients should be instructed to go immediately to the nearest Emergency Room for further medical attention. Medical personnel should be told that a dose of epinephrine has been given and should dispose of the auto-injector properly. Patients should be reminded to store their EpiPen  /EpiPen  Jr in a dark place at room temperature; prolonged temperature extremes (refrigeration or car glove box, trunk) should be avoided for optimal functioning of the auto-injector. Patients should check the EpiPen  /EpiPen  Jr monthly for expiration date and discoloration. If the unit has expired or the drug solution appears brown, the unit should be discarded and replaced immediately. EpiPen  /EpiPen  Jr package instructions. Napa, Calif: Dey, L.P., December 2000.
  • Antihistamines Block H1 and H2 receptors Epinephrine for bronchospasms stimulates the reformation of tight junctions between endothelial cells IV fluids to support blood pressure Desensitization
  • Position. Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure. c Oxygen. Administer oxygen at high flow rates. c Epinephrine. Administer epinephrine to all patients with clinical signs of shock, airway swelling, or definite breathing difficulty. Administer intravenous epinephrine if anaphylaxis is profound and life-threatening and vascular access is available. If vascular access is not available or if anaphylaxis is not profound and life-threatening, administer epinephrine by intramuscular injection. Subcutaneous administration may be used but absorption and subsequent achievement of maximum plasma concentration may be delayed with shock.8—The IM dose of 0.3 to 0.5 mg (1:1000; 1 mL) may be repeated after 5 to 10 minutes if no clinical improvement.—Intravenous epinephrine (1:10 000; 10 mL) 1 to 5 mL or 0.1 to 0.5 mg over 5 minutes should be used only for profound, immediately life-threatening manifestations and when there are no delays in intravenous access.Epinephrine may be diluted to a 1:10 000 solution before infusion. An intravenous infusion (1 mg in 250 mL D5W[4 mg/mL]) at rates of 1 to 4 mg/min may avoid frequent repeat epinephrine injections. 9c Antihistamines. Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). c H2 blockers. Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV).10c Isotonic solutions. Give isotonic crystalloid (normal saline)if hypotension is present and does not respond rapidly to epinephrine. A rapid infusion of 1 to 2 L or even 4 L maybe needed initially. c Inhaled b-adrenergic agents. Provide inhaled albuterol ifbronchospasm is a major feature. If hypotension is present,administer parenteral epinephrine before inhaled albuterol to prevent a possible further decrease in blood pressure.Inhaled ipratropium may be especially useful for treatment of bronchospasm in patients on b-blockers. c Corticosteroids. Infuse high-dose intravenous corticosteroidsslowly or administer intramuscularly after severeattacks, especially for asthmatic patients and those already receiving steroids. The beneficial effects are delayed at least 4 to 6 hours. c Envenomation. Rarely insect envenomation by bees, but not wasps, leaves a venom sac. Immediately scrape away any insect parts at the site of the sting.11 Squeezing is alleged to increase envenomation. Judicious local applicationof ice may also slow antigen absorption. The application of papain (available in meat tenderizers) to the stinger site is a common home remedy that appears to have no therapeutic value.12c Glucagon. For patients unresponsive to epinephrine, especiallythose receiving b-blockers, glucagon may be effective.This agent is short-acting (1 to 2 mg every 5 minutes IM or IV). Nausea, vomiting, and hyperglycemia arecommon side effects. c Observation. Observe closely up to 24 hours. Manypatients do not respond promptly to therapy, and symptomsmay recur in some patients (up to 20%) within 1 to 8 hoursdespite an intervening asymptomatic period.13–15
  • Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV)
  • Rapid Progression to Lethal Airway Obstruction Close observation is required during conventional therapy. Early, elective intubation is indicated for patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling. If respiratory function deteriorates, perform semi elective (awake, sedated) tracheal intubation without paralytic agents. Angioedema. Patients with angioedema pose a particularly worrisome problem because they are at high risk for rapid deterioration. Most will present with some degree of labial orfacial swelling. Patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling are at particular risk for respiratory compromise.Early tracheal intubation. If intubation is delayed, patients can deteriorate over a brief period of time (0.5 to 3 hours),with development of progressive stridor, severe dysphonia oraphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. At this point both tracheal intubation and cricothyrotomy may be difficult or impossible.Attempts at tracheal intubation may only further increase laryngeal edema or compromise the airway with bleeding into the oropharynx and narrow glottic opening. The patient may become agitated as a result of hypoxia and may be uncooperative with oxygen therapy.Paralysis followed by an attempt at tracheal intubation mayprove lethal, because the glottic opening is narrow and difficult to see because of the lingual and oropharyngeal edema and the patient is iatrogenically apneic. If tracheal intubation is not successful, even bag-mask ventilation maybe impossible, because laryngeal edema will prevent air entry and facial edema will prevent creation of an effective seal between the face and bag mask. Pharmacological paralysis at this point may deprive the patient of the sole mechanism for ventilation, ie, spontaneous breathing attempts.
  • During Arrest: Key Interventions and Modifications of BLS/ALS Therapy Death from anaphylaxis may be associated with profound vasodilation, intravascular collapse, tissue hypoxia, and asystole.No data is available on how cardiac arrest procedures. ; should be modified, but difficulties in achieving adequate volume replacement and ventilation are frequent. Reasonable recommendations can be based on experience with non fatalcases.Airway, Oxygenation, and Ventilation Death may result from angioedema and upper or lower airway obstruction. Bag-mask ventilation and tracheal intubationmay fail. Cricothyrotomy may be difficult or impossiblebecause severe swelling will obliterate landmarks. Inthese desperate circumstances, consider the following airwaytechniques:c Fiberoptic tracheal intubationc Digital tracheal intubation, in which the fingers are used toguide insertion of a small (#7 mm) tracheal tubec Needle cricothyrotomy followed by transtracheal ventilationc Cricothyrotomy as described for the patient with massive neck swelling16 Support of Circulation Support of circulation requires rapid volume resuscitation and administration of vasopressors to support blood pressure.Epinephrine is the drug of choice for treatment of both vasodilation/hypotension and cardiac arrest .c Rapid volume expansion is an absolute requirement.—When anaphylaxis occurs, it can produce profound vasodilation that significantly increases intravascular capacity. Very large volumes should be administered over very short periods; typically 2 to 4 L of isotonic crystalloid should be given. c High-dose epinephrine IV (ie, rapid progression to high dose) should be used without hesitation in patients in full cardiac arrest.—A commonly used sequence: 1 to 3 mg IV (3 minutes),3 to 5 mg IV (3 minutes), then 4 to 10 mg/min. c Antihistamines IV. There is little data about the value of antihistamines in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result. c Steroid therapy. Although steroids should have no effectif given during a cardiac arrest, they may be of value in the post resuscitation period. Asystole/PEA Algorithms. Because the arrest rhythm inanaphylaxis is often PEA or asystole, the ILCOR panelrecommended adding the other steps in the Asystole and PEA Algorithms. These include—Administration of atropine—Transcutaneous pacing c Prolonged CPR. Cardiac arrest associated with anaphylaxis may respond to longer therapy than usual.—In these circumstances the patient is often a young person with a healthy heart and cardiovascular system.Rapid correction of vasodilation and low blood volume is required.—Effective CPR may maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reaction resolve.
  • Transcript

    • 1. Emergency Medicine Symposium Hué March 2012 Management of the Anaphylactic Shock Eric Revue1, MD Pr A. Bellou2, MD 1 European Society for Emergency Medicine Head of Emergency Medicine DepartmentDirector of Prehospital Emergency Medicine (SMUR) Louis Pasteur ‘s Hospital, Chartres, France President of European Society for Emergency Medicine 2 Head of Emergency Medicine Department Director of Emergency Medicine Training Program University Hospital, Faculty of Medicine, Rennes, France
    • 2. What is anaphylaxis? An acute systemic allergic reaction The result of a re-exposure to an antigen that elicits an IgE mediated response Usually caused by a common environmental protein that is not intrinsically harmful Often caused by medications, foods, and insect stings It is a Type I hypersensitivity
    • 3. History 1st recorded 2640 BC in hieroglyphics – bee sting of a pharoah Richet & Portier – South Seas – Man-o-war – coined term anaphylaxis
    • 4. IgE Binds irreversible to FcεRI receptors on mast cells, basophils, and eosinophils Is usually for parasitic infections E heavy chain
    • 5. REVISED NOMENCLATURE FOR ANAPHYLAXIS Anaphylaxis Allergic Non-allergic anaphylaxis anaphylaxisIgE- mediated Immunologic,anaphylaxis non-IgE-mediated anaphylaxis Johansson SGO et al JACI 2004,113:832-6
    • 6. Anaphylaxis J Allergy Clin Immunol 2007;120:506-15
    • 7. MEDIATORS
    • 8. Mast Cell Has high affinity for IgE molecules (105 IgE/cell) Originates in the bone marrow, reside in connective tissues Increases host response to parasitic infections Contain immunological mediators in granules ie. Histamine, ECF-A, HMW-NCF 2 populations that vary in granule content and activity  Connective tissue  Mucosal
    • 9. What is happening? Initial exposure sensitizes mast cells. Antigen specific IgE molecules attach to high affinity Fc receptors on the mast cell surface. Cross linking of IgE molecules on surface causes intracellular signaling pathway – Inflammatory mediators are released upon degranulation
    • 10. Mediators Involved Include histamine, proteases, chemotactic factors, leukotrienes, prostaglandin D, and cytokines Primary: released before degranulation – Interleukin 4 used by T cells induces B cell maturation – IL-3 and IL-5 released by T and mast cells are chemo attractants for eosinophils Secondary: come from granules
    • 11. Diagnostic of Anaphylaxis• Anaphylaxis network symposium:J Allergy Clin Immunol 2006 ;117 : 391-7Definition : severe allergic reaction with sudden onset and risk of death
    • 12. Diagnostic of AnaphylaxisCriteria 1 : skin lesions and/or mucosa lesions (urticaria, itching or erythema, lips oedema or tongue-uvula edema). With one or mors following signs : Respiratory troubles (dyspnea, bronchospasm, stridor, decreased of peak flow, hypoxia) Systolic BP<90 mmHg) ou organ dysfunction (hypotonia, syncope, incontinence)
    • 13. Diagnostic of AnaphylaxisCriteria 2 : 2 or more signs after exposition to a probable allergen: skin lesions and/or mucosa lesions (urticaria, itching or erythema, lips oedema or tongue-uvula edema). With one or mors following signs : Respiratory troubles (dyspnea, bronchospasm, stridor, decreased of peak flow, hypoxia) Systolic BP<90 mmHg) ou organ dysfunction (hypotonia, syncope, incontinence) Persistant gastrointestinal troubles (abdominal pain, vomiting)
    • 14. Diagnostic of AnaphylaxisCriteria 3: Decrease of SBP< 90mmHg or more than 30% compared to basal in adults* after exposition to known allergen.*In child decrease of SBP is defined as: SBP < 70 mmHg from 1 month to 1 year, below (70 mmHg + [2 x age]) from 1 to 10 years, <90mmHg from 11 to 17 years.
    • 15. Triggers Drugs causing anaphylaxisCommon causes: • Antibiotics (especially penicillin) • Anaesthetic agents• Foods • Aspirin• Bee and wasp stings • NSAID’S• Drugs • IV Contrast media• Latex rubber • Opioid analgesicsFoods reported as triggers• Peanuts 8 Rare Causes:• Fish• Shellfish • Exercise• Eggs • Semen• Milk • Vaccines• Sesame, Pulses etc• OthersNote:Anaphylaxis may be worse in those on betablockers
    • 16. The Big Eight/Most Common Food Allergens SHELLFISH FISH COWS MILK EGGS SOYA WHEAT PEANUTS TREE NUTS
    • 17. International Food Allergen List Japan 4 of Top 8 *Milk E.U. *EggCanada Top 8 Plus *PeanutsTop 8 Plus + Sesame *Wheat+Sesame + Molluscs Plus +Buckwheat+Molluscs + Sulfites + Buckwheat+Sulfites + Gluten + Another 20+Gluten + Celery allergens are + Mustard recommended + Lupin Hong Kong Top 7 Plus U.S. TOP “8” •Fish +Sulfites •Crustacean +Gluten (in Shellfish place of •Egg wheat) •Milk •Peanuts •Gluten ? Codex •Tree-nuts Top 7 Plus Australia/NZ •Soy + Gluten Top 8 Plus •Wheat (in place +Sesame of wheat) +Molluscs + Sulfites +Sulfites +Gluten
    • 18. INCIDENCE and PREVALENCE• Indicators: - prevalence of all suspected allergic reaction with medical assistance - prevalence of severe reactions - prevalence of severe anaphylaxis complicated by death• Results from different ways: registres, allergy network, hospitals, ED, Schools
    • 19. Prevalence in Emergency Departments Gaeta, 2007-Ann Allergy 12 millions allergic reactions over 12 years (1993 à 2004) in US 1% of all ED visits 1 million per year 12,400 anaphylaxis per year in ED
    • 20. French Allergy Vigilance Network 2000 : 2831 cases 2004 : 3573 cases 22% increaseClin Exp Allergy, 2010
    • 21. Allergy Network Clinical Aspects Children: 34% Adults: 66% ED visits: 80.5% Epinephrine: 44.5% Hospitalisation rate : 59.3% Moneret-Vautrin et al Rev Méd Int 2006;120:S70-72
    • 22. Allergy Network Clinical Aspects Anaphylactic Shock: 47.6% Severe systemic reactions: 36.7% Laryngeal Angio-Edema: 12.4% Severe asthma: 4.4% Moneret-Vautrin et al Rev Méd Int 2006;120:S70-72
    • 23. Clinical Signs Shock Myocardial infarction Cardiac arrest
    • 24. Symptoms Peripheral vasodilation – vascular permeablility (edema) Bronchospasm Cardiac arrhythmias Smooth muscle contractions
    • 25. Laryngeal Angioedema
    • 26. Mortality Review: 4 for 20,381 cases of anaphylaxis cared in ED=2 for 10,000 Moneret-Vautrin, 2005-Allergy 0.65 to 2%=1 to 3 for 1 million in Europe Neugut, 2001-Arch Int Med : 20 for 1 million in US
    • 27. Mortality• Risk Factors: – Delayed adrenalin administration – Beta blokers, AC Inhibitors – Asthma, co-morbidity – Allergen introduced IV 90% of died patients had dyspnea before then cardiac arrest Drug allergy=Shock is the main symptom
    • 28. Anaphylaxis and Food Allergy 32 deaths in patients with age between 2 to 32 ans  - peannut >90% of reations  - history of asthma  - majority didn’t receive epinephrine Bock SA et al. J Allergy Clin Immunol 2001;107:191-3
    • 29. Uniphasic Anaphylaxis Treatment Initial Symptoms 0 TimeAntigen Exposure
    • 30. Biphasic Reaction Treatment Treatment 1 to 38 hours Initial phase Recurrent phaseAllergen contact Time (h) Ellis AK, Day JH, Can Med Ass,2003
    • 31. Meta-analysis 2003 to 2008 : 12 6- Bellou, 2003-Emerg Med J, France1995 to 2001 : 5 7- Brown, 2004-JACI, Australia 8- Clarck, 2004-JACI, USA1- Schwartz, 1995-Allergy 9- Clarck, 2005-JACI, USA Proc : US 10- Haymore, 2005-JACI, USA2- Klein, 1995-JACI 11- De Villiers Smit, 2005-J Emerg US Med3- Stewart, 1995-Q J Med Hong Kong UK 12- Luke, 2006-Ann Emerg Med, USA4- Pastorello, 2001-J Chrom 13- Braganza, 2006-Arch Dis Child Biomed Sc Appl Australia Italy 14- Gaeta, 2007-Ann Allergy, USA5- Brown, 2001-JACI 15- Melville N, 2008-Emerg Med J, UK Australia 16- De Silva IL, 2008-Allergy, Australia 17- Ross MP, 2008-JACI, USA
    • 32. Type of AllergenFood : 33%Hymenoptera Venom : 28%Drugs : 26%
    • 33. Epinephrin Administration in ED 15-Ross MP, USA: 19% 17-Melville N, UK: 5%
    • 34. Epinephrin Self-injected
    • 35. Allergist Follow-up
    • 36. Hospitalisation after ED Care
    • 37. SUMMARY• 75 to 85% of anaphylaxis are cared in EDs +++• 4 guideline recommendations not fully respected: (1) adrenaline at the acute phase, (2) prescription of self-injected adrenaline, (3) education of patient, (4) follow-up by allergist
    • 38. Guidelines Anaphylaxis network symposium :J Allergy Clin Immunol 2006 ;117 : 391-7Self-injected Adrenaline: cardiovascular or respiratory signs and know allergenInformation of patientAllergy follow-up after ED visitMonitoring in ED: 8 to 24 h, hospitalisation for severe or recurrent anaphylaxis, asthmatic patient
    • 39. Guidelines for ED Treatment• Suspicion of severe anaphylaxis• ABC• Diagnostic (definition)• 1e line : Adrenaline + Fluid resuscitation: crystalloïds or saline 0.9%, adult 500 ml to1000 ml ( up to 4000ml), children 20ml/Kg Jasmeet S. Resuscitation 2008;77:157-169.
    • 40. Adrenaline (epinephrine) for the treatment of anaphylaxiswith and without shock (Review)Sheikh A, Shehata YA, Brown SGA, Simons FERThis is a reprint of a Cochrane review, prepared and maintained by TheCochrane Collaboration and published in The Cochrane Library2010, Issue 10http://www.thecochranelibrary.com AUTHORS’CONCLUSIONS • Implications for practice We found no relevant evidence for adrenaline use in the treatment of anaphylaxis. We are, therefore, unable to make any new recommendations based on the findings of this review. Guidelines on the management of anaphylaxis need to be more explicit about the basis of their recommendations regarding the use of adrenaline.
    • 41. Adrenaline (epinephrine) for the treatment of anaphylaxiswith and without shock (Review)Sheikh A, Shehata YA, Brown SGA, Simons FERThis is a reprint of a Cochrane review, prepared and maintained by TheCochrane Collaboration and published in The Cochrane Library2010, Issue 10http://www.thecochranelibrary.com AUTHORS’CONCLUSIONS • Implications for research Although placebo-controlled trials of adrenaline in anaphylaxis would be unethical, it might be possible to conduct randomized controlled trials comparing two different doses of adrenaline, or two different routes of administration of adrenaline, in addition to other standard-of-care treatments (Simons 2008).
    • 42. Epinephrine Injection: IM vs. SQProspective, randomized, blinded study in childrenT-max was 8 ± 2 minutes after injection of epinephrine 0.3 mg from anEpiPen IM in the vastus lateralis vs. 34 ± 14 minutes (range, 5 to 120) afterinjection of epinephrine 0.01 mg/kg SQ in the deltoid region.Simons FER, Gu X, Simons KJ. Epinephrine absorption in adults: intramuscular versus subcutaneous injection. The Journal of Allergy and Clinical Immunology 2001;108:871–3.
    • 43. Adrenaline I.M• Adrenaline IM: dilution 1/1000- Adult : 500 microgramms (0,5ml)- Child > 12 years: 500 microgrammes (0,5ml)- Child 6 to 12 years: 300 microgrammes (0,3ml)- Child < 6 years: 150 microgrammes (0,15ml) Jasmeet S. Resuscitation 2008;77:157-169.
    • 44. Self-injected epinephrine
    • 45. Self-injected epinephrine
    • 46. Self-injected epinephrine
    • 47. Adrenaline I.V• Intravenous adrenaline has been associated with fatal cardiac arrythmias and myocardial infarction, these cases have been associated with too rapid injection, undiluted doses, or excessive doses (Fischer, 1995; Pumphrey, 2000; Brown, 2001; Montanaro and Bardana, 2002).• To minimise these adverse effects, the use of intravenous adrenaline is now recommended at a dilution of 1:10,000 (Project Team of the Resuscitation council, UK, 2005).
    • 48. Adrenaline I.V• IV: dilution 1/10000 (10 ml with 100 microgrammes/ml adrenaline), routinely used by EPs:- Adult: bolus of 50 microgrammes (0.5ml)- Child: bolus of 1 microgramme/Kg- If repeated administration=perfusion by pump (1 to 4 microgrammes/min) Jasmeet S. Resuscitation 2008;77:157-169.
    • 49. Can epinephrine inhalations be substituted for epinephrineinjection in children at risk for systemic anaphylaxis?Simons FE, Gu X, Johnston LM, Simons KJ.Pediatrics. 2000 Nov;106(5):1040-4. • NO • In a study in children, those treated with adrenaline inhalers had blood adrenaline levels no higher than a control group treated with placebos.
    • 50. Glucocorticoids for the treatment of anaphylaxis (Review)Choo KJL, Simons FER, Sheikh AThis This is a reprint of a Cochrane review, prepared and maintained by TheCochrane Collaboration and published in The Cochrane Library2010, Issue 10http://www.thecochranelibrary.comAUTHORS’CONCLUSIONS• Implications for practiceWe found no relevant evidence for the use of glucocorticoids in the treatment of an acute episode of anaphylaxis. We are, therefore, unable to make any new recommendations based on the findings of this review. While we do not necessarily suggest that anaphylaxis guidelines no longer recommend glucocorticoids, these guidelines need to be more explicit about the basis of their recommendations regarding the use of these agents (Alrasbi M, Sheikh A. Comparison of international guidelines for the emergency medical management of anaphylaxis. Allergy 2007; 62:838–41.).
    • 51. Second line treatment• Histamine antagonistsDexchlorpheniramine=against itching• CorticosteroidsHydrocortisone-Methylprednisolone=prevent recurrent anaphylaxis Jasmeet S. Resuscitation 2008;77:157-169.
    • 52. Guidelines for ED Treatment Specific situationsGlucagon : 1-2 mg every 5 min, resistance to adrenaline, patient treaed by β blokersCardiac arrest : follow current guidelines fluid resuscitation=4 to 8l adrenaline : 1 to 3 mg IV (3min), 3 to 5 mg (3min), 4 to 10 microg/min pump perfusion
    • 53. Positive Diagnosis in ED∀ ♦ Medical history to identify allergen∀ ♦ Tryptase - Specific for mast cells degranulation, confirm anaphylactic reaction - Still increased at 6th hour Lieberman PL et al, J Allergy Clin Immunol 2005;115:S483-523
    • 54. Biologic tests in anaphylaxis Plasma histamine Serum tryptase 24-hr Urinary histamine metabolite 0 30 60 90 120 150 180 210 240 270 300 330T1 = after emergency treatment start, T2 = 1 to 2 h after T1 et T3 at 24 h inthe ward. Put serum at -20°C.
    • 55. Anaphylactic Shock 180 160 140 120 100 RT 80 R0 60 40mMABHPg() 20 0 T0 T3 T5 T15 T30 T60 Time (min) Bellou A. Shock, 2003
    • 56. Vasodilatation
    • 57. Effect of NO Synthase, Histamine and Serotonine Inhibition Pathways 500 NIR 400 300 200 IR 100 0 IR+L- u )m R H in a e b s ( / t NAME+DPH+CIM+DH E Time (minutes) Bellou A. Shock, 2003
    • 58. New treatments of Anaphylactic Shock Vasopressin?Anesthesiology, V 106, No 5, May 2007
    • 59. Management of the Anaphylactic shock
    • 60. Management of the Anaphylactic shock Position: Place victims in a position of comfort. If hypotension is present, elevate the legs until replacement fluids and vasopressors restore the blood pressure Oxygen. Administer oxygen at high flow rates. Epinephrine. Administer epinephrine to all patients with clinical signs of shock, airway swelling, or definite breathing difficulty Antihistamines. Administer antihistamines slowly intravenously or intramuscularly (eg, 25 mg of diphenhydramine). H2 blockers. Administer H2 blockers, such as cimetidine(300 mg PO, IM, or IV) Inhaled b-adrenergic agents. Provide inhaled albuterol if bronchospasm is a major feature. If hypotension is present,administer parenteral epinephrine before inhaled albuterol to prevent a possible further decrease in blood pressure.Inhaled ipratropium may be especially useful for treatment of bronchospasm in patients on b-blockers.
    • 61. Management of Anaphylactic Shock Position: Oxygen. Epinephrine. Antihistamines. H2 blockers. Inhaled b-adrenergic agents.
    • 62. Management of the Anaphylactic shock Corticosteroids. Infuse high-dose intravenous corticosteroids slowly or administer intramuscularly after severe attacks, especially for asthmatic patients and those already receiving steroids. The beneficial effects are delayed at least 4 to 6 hours Envenomation. Rarely insect envenomation by bees, but not wasps, leaves a venom sac. Immediately scrape away any insect parts at the site of the sting.Squeezing is alleged to increase envenomation. Judicious local application of ice may also slow antigen absorption. The application of papain (available in meat tenderizers) to the stinger site is a common home remedy that appears to have no therapeutic value. Glucagon. For patients unresponsive to epinephrine, especially those receiving b-blockers, glucagon may be effective.This agent is short-acting (1 to 2 mg every 5 minutes IM or IV). Nausea, vomiting, and hyperglycemia are common side effects. Observation. Observe closely up to 24 hours. Many patients do not respond promptly to therapy, and symptoms may recur in some patients (up to 20%) within 1 to 8 hours despite an intervening asymptomatic period
    • 63. Rapid Progression to Lethal Airway Obstruction Close observation is required during conventional therapy Early, elective intubation is indicated for patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling. If respiratory function deteriorates, perform semi elective (awake, sedated) tracheal intubation without paralytic agents Angioedema. Patients are at high risk for rapid deterioration. Most will present with some degree of labial or facial swelling. Patients with hoarseness, lingual edema, and posterior or oropharyngeal swelling are at particular risk for respiratory compromise Early tracheal intubation. If intubation is delayed, patients can deteriorate over a brief period of time (0.5 to 3 hours),with development of progressive stridor, severe dysphonia oraphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. At this point both tracheal intubation and cricothyrotomy may be difficult or impossible.
    • 64. During Cardiac Arrest: Key Interventions and Modifications of BLS/ALS Therapy Airway, Oxygenation, and Ventilation Death may result from angioedema and upper or lower airway obstruction. Bag-mask ventilation and tracheal intubation may fail. Cricothyrotomy may be difficult or impossible because severe swelling will obliterate landmarks. In desperate circumstances, consider the other airway techniques:  Fiber optic tracheal intubation  Digital tracheal intubation, in which the fingers are used to guide insertion of a small (#7 mm) tracheal tube  Needle cricothyrotomy followed by transtracheal ventilation  Cricothyrotomy as described for the patient with massive neck swelling  Support of Circulation : rapid volume resuscitation and administration of vasopressors to support blood pressure. Epinephrine is the drug of choice for treatment of both vasodilation/hypotension and cardiac arrest. Rapid volume expansion is an absolute requirement.—When anaphylaxis occurs, it can produce profound vasodilation that significantly increases intravascular capacity. Very large volumes should be administered over very short periods; typically 2 to 4 L of isotonic crystalloid should be given
    • 65. During Cardiac Arrest: Key Interventionsand Modifications of BLS/ALS Therapy High-dose epinephrine IV (ie, rapid progression to high dose) should be used without hesitation in patients in full cardiac arrest.—A commonly used sequence: 1 to 3 mg IV (3 minutes),3 to 5 mg IV (3 minutes), then 4 to 10 mg/min. Antihistamines IV. There is little data about the value of antihistamines in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result. Steroid therapy. Although steroids should have no effect if given during a cardiac arrest, they may be of value in the post resuscitation period. Asystole/PEA Algorithms. Because the arrest rhythm in anaphylaxis is often PEA or asystole, the ILCOR panel recommended adding the other steps in the Asystole and PEA Algorithms: Administration of atropine—Transcutaneous pacing Prolonged CPR. Cardiac arrest associated with anaphylaxis may respond to longer therapy than usual.—In these circumstances the patient is often a young person with a healthy heart and cardiovascular system.Rapid correction of vasodilation and low blood volume is required.—Effective CPR may maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reaction resolve
    • 66. CONCLUSION• EPs : critical role=first line• Improve knowledge in Allergy• Use Adrenaline even without hypotension• Collaboration with allergist is essential• Develop research in anaphylaxis Càm on ! erevue@ch-chartres.fr abdelouahab.bellou@chu-rennes.fr