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  • Urticaria
  • Anaphylaxis

    1. 1. Pathophysiology & ManagementScott Cooper B.Sc. (Hons.) Dip. Paramedical Science
    2. 2. Understanding the terminologyPathophysiologySigns and SymptomsClinical Management
    3. 3.  Between 1996 and 2007 there where 112 anaphylaxis fatalities in Australia During those 9 years, food induced anaphylaxis admissions increase by350% Globally, the incidence of allergic related medical conditions related tofood allergies is on the rise In the US there are approximately 150-200 anaphylaxis death annually Hospital admission for anaphylaxis management have increased 7 x inthe last decade in the UK
    4. 4. AnaphylaxisCan be defined as “An exaggerated immune response toa foreign antigen or protein resulting in severe lifethreatening condition”Refers to the physiological events regardless ofactivation mechanism.The term was first used by a couple of FRENCHscientists who where abusing dogs by testing seaanemone antivenin on cute little beagle puppies withsad eyes. It was noted that one of the dogs died withouta perceived reason.
    5. 5. Anaphylaxis continuedAetiologies are grouped into either:Allergic Mediated by Immunoglobulin E (Ig-E) Require previous exposure and sensitization The most common trigger of anaphylaxisNon allergic or anaphylactoid Conflicting evidence as to whether these reaction are activatedby IgE response or not No previous exposure or sensitization required
    6. 6. Anaphylactic ShockShock can be defined as a state of poor systemicperfusionAnaphylactic shock is a state of poor end organperfusion as a direct result of the anaphylacticreactionIn summary anaphylactic shock is just one ofmany possible clinical manifestations resultingfrom a severe allergic reaction.
    7. 7. BasophilsA type of granulocytic white blood cellMake up <1% of WBC countAlthough able to initiate release of chemicalweapons, also possess the ability to initiate mastcells to triggerPredominantly secrete histamine whentriggered.ARE MOBILE!
    8. 8. Mast CellsSimilar to basophils, these cells are locatedthroughout the body bound in connective tissue.Concentrated beneath the skin and the mucousmembranes of the respiratory and digestive tractsCan be considered as storage points for chemicalWMD’sWhen activated, release a multitude of chemicalinflammatory mediators
    9. 9. SensitisationJoe Boggs aged 2 eats his first ever peanut. Certaincells called blah blah blah cells, for some reason,believe this protein to be foreign and dangerousBlah blah blah cells take photographs of the proteinand take it to the bling bling cells who producemassive quantities of an antibody type, IgE. Thisantibody is specific to these proteins.The IgE antibodies bind to mast cells and basophils,ready to attack if this protein shows up again
    10. 10. Stage OneJoe Boggs aged 2 and 26 days eats his second ever peanut.As soon as the protein is absorbed into the blood stream,circulating basophils detect the presence of thisrecognised foreign antigen invader.All hell breaks loose and a cascade of highly complexbiochemical pathways result in the basophils screaming“CODE RED!!” The basophils flow throughout the blood stream, releasing theirchemical weapons as they go, if they havent already been triggered bythe same protein, they also get their bigger mates, the Mast Cells tofire their weaponry as well
    11. 11. Stage TwoBasophils now initiate what is known as a ‘Mastcell-leukocyte-cytokine-cascadeIn normal people, this reaction is controlled bya feedback system ensuring the cascade doesnot get out of hand.In persons with a SAR, this process becomesuncontrolled and results in the release ofmultiple chemical mediators over seconds,minutes and hours
    12. 12. Stage ThreeDisseminated mast cell activation release avariety of noxious mediators including:HistaminesProstaglandinsLeukotriensChemokinesCytokinesThese rapidly synthesized toxic compounds elicit awidespread increase in vascular permeability andvasodilatation
    13. 13. Stage FourThe patient begins to feel unwell as theinflammatory mediators act on the target tissuesThe integumentary, cardiovascular, respiratory,gastro intestinal and central nervous systems canall be affected.If the patient has integumentary involvement(Urticaria, erythema, swelling or pruritis(itching)) AND Respiratory compromise ORhypotension, the patient is said to be inanaphylaxis
    14. 14. Integumentary SystemDue to the high concentration of mast cellsunder the skin, this is often the first sign of animpending reactionHistamine causes vasodilatation of themicorcapillaries resulting in a flushedappearanceAs the capillaries become more permeable,plasma leaks into the interstitial space resultingin urticaria and pruritis due to the irritation ofplasma being outside of the vessel wall
    15. 15. Cardiovascular SystemInflammatory mediators including histamine,Leukotriens and kinins now cause widespreadvasodilatation and vessel wall permeability,As much as 35% of circulating fluid volume canbe lost to the interstitial space, this coupledwith the massive vasodilatation causes a rapiddrop in blood pressure, anaphylactic shock.Baroreceptors in the aortic arch and carotidbulb detect this pressure drop and heart rateincreases.
    16. 16. Cardiovascular System (cont’d)As the blood pressure drops, pre load and afterload decrease, resulting in a potential for poorcardiac perfusion, this is of particular concern inthe elderly or patients with cardiac disease.As the fluid builds up in the interstitial spaces,angioedema begins to cause swelling, particularlyto the eyes, ears, mouth and tongue, throat andlungsThe patient begins to complain of a lump oritching in throat, dysphagia and dyspnoea as theupper airway / tongue swells.
    17. 17. Severe Glossal Oedema
    18. 18. Angelina Jolie or Angiodema…..
    19. 19. Laryngoscope View of Laryngeal oedema
    20. 20. Respiratory SystemAs well as previously discussed upper respiratorytract inflammation due to angioedema, thesmooth muscle of the distal bronchi alsoconstrict, causing a reduction in the lumendiameter, resulting in further airflow resistance.This is a futile protection mechanism to limit theexposure to the antigenAs the patient becomes hypoxaemic, therespiratory rate increases dramaticallyHypoxaemia leads to further vasodilatation andtachycardia, placing more strain on the heart.
    21. 21. GastrointestinalMost gastrointestinal symptoms are due to therelease of serotonin during the reaction, this thebowel to spasm, causing abdominal cramping,induces nausea and diarrhoea.This is an attempt by the body to rid itself of theantagonist, by increasing bowel transit andinducing vomiting.Strong GI symptoms have been associated withan increase in severity and incidence ofanaphylaxis.
    22. 22. Central Nervous SystemMost CNS symptoms are due to hypotensionExpect anxiety, dizziness, confusion, and oftencombative behavior as cerebral blood flow iscompromisedANY GCS less than 15 indicates poor cerebralperfusion and is time critical.Most patients experiencing hypotensiongenuinely believe they are dying, rest andreassurance is an essential aspect of patientmanagement
    23. 23. Primary Survey DRABC find and fix Airway Adrenaline to reduce and arrest the laryngeal / glossal oedema Breathing High flow Oxygen, slow gentle IPPV if required Bronchodilators to assist with bronchospasm Circulation RAISE THE LEGS! Simple but highly effective Fluids to maintain end organ perfusion Adrenaline to increase vascular toneTreatment depends on the symptomsPrepare for the worst i.e. cardiac arrest
    24. 24. It should be remembered that anaphylaxis can beMonophasic, Biphasic or multiphasicMost people recover immediately after aggressiveintervention without experiencing furthersymptoms, some however do, as much as 24 hourslater.Always transport patient for physicianassessment, never leave a patient at homefollowing anaphylaxis, even if asymptomatic
    25. 25. ADRENALINEAdrenaline is a naturally occurring catecholamine which primarilyacts on Alpha1 and Beta1 & 2 adrenergic receptors, locatedmainly in tissues innervated by sympathetic nerves.(β1) increases heart rate Increases the force of myocardial contraction Increases the irritability of the ventricles(β 2) Bronchodilation(α 1) Peripheral vasoconstriction
    26. 26. ADRENALINE (cont’d)There is also anecdotal evidence that adrenaline assists instabilising the mast cells from degranulatingThe net results of adrenaline are: Increase in vascular tone Increase in BP Increase in preload and afterload Decrease in vascular permeability Decrease in swelling Acts as a bronchodilator
    27. 27. ADRENALINE (cont’d) Whilst it is important adrenaline is administered in a timely fashion forpatients in anaphylaxis, it is also prudent to consider the following: Adrenaline can be a dangerous drug! Is this a genuine anaphylaxis (Vasovagal? or anxiety??) Consider age and cardiac health of patient in dosing Best Route IMI (vastus lateralus as more reliable absorption profile) Nebulised (for isolated minor facial and/or tongue swelling thought to beallergic in origin – IMI if stridor present) Ensure adequate monitoring of patient post administration
    28. 28. ADRENALINE (cont’d)ADULT I.M.I. = 250 - 500mcg every 5 minutes until Pt stabilises Consider age of patient, medical condition of patient and severity ofreaction Nebulised = 5mg, single dosePAEDIATRIC I.M.I. = 10mcg / kg (Max 250mcg) every 5 minutes until Ptstabilises for patients equal to or >1 years of age I.M.I. = 100mcg every 5 minutes until Pt stabilises for patientsequal to or <1 years of age Nebulised = 5mg, Single dose
    29. 29. ADRENALINE (cont’d) EpiPen Most people identified as having high risk to anaphylaxis are providedwith an EpiPen If already administered, dose should be taken into account Below table shows the standard dose of EpiPen in AustraliaWeightWeight EpiPen DoseEpiPen DoseChildren < 10kgChildren < 10kg Not usually RecommendedNot usually RecommendedChildren 10-20kgChildren 10-20kg EpiPen Jr. 150mcgEpiPen Jr. 150mcgChildren & Adults >20kgChildren & Adults >20kg EpiPen 300mcgEpiPen 300mcg
    30. 30. FluidsSeverely shocked patient require large volumes of asuitable crystalloid solution to maintain organ perfusion!Adrenaline is the first line drug but fluids also have a vitalrole to play, and may in fact be the only and / or saferintervention required2-3 litres rapid infusion through at least a 16g isrecommended for hypotensive patients, consider
    31. 31. Bronchodilators e.g. SalbutamolThe respiratory symptoms exhibited by patients in anaphylaxisare very similar to those exhibited by asthmatics.Smooth muscle constriction may be relieved bybronchodilators such as salbutamolSalbutamol sulphate is a direct acting sympathomimetic agentwhich mainly effects β2 receptors. As a predominantly β2adrenoreceptor stimulant, Salbutamol bronchodilating action isrelatively more prominent than its cardiac effects
    32. 32. Anti Histamines Generally not recommended for serve allergic reactions Histamine is just one of the many inflammatory mediatorsresponsible for initiating anaphylaxis and is more of an initialmediator than a protracted one. Histamine has been shown to peak early and then return to normaldespite the persistence of severe physiological compromise The main issue of concern is that the major antihistaminepromethazine (phenergan) is a vasodilator and may in fact worsenthe patients outcome. It would therefore seem prudent that phenergan be restricted to thetreatment of skin symptoms and not in patients with realised orpotential haemodynamic compromise
    33. 33. Steroids Inhibit the accumulation of inflammatory cells at inflammation sites Inhibits the release and synthesis of inflammatory mediators Plays a part in suppressing cell mediated immune reactions
    34. 34. Glucagon Glucagon is a hyperglycemic agent but it also acts as a poor mansadrenaline in beta blocked patients! If a patient is beta blocked the efficacy of adrenaline may be severelyreduced due to it’s inability to bind to the beta receptor sites Glucagon works by binding to a different receptor site but still elicitssimilar effects as adrenaline within the cell. Recommended dose = initial load of 1-5mg I.V.I. over 5 minutes NOT RECOGNISED QAS MANAGEMENT, JUST FOR INTEREST
    35. 35. Useful questions to ask your patient:Do you suffer from any of the following?AsthmaBad hay feverSevere allergiesRemember these patient groups are statistically more likely toexperience and anaphylactic reactionAre you taking beta blockers?May explain why adrenaline isn’t working!
    36. 36. Familiarise yourself with adrenaline regularly:When to give itDosagesHow to draw that dose up,How to administer it safely IMI (aspirate)The risks associated with itAlthough anaphylaxis is rare, you never knowwhen you might need it!
    37. 37.  Journal of Emergency medicine July 2002 Anaphylaxis Emergency Medicine Australia 2006 Anaphylaxis: Clinical concepts and research priorities Allergy Notes August 2008 Anaphylactoid Reactions to Intravenous Contrast media New England Journal of Medicine November 2006 Anaphylaxis Prevention via pretreatment Emergency Care in the Streets Nancy Caroline Queensland Ambulance Service Clinical Protocol Manual Drug Therapy protocols Ultravist Drug information Guide And many more!!!!!!!