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Anaphylaxis

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Anaphylaxis
Classification and external resources

A rash on the back of a person with anaphylaxis. ICD-10 DiseasesDB eMedicine#$%&' MeSH med(%#" )***!*! !".#

Anaphylaxis is an acute multi+system severe type , hypersensitivity reaction. he term comes from the -reek words ./ ana 0against1 and 2345678 phylaxis 0protection1.9%: )ue in part to the variety of definitions, between %; and %&; of the population of the <nited =tates can be considered >at risk> for having an anaphylactic reaction if they are exposed to one or more allergens. ?f those people who actually experience anaphylaxis, up to %; may die as a result.9#: Anaphylaxis results in approximately %,&** deaths per year in the <.=.9':9@: ,n Angland, mortality rates for anaphylaxis have been reported as up to *.*& per %**,*** population, or around %*+#* a year.9&: Anaphylactic reactions reBuiring hospital treatment appear to be increasing, with authorities in Angland reporting a threefold increase between %$$@ and #**@.9C: Dased on the pathophysiology, anaphylaxis can be divided into >true anaphylaxis> and >pseudo+anaphylaxis> or >anaphylactoid reaction.> he symptoms, treatment, and risk of death are the sameE however, >true> anaphylaxis is caused by degranulation of mast cells or basophils mediated by immunoglobulin A 0,gA1, and pseudo+anaphylaxis occurs without ,gA mediation.9!:

[edit] Classification
[edit] Biphasic anaphylaxis

Diphasic anaphylaxis is the recurrence of symptoms within !# hours with no further exposure to the allergen. ,t occurs in between %F#*; of cases depending on the study examined.9": ,t is managed in the same manner as anaphylaxis.9$:

[edit] Anaphylactic shock


Anaphylactic shock is anaphylaxis associated with systemic vasodilation which results in low blood pressure. ,t is also associated with severe bronchoconstriction to the point where the individual is unable to breathe.

[edit] Pse doanaphylaxis


Gain article: Hseudoanaphylaxis he presentation and treatment of pseudoanaphylaxis is similar to that of anaphylaxis. ,t however does not involve an allergic reaction but is due to direct mast cell degranulation. 9%*: his can result from morphine, radiocontrast, aspirin and muscle relaxants.9%%:

[edit] Acti!e anaphylaxis


Active anaphylaxis is what is naturally observed. wo weeks or so after an animal, including humans, is exposed to certain allergens, active anaphylaxis 0which is simply called >anaphylaxis>1 would be elicited upon exposure to the same allergens.

[edit] Passi!e anaphylaxis


Hassive anaphylaxis is induced in native animals which receive transfer of the serum experimentally from sensitiIed animals with certain allergens. Hassive anaphylaxis would be provoked in the recipient animals after exposure to the same allergens.9%#:

[edit] Si"ns and sy#pto#s


Anaphylaxis can present with many different symptoms due to the systemic effects of histamine release.9%': hese usually develop over minutes to hours.9$: he most common areas affected include: skin 0"*; to $*;1, respiratory 0!*;1, gastrointestinal 0'*; to @&;1, heart and vasculature 0%*; to @&;1, and central nervous system 0%*; to %&;1.9$:

[edit] Skin
=kin involvement may include generaliIed hives, itchiness, flushing, and swelling of the lips, tongue or throat.9%@:

[edit] $espi%ato%y

Jespiratory symptoms may include shortness of breath, wheeIes or stridor, and low oxygen.9%@:

[edit] &ast%ointestinal
-astrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomiting.
9%@:

[edit] Ca%dio!asc la%


)ue to the presence of histamine releasing cells in the heart coronary artery spasm may occur with subseBuent myocardial infarction or dysrhythmia.9$:

[edit] 'e%!o s syste#


A drop in blood pressure may result in a feeling of lightheadedness and loss of consciousness. here may be a loss of bladder control and muscle tone,9%@: and a feeling of anxiety and >impending doom>.9%&:

[edit] Ca ses
Anaphylaxis can occur in response to any allergen. Kommon triggers include insect bites or stings, foods, medication and latex rubber.9%C:

[edit] (ood
Gany foods can trigger anaphylaxis. he most common are peanut, tree nuts, shellfish, fish, milk, and egg. =evere cases are usually the result of ingesting the allergen.9$:

[edit] Medication
Any medication may potentially trigger anaphylaxis. he most common to do so include antibiotics 0L+lactam antibiotics in particular1, aspirin, ibuprofen, and other analgesics.9$: =ome drugs 0polymyxin, morphine, x+ray contrast and others1 may cause an >anaphylactoid> reaction 0anaphylactic+like reaction1 on the first exposure.9%!: his is usually due to a toxic reaction, rather than the immune system mechanism that occurs with >true> anaphylaxis. he symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. =ome vaccinations are also known to cause >anaphylactoid> reactions.9%":

[edit] )eno#
Menom from stinging or biting insects such as Nymenoptera or Nemiptera may induce anaphylaxis in susceptible people.9$:

[edit] Pathophysiolo"y
Anaphylaxis is a severe, whole+body allergic reaction. After an initial exposure >sensitiIing dose> to a substance like bee sting toxin, the personOs immune system becomes sensitiIed to that allergen. ?n a subseBuent exposure >shocking dose>, an allergic reaction occurs. his reaction is sudden, severe, and involves the whole body. Klassified as a type , hypersensitivity, anaphylaxis is triggered when an antigen binds to ,gA antibodies on mast cells based in connective tissue throughout the body, which leads to degranulation of the mast cells 0the release of inflammatory mediators1.9%$: hese immune mediators cause many symptoms, including common symptoms of allergic reactions, such as itching, hives, and swelling. Anaphylactic shock is an allergic reaction to an antigen that causes circulatory collapse and suffocation due to bronchial and tracheal swelling. )ifferent classes of antibodies are produced by D cells to bind and destroy substances that the immune system has identified as potentially dangerous pathogens. Aach D cell produces thousands of identical antibodies that can attack a single, small part of a pathogen. ,n susceptible individuals, antibodies may be produced against innocuous antigens or allergens, such as components of common foods or plants. ?ne class, the ,gA antibodies, can trigger anaphylaxis. Hroduction of ,gA antibodies may persist for months, even in the complete absence of the allergen. hese ,gA antibodies associate with a receptor on the surface of mast cells. ,f the antibody binds to its specific antigen, then the antibody triggers degranulation of the mast cell. Gast cells become the maPor effector cells for immediate hypersensitivity and chronic allergic reactions.9#*: Gast cells are large cells found in particularly high concentrations in vasculariIed connective tissues Pust beneath epithelial surfaces, including the submucosal tissues of the gastrointestinal and respiratory tracts, and the dermis that lies Pust below the surface of the skin.9%$: hey contain large granules that store a variety of mediator molecules including the vasoactive amine, histamine. Nistamine causes dilation of local blood vessels and smooth+muscle contraction. ?ther molecules in the mast cell granules include lipid inflammatory mediators such as prostaglandin )#Q and leukotriene K@ as well as tumor necrosis factor+5 0 RF+51, a cytokine.9%$: he importance of RF+5 is most noted in the activation of the endothelium. RF+5, the prototype of the RF family cytokines, can induce endothelial cells to present A+selectin and ,KAG+%, both of which are cell adhesion molecules 0KAG1 that mediate the Sroll and stickT mechanism of leukocyte extravasation, termed diapedesis. While this process is essential for the recruit of leukocytes to a localiIed area during an inflammatory response, it can be catastrophic in cases of systemic infection. Hoint in case, the presence of said infection in the bloodstream, or sepsis, is accompanied by the release of RF+5 by macrophages in liver, spleen, and other systemic sites. he systemic release of RF+5 causes vasodilatation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually to shock.9%$:

RF+5, along with the other aforementioned mast cell granule contents become exocytosed upon activation of the mast cell. Activation is achieved only when ,gA, bound to the high+affinity FcU receptors 0FcUJ%1, are cross+linked by multivalent antigen. he FcUJ% is a tetrameric receptor composed of a single 5 chain, responsible for binding the ,gA, associated with a single L chain and a disulfide linked homodimer of V chains that initiate the cell signal pathway.9#%: ?nce the FcUJ% are aggregated by the cross+linking process, the immunoreceptor tryrosine+based activation motifs 0, AGs1 in both the L and V chains are phosphorylated by WXR, a protein tryrosine kinase 0H Y1 belonging to the =rc family. he , AG domain is simply conserved seBuence motif generally composed of two XZZW(, seBuences separated by about six to nine amino acids, where X is tyrosine, W is leucine, , isoleucine and Z any amino acid.9%$: heir phosphorylation in the L and V chains provide high+affinity docking sites for the =N# domains of additional WXR and the =XY 0spleen tyrosine kinasse1, respectively.9##: hese =N# domains 0=rc homology # domian1 are found in a numerous cell+signaling proteins and bind to phosphotyrosine through a very specific seBuence.9%$: As the signal continues to propagate through the pathway, the membrane bound molecule, named linker for activation of cells 0WA 1, is phosphoyraleted by the WXR and =XY and acts as a scaffold protein, organiIing other molecules that complete the degranulation of mast cells, as well as promote further cytokine production.9#': he most notable of these WA affected molecules is Hhospholipase K 0HWK1. As in many cell signaling pathways HWK hydrolyIes the phosphodiester bond in phosphoatidylinositol+@,&+bisphosphate 9H,0@,&1HQQ#: to yield diacylglycerol 0)A-1 and inositol+%,@,&+triphosphate 0,HQQ'1Q. A well+characteriIed second messenger, ,HQ'Q, signals the release of calcium from the endoplasmic reticulum. he influx of cytosolic Ka#[ and phosphoatidylserine further active Hhosphokinase K 0HYK1 bound to )A-. ogether, it is the cytosolic Ka#[ and HYK signal the degranulation of the mast cell.@ Although less well mapped, similarly prevailing cell signaling molecules, such as Jas, a monomeric - protein, =?= 0son of sevenless homologue1 and GAHY 0mitogen+activated protein kinase1 lead to the upregulation of cytokines and the previously mentioned eicosanoids, prostaglandin )#Q and leukotriene K@.9##: While this cell single pathway is sufficient to induce degranulation, it is not the only effective mechanism. =tudies with WXY deficient mice have shown that degranulation is still inducible.9#': KonseBuently, several alternative pathways leading to mast cell degranulation have been mapped. he first of which, dubbed the ScomplementaryT pathway, determined that the crosstalk between WXY and another =rc family H Y, called FXR, is an essential interaction to degranulation, along with the preferential activity of Hhosphoatidylinositol '+kinase 0H,+'Y1 over HWK. =tudies have also elucidated subseBuent pathways that utiliIe the integration of -+protein+coupled receptors to mediate the degranulation and cytokine production mechanism of activated mast cells.9##: ,gA binding to FcUJ% in the absence of a specific antigen still induces the up+regulation of FcUJ% surface expression in mast cells through autocrine signaling of cytokines.9#@: Nowever, not all ,gA are eBually capable of inducing such as secretion. herefore, researchers have divided all invariant ,gAs into two maPor categories: highly

cytokinergic0NK1, where the production and secretion of various cytokines and other activation events including degranulation is inducible, and poorly cytokinergic 0HK1 in which no autocrine signaling is observed. he former, NK ,gA, brings forward a reaction in which cytokines are exocytosed and act as autocrine and paracrine signaling molecules. As such, mast cells with bound NK ,gA attract other mast cells even in the absence of antigen crosslinking.9#%: While the exact structural features that account for the function differences between NK and HK ,gA has yet to be determined their effects are thought to be the result of intracellular cell signaling.9#@: ,gA binding to FcUJ% leads to a greater stability of the mast cell and increased production of surface receptors. he newly expressed FcUJ% then aggregate on the surface, independent of antigen binding. he cell signaling pathway then initiates and appears to involve components used in the alternative mechanisms. Gast cell migration is dependent on soluble factors such as adenosine, leukotriene DQ@ and other chemokines, whose secretion is dependent upon the activity of WXR and =XY. he degranulation of mast cells in the absence of antigen, can then be initiated by -+protein+couple receptors 0-HKJ1 stimulated by soluble factors agonists and completed by downstream activity of H,'Y.9#%:

[edit] Dia"nosis
Anaphylaxis is diagnosed with high likelihood based on clinical criteria. hese criteria are fulfilled when any one of the following three is true:9%@: %. =ymptom onset within minutes to several hours of allergen exposure with involvement of the skin or mucosal tissue and any of the following: hives, itchiness, or swelling of the airwayE plus either respiratory difficulty or a low blood pressure. #. Any two or more of the following symptoms within minutes to several hours of allergen exposure: a. ,nvolvement of the skin or mucosa b. Jespiratory difficulties c. Wow blood pressure d. -astrointestinal symptoms '. Wow blood pressure within minutes to several hours after exposure to known allergen Apart from its clinical features, blood tests for tryptase 0released from mast cells1 might be useful in diagnosing anaphylaxis.9#&: Allergy testing may help in determining what triggered the anaphylaxis. ,n this setting, skin allergy testing 0with or without patch testing1 or JA= blood tests can sometimes identify the cause.

[edit] P%e!ention
,mmunotherapy with Nymenoptera venoms is effective against allergies to bees, wasps, hornets, yellow Packets, white faced hornets, and fire ants.9#C:

he greatest success with prevention of anaphylaxis has been the use of allergy inPections to prevent recurrence of sting allergy. he risk to an individual from a particular species of insect depends on complex interactions between likelihood of human contact, insect aggression, efficiency of the venom delivery apparatus, and venom allergenicity. Menom immunotherapy reduces risk of systemic reactions below ';.9citation needed: ?ne simple method of venom extraction has been electrical stimulation to obtain venom, instead of dissecting the venom sac. A potential vaccine has been developed to prevent anaphylaxis due to peanut and tree nut allergies if they are exposed to a small amount of peanuts or nuts. Although it shows some promise to reduce the likelihood of anaphylaxis in affected individuals, the vaccine has not yet been approved for marketing and distribution.9#!: )esensitiIation techniBues are also being studied for peanut allergies.9#":

[edit] Mana"e#ent
Anaphylaxis is a medical emergency which may reBuire resuscitation measures such as airway management, supplemental oxygen, large volumes of intravenous fluids, and close monitoring.9$: Administration of epinephrine is the treatment of choice with antihistamines and steroids often used as adPuncts. A period of in hospital observation for between C and #@ hours is recommended for people once they have returned to normal due to concerns of biphasic anaphylaxis.9":9#$:

[edit] *pineph%ine
Apinephrine 0adrenaline1 is the primary treatment for anaphylaxis with no absolute contraindication to its use.9$: Apinephrine improves airway patency, improves blood pressure, and may be life+saving. he recommended dose is &** \g 0or *.& mW adrenaline inPection % in %***1 given intramuscularly.9'*: A dose of '** \g 0*.' mW adrenaline inPection % in %***1 may be appropriate for immediate self+administration.9'*: he dose is repeated if necessary at &+minute intervals according to blood pressure, pulse and respiratory function.9'*: ,f necessary, it can also be given intravenously using dilute solution.9'*: Apinephrine autoinPector is provided for self+prescription.

[edit] Int%a!eno s fl ids


Anaphylaxis can lead to massive losses of intravascular fluids. hus large amounts of intravenous fluids maybe reBuired.9#$:

[edit] Ad+ ncts


Antihistamines

Antihistamines while commonly used and assumed effective based on theoretical reasoning are poorly supported by evidence. A #**! Kochrane review did not find any good Buality studies upon which to base recommendations.9'%: =teroids Korticosteroids, are unlikely to make a difference in the current episode of anaphylaxis, but may be used in the hope of decreasing the risk of biphasic anaphylaxis. Now effective they are at achieving this, however, is uncertain.9":

[edit] P%epa%edness
Heople prone to anaphylaxis are advised to have an >allergy action plan>, and parents are advised to inform schools, etc., of their childrenOs allergies and what to do in case of an anaphylactic emergency.9'#: he action plan usually includes use of epinephrine auto+ inPectors, the recommendation to wear a medical alert bracelet, and counseling on avoidance of triggers.9'':. ,mmunotherapy is available for certain triggers to prevent future episodes of anaphylaxis. A multiFyear course of subcutaneous desensitiIation has been found effective against stinging insects while oral desensitiIation is effective for many foods.9$:

[edit] *pide#iolo"y
he rate of anaphylaxis appears to be increasing. he rate in the %$"*s was #% per %**,*** per year while in the %$$*s it had increased to &* per %**,*** per year.9$: he risk is greatest in young people and females. he trigger in the young is usually food related while in adults, medications and insect venoms are more common causes.9$: )ue in part to the variety of definitions, between %; and %&; of the population of the <nited =tates can be considered >at risk> for having an anaphylactic reaction if they are exposed to one or more allergens, especially penicillin and insect stings. Gost of these people successfully avoid their allergens and will never experience anaphylaxis. ?f those people who actually experience anaphylaxis, up to %; may die as a result.9#: Anaphylaxis results in approximately %,&** deaths per year in the <.=.9': 0one out of every %,C** of the #.@ million deaths from all causes each year in the <.=.E9@:1. he most common presentation includes sudden cardiovascular collapse 0""; of reported cases of severe anaphylaxis1. ,n Angland, mortality rates for anaphylaxis have been reported as up to *.*& per %**,*** population, or around %*+#* a year.9&: Anaphylactic reactions reBuiring hospital treatment appear to be increasing, with authorities in Angland reporting a threefold increase between %$$@ and #**@.9'@:

[edit] $efe%ences
%. , >anaphylaxis>. merriam+webster.com. http:((www.merriam+ webster.com(dictionary(anaphylaxis. Jetrieved #**$+%%+#%.

#. ] a b Reugut A,, -hatak A , Giller JW 0January #**%1. >Anaphylaxis in the <nited =tates: an investigation into its epidemiology>. Arch. Intern. Med. 1-1 0%1: %&F#%. doi:%*.%**%(archinte.%C%.%.%&. HG,) %%%@CC$@. http:((archinte.ama+ assn.org(cgi(content(full(%C%(%(%&. '. ] a b Gatasar GJ, Reugut A, 0January #**'1. >Apidemiology of anaphylaxis in the <nited =tates>. Curr Allergy Asthma Rep . 0%1: '*F&. doi:%*.%**!(s%%""#+**'+ ***!+". HG,) %#&@#$$*. @. ] a b >)eaths(Gortality>. Rational Kenter for Nealth =tatistics. #**"+*'+'%. http:((www.cdc.gov(nchs(fastats(deaths.htm. Jetrieved #**"+*@+##. &. ] a b A Jeview of =ervices for Allergy. )epartment of Nealth. #**C. =ee sections #.C*+C' and #."C. C. , A Jeview of =ervices for Allergy. )epartment of Nealth. #**C. =ee sections #.&@+&&. !. , Wimmer ), Gistovich JJ, Yrost W= 0Rovember %!, #**&1. >Anaphylactic and Anaphylactoid Jeactions ++ Hrehospital Hathophysiology>. AG=Jesponder.com. http:((publicsafety.com(article(article.Psp^id_#%C&`site=ection_C. Jetrieved #**!+%%+#!. ". ] a b c Wieberman H 0=eptember #**&1. >Diphasic anaphylactic reactions>. Ann. Allergy Asthma Immunol. /0 0'1: #%!F#CE BuiI ##C, #&". doi:%*.%*%C(=%*"%+ %#*C0%*1C%#%!+'. HG,) %C#**"%%. $. ] a b c d e f g h i j k l =imons FA 0?ctober #**$1. >Anaphylaxis: Jecent advances in assessment and treatment>. J. Allergy Clin. Immunol. 112 0@1: C#&F'CE BuiI C'!F ". doi:%*.%*%C(P.Paci.#**$.*".*#&. HG,) %$"%&%*$. %*. , Joris, ,sabelleE GaPno, -uido 0#**@1. Cells, tissues, and disease: principles of general pathology. ?xford 9?xfordshire:: ?xford <niversity Hress. pp. &'"F&'$. ,=DR *+%$+&%@*$*+!. %%. , >John Wibbey Aurotext : aditions mbdicales et scientifiBues France : revues, mbdicales, scientifiBues, mbdecine, santb, livres + exte intbgral de lOarticle> 0H)F1. http:((www.Pohn+libbey+eurotext.fr(e+ docs(**(*@('"(C*(verscalt(MersionH)F.pdf. %#. , =ell = 0%$$%1. >,mmunopathology,> In )ulbecco J 0ed.1 Encyclopedia of Human iology, !ol. ". pp. @*%+@%', =an )iegoE Academic Hress, ,=DR *%###C!&@*. %'. , ?swalt GW, Yemp =F 0Gay #**!1. >Anaphylaxis: office management and prevention>. Immunol Allergy Clin #orth Am 13 0#1: %!!F$%, vi. doi:%*.%*%C(P.iac.#**!.*'.**@. HG,) %!@$'@$!. %@. ] a b c d e =ampson NA, GudoI+Furlong A, Kampbell JW, et al. 0February #**C1. >=econd symposium on the definition and management of anaphylaxis: summary report++=econd Rational ,nstitute of Allergy and ,nfectious )isease(Food Allergy and Anaphylaxis Retwork symposium>. J. Allergy Clin. Immunol. 113 0#1: '$%F!. doi:%*.%*%C(P.Paci.#**&.%#.%'*'. HG,) %C@C%%'$. %&. , >Anaphylaxis 0=evere Allergic Jeaction1 =ymptoms, Kauses, )iagnosis, reatment, and Hrevention on GedicineRet.com>. http:((www.medicinenet.com(anaphylaxis(page'.htm. %C. , Awan HW 0Gay %$$"1. >Anaphylaxis>. MJ .1- 0!%@#1: %@@#F&. HG,) $&!#!C*.

%!. , >Gastocytosis: Allergic Jeactions: Gerck Ganual Nome Adition>. http:((www.merck.com(mmhe(sec%C(ch%"&(ch%"&e.html. Jetrieved #**!+%%+#!. %". , Rational Advisory Kommittee on ,mmuniIation 0RAK,1 + =<HHWAGAR AJX = A AGAR GGJ MAKK,RA AR) ARAHNXWAK ,K NXHAJ=AR=, ,M, X ? A-- ?J A--+JAWA A) AR ,-AR= + KK)J Molume ## %$. ] a b c d e f Gurphy, Yenneth 0Rovember #!, #**!1. Jane$ay%s Immuno&iology 0!th ed.1. Rew Xork: -arland =cience. ,=DR *+"%&'+@%#'+!. #*. , Yitaura J, Yinoshita , Gatsumoto G, et al. 0April #**&1. >,gA+ and ,gA[Ag+ mediated mast cell migration in an autocrine(paracrine fashion>. lood 100 0"1: '###F$. doi:%*.%%"#(blood+#**@+%%+@#*&. HG,) %&C'!%'&. HGK %@C@@*C. http:((bloodPournal.hematologylibrary.org(cgi(content(full(%*&("('###. #%. ] a b c Haolini J, Jouvin GN, Yinet JH 0?ctober %$$%1. >Hhosphorylation and dephosphorylation of the high+affinity receptor for immunoglobulin A immediately after receptor engagement and disengagement>. #ature .0. 0C'@!1: "&&F". doi:%*.%*'"('&'"&&a*. HG,) %"'@$@C. ##. ] a b c -ilfillan AG, kacIyk K 0Garch #**C1. >,ntegrated signalling pathways for mast+cell activation>. #at. Re'. Immunol. - 0'1: #%"F'*. doi:%*.%*'"(nri%!"#. HG,) %C@!*##C. #'. ] a b Harravicini M, -adina G, Yovarova G, et al. 0August #**#1. >Fyn kinase initiates complementary signals reBuired for ,gA+dependent mast cell degranulation>. #at. Immunol. . 0"1: !@%F". doi:%*.%*'"(ni"%!. HG,) %#*"$&%*. #@. ] a b Yitaura J, =ong J, sai G, et al. 0?ctober #**'1. >Avidence that ,gA molecules mediate a spectrum of effects on mast cell survival and activation via aggregation of the FcepsilonJ,>. (roc. #atl. Acad. )ci. *.).A. 100 0##1: %#$%%FC. doi:%*.%*!'(pnas.%!'&&#&%**. HG,) %@&C$*#%. HGK #@*!%". http:((www.pnas.org(cgi(content(full(%**(##(%#$%%. #&. , =chwartI WD 0August #**C1. >)iagnostic value of tryptase in anaphylaxis and mastocytosis>. Immunology and allergy clinics of #orth America 1- 0'1: @&%FC'. doi:%*.%*%C(P.iac.#**C.*&.*%*. HG,) %C$'%#"". #C. , DousBuet J, Geller <J, )reborg =, et al. 0%$"!1. >,mmunotherapy with Nymenoptera venoms. Hosition paper of the Working -roup on ,mmunotherapy of the Auropean Academy of Allergy and Klinical ,mmunology>. Allergy 21 0C1: @*%F%'. doi:%*.%%%%(P.%'$"+$$$&.%$"!.tb**'&&.x. HG,) ''%*!%@. #!. , Heanut Allergy. Website of the Allergic Khild Hublishing -roup. #". , 9%: #$. ] a b >Amergency treatment of anaphylactic reactions ++ -uidelines for healthcare providers> 0H)F1. Jesuscitation Kouncil 0<Y1. January #**". http:((www.resus.org.uk(pages(reaction.pdf. Jetrieved #**"+*@+##. '*. ] a b c d e+radiography.net f Allergic Amergencies 0From DRF Website1 Wast <pdate %%(*%(%* '%. , =heikh A, en Droek M, Drown =-, =imons FA 0August #**!1. >N%+ antihistamines for the treatment of anaphylaxis: Kochrane systematic review>. Allergy -1 0"1: "'*F!. doi:%*.%%%%(P.%'$"+$$$&.#**!.*%@'&.x. HG,) %!C#**C*.

'#. , >Asthma and Allergy Foundation of America + ,nformation About Asthma, Allergies, Food Allergies and Goreg>. http:((www.aafa.org(display.cfm^ id_@`sub_"%`cont_'$#. Jetrieved #**!+%%+#!. ''. , >Anaphylaxis + AKAA,>. http:((www.acaai.org(public(advice(anaph.htm. '@. , A Jeview of =ervices for Allergy. )epartment of Nealth. #**C. =ee sections #.&@+&&.

Se!e%e Alle%"ic $eaction 4Anaphylactic Shock5


%* Kommon Allergy riggers =lideshow ake the huiI on Allergies Rasal Allergy Jelief =lideshow

Se!e%e Alle%"ic $eaction 6!e%!ie7


Anaphylaxis is a severe allergic reaction that occurs rapidly and causes a life+threatening response involving the whole body. his reaction can lead to difficulty breathing and shock ultimately leading to death. For an anaphylactic reaction to occur, you must have been exposed in the past to the substance that causes the reaction, called the antigen. his is called >sensitiIation.>

A bee sting, for example, may not cause an allergic reaction the first time. Another bee sting may produce a sudden, severe allergic reaction known as anaphylaxis or anaphylactic shock.

hese reactions usually occur within seconds to minutes of exposure. ?ccasionally, they are delayed. Xou may develop sensitivity and anaphylaxis to a substance that you have been exposed to many times in the past without a reaction, and often people donOt recall the previous exposure.

Se!e%e Alle%"ic $eaction Ca ses


An anaphylactic reaction occurs when the bodyOs immune system overreacts to an antigen, which it recogniIes as an >invader> or foreign substance.

he bodyOs white blood cells produce substances called antibodies as a reaction to that antigen. he antibodies circulate in the bloodstream and attach themselves to certain cells in the body.

o o

,n an allergic reaction, the antibody is called immunoglobulin A, or ,gA. When the antibodies come in contact with the antigen, they signal other cells to produce certain chemicals called >mediators.> Nistamine is an example of a mediator. he effects of these mediators on organs and tissues of the body cause the symptoms of the reaction.

riggers of anaphylaxis include many substances. ?nly a trace amount of the trigger may be needed to cause a severe reaction. riggers of allergic reactions, including anaphylaxis, may include: o Hrescription and over+the+counter medications 0see )rug allergy1 o Menom of stinging insects such as yellow Packets, bumble bees, honey bees, wasps, fire ants 0see Allergy: =tinging ,nsect Menom1 o Foods, especially high+protein foods + most commonly, shellfish, fish, nuts, fruit, wheat, milk, eggs, soy products 0see Food allergy1 o Food additives, such as sulfites o ransfusion of blood or blood products o Rumerous other substances such as latex 0natural rubber1 o )yes and contrast materials used during radiologic procedures or tests =ometimes the trigger of the reaction is obvious++a bee sting, or a new prescription drug. ?ften, however, the trigger is unknown.

Heople with asthma, ecIema, or hay fever are slightly more likely to have an anaphylactic reaction than people who do not have these conditions.

Se!e%e Alle%"ic $eaction Sy#pto#s


he symptoms of anaphylaxis can vary. ,n some people, the reaction begins very slowly, but in most the symptoms appear rapidly and abruptly.

he most severe and life+threatening symptoms are difficulty breathing and loss of consciousness. )ifficulty breathing is due to swelling and(or spasm in the airways 0which can include swelling of the tongue or the airways1. ,n very rare cases, breathing can stop altogether. o Woss of consciousness is due to dangerously low blood pressure, which is called >shock.> o ,n the most serious cases, the heart can stop pumping altogether. o hese events can lead to death from anaphylaxis. While some symptoms are life threatening, others are merely uncomfortable. -enerally, a reaction must involve at least two different body systems, such as skin and heart, to be considered anaphylaxis. o Skin8 Gost anaphylactic reactions involve the skin.
o

Nives, welts, or wheals 0raised bumps1: Nives can cause severe itching -eneraliIed erythema 0redness1 =welling in the face, eyelids, lips, tongue, throat, hands, and feet B%eathin"8 =welling of the surrounding tissues narrows the airways. )ifficulty breathing, wheeIing, chest tightness Koughing, hoarseness Rasal congestion, sneeIing Ca%dio!asc la%8 Dlood pressure may drop to dangerously low levels. Japid or irregular heart beat )iIIiness, faintness Woss of consciousness, collapse &ene%al ingling or sensation of warmth + ?ften the first symptom )ifficulty swallowing Rausea, vomiting )iarrhea, abdominal cramping, bloating Anxiety, fear, feeling that you are going to die Konfusion

9hen to Seek Medical Ca%e


Act Buickly if someone experiences the symptoms of an anaphylactic reaction. rue anaphylaxis is a medical emergency and reBuires immediate treatment in an emergency department of a hospital, where the person can be watched closely and life+saving treatment can be given.

,t is impossible to predict how severe the allergic reaction will be. Any person who shows symptoms of anaphylaxis must be transported to a hospital emergency department.

,f swelling develops rapidly, particularly involving the mouth or throat, and you have trouble breathing or feel diIIy, light+headed, or faint, call $%% for ambulance transport to the hospital.

While awaiting the ambulance, administer self+treatment.

*xa#s and :ests


Anaphylactic reactions are diagnosed solely on the basis of signs and symptoms.

Ro specific tests are helpful.

Xour health care provider may order tests to rule out other conditions.

Se!e%e Alle%"ic $eaction :%eat#ent Self-Ca%e at Ho#e


)o not attempt to treat severe reactions or to >wait it out> at home. -o immediately to the nearest emergency department or call an ambulance. While waiting for the ambulance, try to stay calm.

,f you can identify the cause of the reaction, prevent further exposure.

ake an antihistamine 0one to two tablets or capsules of diphenhydramine 9Denadryl:1 if you can swallow without difficulty.

,f you are wheeIing or having difficulty breathing, use an inhaled bronchodilator such as albuterol 0Hroventil1 or epinephrine 0Hrimatene Gist1 if one is available. hese inhaled medications dilate the airway.

,f you are feeling light+headed or faint, lie down and raise your legs higher than your head to help blood flow to your brain.

,f you have been given an epinephrine kit, inPect yourself as you have been instructed or have someone else perform the inPection. he kit provides a premeasured dose of epinephrine, a prescription drug that rapidly reverses the most serious symptoms of anaphylaxis 0see Follow+up1.

Dystanders should administer KHJ to a person who becomes unconscious and stops breathing or does not have a pulse.

,f at all possible, you or your companions should be prepared to tell medical personnel what medications you take and your allergy history.

Medical :%eat#ent

he first priority in the emergency department is to protect the airway 0breathing1 and maintain adeBuate blood pressure. he emergency team will make sure that your airway is open and that you are getting adeBuate oxygen.

?xygen may be given through tubes into the nose or by face mask.

,n severe respiratory distress, mechanical ventilation may be reBuired. ,n this situation, a tube is placed via the mouth into the air passages to keep the airway open. he tube is connected to a ventilator 0 providing oxygen directly into the lung 1

,n rare cases, a simple surgery is performed to open an airway.

,f blood pressure is dangerously low, medication to increase blood pressure will be given.

An intravenous 0,M1 catheter may be inserted

his is used to give saline solution to help boost blood pressure.

he ,M line may also be used to give medication.

Xou may need to be admitted to the hospital for further monitoring and treatment.

Medications

Apinephrine + -iven in severe allergic reactions, epinephrine is extremely effective and fast+actingE it acts by constricting blood vessels, which increases blood pressure, and widening the airway. Apinephrine is given by inPection into the muscle, through an ,M line, or by inPection under the skin. N%+receptor blockers(antihistamines + <sually diphenhydramine 0Denadryl1E these drugs do not stop the reaction but relieve some of the symptoms. hey may be given by ,M, by inPection in the muscle, or by mouth ,nhaled beta+agonists 0albuterol1 + <sed to treat bronchospasm 0spasms in the lung1 and dilate the airwaysE inhaled N#+receptor blockers + <sually cimetidine 0 agamet1E given by ,M or by mouth

Korticosteroids 0examples are prednisone, =olu+Gedrol1 + hese drugs help decrease the severity and recurrence of symptomsE may be given orally, inPected in muscle, or by ,M line ,f low blood pressure does not improve, additional medications, such as dopamine, may be given.

'ext Steps (ollo7- p


Xou will usually be observed for at least six hours after the beginning of the reaction. ?ccasionally, a reaction will seem to get better and then recur, and even worsen, in a few hours. =ometimes the severity of the reaction will reBuire admission to the hospital. <pon leaving the hospital emergency department, you should immediately obtain the medication prescribed for you. Xou should carry these at all times to prevent another reaction or lessen its severity.

he epinephrine kit 0known as ApiHen or Ana+Yit1 should be kept with you at all times in case you are exposed to the antigen that caused the first reaction.

he kit contains a premeasured dose of epinephrine in an easy+to+use syringe. As soon as an exposure occurs, you immediately inPect the epinephrine into your thigh muscle. his is extremely effective and fast+acting.

Anyone who has experienced an anaphylactic reaction should carry one of these kits after consulting with your physician.

Gedical attention is always reBuired right away, even if you have treated yourself with epinephrine.

P%e!ention
=trictly avoid contact with the substance 0allergen1 that was the trigger.

,f the trigger is a food, you must learn to read food labels carefully. When ordering foods at restaurants or eating in friendsO homes, ask about ingredients. De aware of ingredients that may contain triggers. Avoid eating foods if you canOt confirm their ingredients. ,f your reactions are severe, contact the manufacturer to

assure that the triggering food was not processed in the same area as a food to which you are allergic.

,f the trigger is a drug, inform all health care providers of the reaction. De prepared to report what happened when you had the reaction. Wear a tag 0necklace or bracelet1 that identifies the allergy.

,nsect stings are more difficult to avoid. Wear long+sleeved clothing outdoors. Avoid bright colors and perfumes that attract stinging insects. <se caution with sweetened beverages outdoors, such as uncovered soft drinks.

Heople who are likely to be re+exposed to 0or are unable to avoid1 an allergen that has caused them a severe anaphylactic reaction in the past should see an allergist for desensitiIation. =kin testing may be reBuired to help identify the allergen.

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