Anafilaksis revisi 2007

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Curriculum Vitae-Daftar Riwayat Hidup Singkat Dr. E.M Dadi Suyoko Spa(K). Konsultan Allergi Immunologi anak  Tamat dokter umum Fakultas Kedokteran Universitas Indonesia (FKUI) tahun 1970. Staf pengajar bagian Ilmu Kesehatan Anak FKUI tahun 1971-sekarang. Dokter spesialis anak FKUI tahun 1976. Staf pengajar FKUI yang ditempatkan di RSU Tangerang tahun 1977-sekarang. Staf sub-bagian Alergi Immunologi IKA FKUI tahun 1986-sekarang. Dokter spesialis anak Konsultan Alergi Immunologi tahun1991. Mengikuti berbagai kegiatan dalam bidang ilmu kesehatan anak umumnya dan Alergi immunologi pada khususnya baik di dalam maupun di luar

Transcript of Anafilaksis revisi 2007

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Curriculum Vitae-Daftar Riwayat Hidup SingkatDr. E.M Dadi Suyoko Spa(K).

Konsultan Allergi Immunologi anak 

Tamat dokter umum Fakultas KedokteranUniversitas Indonesia (FKUI) tahun 1970.

Staf pengajar bagian Ilmu Kesehatan Anak FKUI

tahun 1971-sekarang. Dokter spesialis anak FKUI tahun 1976. Staf pengajar FKUI yang ditempatkan di RSU

Tangerang tahun 1977-sekarang. Staf sub-bagian Alergi Immunologi IKA FKUI

tahun 1986-sekarang. Dokter spesialis anak Konsultan Alergi

Immunologi tahun1991. Mengikuti berbagai kegiatan dalam bidang ilmu

kesehatan anak umumnya dan Alergi immunologipada khususnya baik di dalam maupun di luar

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General Treatment ofAnaphylaxis

E.M. Dadi Suyoko Sp A(K)Division of Allergy Immunology

Dept, of Child Health

Faculty of MedicineUniversity of Indonesia

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Introduction

Definition Anaphylaxis,Consequencies of IgE mediatedrelease of potent biologically active substancesfrom mast cell and basophil, upon a given target

organ Anaphylactoid clinically indistinguishable but donot involve antigen- spesific IgE

Systemic and local form of anaphylaxis Systemic : Happened upon more than one

target organ, sites distant from initial antigenpresentation.

Systemic anaphylaxis is the most urgent andpotentially serious

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Introduction

The potentially lethal : acute upperrespiratory obstruction, bronchospasm, shock with vascular collapse. 

Successful management

Require: recognition of symptoms, aggressive

therapeutic intervention, identification of precipitating factors and prevention of futureepisodes.

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Data of incidence of anaphylaxis is still limited

-  Anaphylaxis occurs in all age groups but is morecommon in adults, and older children.

- The incidence of anaphylaxis in children isunknown not a reportable condition.

- Combining data from several studies average

age of anaphylaxis, 9 years. -  Atopics are greater risk of experincing

anaphylaxis? Still unclear !

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Pathophysiology of generalized reactions

 A. Mechanism

1.Immunoglobulin E-mediated processes

2.Complement system activation

3.Direct mast cell degranulation ( anaphylactoid rx )

4.Abnormalities of arachidonic acid metabolism

5.Unknown

B.Mediators

Histamin

Other mediator

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Pathology

 Anatomical findings in anaphylaxis

laringeal oedema, acute bronchospasm,

hyperinflation, pulmonary oedema, parenchymal

haemorrhage and visceral congestion

Laboratory test

No pathognomonic laboratory test to establish the

diagnosis of anaphylaxis. Assays for mast cellmediators may be useful; serum tryptase, urinary

histamine and plasma histamine.

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Pathophysiology of Anaphylaxis

IgE-mediated anaphylaxis

From re-exposure to the antigen, there ismassive release of potent biochemicalmediators from mast cells and basophilsdue to bridging of antigen specific IgEmolecules located on the cell surface.

Early reaction abruptly Histamine.

Late reaction inflammatory mediators.

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Pathophysiology of Anaphylaxis

Immune complex complement mediatedanaphylaxis

- Can be seen in transfusion reaction

 Anaphilaxis due to presumptiveabnormalities of arachidonic acid

metabolism-  Anaphylaxis reactions due to aspirin

- Occur in 1 % of general population

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 Anaphylaxis associated with direct mastcell degranulating agents

- example: opiate, curariform agent,dextran, pentamide,radiocontrast media

- Contrast with igE mediated mechanism, can behappened in initial exposure to such agents

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 Anaphylaxis associated with physicalstimuli

- Cold induced urticaria

can be life threatened if happened in a large surfacearea of the skin

- Cholinergic urticaria

- Exercise induced anaphylaxis

elevation of plasma histamine levels and ultra structuralevidence of mast cell degranulation

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Common causes of anaphylaxis in children

Food : peanuts, milk, eggs, fish, shellfish, grains.

Drugs : penicillins, cephaloceporins,sulfonamides, non steroidal anti inflammatoryagents, opiats.

Hymenoptera venom.

Latex.

 Vaccinations: tetanus, measles, mumps, influenza Miscellaneous : radiocontrast media,

gammaglobulin, blood products, cold temperature

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Clinical Presentation

Symptoms may range from mild to severe,differ from case to case.

Skin: cutaneous warmth, flushing,pruritus, urticaria or/and angioedema.

Upper airway: rhinorrhea, nasalcongestion, sneezing, nasal / ocular

pruritus. Angioedema may be associatedin severe cases respiratory arrest.

Lower airway: bronchoconstrition,

airway oedema.

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Clinical Presentation

Gastrointestinal: abdominal pain, nausea,vomiting, and diarrhea, occasionally frank rectal bleeding.

Cardiovascular: cardiac arrhytmia, chest pain;hypotension and shock the most fearedcomplication of anaphylaxis.

Fatalities : United States; approximately 1500deaths, most commonly caused by penicillin,Hymenoptera stings, and food allergy.

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Symptoms Treatment

Cardiac and/or 

respiratory arrest

Shock

Cyanosis

RR ↓, Tachycardia

Dyspnea

G.I Symptoms

Urticaria

Flush

Resuscitation

“ABC” rule 

Volume

O2

Epinephrine (1:1000) 0.3-1 ML

Glucocorticosteroide 100mg 

Theophylline 0.24 g i.v 

Antihistamines i.v 

Stop Antigen-(eliciting agent)! i.v catheter  

I II III IV 

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Diagnosis

Diagnosis of systemic anaphylaxis is establishedon clinical grounds, and is usuallystraightforward.

Signs and symptoms of : upper and lowerrespiratory tract, cardiovascular andgastrointestinal tract.

Doubt/not sure about the diagnosis treat asan anaphylaxis, don’t delay. 

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 Anaphylaxis management

1. Adrenaline, 1 : 1000, 0,3-0,5 mlsubcutaneously / intramuscularly.Children 0,01 ml/kg bw max 0,3 ml.

Usually a single injection may besufficient, but if necessary repeated after20 minutes. The pivotal role in therapy.

2. Oxygenation,maintenance of airway.

3. H1 and H2 antihistamine.4. Corticosteroids.

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  5. Inhaled beta-adrenergicagonist/aminophyllin.

6. Fluids Establish intravenous

volume replacement.

7. For refractory hypotension  

intravenous dopamine.

8. Intubation if necessary.

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Prevention/Prophylaxis

Prevention of future episodes is a key componentof long-term management.

Medical history to suspected antigens ( especially a

parenteral medication ).

Careful follow-up.

Referral to an allergist-immunologist, should be made inmost cases, for definitive diagnostic testing andtreatment.

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Prophylaxis ……. 

Observation of the patient in the firstminute after parenteral drug ( 20 -30minutes ) administration is the basis of 

prophylaxis

General rule : The more severe theanaphylactic symptoms to be expected the

sooner they will become manifest !

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…Prophylaxis 

Patient with previous immediate-typereactions to radiocontrast media  significant risk for anaphylaxis on re-

exposure reduced by pre-treatmentwith corticosteroids, H1 antagonist & ephedrine/adrenaline.

Latex anaphylaxis the process appearsto represent IgE-mediated hypersensitivityto the natural latex protein use non

latex surgical & examination gloves

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…..Prophylaxis 

Seminal plasma anaphylaxis an unusual cause avoidance of contact with ejaculate  immunotherapy facilitates & accelerates theinduction of tolerance

Hymenoptera anaphylaxis use dark-coloredclothes to diminish of sting

Food-associated anaphylaxis, cold, inhalant,exercise avoidance

One or more episodes without a defined aetiology are described idiophatic anaphylaxis

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….. Prevention 

 A number of patients require maintenancetherapy with H1 and H2 antagonist in some

cases daily or alternate-day corticosteroids to

control recurrent life threatening episodes

Patients as well as others at increased risk of anaphylaxis should avoid the use of ß-adrenergic blocking drugs associated risk of severe or refractory anaphylaxis 

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Desensitization

 Acute desensitization to a drug should beconsidered in children who have allergy to amedication and no acceptable alternate treatmentis available.

Rapid desensitization render mast cell

unresponsive ; the exact immunologic mechanismis unknown.

Desensitization can be performed either by theoral or intravenous route.

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……Desensitization 

First, the amount of drug the patient toleratedduring skin testing, determines a safe initial dosefor desensitization, which generally translate to1/10.000 of the full therapeutic dose.

Second, doubling the dose every 15 minutes untilthe recommended dose reached.

Rapid desensitization should be performed onlyby physician experience in the procedure, in ahospital setting, with intravenous access andnecessary medication.

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…..Prevention 

Patients with radiocontrast sensitivity :

1. Use of low osmolarity contrast media

2. Prednisone, 1-2 mg/kg bw, p.o. 13, 7, and 1hour before the procedure.

3. Dypenhydramine, 1-2 mg/kg bw, p.o. 1 hourbefore the procedure.

4. Albuterol, 1 hour before the procedure. 5. Have emergency therapy available.

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Prevention

Drug allergy : Children commonly labeled asbeing allergic to various medications thoroughallergy evaluation determine truly at risk.

The ideal time to evaluate drug allergy in childrenis when they are well and not in acute need of treatment.

To prove the savety of drugs to the parents, andthe referring physician, an oral chalenge should

be taken.

Desensitization can be used in situations wherethere is no substitution.

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Prognosis 

The prognosis after an anaphylaxis attack is contingent upon early recognation & prompt institution of appropriate therapy

route of drug administration, sensitivityof the recipient & the duration of thelatent period provide

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Conclusion

 Anaphylaxis is a life threatening multi organsystem reaction.

Cutaneous, respiratory, cardiovasculair,and GI

tract system, are the most commonly occuring.

The pivotal treatment of acute anaphylaxis isephinephrine.

H1, H2 antagonist, systemic corticosteroids, andbronchodilators are secondary medications to begiven after ephinephrine has been administered.

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Conclusion

Of fatal anaphylaxis, 50 % occurs within the firsthour.

The most important risk factor for a fatal outcomeis the delay of administration of epinephrine.

Of patients with anaphylaxis, 5% to 20% havebiphasic anaphylaxis, a late phase, usuallyoccuring 4 to 6 hours after acute reaction.

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Conclusion

Patients with anaphylaxis need a thorough,comprehensive allergy-immunology evaluation todiagnose the spesific etiology.

Succesful avoidance strategies and educationremain the mainstay of management.