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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.