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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

General Treatment of Anaphylaxis


E.M. Dadi Suyoko Sp A(K) Division of Allergy Immunology Dept, of Child Health Faculty of Medicine University of Indonesia

Introduction

Definition

Anaphylaxis,Consequencies of IgE mediated release of potent biologically active substances from mast cell and basophil, upon a given target organ Anaphylactoid clinically indistinguishable but do not involve antigen- spesific IgE

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

target organ, sites distant from initial antigen presentation. Systemic anaphylaxis is the most urgent and potentially serious

Introduction
The potentially lethal : acute upper respiratory obstruction, bronchospasm, shock with vascular collapse. Successful management

Require: recognition of symptoms, aggressive therapeutic intervention, identification of precipitating factors and prevention of future episodes.

Data of incidence of anaphylaxis is still limited


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Anaphylaxis occurs in all age groups but is more common in adults, and older children. The incidence of anaphylaxis in children is unknown not a reportable condition. Combining data from several studies average age of anaphylaxis, 9 years.

Atopics are greater risk of experincing anaphylaxis? Still unclear !

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

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 cell mediators may be useful; serum tryptase, urinary histamine and plasma histamine.

Pathophysiology of Anaphylaxis

IgE-mediated anaphylaxis From re-exposure to the antigen, there is massive release of potent biochemical mediators from mast cells and basophils due to bridging of antigen specific IgE molecules located on the cell surface. Early reaction abruptly Histamine. Late reaction inflammatory mediators.

Pathophysiology of Anaphylaxis

Immune complex complement mediated anaphylaxis


Can be seen in transfusion reaction

Anaphilaxis due to presumptive abnormalities of arachidonic acid metabolism


Anaphylaxis reactions due to aspirin Occur in 1 % of general population

Anaphylaxis associated with direct mast cell degranulating agents


example: opiate, curariform agent,dextran, pentamide, radiocontrast media Contrast with igE mediated mechanism, can be happened in initial exposure to such agents

Anaphylaxis associated with physical stimuli


Cold induced urticaria can be life threatened if happened in a large surface area of the skin Cholinergic urticaria Exercise induced anaphylaxis elevation of plasma histamine levels and ultra structural evidence of mast cell degranulation

Common causes of anaphylaxis in children


Food : peanuts, milk, eggs, fish, shellfish, grains. Drugs : penicillins, cephaloceporins, sulfonamides, non steroidal anti inflammatory agents, opiats. Hymenoptera venom.

Latex. Vaccinations: tetanus, measles, mumps, influenza Miscellaneous : radiocontrast media, gammaglobulin, blood products, cold temperature

Clinical Presentation

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

cutaneous warmth, flushing, pruritus, urticaria or/and angioedema. airway: rhinorrhea, nasal congestion, sneezing, nasal / ocular pruritus. Angioedema may be associated in severe cases respiratory arrest. airway: bronchoconstrition, airway oedema.

Upper

Lower

Clinical Presentation

Gastrointestinal: abdominal pain, nausea, vomiting, and diarrhea, occasionally frank rectal bleeding. Cardiovascular: cardiac arrhytmia, chest pain; hypotension and shock the most feared complication of anaphylaxis. Fatalities : United States; approximately 1500 deaths, most commonly caused by penicillin, Hymenoptera stings, and food allergy.

Symptoms

Treatment
Resuscitation ABC rule

Cardiac and/or respiratory arrest Volume Shock Cyanosis O2 Epinephrine (1:1000) 0.3-1 ML

RR , Tachycardia Dyspnea
G.I Symptoms

Glucocorticosteroide 100mg Theophylline 0.24 g i.v

Antihistamines i.v Urticaria Flush Stop Antigen-(eliciting agent)! i.v catheter I II III IV

Diagnosis

Diagnosis of systemic anaphylaxis is established on clinical grounds, and is usually straightforward.

Signs and symptoms of : upper and lower respiratory tract, cardiovascular and gastrointestinal tract.
Doubt/not sure about the diagnosis treat as an anaphylaxis, dont delay.

Anaphylaxis management

1. Adrenaline, 1 : 1000, 0,3-0,5 ml subcutaneously / intramuscularly. Children 0,01 ml/kg bw max 0,3 ml. Usually a single injection may be sufficient, but if necessary repeated after 20 minutes. The pivotal role in therapy. 2. Oxygenation,maintenance of airway. 3. H1 and H2 antihistamine. 4. Corticosteroids.

5. Inhaled beta-adrenergic agonist/aminophyllin. 6. Fluids Establish intravenous volume replacement. 7. For refractory hypotension intravenous dopamine. 8. Intubation if necessary.

Prevention/Prophylaxis

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

Medical history to suspected antigens ( especially a parenteral medication ). Careful follow-up. Referral to an allergist-immunologist, should be made in most cases, for definitive diagnostic testing and treatment.

Prophylaxis .
Observation of the patient in the first minute after parenteral drug ( 20 -30 minutes ) administration is the basis of prophylaxis General rule : The more severe the anaphylactic symptoms to be expected the sooner they will become manifest !

Prophylaxis

Patient with previous immediate-type reactions to radiocontrast media significant risk for anaphylaxis on reexposure reduced by pre-treatment with corticosteroids, H1 antagonist & ephedrine/adrenaline.

Latex anaphylaxis the process appears to represent IgE-mediated hypersensitivity to the natural latex protein use non latex surgical & examination gloves

..Prophylaxis

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

Hymenoptera anaphylaxis use dark-colored clothes to diminish of sting

Food-associated anaphylaxis, cold, inhalant, exercise avoidance One or more episodes without a defined a etiology are described idiophatic anaphylaxis

.. Prevention

A number of patients require maintenance therapy 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 adrenergic blocking drugs associated risk of severe or refractory anaphylaxis

Desensitization

Acute desensitization to a drug should be considered in children who have allergy to a medication and no acceptable alternate treatment is available.

Rapid desensitization render mast cell unresponsive ; the exact immunologic mechanism is unknown.
Desensitization can be performed either by the oral or intravenous route.

Desensitization

First, the amount of drug the patient tolerated during skin testing, determines a safe initial dose for desensitization, which generally translate to 1/10.000 of the full therapeutic dose.

Second, doubling the dose every 15 minutes until the recommended dose reached.
Rapid desensitization should be performed only by physician experience in the procedure, in a hospital setting, with intravenous access and necessary medication.

..Prevention

Patients with radiocontrast sensitivity :

1. Use of low osmolarity contrast media 2. Prednisone, 1-2 mg/kg bw, p.o. 13, 7, and 1 hour before the procedure. 3. Dypenhydramine, 1-2 mg/kg bw, p.o. 1 hour before the procedure. 4. Albuterol, 1 hour before the procedure. 5. Have emergency therapy available.

Prevention

Drug allergy : Children commonly labeled as

being allergic to various medications thorough allergy evaluation determine truly at risk. The ideal time to evaluate drug allergy in children is when they are well and not in acute need of treatment. To prove the savety of drugs to the parents, and the referring physician, an oral chalenge should be taken. Desensitization can be used in situations where there is no substitution.

Prognosis

The prognosis after an anaphylaxis attack is contingent upon early recognation & prompt institution of appropriate therapy route of drug administration, sensitivity of the recipient & the duration of the latent period provide

Conclusion

Anaphylaxis is a life threatening multi organ system reaction. Cutaneous, respiratory, cardiovasculair,and GI tract system, are the most commonly occuring. The pivotal treatment of acute anaphylaxis is ephinephrine.

H1, H2 antagonist, systemic corticosteroids, and bronchodilators are secondary medications to be given after ephinephrine has been administered.

Conclusion

Of fatal anaphylaxis, 50 % occurs within the first hour. The most important risk factor for a fatal outcome is the delay of administration of epinephrine. Of patients with anaphylaxis, 5% to 20% have biphasic anaphylaxis, a late phase, usually occuring 4 to 6 hours after acute reaction.

Conclusion

Patients with anaphylaxis need a thorough, comprehensive allergy-immunology evaluation to diagnose the spesific etiology. Succesful avoidance strategies and education remain the mainstay of management.