SYOK ANAFILAKTIK

SYOK
Hipovolemik
Sindrom klinis akibat kegagalan
sistem sirkulasi dalam
mencukupi kebutuhan nutrien
dan oksigen (pasokan maupun
utilisasinya) metabolisme
Distributif
Kardiogenik
seluler jaringan tubuh  (increased vascular capacitance
defisiensi akut oksigen di with normal circulating volume)
tingkat seluler
Distributif
(PPM IDAI)
Syok Distibutif
 Dapat terjadi akibat berbagai sebab : syok neurogenik, anafilaksis, sepsis

 Penurunan resistensi vaskular akan berakibat penumpukan darah dalam

pembuluh darah perifer dan penurunan tekanan vena sentral (venous
pooling)
 SYOK ANAFILAKTIK
 Syok yang terjadi karena reaksi hipersensitivitas (tipe 1) atau reaksi alergi

 Manifestasi sistemik yang terjadi akibat pelepasan mediator-mediator

inflamasi yang cepat
Etiology
 Foods (most common cause in children) – Milk, eggs, wheat, soy, fish, shellfish,
legumes (peanuts), tree nuts

 Medicinals – Antibiotics (penicillins, cephalosporins), local anesthetics

(lidocaine), analgesics (aspirin, nonsteroidal anti-inflammatory drugs [NSAIDS]
[ibuprofen], opiates [codeine, morphine]), dextran, radiocontrast media

 Biologics – Venoms (bee sting, ant or snake bite), blood and blood products,
vaccines, allergen extracts

 Preservatives and additives – Metabisulfite, monosodium glutamate Other –

Latex, unknown/idiopathic
 IgE Mediated
 Reexposure with antigen (body already has produced specifis IgE
antobody)  IgE antibodies bind to the high-affinity IgE receptor
(FcεRI) on the surface of mast cells and basophils allergen may
cross-link the mast cell or basophil surface-bound allergen-specific
IgE  cellular degranulation & synthesis of mediators.
 Histamine  primary mediator of anaphylactic shock. Many of the signs and
symptoms of anaphylaxis are attributable to binding of histamine to its receptors;
binding to H1 receptors mediates pruritis, rhinorrhea, tachycardia, and
bronchospasm. On the other hand, both H1 and H2 receptors participate in
producing headache, flushing, and hypotension.
  Arachadonic acid( prostaglandins and leukotrienes).
 PGD2  bronchospasm and vascular dilatation, principle manifestations of
anaphylaxis.
 LTC4  converted into LTD4 and LTE4  hypotension, bronchospasm, and
mucous secretion during anaphylaxis in addition to acting as chemotactic
signals for eosinophils and neutrophils.
 Complement system, the kallikrein-kinin system, the clotting cascade, and the
fibrinolytic system.

 Specific lymphocyte subtypes (CD4+ Th2 T-cells)  induction of the IgE

response. Th2 responses are important in humoral immunity and critical for
the allergic response. Th2 cells produce interleukin (IL)-4, IL-5, IL-9, and IL-
13. IL-4  B cells to begin producing IgE.
Non- IgE Mediated
 Triggered by several different mechanisms
 Stimulation of the complement cascade to produce C3a, C4a, and C5a
anaphylatoxin, neuropeptide and cytokine activity, and direct contact (kallikrein-
kinin system) stimulation by certain agents (eg, opiates, radiocontrast media).
 Manifetasi Klinis

 Takikardia

 Akral hangat

 Penurunan kesadaran

 Hipotensi

 Penurunan produksi urine

 Hipovolemia efektif  krn vascular/ venous pooling dan peningkatan

permeabilitas kapiler
Tanda and Gejala
 Dapat dibagi menjadi 4 kategori (Medscape)

Mucocutaneous Respiratory Cardiovascular Gastrointestinal

• Urticaria • dyspnea • hypotension • nausea

• Angioedema • throat • tachycardia • vomiting
• Pruritis tightness • syncope • abdominal
• Flushing • stridor cramps
• wheezing • diarrhea
• rhinorrhea
• hoarseness
• cough
 The Second National Institute of Allergy and Infectious Disease (NIAID) /
FAAN symposium proposed diagnostic criteria that would identify at least
95% of the patients with anaphylaxis.
 The primary clinical diagnostic criteria : acute onset of skin and/or mucosal
symptoms along with either respiratory compromise (eg, bronchospasm, stridor,
shortness of breath) and/or reduced blood pressure or associated symptoms of
end-organ dysfunction (eg, hypotonia, syncope, incontinence).
 Often, a history of exposure to a known trigger is given. At times, the inciting
agent may be unknown or unclear.
 Symptoms may develop slowly and insidiously over several hours or may rapidly
progress over several minutes.
 Parenteral agents generally have a faster onset of symptoms than ingested ones.
 Anaphylaxis may result in respiratory failure, shock, multiorgan system failure, and
disseminated intravascular coagulation.
 Between 5% and 20% of patients may experience a recurrence of anaphylaxis 8-12
hours after the initial presentation.
 Prolonged symptoms can last up to 32 hours despite treatment.
Diagnosis
 Pemeriksaan lab umumnya tidak berguna untuk keadaan akut

 Pemeriksaan yang dapat dilakukan untuk menegakkan diagnosis:

 Serum histamin
 Serum triptase
 Tatalaksana Syok (PPM IDAI)
 Airway
 Pertahankan jalan napas

 Breathing
 Berikan oksigen (FiO2 100%), bila perlu berikan tunjangan ventilator

 Circulation
 Pasang akses vaskuler secepatnya (60 – 90 detik)
 Berikan cairan kristaloid 20 ml/kgBB (dalam waktu < 10 menit)
 Nilai respon : perubahan denyut nadi? Perfusi jaringan?
 Respon baik  penurunan denyut nadi, perbaikan perfusi jaringan, perbaikan
tekanan daran bila terdapat hipotensi sebelumnya
 Pasng kateter urin untuk menilai sirkulasi dengan memantau produksi urin
 Penggunaan koloid, dalam jumlah terukur, dapat dipertimbangkan untuk mengisi
volume intravaskular
 Pemberian cairan resusitasi dapat diulang bila syok belum teratasi, hingga
volume intravaskular optimal. Target resusitasi :
 CRT < 2s
 Kualitas nadi perifer = nadi sentral
 Akral hangat
 Produkasi urin > 1 ml/kgBB/ jam
 Kesadaran normal

 Pemberian cairan resusitasi dihentikan bila:

 Penambahan volume tidak lagi mengakibatkan oerbaikan hemodinak
 Terdapatnya rhonki basah halus tidak nyaring
 Peningkatan JVP
 Pembesaran hati akut
 Periksa dan atasi gangguan metaboli (hipoglikemi, hipokalsemi, asidosis)

 Sedasi atau pemasangan ventilator u/ mengurangi konsumsi O2 dapat

dipertimbangkan

 Bila syok belum teratasi :

 Pemasangan CVP. Bila tekanan vena sentral < 10 mmHg, pemberian cairan dapat
dilanjutkan mencapai 10 mmHg

 Bila syok belum teratasi setelah pemasangan CVP :

 Dopamin 2 – 10 ug/kg/menit

 Bila syok belum teratasi setelah inj dopamin :

 norepinefrin 0.05 – 2 ug/kg/menit
 Bila syok belum teratasi setelah inj norepinefrin :
 Pertimbangkan pemberian Terutama pada anak yang
 Hidrokortison : 2 mg/kg, atau sebelumnya mendapatkan
 Metil-prednisolon : 1.3 mg/kg, atau terapi steroid lama (asma,dll)
 Dexamethason : 0.2 mg/kg

 Bile syok belum teratasi :

 Dibutuhkan pemasangan pulmonary artery catheter untuk pengukuran dan
intervensi lebih lanjut.
 CO , SVR   inotropik dan vasodilator
 CO , SVR   vasopresor
 CO , SVR   inotropik dan vasopresor
 Target terapi :
 Cardiac Index >3.3 dan < 6 l/min/M2

 Perfusion pressure (MAP-CVP) normal  < 1 th : 60 cmH20, >

1 th : 65 cmH20
 Saturasi vena sentral > 70%

 Kadar laktat < 2 mmol/l

 Bila kadar laktat > 2 mmol/l, saturasi vena sentral < 70%, dan Ht
< 30%, dapat transfusi PRC disertai upaya untuk menurunkan
konsumsi oksigen
 Efek Obat Dosis

Inotropik Dopamine 5 – 10 mg ug/kg/menit

Dobutamine 1 – 20 mg ug/kg/menit
Amrinone < 4 minggu : 4 mg/kg dalam 1 jam (bolus)  3-5 ug/kg/min
> 4 minggu : 1-3 mg/kg dlm 1 jam (bolus) 5-15
Milrinone ug/kg/min
50 ug/kg/ bolus (dlm 10 min)  0.25 – 0.75 ug/kg/hari
Epinephrine Dosis max : 1.13 ug/kg/ hari
0.05 – 0.3 ug/kg/min
Vasopresor Dopamin 10 - 20 ug/kg/min
NE 0.05 - 2 ug/kg/min
Phenylaphrine 2 - 10 ug/kg/min (bolus)  1 - 5 ug/kg/min
Epinephrine 0.3 - 2 ug/kg/min

Vasodilator Nitropruside 0.5 - 10 ug/kg/min. Dosis max/ 24 jam bila fungsi injal
normal = 70 mg/kg/hari. Bila digunakan > 24 jam dosis max
= 4 mg/kg/hari
Nitroglyserine 1 - 10 ug/kg/min
Phentolamine 0.1 mg/kg (bolus)  5 - 50 ug/kg/min
Thank You 