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Diterbitkan olehDevi Gunawan Telah diubah "7 tahun yang lalu
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ACUTE RESPIRATORY DISTRESS SYNDROME ( ARDS )
Oea Khairsyaf
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Acute Respiratory Distress Syndrome
Defenisi “Non-cardiogenic Pulmonary Oedema” Ashbaugh, Bigelow et al, 1967 “Adult Respiratory Distress Syndrome” Petty and Ashbaugh, 1971 “Shock Lung” Staub, 1974 “Acute Respiratory Distress Syndrome” American-European Consensus Committee, 1992
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Tekanan arteri pulmonale
Consensus Conference Definitions for Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) waktu Oxsigenasi (astrup) X-ray Tekanan arteri pulmonale ALI Kriteria Akut PaO2 / FIO2 ≤ 300 mmHg (fraksi oksigen 21%) Infiltrat bilateral ≤ 18 mmHg ARDS Kriteria PaO2 / FIO2 ≤ 200 mmHg (fraksi oksigen 21%) Bilateral
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ETIOLOGI ARDS Asma bronkial PPOK Pneumonia Aspirasi makanan
SECARA LANGSUNG TIDAK LANGSUNG Asma bronkial PPOK Pneumonia Aspirasi makanan Pulmonary contusion Near-drowning Inhalational injury DLL Sepsis Severe trauma with shock Drug overdose Acute pancreatitis Transfusion of blood products
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Acute Respiratory Distress Syndrome
Gambaran klinis: Awal “shock” responsif terhadap resusitasi. Periode latent : beberapa jam, biasanya beberapa hari (12-48 jam). Insidious tachypnoea, pasien jadi gelisah . Paru tidal volume kecil, napas cepat, hipoksemia refrakter. Mula-mula alkalosis respiratorik asidosis respiratorik Ventilasi mekanis
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Patogenesis 3 fase dari lung injury:
Fase exudatif ( edema and perdarahan ) Fase inflammatory and repair Fase fibrotic
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Acute Respiratory Distress Syndrome
Exudative Phase, 0-5 hari. Ruang alveoli terisi cairan, protein dan inflammatory cells. Necrosis sel-sel pneumocyte type 1, fibrin, platelet thrombi. Inflammatory Phase, 5-10 hari. Proliferasi fibroblasts dan sel-sel pneumocyte type 2. Squamous metaplasia dan pembentukan hyaline membranes. Fibroproliferative Phase, 10 hari sampai sembuh atau mati. Fibrosis interstital dan intra-alveolar. Thrombosis dan obliterasi vaskuler. Collagen paru meningkat.
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Pathogenesis ARDS / ALI
Precipitating Event Inflammatory Response Neutrophil activation ROS Reactive Oxygen Species Superoxide / Hydroxyl Neutrophils in BAL Histology appearances Alveolar / capillary permeability Protein levels in BAL Pulmonary Oedema Lung Water ARDS / ALI
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Patogenesis ARDS / ALI REDOX Balance Generation of Antioxidant Oxidant
species Antioxidant Protection Superoxide dismutase Catalase Glutathione Transferrin Ceruloplasmin Vit E Vit C Beta-carotene ROS H2O2 Superoxide (O2.-) Hydroxyl radical (OH-) RNS Nitric oxide (NO) Peroxynitrite (ONOO-) Normal
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Patogenesis ARDS / ALI Oxidative Stress Depletion of antioxidants
ROS formation & Oxidative damage
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The Pathogenesis of ARDS / ALI
Precipitating Event Predisposition? Inflammatory Response (Respiratory Burst) Inflammatory mediators ROS RNS Ventilatory support Inhaled NO signalling Molecular Damage and Dysfunction Alveolar / capillary permeability Inflammatory mediators Pulmonary Oedema ARDS/ALI
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Faktor-faktos seluler dan humoral pada ALI/ARDS
Neutrophils. ROS dan proteases. Resting, activated, primed and unresponsive. Cytokines (polypeptides). TNF-, macrophages, monocytes, neutrophils. IL-1, macrophages, endothelial cells GM-CSF, monocytes, macrophages, fibroblasts epithelial, endothelial dan smooth muscle cells. Chemokines (chemotactic cytokines). IL-8. Eicosanoids (prostaglandin, leucotrienes, thromboxanes), complement, endotoxins, adhesion molecules, PAF, endothelins, NO.
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Pathogenesis Influx cairan edema kaya protein alveoli (permeabilitas alveolar-capillary barrier ) Kerusakan Type 2 cells gangguan epithelial fluid transport gangguan pengeluaran cairan dan produksi surfactant abnormal Bila kerusakan hebat gangguan epithelial repair fibrosis Neutrophils merupakan sel yang dominant Cytokines dan proinflammatory compounds mengawali dan memperkuat respons inflammatory
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Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349
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Fibrosing-alveolitis phase
Hyaline membr Collagen Exudative phase (A & D) Fibrosing-alveolitis phase (B, C & E) Ware LB, Matthay MA. N Engl J Med 2000;342:
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Fibrosing-alveolitis phase
Exudative phase Fibrosing-alveolitis phase Ware LB, Matthay MA. N Engl J Med 2000;342:
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ARDS
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PENATALAKSANAAN Obati penyakit dasar Antibiotika Kortikosteroid
oksigenasi Anti oksidan
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Keluaran (outcome) Tahun 1967 - 1979 Tahun 1980 - 1989
Asbaugh (1967) : survival 42% Survival : 18 – 38% Tahun Survival (< 1985) : 32 – 36% Survival (> 1985) : % (European Collaborative Study 41%) Tahun 1990 – 2000 Survival : 41 – 60% NIH ARDS study : mortality 40% vs 30% (penurunan 25%, antara VT 12 mL/kg vs 6 mL/kg)
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Outcome Jangka Panjang pada Survivors (1-1,5 tahun pasca ARDS)
Sequelae pulmoner Majoritas, fungsi paru kembali hampir normal Gangguan residual: restrictive ventilatory defect (biasanya ringan), Hipertensi pulmoner (ringan), airflow limitation ( bronchial hyperactivity) Gangguan pada exercise testing lebih bermakna (setara pasien COPD berat) Derajat gangguan ~ umur, riwayat merokok, ventlasi mekanis berkepanjangan
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Survival 10 tahun terakhir, mortalitas turun 20% Mortalitas:
Umur : 75% (≥ 60 th) vs 37% (< 60 th) Faktor resiko : 64% (sepsis) vs 42% (trauma) Penyulit : 86% (sepsis) vs 38% (tanpa sepsis) Response thd PEEP : PaO2/FiO2 > 150 mmHg mortalitas 23%
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TERIMA KASIH TERIMA KASIH
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