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SYNDROME ( ARDS )
Acute Respiratory Distress Syndrome
Defenisi
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
Patogenesis
3 fase dari lung injury:
1. Fase exudatif ( edema and perdarahan )
2. Fase inflammatory and repair
3. Fase fibrotic
Acute Respiratory Distress Syndrome
Precipitating Event
ARDS / ALI
Patogenesis ARDS / ALI
REDOX Balance
Generation of Antioxidant
Oxidant Protection
species
ROS
signalling RNS
Molecular Damage
and Dysfunction
Inflammatory
Alveolar / capillary
mediators
permeability
ARDS/ALI
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.
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
Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349
Hyaline membr Collagen
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
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%