highlight in acute respiratory...
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Highlight in acute respiratory failure
Yusup Subagio Sutanto
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Acute Respiratory Distress Syndrome
• “Non-cardiogenic Pulmonary Oedema”– Ashbaugh, Bigelow et al, 1967
• Hipoksemia berat : PaO2/FiO2 <200, infiltrat bilateral, tanpa edema paru kardiogenik– American-European Consensus Committee, 1994
• Berlin kriteria menambahkan kriteria dari AECC dengan mengekslusikan hipoksemia oleh atelektasis dan PEEP > 5 cmH2O
Definisi
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Kriteria Berlin
Acute Respiratory Distress Syndrome
Onset Dalam 1 minggu pada penyakit dasar atauperburukan gejala respirasi
Fototoraks
- Opasitas bilateral- Tanpa efusi pleura- Kolaps lobular- nodul
Origin of edema
Edema paru non kardiogenik, membutuhkanpenilaian obyektif (ekokardiografi)
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Kriteria Berlin
Ringan Sedang Berat
Oksigenasi (mmHg)
200<PaO2/FiO2≤300
100<PaO2/FiO2≤200
PaO2/FiO2≤100
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ETIOLOGI ARDS
• 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
SECARA LANGSUNG TIDAK LANGSUNG
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Acute Respiratory Distress Syndrome
Gambaran klinis:
▪ Awal “shock” responsif terhadap resusitasi.
▪ Periode latent : beberapa jam, biasanyabeberapa 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:
1. Fase exudatif ( edema and perdarahan )
2. Fase inflammatory and repair
3. 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 ataumati.
▪ Fibrosis interstital dan intra-alveolar.
▪ Thrombosis dan obliterasi vaskuler.
▪ Collagen paru meningkat.
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Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349
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Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349
Exudative phase(A & D)
Fibrosing-alveolitis phase(B, C & E)
Hyaline membr Collagen
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Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349
Exudative phase Fibrosing-alveolitis phase
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ARDS
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Terapi terkini ARDS
▪ Obati penyakit dasar
▪Hindari cedera paru sekunder: Aspirasi,
barotrauma, infeksi nosokomial atau toksisitas
oksigen
▪ Hantaran oksigen yang adekuat ke end-organ
dengan meminimalkan angka metabolik
▪ optimalisasi fungsi kardiovaskuler
▪Dukungan nutrisi
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Terapi eskalasi ARDS
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Terapi terkini ARDS
• Oksigen nasal kanul high-flow
• Cough assistant
• High-frequency chest wall oscillation
• Extracorporeal CO2 removal (ECCO2R)
• Terapi untuk hipoksemia berulang:
– Prone ventilation
– Neuromuscular blockage
– Artificial lung: extracorporeal membrane oxygenation
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Kesimpulan
• Berlin kriteria
– Onset (1 minggu /perburukan gejala
– Thorax (opasitas bilateral, tanpa efusi pleura, kolaps lobular atau nodul)
– Edema paru non kardiogenik
– ARDS ringan (200<PaO2/FiO2 ≤ 300 mmHg), sedang (100<PaO2/FiO2≤ 200 mmHg), berat (PaO2/Fio2 ≤ 100 mmHg)
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• Patogenesis ALI/ARDS : kerusakan epitelium alveolar dan endotelium mikrovaskular
• Faktor risiko dapat berasal dari paru mapun di luar paru
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