ACUTE RESPIRATORY DISTRESS

SYNDROME ( ARDS )

Steven HK 102016280
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
Consensus Conference Definitions for Acute Lung Injury (ALI) and
Acute Respiratory Distress Syndrome (ARDS)

Oxsigenasi Tekanan arteri

waktu X-ray
(astrup) pulmonale

ALI Akut PaO2 / FIO2 Infiltrat 18 mmHg

Kriteria 300 mmHg bilateral
(fraksi oksigen
21%)

ARDS Akut PaO2 / FIO2 Infiltrat 18 mmHg

Kriteria 200 mmHg Bilateral
(fraksi oksigen
21%)
ETIOLOGI ARDS
SECARA LANGSUNG TIDAK LANGSUNG

Asma bronkial Sepsis

PPOK Severe trauma with shock
Drug overdose
Pneumonia
Acute pancreatitis
Aspirasi makanan
Transfusion of blood products
Pulmonary contusion
Near-drowning
Inhalational injury
DLL
 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
Patogenesis

3 fase dari lung injury:

1. Fase exudatif ( edema and perdarahan )
2. Fase inflammatory and repair
3. Fase fibrotic
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.
 Pathogenesis ARDS / ALI

Precipitating Event

Inflammatory Response Neutrophils in BAL

ROS Neutrophil activation Histology appearances
Reactive Oxygen Species
Superoxide / Hydroxyl
Alveolar / capillary
permeability Protein levels in BAL

Pulmonary Oedema Lung Water

ARDS / ALI
Patogenesis ARDS / ALI

REDOX Balance

Generation of Antioxidant
Oxidant Protection
species

ROS Superoxide dismutase

H2O2 Catalase
Superoxide (O2.-) Glutathione
Hydroxyl radical (OH-) Transferrin
RNS Ceruloplasmin
Vit E
Nitric oxide (NO) Normal Vit C
Peroxynitrite (ONOO-)
Beta-carotene
Patogenesis ARDS / ALI

Oxidative Stress
Depletion of
antioxidants

ROS formation &

Oxidative damage
 The Pathogenesis of ARDS / ALI
Precipitating Event
Predisposition?
Inflammatory Response
Inflammatory (Respiratory Burst)
mediators

ROS
signalling RNS

Molecular Damage
and Dysfunction

Inflammatory
Alveolar / capillary
mediators
permeability

Pulmonary Oedema Ventilatory support

Inhaled NO

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

Exudative phase Fibrosing-alveolitis phase

(A & D) (B, C & E)

Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349

Exudative phase Fibrosing-alveolitis phase

Ware LB, Matthay MA. N Engl J Med 2000;342:1334-1349

ARDS
PENATALAKSANAAN

Obati penyakit dasar

Antibiotika
Kortikosteroid
oksigenasi
Anti oksidan
Keluaran (outcome)

Tahun 1967 - 1979

Asbaugh (1967) : survival 42%
Survival : 18 38%
Tahun 1980 - 1989
Survival (< 1985) : 32 36%
Survival (> 1985) : 41 - 52% (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)
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
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%