JEMBER

Keindahan Alam Indonesia

Acute Respiratory Distress
Syndrome
[ARDS]
Oleh :
dr. Edi Nurtjahja, Sp.P

SMF PARU
RSD dr. Soebandi Jember
 ARDS
 1988  definisi ARDS
1. Akut / kronik
2. Risk factor : sepsis
3. Survey pulmonary disfunction (L.I.S):
- hipoksemia
- level PEEP
- respiratory system compliance
- kelainan radiologi
 score > 2,5 ARDS
 ARDS
 Causa primer ARDS  LUNG
 Concensus A.E Investigation
- syndrome acute
- bilateral infiltrate
- oedema paru
- pulmonary artery oclution preasure ≤ 18 mmHg
- hipoksemia
- PaO2 / FiO2
 ALI <300
 ARDS <200
 ARDS

 AECC  Ro
 Bilateral infection
Oedema paru

 Pemeriksaan
 β – Agpi typenatriuretic
 DD  cardiogenic pulmonary oedema
 American-Eropean Consensus Conference
Criteria for Acute Respiratory Distress
Syndrome
Timing Oxygenation Frontal Chest Pulmonary Artery
Radiograph Wedge Pressure
Acute lung Acute PaO2/FlO2 Bilateral ≤18 mmHg if measured, or
injury ≤300mmHg infiltrates no clinical evidence of left
atrial hypertension
ARDS Acute PaO2/FlO2 Bilateral ≤18 mmHg if measured, or
≤200mmHg infiltrates no clinical evidence of left
atrial hypertension
 ARDS
 Insidensi > 5/100.000 – 1,5/100.000
 ARDS/ALI  22 cases/100.000

 Risk factor
1. Sepsis
2. 40 % sepsis  ARDS
3. Aspirasi gastric content
4. Multiple blood transfution (>15 unit/24 jam)
5. Masif blood transfution
6. Multipel trauma
 Conditions Associated with Acute Respiratory
Distress Syndrome, by Possible Mechanisms of Injury

Indirect Injury Direct Injury

Sepsis Pnemonia
Mayor trauma Aspiration
Multiple blood transfutions Pulmonary contusion
Pancreatitis Toxic inhalation
Cardiopulmonary bypass Near-drowning
Drug overdose Reperfution injury (e.g., post
lung transplant)
Adverse effect of medication
 ARDS

 Causa:
 Sevire trauma
 Viral infection
 Onset cepat
 Respiratory distress:48-72 jam
 Patologi
 Fase 1 : Exudatif phase of lung injuries
 difuse alveolar damage
 Didapatkan antara lain : adanya hialin membran dan protein rich edema
fluid di alveolar space
 Kerusakan epitel
 influitrasi neutrophil dan makrofag
 perdarahan di alveoli
 Proses berlangsung 5 sampai 7 hari
 Fase 2 : Proliferasi phase
 Membran hialin mengalami fibrosis .
 Terjadi :
obliterasi pulmonare kapiler
Timbunan kolagen di ruang intersitial dan alveoli
Penurunan neutrophil
Perluasan edema paru
 Patologi

 Fase 3 : fibrosis phase.

 Pada pemeriksaan bal didapat peningkatan kadar N – terminal
prokolagen peptida III. Adanya proliferasi fibroglas.

 Alveolar capilare membran

Patofisiologis proses pada ALDS :

 Adanya peningkatan permeabilitas alveolar kapelare membran
 Adanya proses pada pulmonare mikrovaskular indotelium
 Adanya proses pada alveolar epitelium
 Kerusakan apda epitel alveoli meningkatkan permeabilitas alveolar
kapilare membran pada ALDS
 Alveolar capilare membran

 Pada keadaan normal sel epitel paru lebih resisten terhadap efek
injuries dari sirkulatori endotoksin dari pada sel endotel
 Pada ARDS hal ini berubah sehingga terjadi alveolar floading
 Pada alveolar epitelium pneumocyte tipe 2 berdiferensi ke
pneumocyte tipe 1 utk membantu mengatasi proses perubahan pada
permukaan epitel terjadi peningkatan Na.K+ ATP ase utk
mengatasi cairan edema di alveoli
 Injuries pada pneumocyte tipe 2 akan mempengaruhi produksi
surfaktan

 Surfactan

 Adalah complex micture of phospholipids dan

surfaktan protein dimana berfungsi untuk
mengurangi tegangan permukaan alveoli
 Pada ARDS terjadi perubahan pada lipids dan
protein dari surfactan, dan penurunan dipalmytoil
phosphatidylcholine dan phosphatidylglyserol.
 Gangguan fungsi surfactan dapat terjadi alveolar
kolaps
 Surfactan protein juga mempunyai sifat
antimikrobial
 Neutrophils

Merupakan sentral patogenesis dari ALI

 cells in innate immunity, neutrophils
generate an array of cytotoxic
 Mortality dan Complications

Menurun dari 60 ke 40 % sejak tahun 1993

 Terapi suportiv care
 Hemodinamic manajemen
 Nutrisi
 Farmakoterapi
 mekanikal ventilasi
 Key Points

 ARDS is a syndrome defined by acute hypoxemia,

bilateral infiltrates on chest radiograph, and the
absence of left atrial hypertension.
 ARDS has been associated with diseases that directly
involved the lungs (e.g. pnemonia) and also with
diseases that do not obviously involve the lungs (e.g.
pancreatitis).
 The pathogenesis of ARDS is not clear, but increased
permeability of the alveolar-capillary membrane due
to neutrophilic infiltration of the lungs is thought to
be an important factor.
 ARDS is a syndrome, not a spesific diagnosis; clinicians
must, therefore, look for the cause in order to institute
spesific therapy.
 The mortality rate for ARDS has fallen since the 1980s
and in now about 40%.
 Mechanical ventilation is lifesaving but, when
inappropiartely applied, can incuded or aggravate lung
injury.
 Most deaths is patiens with ARDS are from multiorgan
failure rather than hypoxia per se.
 No pharmacologic therapies have been shown to
improve survival in ARDS; thus, management consists
of treating the underlying cause, lung-protective
ventilation, conservative management of fluids, and
excellent supportive care.
 Many survivors of ARDS suffer fro reduced quality of
life and cognitive impairment.