Download - ARDS [Dr. Edi Nurtjahja_ Sp.P]
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JEMBER
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Keindahan Alam Indonesia
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Acute RespiratoryDistress Syndrome
[ARDS]Oleh :dr. Edi Nurtjahja, Sp.P
SMF PARU
RSD dr. Soebandi Jember
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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 > 2,5ARDS
ARDS
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Causa primer ARDS LUNG
Concensus A.E Investigation
- syndrome acute
- bilateral infiltrate
- oedema paru
- pulmonary artery oclution preasure 18 mmHg
- hipoksemia
- PaO2 / FiO2
ALI
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AECC Ro
Bilateral infection
Oedema paru
Pemeriksaan
Agpi typenatriuretic DD cardiogenic pulmonary oedema
ARDS
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Timing Oxygenation Frontal Chest
Radiograph
Pulmonary Artery
Wedge Pressure
Acute lung
injury
Acute PaO2/FlO2
300mmHg
Bilateral
infiltrates
18 mmHg if measured, or
no clinical evidence of leftatrial hypertension
ARDS Acute PaO2/FlO2
200mmHgBilateral
infiltrates18 mmHg if measured, or
no clinical evidence of leftatrial hypertension
American-Eropean Consensus ConferenceCriteria for Acute Respiratory Distress
Syndrome
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Insidensi > 5/100.000 1,5/100.000 ARDS/ALI 22 cases/100.000
Risk factor1. Sepsis
2. 40 % sepsis ARDS
3. Aspirasi gastric content
4. Multiple blood transfution (>15 unit/24 jam)
5. Masif blood transfution
6. Multipel trauma
ARDS
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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., postlung transplant)
Adverse effect of medication
Conditions Associated with Acute RespiratoryDistress Syndrome, by Possible Mechanisms of Injury
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Causa:
Sevire trauma
Viral infection
Onset cepatRespiratory distress:48-72 jam
ARDS
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Patologi Fase 1 : Exudatif phase of lung injuries
difuse alveolar damage
Didapatkan antara lain : adanya hialin membran dan protein rich edemafluid 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
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Patologi
Fase 3 : fibrosis phase.
Pada pemeriksaan bal didapat peningkatan kadar N terminalprokolagen peptida III. Adanya proliferasi fibroglas.
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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 alveolarkapilare membran pada ALDS
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Surfactan
Adalah complex micture of phospholipids dansurfaktan protein dimana berfungsi untuk
mengurangi tegangan permukaan alveoli Pada ARDS terjadi perubahan pada lipids dan
protein dari surfactan, dan penurunan dipalmytoilphosphatidylcholine dan phosphatidylglyserol.
Gangguan fungsi surfactan dapat terjadi alveolarkolaps
Surfactan protein juga mempunyai sifat
antimikrobial
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Neutrophils
Merupakan sentral patogenesis dari ALI
cells in innate immunity, neutrophilsgenerate an array of cytotoxic
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Mortality dan Complications
Menurun dari 60 ke 40 % sejak tahun 1993
Terapi suportiv care Hemodinamic manajemen
Nutrisi
Farmakoterapi
mekanikal ventilasi
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ARDS is a syndrome defined by acute hypoxemia,bilateral infiltrates on chest radiograph, and theabsence of left atrial hypertension.
ARDS has been associated with diseases that directlyinvolved the lungs (e.g. pnemonia) and also withdiseases that do not obviously involve the lungs (e.g.pancreatitis).
The pathogenesis of ARDS is not clear, but increasedpermeability of the alveolar-capillary membrane dueto neutrophilic infiltration of the lungs is thought tobe an important factor.
Key Points
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ARDS is a syndrome, not a spesific diagnosis; cliniciansmust, 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 lunginjury.
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Most deaths is patiens with ARDS are from multiorganfailure rather than hypoxia per se.
No pharmacologic therapies have been shown toimprove survival in ARDS; thus, management consistsof treating the underlying cause, lung-protectiveventilation, conservative management of fluids, andexcellent supportive care.
Many survivors of ARDS suffer fro reduced quality oflife and cognitive impairment.