ards [dr. edi nurtjahja_ sp.p]

7/28/2019 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.

ards [dr. edi nurtjahja_ sp.p]

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