ACUTE

RESPIRATORY DISTRESS
SYNDROME
Tatar Sumandjar
Div. Tropical and Infectious disease, Dept.
Internal Medicine, Moewardi Hospital/Faculty of
Medicine, UNS
 Curriculum Vitae

Name : Tatar Sumandjar

Institution : Medical Staff Division Tropical Medicine and
Infectious Diseases, Dept. of Internal Medicine
Medical Faculty University of Sebelas Maret/
Dr. Moewardi Hospital, Surakarta
Graduates:
MD : FK UGM : 1983
Internist : FK UGM : 2000
Consultant : FK UI : 2008
Occupation:
Puskesmas in Purworejo, Central Java 1984 - 1990
Internal Medicine Department Merauke Hospital 2000 – 2001
Internal Medicine Department Moewardi Hospital: 2001- recently
 Introduction
• 1967: The initial description of acute respiratory
distress syndrome (ARDS) by Ashbaugh et al.

• “A syndrome of acute respiratory failure in adults

characterized by non-cardiogenic pulmonary
edema manifested by severe hypoxemia caused
by right to left shunting through collapsed or fluid-
filled alveoli.”
• 1994: American-European Consensus Con-
ference (AECC) definition of ARDS:

² acute onset of hypoxemia PaO2/FIO ≤

200 mm Hg
² bilateral infiltrates on frontal chest
radiograph
² no evidence of left atrial hypertension.
•2012 : The Berlin Definition:
• “An acute, diffuse, inflammatory lung injury
that leads to increased pulmonary vascular
permeability, increased lung weight, and a loss
of aerated tissue.”

• The ARDS Definition Task Force. Acute Respiratory Distress

Syndrome: The Berlin Definition.JAMA 2012; May 21, 2012:Epub
ahead of print.)
The Berlin Definition of ARDS- 2012
Within 1 week of a known clinical
Timing insult or new or worsening
respiratory symptoms

Chest Bilateral opacities—not fully explained

by effusions, lobar/lung collapse, or
imaging nodules

Origin of Respiratory failure not fully explained by cardiac failure or fluid

overload. Need objective assessment (eg, echocardiography) to
edema exclude hydrostatic edema if no risk factor present

Oxygenation Mild Moderate Severe

(with PEEP > 5 cm PaO2/FIO2 PaO2/FIO2 PaO2/FIO2
H2O) 200-300 mm Hg 100- 200 mm Hg <100 mm Hg

JAMA. 2012;307(23) Published online May 21, 2012

Staging and severity of ARDS
 Cardiogenic vs. Non-Cardiogenic
Edema via CXR
Cardiogenic Non-Cardiogenic

Bilateral infiltrates Diffuse Bilateral patchy infiltrates

predominately in lung bases. homogenously distributed
Kerley B’s. Cardiomegaly. throughout the lungs. Positive tube
sign. No Kerley B’s.
 Clinical Disorders Associated with the
Development of ALI/ARDS
Direct insult Indirect insult
Common Common
Aspiration pneumonia Sepsis
Pneumonia Severe trauma
Shock
Less common
Inhalation injury Less common
Pulmonary contusions Acute pancreatitis
Fat emboli Cardiopulmonary bypass
Near drowning Transfusion-related TRALI
Reperfusion injury Disseminated intravascular
coagulation
Burns
Head injury
Drug overdose

Atabai K, Matthay MA. Thorax. 2000.

Frutos-Vivar F, et al. Curr Opin Crit Care. 2004.
 Pathophysiology

INJURY EXUDATIVE PROLIFERATIVE FIBROTIC

DIRECT
EDEMA INTERSTITIALS
Viral infection INFLAMMATION
HYALINE INTERSTITIAL
FIBROSIS
Pnemonia MEMBRANES FIBROSIS
Aspiration

INDIRECT
Sepsis
Day 0-7 14 21..
Trauma
Burn

Lancet 2007; 369:1553-65

EXUDATIVE : Up to 1 week

1. Direct or indirect injury to

the alveolus causes
alveolar macrophages to
release pro-inflammatory
cytokines

Ware et al. NEJM 2000; 342:1334

EXUDATIVE : Up to 1 week

2. Cytokines attract
neutrophils into the alveolus
and interstitum, where they
damage the alveolar-capillary
membrane (ACM).

Ware et al. NEJM 2000; 342:1334

EXUDATIVE : Up to 1 week

3. ACM integrity is lost,

interstitial and alveolus fills with
proteinaceous fluid, surfactant
can no longer support alveolus

Ware et al. NEJM 2000; 342:1334

 PROLIFERATIVE FIBROTIC

Beyond 3rd week

2 to 3rd week

Remodeling by
organization of collagenous tissue,
alveolar arterial thickening,
exudates,Type I obliteration of pre-
alveolar cells get capillary vessels.
replaced by type 2
abnormal tissue
alveolar cells
repair,
Lymphocytes Type III collagen

Long term MV
support and O2
Most patients get therapy
recovered Increased morbidity
and mortality
 MANAGEMENT
1. Main therapy : mechanical ventilation
“ Lung protective mechanical ventilation “

2. Supportive therapy
Treatment of cause : e.g. antibiotics for pneumonia
Fluid & Hemodinamic management

3. Pharmacological treatment
Steroids, vasodilators, surfactant, anti inflammatory

4. “RESCUE” THERAPY
 Ventilasi mekanis pada ARDS

üGunakan PEEP → menurunkan

intrapulmonary shunting
üTidal volume lebih kecil → mencegah
overdistensi
üPplat < 30 cmH2O → mencegah
overdistensi
üMenerima hypercapnia
üMinimalisasi FiO2 < 0.6 → menurunkan
resiko keracunan oksigen