ACUTE RESPIRATORY
DISTRESS SYNDROME
(ARDS)
Dewa Artika
DEVISI PARU / [Link]
FK UNUD RSUP Sanglah
INTRODUCTION
Acute Respiratory Distress Syndrome (ARDS) is
an acute and severe breathing failure syndrome,
indicated by acute breathing distress, with
oxygenation disorder caused by non cardiogenic
lung oedem.
Distinguished by Acute Lung Injury (ALI) which is
a series of pathologic process, while ARDS is an
end of this process which has more severe
characteristics.
Asbough, 1967 introduced it for the first
time
Murray, 1988 defined it using scoring
system
In year 1994, AECC (American European
Consensus Conference) on ARDS
recommended a new definition
ARDS spectrum
DEFINITION
ALI or ARDS is a kind of inflammation
syndrome causing increase of permeability
with lung oedem clinical, radiological
and physiological defect was occured that
is not due to left side heart failure.
ALI distinguished from ARDS
On ALI PaO2/FiO2 < 300
while ARDS PaO2/FiO2 < 200
EPIDEMIOLOGY
In the US in 1972 : 150.000 cases/year or
75 cases / 100.000 population
In Scandinavia, 17.9/100.000/year for ALI
and 13.5/ 1000.000/year for ARDS
Survey by Intensive Care Unit in AS : 9%
from Intensive Care Unit filled by ARDS
patients
RISK FACTOR
Direct lung injury
Digestive aspiration, thorax trauma, severe lung
infection, toxic gas inhalation, drown.
Indirect lung injury
Severe sepsis, non thorax trauma, transfusion,
acute pancreatic, medication overdose.
Generally, sepsis very much related to ARDS
creation, where incidence 40 %.
PATHOPHYSIOLOGY
The principal of ARDS occurrence, liquid
overflowing from capillary to alveoli, therefore
lung oedema occurred.
Normal, liquid in alveoli is regulated by
Hydrostatics pressure & osmotic capillary
Interstitial lymphatic
Tight junction between alveolar epithelium cell
On ARDS, / permeability barrier alv capillary
occurred, due to cell endothelia capillary or
epithelium alveoli injury
Disintegrity of epithelium causing :
Oedema alveoli
Disturbing transportation of epithelium liquid
Reducing the production of surfactant
In pneumonia septic shock can happen
There are 4 stages of ARDS pathophysiology :
1. Degradation of alv-cap membrane interstitial
fluid accumulation.
1. Lung become stiff ventilation disorder and V/Q
mismatch heavy hypoxemia
2. Liquid entered into alveoli area no ventilation,
proportion of V/Q become 0 shunt
3. Closing of terminal airway occurred atelectasis,
so los of lung volume which causing decreasing of
artery oxygen pressure.
Picture 1
PATHOLOGY
Exudative phase (day 1 7)
Edema interstitial and intra alveolar
Bleeding
Leuco-aglutination
Necrosis (pneumocite 1 and endothelium cell)
Hyalin membrane
Trombus fibrin platelet
Proliferative phase (day 7 21)
Interstitial myofibroblast reaction
Organization of fibrosis lumenal
Chronic inflammation
Parenchyma necrotic
Hyperplasia pneumocite II
Endarteritis obliterative
Macro thrombi
Fibrotic phase ( > day 21)
Fibrosis collagen
Microcystic honeycombing
Bronchiektasis traction
Artery pulls
Fibrosis mural
Hypertrophy medial
CLINICAL MANIFESTATION
During acute phase or exudative
Complaint: high fever, abdominal pain, shock,
pulmonary dysfunction such as dispnea, hypoxemia,
coughing, chest pain, uncomfortable feeling.
Physic: cyanosis, tachicardia, tachipnea, ronchi
Lab: blood gas analysis, alkalosis respiratoric,
increase of PaO2/PAO2 ratio, severe hypoxemia.
Hematologis dis; anemia, leucositosis, leucopenia,
trombositopenia, while DIC rarely found.
On BAL examination, it biochemistry and
cellular abnormality were observed
On thorax photo, early stage may still be
normal. After 12 24 hours there will be
cloudy bilateral opacities. After 24 hours,
opacities become more compacted.
Abnormality of kidney and liver occured.
THORAX PHOTO
On chronic phase, severity tending to fibrosis
alveolitic occurred with persistent hypoxemia.
Pulmonal hypertension occurred failure of
right side ventricle. In this phase, there is a
complication of nosokomial infection and multi
organ failure.
- On thorax photo it appear as steady opacity
- CT scan examination on thorax showing
opacities reticuler, difuse ground glass to
both lung areas and bula picture.
MANAGEMENT
General care
a. Identification and handling of the basic
cause such as infection, sepsis with correct
antimicrobial
b. Profilaxis / nosokomial infection therapy
c. Adequate nutrition
d. Profilaxis for GI organ bleeding with H2
blocker, antacid or sukralfat
e. Profilaxis tromboemboli
Medication for hypoxemia
a. Need high FiO2 to overcome severe
hypoxemia. For that, we need intubations
using Ventilator
b. Reduce consumption and improve oxygen
transportation
c. Mechanical ventilation
Exhalation technique (using PEEP)
Inhalation technique
Procedure for liquid and haemodynamic
Limitation of liquid to reduce lung oedema
Intravascular volume will be maintain, which is able to
support systemic perfusion
If perfusion do not achieved, can be given vasopresor
such as shock septic
Surfactant therapy
The main function is to regulate surface retention of
alveoli, so atelectasis will not be occurred.
Using exogenous surfactant results is not good
enough, therefore aerosol therapy will be preferred
Nitric-Oxide (NO) inhalation
A potential vasodilator
Able to improve artery oxygenation
Has an anti inflammation function
Glucokortikoid
Has an anti inflammation characteristics
Can be given at the end phase of ARDS
High dose prescription in a short time period
as a rescuer for patient with severe
disease who do not shows any improvement
Resolution acceleration
Can be achieved with oedema alveoli liquid
transfer using catecholamine or non
catecholamine
non catecholamine group (beta agonist)
has been extensively applied
can also increase surfactant and anti
inflammation effect
Recently Keratinocyte growth factor has been
attempted, where it can help epithelium
alveoli II cell proliferation shield for lung
injury
Learning task
A patient was brought to Emergency Unit by their family with complaint of
sudden breathing difficulties and decrease in consciousness. Five days before
the patient suffered from high temperature until shivering together with purulent
cough and breathing difficulties. Vital sign it was found BP:100/70, N. 120/m,
RR. 30 times/m temp. 39oC. On physical examination it was found ronchi
diffuse, wheezing. On the thorax photo it was found opacity covering on the two
lung areas and consolidation in the center-right side part. Examination of blood
gas analyses it was found PaO2, 45 mmHg while PaCO2 65 mmHg, PH 7,25.
Self Assessment
- Discuss about that case assessment
- Other recommended examination
- What is the diagnostic procedure
- How is the pathophysiology of ARDS
- How is the management of ARDS
THANK - YOU
