ACUTE RESPIRATORY

DISTRESS SYNDROME
(ARDS)
Farida A. Soetedjo
Fakultas Kedokteran
Universitas Wijaya Kusuma Surabaya
2013

ARDS: Definitions
First described in 1967 as Adult

Respiratory Distress Syndrome

American-European Consensus Conference
Committee (1994) criteria:
Acute onset
Bilateral infiltrates in chest radiography
Pulmonary-artery wedge pressure < 18 mmHg
Acute lung injury PaO2/FiO2 < 300
Acute respiratory distress syndrome PaO2/FiO2

< 200

ARDS: Causes

ARDS: Epidemiology
Incidence: 80 per 100,000
Outcomes:
Traditionally 40-60% mortality
Majority of deaths due to MSOF
Low tidal volume ventilation decreases

mortality
Other critical care improvements may be
involved
Predictive factors for death: CLD, non
pulmonary organ dysfunction, sepsis and
advance age
Survivors: Most of them will have normal

ARDS: Pathogenesis
ARDS is the manifestation of SIRS in the

lungs
Influx of protein rich edema into the air

spaces due to increased permeability of the

alveolar-capillary barrier

Endothelial damage pathophysiology is

similar to that of SIRS/SEPSIS

ARDS: Pathogenesis
Epithelial damage
Loss

of epithelial integrity which in normal

conditions less permeable than endothelium
Type II cells injury
disrupts normal epithelial fluid transport
reduces production of surfactant
May lead to septic shock in patients with
pneumonia
Severely injured epithelium lead to
disorganized repair and fibrosis

ARDS: Pathogenesis
Neutrophils
Cytokines
Unbalanced production of pro-inflammatory

and anti-inflammatory cytokines

Ventilator induced injury

High FiO2
Overdistention
Recruitment/De-recruitment
May exacerbate and perpetuate ARDS/ALI as

well as SIRS/Sepsis/MSOF

ARDS: Exudative Phase

The definition applies for the acute exudative

phase
Rapid onset
Hypoxemia refractory to supplemental oxygen
CXR similar to pulmonary edema
CT Scan: Alveolar filling, consolidation and
atelectasis in the dependent lung zones
Pathologic findings:
diffuse alveolar damage with capillary injury and
disruption of the alveolar epithelium
hyaline membranes
protein rich fluid edema with neutrophils and
macrophages

ARDS: Pathogenesis

ARDS: Exudative Phase

CT Scan During Acute Phase

ARDS: Fibroproliferative phase

Some patients progress to fibrosing

alveolitis with persistent hypoxemia,

increase alveolar dead space and further
decrease in pulmonary compliance
The process may start as early as 5-7
days
The alveolar space becomes filled with
mesenchymal cells and their products as
well as new blood vessels

ARDS: Fibroproliferative phase

Pulmonary HTN due to obliteration of

pulmonary bed may lead or worsen RV

dysfunction
CXR shows linear opacities.
PTX and bullae are common
Histologically, there is fibrosis and partial
resolution of the pulmonary edema
Mortality is 80% if this phase persists

ARDS: Fibroproliferative phase

CT Scan during fibroproliferative phase.
Diffuse interstitial opacities and bullae

ARDS: Pathogenesis

ARDS: Clinical Features

Tachypnea, tachycardia, hypoxia, and

respiratory alkalosis are typical early clinical

manifestations
Usually followed by the appearance of diffuse
pulmonary infiltrates and respiratory failure
within 48 hours.

ARDS: Radiographic
abnormalities
Due to alveolar epithelial injury, or diffuse

alveolar damage, that causes leakage of

protein-rich fluid into the alveolar spaces.

ARDS: Chest X-ray

Exudative phase: progression from diffuse

bilateral interstitial infiltrates to diffuse,

fluffy, alveolar opacities +/- air
bronchograms
White out
Ground glass opacities

Proliferative and fibrotic phase: a more

heterogeneous, linear or reticular pattern.

ARDS: Chest X-Ray

To help distinguish from cardiogenic

pulmonary edema: often a lack

cardiomegaly, obvious pleural effusions, and
vascular redistribution.
Radiographic findings tend to stabilize and if
further worsening occurs after 5-7 days,
another process should be considered.

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ards.htm

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Inc.

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ARDS: CT Scan
The diffuse and nonspecific consolidation on

CXRs is revealed to actually be more

heterogeneous on CT scans.
Alveolar opacities in the gravity-dependent
areas of the lung
ARDS due to pulmonary disease tends to be
asymmetric, with a mix of consolidation and
ground-glass opacification
ARDS due to extrapulmonary causes has
predominantly symmetric ground-glass
opacification.
Pleural effusions and air bronchograms are
common with both

ARDS: Treatment

Recent decrease of mortality

Treatment of underlying cause
Better supportive ICU Care

Prevention of infections
Appropriate nutrition
GI prophylaxis
Thromboembolism prophylaxis

ARDS: Treatment
Mechanical ventilation
Buys time for the lungs to heal and solve the

inciting cause
New ventilator strategies

Recognition of ventilator induced injury (VILI)

Overdistention
Recruitment/de-recruitment
Mechanical ventilation induces cytokine response
which is worse with alveoli overdistention and
recruitment/ de-recruitment of the lung (Ranieri
et al JAMA 1999;282: 54-61)

ARDS: Treatment

ARDS: Treatment
Protective

ventilation

Smaller

tidal volumes
Avoid overdistention
Tolerate permissive hypercarbia

Open

lung ventilation
Avoid alveolar collapse and reopening

ARDS: Treatment
Recruiting maneuvers
Prone positioning
Steroids
APRV
Volume cycle vs. pressure cycle
Inverse-Ratio Ventilation
Non invasive Positive Pressure Ventilation
High-Frequency Ventilation
Tracheal Gas Insufflation
Extracorporeal gas exchange
Fluorocarbon Liquid Gas Exchange

Recruitment maneuvers
Lung recruitment in patients with ARDS

Gattinoni

NEJM 2006;354:1175-86

Sixty eigt patients with ALI/ARDS underwent

whole lung CT Scan during breath holding

session at airway pressures of 5, 15 and 45 cm
of water
The percentage of potentially recruitable lung
was defined as the proportion of lung tissue in
which aeration was restored (Recruited)

Recruitment
The potentially recruitable lung was

significantly variable but highly correlated

with the percentage of lung tissue in
which aeration was maintained with PEEP
Patients with more recruitable lung were
sicker
Greater lung weight
Poorer oxygenation
Poorer compliance
Higher levels of death space
Higher mortality

Recruitment
Knowing the % of recruitable lung might be

the key to the effects of PEEP

PEEP in patients with limited recruitable
areas might be of little benefit or harmful
Overdistention
Worsening of Shunt
Authors suggest PEEP of 15 for those

recruitables and 10 for those who are not

ARDS: Treatment
Prone positioning
In about 70% of ARDS patients, prone

positioning improves the PaO2 by > 20%

Consider a lung recruitment strategy, since

allows a decrease in FiO2 and PEEP

A more uniform distribution of pleural

pressure gradients, result in greater

ventilation of dependent lung than in supine
positioning

ARDS: Treatment
Gattinoni et al, NEJM 2001;345:568-573
304 patients with ARDS
Prone group: at least six hours/day for ten days
Better oxygenation in the prone patients
Similar incidence of complications
No improvement in survival
However patient only prone for 7 hours a day

and up to 10 days

TURNING PATIENT PRONE ON VOLLMAN

PRONE POSITIONER

Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli

35

PATIENT LYING PRONE ON VOLLMAN PRONE

POSITIONER

Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli

36

LATERAL ROTATION THERAPY BED

Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli

37

ARDS: Treatment
Fluid and hemodynamic management
Optimal fluid management is controversial
There is data supporting fluid restriction as a mean
to minimize lung edema
However maintenance and preservation of oxygen
delivery may require fluid administration
Euvolemia, judicious use of vasopressors
Effects of ventilation in circulation
To Swan or not to Swan

ARDS: Treatment
APRV

It uses a release of airway pressure from an

elevated baseline to simulate expiration.

The elevated baseline facilitates oxygenation
avoids collapsing of alveoli and the timed
releases aid in carbon dioxide removal.
Potential advantages of APRV include lower
airway pressures, lower minute ventilation,
minimal adverse effects on cardio-circulatory
function.
Airway pressure release ventilation is consistent
with lung protection strategies that strive to limit
lung injury associated with
mechanical
ventilation, particularly
recruitment/derecruitment
More (larger) studies are needed to define its role
in ALI/ARDS

ARDS: Treatment
Inhaled nitric oxide and other

vasodilators
Most ARDS/ALI patient may have mild to

moderate pulmonary HTN

Improvement in oxygenation was small and
not sustained
No change on mortality or duration of
mechanical ventilation
May be used as rescue therapy

Surfactant
Successful in neonatal respiratory distress

syndrome

ARDS: Treatment
Glucocorticoids
No benefits in acute phase
Some evidence of improvement during

proliferative phase (Meduri et al JAMA

1998;280:159-165)
Methylprednisolone 2mg/kg initially for 32 days
Improvement in Lung injury scores, MOSD scores
and mortality
Benefits may be noticed by day 3

High risk of infection

? May consider a short course of high dose

as rescue therapy

ARDS: Treatment
Steroids

Efficacy and safety of corticosteroids for

persistent acute respiratory distress

syndrome NEJM 2006.354: 1671-84
180 patients
Mortality at 60 days
28.9% mortality in the placebo group and 29.2% in the
methylprednisolone group
Methylprednisolone increased the number of ventilator
free and shock free days during the first 28 days in
association with an improvement in oxygenation,
respiratory system compliance and blood pressure with
fewer vasopressor days
But methylprednisolone was associated with a significant
increase 60-180 days mortality in patients enrolled at
least 14 days after the onset of ARDS

ARDS: Treatment
Anti-inflammatory Strategies
Prostaglandin agonist/inhibitors
Lisofylline and pentoxifylline
Anti IL-8
Antioxidant therapy
Enhanced resolution of pulmonary edema
Enhanced repair of alveolar epithelial

barrier

THANK YOU