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 pulmonary
function within a year
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: 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

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Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
 PATIENT LYING PRONE ON VOLLMAN PRONE POSITIONER

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Mr sanjay. M. Peerapur, Principal, KLES Institute of Nursing Sciences, Hubli
 LATERAL ROTATION THERAPY BED

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