Acute respiratory distress syndrome

(ARDS)
Acute respiratory distress syndrome (ARDS), also known as
respiratory distress syndrome (RDS) or adult respiratory
distress syndrome is a serious reaction to various forms of injuries
to the lung This is the most important disorder resulting in increased
permeability pulmonary edema.
ARDS is a severe lung disease caused by a
- variety of direct and indirect insults.
It is characterized by
- inflammation of the lung parenchyma leading to
impaired gas exchange
- with concomitant systemic release of inflammatory
mediators causing inflammation, hypoxemia
- and frequently resulting in multiple organ failure.
This condition is life threatening and often lethal, usually requiring
- mechanical ventilation and admission to an intensive care
unit.
 Consensus after 1967 and 1994

ARDS is characterized by:

Acute onset
Bilateral infiltrates on chest radiograph
Pulmonary artery wedge pressure < 18
mmHg (obtained by pulmonary artery
catheterization )
 Patient presentation and diagnosis

ARDS usually occurs within 24 to 48 hours of the initial

injury or illness Evaluasi Chest X ray

Plain Chest X-rays are sufficient to document bilateral

alveolar infiltrates in the majority of cases.

The patient usually presents with shortness of breath,

tachypnea, and symptoms related to the underlying cause,
i.e. shock.

An arterial blood gas analysis and chest X-ray allow formal

diagnosis by inference using the aforementioned criteria.
 Pathophysiology

ARDS is characterized by
- Diffuse inflammation of lung parenchyma.
- The triggering insult to the parenchyma usually
results in an initial release of cytokines and other
inflammatory mediators, secreted by local
epithelial and endothelial cells.
Neutrophils and some T-lymphocytes quickly migrate
into the inflamed lung parynchema and contribute in the
amplification of the phenomenon.
Typical histological presentation involves diffuse alveolar
damage and hyaline membrane formation in alveolar
walls.
 Progression

If the underlying disease or injurious factor is not removed,

the amount of inflammatory mediators released by the
lungs in ARDS may result in a systemic inflammatory
response syndrome (or sepsis if there is lung infection).
The evolution towards shock and/or multiple organ failure
follows paths analogous to the pathophysiology of sepsis.
This adds up to the impaired oxygenation, the real
mainstay of ARDS, and respiratory acidosis, often caused
by the ventilation techniques indicated in ARDS.
The result is a critical illness in which the 'endothelial
disease' of severe sepsis/SIRS is worsened by the
pulmonary dysfunction, which further impairs oxygen
delivery.
 Treatment

General
Acute respiratory distress syndrome is usually treated with
mechanical ventilation in the Intensive Care Unit.
Ventilation is usually delivered through oro-tracheal
intubation, or tracheostomy whenever prolonged ventilation
(2 weeks) is deemed inevitable.
Appropriate antibiotic therapy must be administered as
soon as microbiological culture results are available.
The origin of infection, when surgically treatable, must be
operated on. When sepsis is diagnosed, appropriate local
protocols should be enacted.
Mechanical ventilation
PEEP (positive end-
expiratory pressure, to
maintain maximal recruitment
of alveolar units)
Prone position
Distribution of lung infiltrates in acute
respiratory distress syndrome is non-
uniform. Repositioning into the prone
position (face down) might improve
oxygenation by relieving atelectasis and
improving perfusion.
Fluid management
Several studies have shown that pulmonary
function and outcome are better in patients
that lost weight or wedge pressure was
lowered by diuresis or fluid restriction.
Corticosteroids
Patients with ARDS do not benefit from high-dose
corticosteroids. Meduri et al however did find significant
improvement using modest doses. This is probably
because of a suppression of ongoing inflammation during
the fibroproliferative phase of ARDS.
The initial regimen consists of methylprednisolone 2 mg/kg
daily. After 3-5 days a response must be apparent. In 1-2
weeks the dose can be tapered to methylprednisolone 0.5-
1.0 mg daily.
In the absence of results steroids can be discontinued.
Nitric oxide
Inhaled nitric oxide (NO) potentially acts as selective
pulmonary vasodilator. Rapid binding to hemoglobin
prevents systemic effects. It should increase perfusion of
better ventilated areas. There are no large studies
demonstrating positive results. Therefore its use must be
considered individually.
Almitrine bismesylate stimulates chemoreceptors in carotic
and aortic bodies. It has been used to potentiate the effect
of NO, presumably by potentiating hypoxia-induced
pulmonary vasoconstriction. In case of ARDS it is not
known whether this combination is useful