Acute respiratory distress

syndrome
(ARDS)
 DEFINITION
• Acute respiratory distress syndrome is a
clinical syndrome of severe dyspnoea of rapid
onset, hypoxaemia and diffuse pulmonary
infiltrates leading to respiratory failure.
CAUSES
DIAGNOSTIC CRITERIA
 PATHOPHYSIOLOGY
• ARDS consists of three phases:
A. Exudative phase:
• This phase lasts for about seven days.
• Injury involving alveolar capillary endothelial cells
and type I pneumocytes cause exudation of highly
proteinaceous fluid into the interstitial and alveolar
spaces.
• The oncotic pressure is normal.
• B. Proliferative phase:
• This phase lasts for about two weeks (8th-21st
days)
• This phase is characterised by prominent
interstitial inflammation and early
fibrosis
• C. Fibrotic phase:
• Many ARDS patients recover lung
function four weeks after initial lung injury.
• Some will enter a fibrotic phase that may
require long term support on mechanical
ventilation
• Secondary effects include loss of surfactant and
impaired surfactant production.
• The net effect is alveolar collapse and reduced lung
compliance, most marked in dependent regions of
the lung (mainly dorsal in supine patients).
The affected airspaces become fluid-filled and can
no longer contribute to ventilation, resulting in
hypoxaemia and hypercapnia (due to inadequate
ventilation
in some areas of the lung): that is, ventilation–
perfusion mismatch
 CLINICAL FEATURES
• Tachypnoea followed by
• dyspnoea,
• cyanosis,
• extensive
crackles over both lung fields.
 INVESTIGATIONS
• Investigations
1. ABG analysis: Demonstrates hypoxaemia.

2. Chest X-ray: Diffuse, extensive alveolar

shadowing bilaterally and more peripherally.
• 3. Haemodynamic measurements: Pulmonary
capillary wedge pressure < 18 mm Hg;
• Pcwp > 18 mm Hg suggests hydrostatic
pulmonary oedema.

4. Investigations to determine specific cause

 DIFFERENTIAL DIAGNOSIS
 cardiogenic pulmonary edema,(most common)
 diffuse pneumonia, and
 alveolar hemorrhage.
Less common diagnoses:
acute interstitial lung diseases ,
acute immunologic injury (e.g., hypersensitivity
pneumonitis; ),
toxin injury (e.g., radiation pneumonitis)
and neurogenic pulmonary edema
 TREATMENT
• 1. Treat the cause
2. Oxygen inhalation
3. Respiratory support with Mechanical
Ventilation
• Set PEEP to minimize Fio2 and optimize Pao2.
• PEEP helps in the redistribution of capillary
blood flow resulting in improved V/Q
matching and the recruitment of previously
collapsed alveoli and prevention of their
collapse during exhalation
• Oxygenation can also be improved by
increasing mean airway pressure with inverse
ratio ventilation(Inspiration: Expiration ratio >
1:1).
• Prone position ventilation can also be tried
• Sedation and muscle paralysis to prevent the
patient from fighting the ventilator and oxygen
utilisation.
• If cardiac output cannot be preserved, inotropic
agents, vasodilators or both can be used.
• Cyclo-oxygenase inhibitors, protease inhibitors,
antioxidant therapy, antitumour necrosis factor
orinterleukin-1 receptor antagonists are being
evaluated
• Nitric oxide inhalation (reduces pulmonary artery
pressure and improves oxygenation)
• Current evidence does not support the use of
high-dose glucocorticoids in the care of ARDS
patients.
 PROGNOSIS
• Mortality in ARDS is largely attributable to
nonpulmonary causes, with sepsis and
nonpulmonary organ failure accounting for
>80% of deaths.
• FACTORS ASSOCIATED WITH INCREASED
MORTALITY
 Advanced age
 Sepsis
 Preexisting organ dysfunction from chronic
medical illness—chronic liver disease,cirrhosis,
chronic alcohol abuse, chronic
immunosuppression, sepsis, chronic renal
disease.
 ARDS arising from direct lung
injury (including pneumonia, pulmonary
contusion, and aspiration)
 An early (within 24 h of presentation)
elevation in pulmonary dead space (>0.60)
and severe arterial hypoxemia (Pao2/Fio2,
<100 mmHg)