This lecture was conducted during the Nephrology Unit Grand
Ground by Medical Student under Nephrology Division under
the supervision and administration of Prof. Jamal Al Wakeel,
Head of Nephrology Unit, Department of Medicine and Dr.
Abdulkareem Al Suwaida, Chairman of Department of
Medicine and Nephrology Consultant. Nephrology Division is
not responsible for the content of the presentation for it is
intended for learning and /or education purpose only.
Presented By:
Abdulrahman Al Aseem
Medical Student
Definition
 It is a clinical syndrom characterized by sever
respiratory distress, hypoxemia, noncardiogenic
pulmonary edema.
 Severe, acute lung injury involving diffuse alveolar
damage, increased microvascular permeability and non
cardiogenic pulmonary edema with acute refractory
hypoxemia.
 mortality- 30-40%
American European consesnsu conference
(1994) criteria for ARDS:
Acute onset of respiratory distress.
2. CXR: New bilateral, diffuse infiltrates.
3. PCWP <18 if measured or no clinical effidence of
increased left atrial pressure.
4. Refractory hypoxemia based on PaO2/FiO2 (arterial
oxygen tension/fractional inspiratory oxygen)ratio:
1.
-ARDS: PaO2/FiO2 < 200mmHg
-ALI : PaO2/FiO2 < 300mmHg
Etiology & Risk factors
 May result from direct or indirect (secondary) lung injury
 Indirect causes:
a) sepsis/ septic shock
b) severe trauma, burns, pancreatits w/ shock
hypoperfusion
c) drug over dose
d) cardiopulmonary bypass
e) acute pancreatitis
f) transfusion of multp blood products
g) fat or amniotic fluid embolism
Etiology & Risk factors
 Direct causes:
a) pneumonia
b) aspiration of gastric contents
or other causes of chemical pneumonitis
c) pulmonary contusion, penetrating lung injury
d) fat emboli
e) near drowning
f) inhalation injury
Pathogenesis
 Activation of inflammatory mediators and cellular
components resulting in damage to capillary
endothelial and alveolar epithelial cells
 Increased permeability of alveolar capillary
membrane
 Influx of protein rich edema fluid and
inflammatory cells into air spaces
 Dysfunction of surfactant
How the patient present??
 Unexplained tachypnea ( the 1st sign often).
 Breathlessn
 Increasing hypoxaemia with central cynosis.
 Bilateral fine Inspiratory crackles thoughout lung
field.
 CXR: bilateral diffuse shadowing diffuse, interstitial at
first but subsequently alveolar pattern and air
bronchogram. May progress to a picture of complete
“white-out”.
DDx??
Investigations:
 Blood: CBC, U&E, amylase, clotting , CRP, Blood culturs.
 ABG
 CXR
 Pulmonary artery catheter to measure
PCWP(Pulmanary capillary wedge pressure
Management:
 Admit to ICU
 Give supportive therapy (respiratory support,
circulatory support, nutritional support)
 Treat the underlying cause (e.g sepsis )
 Avoid complications (such as ventilator – associated
pneomonia)
Respiratory support
 In early ARDS, CPAP with 40-60% O2 may be adequate to
maintain oxygenation.
 However, most pts need mechanical ventilation
 Indications for ventilation: PaO2<8.3kPa despite 60% O2
 A low- tidal –volume, pressure limited approach, with
either loe or moderate high PEEP improves the outcomes.
Circulatory support
 Invasive haemodynamic monitring
 Conservative fluide management approach improves
outcomes
 Inotrops (eg. Dobutamine ) to maintaine CO and O2
delivery
 Nitric Oxide
Thank you