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Acute Respiratory Distress
Syndrome (ARDS)
Acute respiratory distress syndrome
:
Acute respiratory distress syndrome (ARDS) is
a clinical syndrome caused by diffuse alveolar
capillary and epithelial damage, it’s a condition
that prevents enough oxygen from getting to the
lungs and into the blood.
The usual course is characterized by
respiratory insufficiency, cyanosis, and severe
arterial hypoxemia that is refractory to oxygen
therapy and may progress to multisystem organ
failure.
The histologic manifestation of ARDS
in the lungs is known as diffuse
alveolar damage (DAD).
ARDS can be caused by any major direct or
indirect injury to the lung:
Pathogenesis:
 The alveolar-capillary membrane is formed by two
separate barriers: the microvascular endothelium
and the alveolar epithelium. In ARDS, the integrity
of this barrier is compromised by either
endothelial or epithelial injury, or, more commonly,
both.
The acute consequences of damage to the
alveolar capillary membrane include increased
vascular permeability and alveolar flooding, loss
of diffusion capacity, and widespread surfactant
abnormalities caused by damage to type II
pneumocytes.
 As early as 30 minutes after an acute insult, there is
increased synthesis of interleukin 8 (IL-8), a potent
neutrophil
chemotactic and activating agent, by pulmonary
macro- phages. Release of this and similar mediators,
such as IL-1 and tumor necrosis factor (TNF), leads to
endothelial activation as well as sequestration and
activation of neutrophils in pulmonary capillaries.
Activated neutrophils release a variety of products
(e.g., oxidants, proteases, platelet-activating factor,
leukotrienes) that cause damage to the alveolar
epithelium and endothelium. Combined assault on the
endothelium and epithelium perpetuates vascular
leakiness and loss of surfactant that render the
 In the organizing stage, proliferation of type II
pneumocytes occurs in an attempt to regenerate
the alveolar lining. Resolution is unusual; more
commonly, there is organization of the fibrin
exudates, with resultant intra-alveolar fibrosis.
Marked thickening of the alveolar septa ensues,
caused by proliferation of interstitial cells and
deposition of collagen.
Morphology:
 In the acute phase of ARDS, the lungs are dark
red, firm, airless, and heavy.
Microscopic examination reveals capillary
congestion, necrosis of alveolar epithelial cells,
interstitial and intra-alveolar edema and
hemorrhage, and (particularly with sepsis)
collections of neutrophils in capillaries. The most
characteristic finding is the presence of hyaline
membranes, particularly lining the distended
alveolar ducts, such membranes consist of fibrin-
rich edema fluid mixed with remnants of necrotic
epithelial cells.
Exams and Tests:
 Listening to the chest with a stethoscope
(auscultation) reveals abnormal breath sounds,
such as crackles, which may be signs of fluid in
the lungs. Often, blood pressure is low.
Tests used to diagnose ARDS include:
 Arterial blood gas
 Blood and urine cultures
 Bronchoscopy
 Chest X-ray
 Sputum cultures and analysis
Possible Complications:
 Failure of many organ systems
 Lung damage due to injury from the breathing
machine needed to treat the disease
 Pulmonary fibrosis (scarring of the lung)
 Ventilator-associated pneumonia
Treatment:
ARDS often needs to be treated in an intensive
care unit (ICU).
The goal of treatment is to provide breathing
support and treat the cause of ARDS. This may
involve medicines to treat infections, reduce
inflammation, and remove fluid from the lungs.
A ventilator is used to deliver high doses of oxygen
and continued pressure (positive end-expiratory
pressure, or PEEP) to the damaged lungs. Patients
often need to be deeply sedated with medicines.
During treatment, doctors and nurses make every
effort to protect the lungs from further damage

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Acute respiratory distress syndrome

  • 2. Acute respiratory distress syndrome : Acute respiratory distress syndrome (ARDS) is a clinical syndrome caused by diffuse alveolar capillary and epithelial damage, it’s a condition that prevents enough oxygen from getting to the lungs and into the blood. The usual course is characterized by respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy and may progress to multisystem organ failure.
  • 3. The histologic manifestation of ARDS in the lungs is known as diffuse alveolar damage (DAD).
  • 4.
  • 5. ARDS can be caused by any major direct or indirect injury to the lung:
  • 6. Pathogenesis:  The alveolar-capillary membrane is formed by two separate barriers: the microvascular endothelium and the alveolar epithelium. In ARDS, the integrity of this barrier is compromised by either endothelial or epithelial injury, or, more commonly, both. The acute consequences of damage to the alveolar capillary membrane include increased vascular permeability and alveolar flooding, loss of diffusion capacity, and widespread surfactant abnormalities caused by damage to type II pneumocytes.
  • 7.  As early as 30 minutes after an acute insult, there is increased synthesis of interleukin 8 (IL-8), a potent neutrophil chemotactic and activating agent, by pulmonary macro- phages. Release of this and similar mediators, such as IL-1 and tumor necrosis factor (TNF), leads to endothelial activation as well as sequestration and activation of neutrophils in pulmonary capillaries. Activated neutrophils release a variety of products (e.g., oxidants, proteases, platelet-activating factor, leukotrienes) that cause damage to the alveolar epithelium and endothelium. Combined assault on the endothelium and epithelium perpetuates vascular leakiness and loss of surfactant that render the
  • 8.
  • 9.  In the organizing stage, proliferation of type II pneumocytes occurs in an attempt to regenerate the alveolar lining. Resolution is unusual; more commonly, there is organization of the fibrin exudates, with resultant intra-alveolar fibrosis. Marked thickening of the alveolar septa ensues, caused by proliferation of interstitial cells and deposition of collagen.
  • 10.
  • 11. Morphology:  In the acute phase of ARDS, the lungs are dark red, firm, airless, and heavy. Microscopic examination reveals capillary congestion, necrosis of alveolar epithelial cells, interstitial and intra-alveolar edema and hemorrhage, and (particularly with sepsis) collections of neutrophils in capillaries. The most characteristic finding is the presence of hyaline membranes, particularly lining the distended alveolar ducts, such membranes consist of fibrin- rich edema fluid mixed with remnants of necrotic epithelial cells.
  • 12. Exams and Tests:  Listening to the chest with a stethoscope (auscultation) reveals abnormal breath sounds, such as crackles, which may be signs of fluid in the lungs. Often, blood pressure is low. Tests used to diagnose ARDS include:  Arterial blood gas  Blood and urine cultures  Bronchoscopy  Chest X-ray  Sputum cultures and analysis
  • 13. Possible Complications:  Failure of many organ systems  Lung damage due to injury from the breathing machine needed to treat the disease  Pulmonary fibrosis (scarring of the lung)  Ventilator-associated pneumonia
  • 14. Treatment: ARDS often needs to be treated in an intensive care unit (ICU). The goal of treatment is to provide breathing support and treat the cause of ARDS. This may involve medicines to treat infections, reduce inflammation, and remove fluid from the lungs. A ventilator is used to deliver high doses of oxygen and continued pressure (positive end-expiratory pressure, or PEEP) to the damaged lungs. Patients often need to be deeply sedated with medicines. During treatment, doctors and nurses make every effort to protect the lungs from further damage