Acute Respiratory Distress Syndrome (ARDS) is also known as shock lung, diffuse alveolar damage, or acute lung injury.
Severe acute lung injury is caused by toxic insults.
ARDS is characterized by the rapid onset of severe, life-threatening respiratory insufficiency (dyspnea and tachypnea), cyanosis, and
Chest radiographs are intially normal but soon show diffuse alveolar infiltration and bilateral opacities. As this can mimic heart failure, clinical correlates are also required for diagnosis.
Severe arterial hypoxemia and decreased PaO2, with a PaO2/FiO2 ratio less than 200, refractory to oxygen therapy.
Pulmonary arterial wedge pressure (surrogate for left atrial pressure) is <18 mmHg, suggesting no clinical evidence of left heart failure.
Histologically, hyaline membranes are present
ARDS results from diffuse alveolar capillary damage. Alveolar flooding leads to loss of diffusion capacity, and type II pneumocytes become damaged.
During the acute phase, epithelial and endothelial injury lead to edema and hyaline membranes form.
During the organizing phase, alveolar collapse, fibroblast proliferation, and fibrosis occurs. Diffuse tissue destruction is not easily repaired, and scarring results.
IL-1 and TNF recruit neutrophils, and NF-kB-mediated genes are transcribed.
ARDS has many causes:
infection
trauma and injury: fractures and fat emboli, burns, radiation
gas and chemical injury
multiple transfusions
disseminated intravascular coagulation
pancreatitis
uremia
cardiopulmonary bypass
hypersensitivitry reactions
idiopathic ARDS is referred to as acute interstitial pneumonia
Positive expiratory pressure (PEP) keeps the airways open and keeps them from filling with fluids.
Respiratory acidosis can develop.
Mortality rate is about 60%.