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Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. [1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). [ 1 ]
The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]
Acute respiratory distress syndrome : a potentially life-threatening condition where the alveoli are damaged thereby letting fluid leak into the lungs which makes it difficult to exchange gases and oxygenate the blood. [3] It is the general practice of the medical community to use the Berlin criteria to diagnose ARDS.
There are multiple causes of noncardiogenic edema with multiple subtypes within each cause. Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Although ARDS can present with pulmonary edema (fluid accumulation), it is a distinct clinical syndrome that ...
Acute interstitial pneumonitis is often categorized as both an interstitial lung disease and a form of acute respiratory distress syndrome (ARDS). In uncommon instances, if ARDS appears acutely, in the absence of known triggers, and follows a rapidly progressing clinical course, the term "Acute interstitial pneumonia" is used. [ 1 ]
Both the release of fatty acids and the inflammation causes damage to the capillary beds [6] of the lungs and other organs, causing interstitial lung disease, chemical pneumonitis, [7] and acute respiratory distress syndrome (ARDS). [6] This theory can help to explain non-traumatic causes of fat embolism. [7]
The cause of TRALI is currently not fully understood. 80–85% of cases are thought to be immune mediated. [5] [6] Antibodies directed toward human leukocyte antigens (HLA) or human neutrophil antigens (HNA) have been implicated, with transfused antibodies shown to bind antigens expressed on pulmonary endothelial cells to initiate acute inflammation in the lungs.
It is usually caused by respiratory syncytial virus (RSV), which is spread when an infant touches the nose or throat fluids of someone infected. [26] The virus infects the cells causing ciliary dysfunction and death. The debris, edema, and inflammation eventually leads to the symptoms. [27]