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It is often impossible to distinguish TRALI from acute respiratory distress syndrome (ARDS). The typical presentation of TRALI is the sudden development of shortness of breath, severe hypoxemia (O 2 saturation <90% in room air), low blood pressure, and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours.
Flash Pulmonary Edema or Crash Pulmonary Edema is a clinical characterization of acute heart failure with a dramatic presentation. [4] It is an acute cardiac disease precipitated by cardiac events and usually associated with severe hypertension.
Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs. [1] This leads to impaired gas exchange , most often leading to shortness of breath ( dyspnea ) which can progress to hypoxemia and respiratory failure .
Alcohol excess appears to increase the risk of ARDS. [47] Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema. [48] [49] Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.
Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. [3] [4] Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase.
NPPE develops as a result of significant negative pressure generated in the chest cavity by inspiration against an upper airway obstruction. These negative pressures in the chest lead to increase venous supply to the right side of the heart while simultaneously creating more resistance for the left side of the heart to supply blood to the rest of the body (). [4]
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]
Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic shock). Lactic acidosis and anemia can also result in type 4 respiratory failure. [1] However, type 1 and 2 are the most widely accepted. [1] [4] [5]