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Pulmonary edema has multiple causes and is traditionally classified as cardiogenic (caused by the heart) or noncardiogenic (all other types not caused by the heart). [2] [3] Various laboratory tests (CBC, troponin, BNP, etc.) and imaging studies (chest x-ray, CT scan, ultrasound) are often used to diagnose and classify the cause of pulmonary edema.
High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). [2] HAPE is a severe presentation of altitude sickness. Cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in people who ...
Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, is a life threatening condition that occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).
Other causes of pulmonary edema that require rapid intervention and should be considered first include fluid overload, brain injury, and anaphylaxis. If when considering these differentials, there is no evidence for administration of excessive fluids, no focal signs suggesting a brain injury, and so signs of allergic reaction, one can then ...
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.
Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. [4] [5] Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase.
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.
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]
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