In children, pulmonary edema can be secondary to increased hydrostatic pressure This can be seen in cardiac conditions including congenital anomalies that are associated with left-sided heart failure, such as hypoplastic left heart syndrome, cor triatriatum, mitral stenosis, severe aortic stenosis, coarctation of the aorta, or acquired myocardial disease Pulmonary edema from overcirculation within the pulmonary vasculature secondary to left-to-right vascular shunting can occur with patent ductus arteriosus, ventricular septal defects, and iatrogenic cardiac shunts Beyond cardiac disease, increased hydrostatic pressures from overaggressive administration of IV fluids can also cause pulmonary edema Neurogenic pulmonary edema may be seen with seizure activity or increased intracranial pressure Although the mechanism is not entirely understood, it likely results from increased capillary hydrostatic pressures after acute sympathetic discharge in these patients The possibility of concomitant capillary leak in neurogenic pulmonary edema has also been proposed Decreased plasma oncotic pressure is also associated with pulmonary edema This condition is seen with lowered levels of circulating plasma proteins, such as occurs with nephrosis, protein-losing enteropathies, massive burns, and severe malnutrition Any breakdown in the alveolar–capillary barrier can result in accumulation of protein-rich fluid in the interstitium This is the initial and major manifestation of ARDS Lung insult leads to tissue destruction and increased permeability of the alveolar–capillary membrane In addition to ARDS, a variety of other clinical conditions can similarly lead to capillary leak syndromes Circulating toxins, such as snake venom and endotoxins from gram-negative sepsis, are examples In addition, altered permeability can lead to pulmonary edema from asthma, hypersensitivity pneumonitis, Goodpasture syndrome, and SLE Inhaled environmental exposures can have a similar effect Noxious gases from fires, hydrocarbons, oxides from sulfur and nitrogen, and inhalation of some herbicides (e.g., paraquat) can denature proteins and cause cellular damage with development of pulmonary edema Postobstructive pulmonary edema, also known as negative-pressure pulmonary edema, is associated with upper airway obstruction ( Fig 99.5 A–C ) It is thought to result from exaggeration of the transmural pulmonary vascular hydrostatic pressure gradient Re-expansion pulmonary edema can also occur following rapid drainage of a large pneumothorax or pleural effusion Pulmonary edema can also result from travel to high altitudes This characteristically affects young people who are exposed to altitudes above 2,700