Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gas can enter arteries (arterial gas embolism) due to alveolar-capillary disruption (caused by pulmonary overpressurization, e.g., breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is sub-atmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces strokelike manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries. However, VGE can cause pulmonary edema, cardiac "vapor lock" and AGE due to transpulmonary passage or right-to-left shunt through a patent foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.
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PMID:Hyperbaric oxygen treatment for air or gas embolism. 2485 54

Swimming-induced pulmonary edema (SIPE) may develop during strenuous physical exertion in water. This case series reports on three cases of suspected late-presenting SIPE during the Norseman Xtreme Triathlon. A 30-year-old male professional (PRO) triathlete, a 40-year-old female AGE GROUP triathlete and a 34-year-old male AGE GROUP triathlete presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. All three athletes reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. The PRO athlete had a thoracic computed tomography, and the scan showed bilateral ground glass opacity in the peripheral lungs. The male AGE GROUP athlete had a normal chest x-ray. Both athletes were admitted for further observation and discharged from hospital the following day, with complete regression of symptoms. The female athlete recovered quickly following pre-hospital oxygen treatment. Non-cardiogenic pulmonary edema associated with endurance sports is rare but potentially very dangerous. Knowledge and awareness of possible risk factors and symptoms are essential, and the results presented in this report emphasize the importance of being aware of the possible delayed development of symptoms. To determine the presence of pulmonary edema elicited by strenuous exercise, equipment for measuring oxygen saturation should be available for the medical staff on site.
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PMID:Late-Presenting Swimming-Induced Pulmonary Edema: A Case Report Series from the Norseman Xtreme Triathlon. 3116 77

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac "vapor lock" and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence based review of adjunctive therapies is presented.
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PMID:Hyperbaric treatment of air or gas embolism: current recommendations. 3168 67