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)

It is well known that inhalation of pyrolysis products of perfluorinated hydrocarbons (e.g. Teflon) may result in polymer-fume fever and even pulmonary oedema. A new type of ski wax has recently been introduced, a powder consisting of low-molecular perfluorinated hydrocarbons. We report a case history of a man who developed an attack of polymer-fume fever and pulmonary oedema after smoking cigarettes contaminated with this ski wax. Inhalation of vapour from ski waxes melted at low temperatures may also be harmful to the lungs.
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PMID:[Pulmonary damage caused by ski waxing]. 226 59

When possible, the management of acute cardiogenic pulmonary edema should be started before the patient reaches the hospital. Simple measures such as having the patient sit up with the legs dependent, administering oxygen by nasal prongs, giving sublingual nitroglycerin and small doses of morphine, and rotating tourniquets on the limbs may reduce the need for more intensive procedures. Digoxin and other inotropic agents, aminophylline, furosemide, and vasodilators are given as appropriate during hospitalization. A minority of patients need endotracheal intubation and pressure monitoring with a Swan-Ganz catheter. If the arterial PO2 cannot be maintained at 60 mm Hg or more during face mask ventilation, the PCO2 rises, and the arterial pH declines, the patient should be intubated. Pressure monitoring with a Swan-Ganz catheter is indicated if the patient does not immediately respond to treatment or in special situations such as cardiogenic shock with pulmonary edema. Pulmonary edema caused by diastolic dysfunction is managed differently than that caused by systolic dysfunction. The cause and precipitating factors of the acute pulmonary edema should be sought and treated as early as possible to prevent recurrences.
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PMID:Treatment of acute pulmonary edema. 792 65

A 45-year-old, healthy, well-trained man climbed within 12 hours from 300 m above sea level to a shelter at 2500 m in the Tyrolean Alps. During the following 3 days he undertook ski tours to the surrounding mountains up to 3356 m. On the 4th day he suddenly suffered from headache, coughing and very severe dyspnoea even at rest, accompanied by loss of appetite and the feeling of suffocation. The following day he was rescued by a helicopter and taken to hospital. At the time of admission the patient was severely hypoxaemic (capillary PO2 = 25.7 mmHg), and the chest X-ray revealed signs of bilateral alveolar pulmonary edema localised predominantly in the right lung. High-altitude pulmonary edema (HAPE) was diagnosed because of the typical clinical course. Pulmonary gas exchange normalised within hours, and complete restitution was achieved within 2 days. The chest X-ray was normal on the 4th day after admission. HAPE is a non-cardiogenic pulmonary edema which develops in healthy individuals usually above 3000 m. Among the predisposing factors are rapid ascent, severe physical effort, diminished hypoxic ventilatory response and abnormal fluid balance. The treatment of choice is descent to a lower altitude, administration of oxygen and of nifedipine and expiratory positive airway pressure.
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PMID:[High altitude pulmonary edema at a medium height. A case report]. 817 68

Ten cases of acute renal failure (ARF) were seen in the period from July 1990 to August 1991 in the Nephrology Department of the SIMS Hospital, Srinagar. All were males in the age group of 18-28 years and in apparent good health when apprehended by the police. There was alleged history of physical torture of different types. All had been beaten on the buttocks, back and limbs; in addition, 2 cases had been given repeated electric shocks and 1 case put to 'sit-and-stand' exercise for about 3 h. The interval between the first day of torture till they came to our observation varied from 4 to 11 days. The main clinical features at the time of presentation were generalized aches and weakness (10), oligoanuria (9), vomiting (8), hypertension (6), acidosis (10), facial puffiness and pedal edema (6), fever and shivering (3), pulmonary edema (2), stupor (4), and hyperkalemia (5). All the cases had an established ARF (serum creatinine 668-1,997 mumol/l and serum urea 21.8-71.8 mmol/l) when first seen. Muscle enzymes, creatine phosphokinase, lactic dehydrogenase and serum glutamic oxaloacetic transaminase were all significantly raised indicating rhabdomyolysis. All showed evidence of myoglobin casts in urine. Nine had oliguric and 1 had nonoliguric ARF. All except the 1 case with nonoliguric ARF were managed with peritoneal dialysis and/or hemodialysis. All recovered. Early recognition of ARF is important since the main attention in such cases is directed towards the surgical aspect.
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PMID:Acute renal failure following physical torture. 845 79

Medical records of 150 patients with high-altitude pulmonary edema seen over a 39-month period in a Colorado Rocky Mountain ski area at 2,928 m (9,600 ft) (mean age 34.4 years; 84% male) were reviewed. The mean time to the onset of symptoms was 3 +/- 1.3 days after arrival. Common symptoms were dyspnea, cough, headache, chest congestion, nausea, fever, and weakness. Orthopnea, hemoptysis, and vomiting were rare, occurring in 7%, 6%, and 16%, respectively. Symptoms of cerebral edema occurred in 14%. A temperature exceeding 100 degrees F occurred in 20%, and 17% had a systolic blood pressure of 150 mm of mercury or higher. Blood pressures were higher in patients older than 50 years (142 mm of mercury). Rales were present in 85%, and a pulmonary infiltrate was present in 88%; both were most commonly bilateral or on the right side. The amount of infiltrate was mild. Men appeared to be more susceptible than women to high-altitude pulmonary edema. Pulse oximetry in 45 patients showed a mean oxygen saturation of 74% (38% to 93%). Treatment methods depended on severity and included a return to quarters for portable nasal oxygen, an overnight stay in the clinic for continuing oxygen, or a descent to Denver for recovery or admission to a hospital. All patients received oxygen for 2 to 4 hours in the clinic. There were no deaths or complications.
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PMID:High-altitude pulmonary edema at a ski resort. 877 33

High altitude retinal hemorrhages are commonly seen at altitudes above 4270 m. While these hemorrhages are generally asymptomatic, macular involvement may result in permanent visual acuity deficit. We present the case of a 29-year-old male recreational skier who traveled to a ski resort at 2930 m, ascended to 3470 m, and developed acute mountain sickness, high altitude pulmonary edema, and bilateral retinal hemorrhages. A funduscopic examination to determine if macular retinal hemorrhage is present may be performed by clinicians in the final assessment of patients following altitude illness.
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PMID:High altitude retinal hemorrhages in a Colorado skier. 1180 95

A 34-year-old man presented to a clinic at a ski resort in the Rocky Mountains at 9000 feet (2743 m) with shortness of breath and fatigue, a few days after arriving to altitude from sea level. He was found to be hypoxic with radiographic findings consistent with high altitude pulmonary edema (HAPE). He was treated with high flow oxygen, steroids, and calcium channel blockers and transferred to a lower altitude tertiary care hospital for intensive care unit monitoring and further treatment. During his diagnostic evaluation, he was found to have both a patent foramen ovale and influenza B infection. While patent foramen ovale is a known risk factor for HAPE, there is also some evidence that upper respiratory tract infections in general and influenza in particular may also be risk factors for HAPE. The 2 diseases may share an underlying pulmonary pathophysiology, as both cause noncardiogenic pulmonary edema and alveolar hemorrhage. We report an unusual case of influenza B virus compounded by previously undiagnosed patent foramen ovale, travel to high altitude, and subsequent development of HAPE.
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PMID:Influenza B infection complicated by patent foramen ovale and high altitude pulmonary edema. 2302 59

Our hypothesis is that symptoms of high altitude syndromes are detectable even at intermediate altitudes, as commonly encountered under Australian conditions (<2500 m above sea level). High altitude medicine has long recognised several syndromes associated with rapid ascent to altitudes above 2500 m, including high altitude pulmonary oedema (HAPE), high altitude cerebral oedema (HACE) and high altitude flatus expulsion (HAFE). Symptoms of high altitude syndromes are of growing concern because of the global trend toward increasing numbers of tourists and workers exposed to both rapid ascent and sustained physical activity at high altitude. However, in Australia, high altitude medicine has almost no profile because of our relatively low altitudes by international standards. Three factors lead us to believe that altitude sickness in Australia deserves more serious consideration: Australia is subject to rapid growth in alpine recreational industries; altitude sickness is highly variable between individuals, and some people do experience symptoms already at 1500 m; and there is potential for an occupational health and safety issue amongst workers. To test this hypothesis we examined the relationship between any high altitude symptoms and a rapid ascent to an intermediate altitude (1800 m) by undertaking an intervention study in a cohort of eight medical clinic staff, conducted during July of the 2012 (Southern Hemisphere) ski season, using self-reporting questionnaires, at Mansfield (316 m above sea level) and at the Ski Resort of Mt Buller (1800 m), Victoria, Australia. The intervention consisted of ascent by car from Mansfield to Mt Buller (approx. 40 min drive). Participants completed a self-reporting questionnaire including demographic data and information on frequency of normal homeostatic processes (fluid intake and output, food intake and output, symptoms including thirst and headaches, and frequency of passing wind or urine). Data were recorded in hourly periods extending over 18 h before and 18 h after ascent. We found that the frequency of flatus production more than doubled following ascent, with a post-ascent frequency of approximately 14 expulsions per person over the 18 h recording period (Rate Ratio 2.31, CI 1.33-3.99, p=0.003). The frequency and severity of headaches also increased following ascent. These results support the hypothesis that high altitude symptoms can be significant issues even at the relatively lower altitudes encountered in Australian alpine regions. Increased awareness amongst clinicians of this possibility could contribute to a reduction in the disease burden from high altitude syndromes at intermediate altitudes.
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PMID:High altitude syndromes at intermediate altitudes: a pilot study in the Australian Alps. 2389 Oct 43

Every year thousands of ski, trekking or climbing fans travel to the mountains where they stay at the altitude of more than 2500-3000m above sea level or climb mountain peaks, often exceeding 7000-8000m. High mountain climbers are at a serious risk from the effects of adverse environmental conditions prevailing at higher elevations. They may experience health problems resulting from hypotension, hypoxia or exposure to low temperatures; the severity of those conditions is largely dependent on elevation, time of exposure as well as the rate of ascent and descent. A disease which poses a direct threat to the lives of mountain climbers is high altitude pulmonary edema (HAPE). It is a non-cardiogenic pulmonary edema which typically occurs in rapidly climbing unacclimatized lowlanders usually within 2-4 days of ascent above 2500-3000m. It is the most common cause of death resulting from the exposure to high altitude. The risk of HAPE rises with increased altitude and faster ascent. HAPE incidence ranges from an estimated 0.01% to 15.5%. Climbers with a previous history of HAPE, who ascent rapidly above 4500m have a 60% chance of illness recurrence. The aim of this article was to present the relevant details concerning epidemiology, pathophysiology, clinical symptoms, prevention, and treatment of high altitude pulmonary edema among climbers in the mountain environment.
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PMID:High altitude pulmonary edema in mountain climbers. 2529 Nov 81

High intensity exercise is associated with several potentially thrombogenic risk factors, including dehydration and hemoconcentration, vascular trauma, musculoskeletal injuries, inflammation, long-distance travel, and contraceptive usage. These are well documented in case reports of venous thrombosis in track and field athletes. For mountaineers and those working at high altitude, additional risks exist. However, despite there being a high degree of vigilance for "classic" conditions encountered at altitude (eg, acute mountain sickness, high altitude pulmonary edema, and high altitude cerebral edema), mainstream awareness regarding thrombotic conditions and their complications in mountain athletes is relatively low. This is significant because thromboembolic events (including deep vein thrombosis, pulmonary embolism, and cerebral vascular thrombosis) are not uncommon at altitude. We describe a case of deep vein thrombosis and pulmonary embolism in a male mountain guide and discuss the diagnostic issues encountered by his medical practitioners. Potential risk factors affecting blood circulation (eg, seated car travel and compression of popliteal vein) and blood hypercoagulability (eg, hypoxia, environmental and psychological stressors [avalanche risk, extreme cold]) relevant to the subject of this report and mountain athletes in general are identified. Considerations for mitigating and managing thrombosis in addition to personalized care planning at altitude are discussed. The prevalence of thrombosis in mountain athletes is uncharted, but lowlanders increasingly go to high altitude to trek, ski, or climb. Blood clots can and do occur in physically active people, and thrombosis prevention and recognition will demand heightened awareness among participants, healthcare practitioners, and the altitude sport/leisure industry at large.
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PMID:Deep Vein Thrombosis and Pulmonary Embolism in a Mountain Guide: Awareness, Diagnostic Challenges, and Management Considerations at Altitude. 2672 46


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