Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Acute pulmonary oedema has been described in individuals participating in three aquatic activities: (i) scuba diving; (ii) breath-hold diving; and (iii) endurance swimming. In this review, 60 published cases have been compiled for comparison. Variables considered included: age; past medical history; activity; water depth, type (salt or fresh) and temperature; clinical presentation; investigations; management; and outcome. From these data, we conclude that a similar phenomenon is occurring among scuba, breath-hold divers and swimmers. The pathophysiology is likely a pulmonary overperfusion mechanism. High pulmonary capillary pressures lead to extravasation of fluid into the interstitium. This overperfusion is caused by the increase in ambient pressure, peripheral vasoconstriction from ambient cold, and increased pulmonary blood flow resulting from exercise. Affected individuals are typically healthy males and females. Older individuals may be at higher risk. The most common symptoms are cough and dyspnoea, with haemoptysis also a frequent occurrence. Chest pain has never been reported. Radiography is the investigation of choice, demonstrating typical findings for pulmonary oedema. Management is supportive, with oxygen the mainstay of treatment. Cases usually resolve within 24 hours. In some cases, diuretics have been used, but there are no data as to their efficacy. Nifedipine has been used to prevent recurrence, but there is only anecdotal evidence to support its use.
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PMID:Pulmonary oedema of immersion. 1573 Mar 35