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Study Zeroes In on Fatal Altitude Illness

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ASSOCIATED PRESS

Climbers who hiked the highest mountain in Switzerland have led researchers to a new understanding of a potentially fatal condition that strikes at high altitudes.

The study discovered a trigger that sets off high altitude pulmonary edema, known as HAPE, in which leaks from blood vessels fill the lungs with fluid.

HAPE apparently results from a buildup of pressure in capillaries in the lungs, the study found.

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“You need to know the capillary pressure, and then you can distinguish between those who get the condition and those who don’t,” said Dr. Marco Maggiorini, lead author of the paper in the journal Circulation.

Maggiorini and his colleagues compared 16 climbers who had experienced HAPE previously with 14 who had never developed it. All received right heart catheterization. In this procedure, a long tube is threaded through the heart to the pulmonary artery, which brings blood from the heart to the lungs.

The researchers inflated a tiny balloon at the tip of the catheter and checked for changes in pressure in the pulmonary capillaries, tiny vessels in which blood picks up oxygen from the lungs. The researchers also used irradiated red blood cells to check the capillaries’ permeability--their capacity to let oxygen molecules pass through.

The climbers were first tested at the University Hospital of Zurich, where the altitude is around 1,617 feet above sea level--far too low to trigger HAPE. Within three weeks of the initial exam, the climbers trekked up Monte Rosa--a 24-hour trip including an overnight stop and a walk on a glacier.

The climbers wound up at a research lab at 15,045 feet, near the top of the mountain and well above the 8,250-foot level at which HAPE can occur. There they were given new right heart catheterizations.

Nine of the previous HAPE sufferers developed the condition again. All nine had the highest capillary pressures. Climbers who had suffered HAPE before, but not this time, had lower pressure. Controls who had never suffered HAPE had the lowest pressure.

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There was no meaningful difference in the ability of the climbers’ capillaries to let oxygen pass through to blood cells. And there was no sign of inflammation, which had been considered a possible trigger of HAPE.

Capillary pressure was the only thing that seemed to make a difference, and this may be enough to trigger the leakage that fills the lungs with fluid, Maggiorini said.

“The idea that it’s high pressure and not inflammation is an important advance,” said Dr. John D. Reeves, professor emeritus at the University of Colorado Health Sciences Center in Denver.

The Swiss research underscores the value of treating HAPE with drugs to dilate the blood vessels, although anti-inflammatory drugs may be needed if inflammation develops later, said Dr. John B. West, a professor at the University of San Diego Medical School.

Vessel-dilating drugs can be used to prevent HAPE as well as treat it, and mountaineers who are susceptible to HAPE should ask their doctors for them, Maggiorini said. He suggested nifedipine, a common circulatory system drug. It is sold in the United States under the names Procardia and Adalat.

While drug treatment is valuable, it should not be needed if someone spots HAPE’s symptoms quickly and takes the victim below 8,000 feet, Reeves said. Symptoms include extreme listlessness, coughing up blood or sputum, and a feeling in the chest that the victim might describe as “strange.” Foggy thinking also is a symptom, so a HAPE sufferer might not realize he or she is ill.

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HAPE may be prevented if people take several days to go up to the higher altitude, Reeves said. Similarly, some time under about 8,000 feet can give a HAPE sufferer time to adjust, he said.

HAPE is far less common than mountain sickness, which also afflicts people who ascend quickly to high altitude. Symptoms include listlessness and headache. But mountain sickness is not fatal, and it passes as people adjust to the high altitude.

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