HIGH on Broad Peak in the mountains of Pakistan, Pete Thexton realised he was in trouble. As a doctor, he recognised the signs of fluid building up in his lungs. He told his partner that it felt as if his diaphragm had stopped working and asked whether his lips were blue. They were. The pair began descending, but it was too late. Less than 12 hours later, Thexton was dead.
Doctors in Switzerland have now shown just what leads to high altitude pulmonary oedema (HAPE), the condition that killed Thexton in 1984, and why some people are probably genetically susceptible. They hope their work could make it possible to identify those at risk, as well as improving prevention and treatment.
The primary cause of HAPE has long been understood. Above 2500 metres, the body compensates for the low oxygen levels by increasing blood pressure in the lungs, which forces more fluid into the air sacs, or alveoli. Most people can clear their lungs of this fluid, but in some it builds up to dangerous levels. Careful acclimatisation reduces the risk substantially but HAPE can still occur in fit individuals who have been at altitude for some time.
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The Swiss team, based at the Centre Hospitalier Universitaire Vaudois in Lausanne, suspected that susceptibility to HAPE might be connected with the efficiency of sodium pumps in the cells lining lung alveoli. These help rid the lungs of excess fluid by pumping sodium ions out of the fluid into the surrounding tissue. The resulting concentration difference draws water out of the lungs by osmosis. In 2002, the team showed that an asthma drug called salmeterol, which boosts the activity of sodium pumps, halves the risk of HAPE.
Now the researchers have provided further evidence. The team enlisted 21 mountaineers who had suffered HAPE in the previous five years, and 29 who, despite long careers involving climbing above 4000 metres, had not. To test the efficiency of sodium pumps within the respiratory tract, they measured the potential difference across one part of the nasal membrane. Since sodium ions are positively charged, the more effectively the pumps are working, the higher potential difference (PD) should be. Sure enough, the climbers who had suffered from HAPE in the past had a lower nasal PD on average.
Next the climbers were taken from sea level to a research centre on Monte Rosa in the Italian Alps, at 4556 metres the highest mountain hut in Europe. After just 16 hours at altitude, 13 of the 21 climbers prone to HAPE developed signs of the condition, and their nasal PDs had fallen significantly. By contrast, all 29 HAPE-resistant climbers remained healthy, and their nasal PDs remained high (The European Respiratory Journal, vol 23, p 916).
Team member Urs Scherrer hopes the findings will lead to a test for identifying those susceptible to HAPE before they go to high altitudes. 鈥淧eople underestimate the number of those who will develop this condition,鈥� he said. 鈥淚f you took a group off the streets of London and took them straight to 4500 metres, then 10 per cent would develop HAPE.鈥�
Measuring nasal PD alone would not be a very accurate predictor, as at low altitudes there is some overlap between the scores of those who are and are not susceptible. But this test could be combined with other predictive measures, such as blood pressure in the lungs. It might also be possible to identify the underlying genetic variations. Those found to be susceptible could take salmeterol during climbs as a preventive measure.
In the meantime, Scherrer stresses the importance of acclimatisation. He also advises climbers to continue carrying the angina drug nifedipine.