Travellers are drawn to high altitude places in ever increasing numbers - Nepal alone now receives more than one hundred thousand trekkers from around the world every year. It can be easy to under-estimate the dangers of altitude illness; deaths from these conditions are all the more tragic because they are entirely preventable.

Mountain climbers, serious trekkers, romantics sauntering through the foothills of the Himalayas, native porters, skiers in North America and Europe, pilgrims to high altitude shrines, diplomats posted to La Paz or Lhasa, miners in South America, and Everest marathon runners have something in common: they are all exposed to the effects of high altitude, and may be at risk from a potentially fatal but eminently preventable problem: acute mountain sickness, commonly referred to just as AMS. 

AMS consists of headache plus any one of the following symptoms in different degrees: nausea, tiredness, sleeplessness or dizziness, occurring at altitudes of around 8000 ft or higher where pathophysiological changes due to lack of oxygen may manifest. Another term, "altitude illness", is also widely used - an umbrella term that includes the benign acute mountain sickness and its two life-threatening complications, water accumulation in the brain (high altitude cerebral oedema, HACE) or high altitude pulmonary oedema (HAPE, water accumulation in the lungs). The latter two complications may follow AMS, especially when people continue to ascend in the face of increasing symptoms. In keeping with the Jesuit tradition of painstaking documentation, Father Joseph de Acosta, a sixteenth century Spanish Jesuit priest, is credited with having first described the effects of high altitude in humans. In vernacular Nepali, mountain sickness is called "lake lagne"; in Sanskrit it is aptly called "damgiri" ("dam" means breathlessness and "giri" means mountain).

Those most at danger from complications are people who do not "listen to their body", and heed the early warning signals of AMS; they can go on to suffer from HAPE and HACE and may even die - a process that has been carefully documented in important autopsy studies performed by Walter Bond and John Dickinson during the Seventies in the old Shanta Bhawan hospital in Nepal. 

Chronic mountain sickness is an entirely different condition, recognized by Carlos Monge Medrano in high altitude long-term residents of South America during the Twenties. Such maladaptation is seldom found in the Sherpas or Tibetans, possibly due to thousands of years of exposure to high altitude living. (South Americans populations are relative newcomers to high altitude.)
The present discussion will be confined to acute exposure to altitude in short-term sojourners.

If a participant on an Everest trek suffers from a mild headache and nausea at Namche Bazaar (12,300ft), he might take an aspirin and wait for these symptoms to go away; however if the symptoms progress to vomiting and a splitting headache, he must assume that he is suffering from AMS and make plans to descend. It is amazing how many people in this situation ignore the dangers and continue to ascend with their friends, trying to blame their symptoms on poor fitness or flu. For some people, it's the high investment of time, effort and money, for others perhaps it's peer pressure or reluctance to accept defeat. A further problem is that many in the burgeoning adventure travel industry are clueless about mountain sickness. 

AMS may set in within hours to days of arrival at high altitude: the onset of symptoms is usually gradual, which is why it is so vital to watch out for early warnings: does a person feel excessively tired; is she the last one to drag herself in to camp?

AMS is caused by a lack of oxygen. Although the proportion of oxygen in the atmosphere always remains the same (21%), as we go higher the "driving pressure" decreases. The driving pressure depends directly on the barometric pressure, and forces
oxygen from the atmosphere into the capillaries of the lungs. Reduced driving pressure results in decreased saturation of oxygen in the blood and throughout the tissues. 

Just what causes some people to suffer from AMS but not others is largely unknown, but there are clear-cut and important preventive factors that are now well established (see below). The exact mechanism (pathophysiology) of AMS has similarities to that of HACE.

Our trekker in the above example would probably go on to suffer from HACE if he continued to ascend despite the headache and vomiting; the symptoms of HACE are an extension of those of AMS. 

From fatigue, there is progression to lethargy and then to coma. Or there may be confusion and disorientation. A useful test is to see if the person can walk a straight line. If he walks like a drunk or is unsteady, it has to be assumed that he has life-threatening HACE and needs to descend promptly with assistance. This situation is serious enough to justify immediate helicopter evacuation.

HACE is probably caused by shifts of fluid into the tissues of the brain. Reduced oxygen levels cause swelling within the confines of the bony skull. The resulting rise in pressure may lead to lethargy and eventually coma.

This disease may follow AMS, but often it may appear independently. The typical scenario would be a trekker who has no headache or nausea, but finds he has a harder time walking uphill, that he is out of breath on slight exertion compared with the initial days of the trek. There may be a nagging cough and he too may have ascribed these symptoms to a cold. He may be suffering from subclinical or early HAPE, a well-recognized entity. With further ascent this may progress to shortness of breath
even at rest - descent is now obligatory, or the outcome may be fatal. Low oxygen causes the pulmonary artery to narrow and this results in exudation of blood near the smaller branches of the lungs (the alveoli). If the exudation continues, blood may
escape into the alveoli leading to a cough with watery, blood-tinged phlegm. Such exudation, or "water logging" of the lung tissue interferes further with oxygenation. A popular, compact device called a pulse oximeter can measure the oxygen level in
the blood simply and rapidly, using a sensor attached to the index finger. It can be very helpful in confirming if HAPE is present.

Acclimatization is a state of physiological "truce" between the body of a visitor and the hostile low-oxygen environment of high altitude. This truce permits the trekker to ascend gradually. (This is distinct from "adaptation" - permanent change to the organism, perhaps over thousands of years, perhaps even at a genetic or evolutionary level, to facilitate survival at altitude.
Scientists are trying to decipher if the Sherpas or Tibetans have made such an adaptation.) For acclimatization to take place the single most important step is hyperventilation - the trekker unconsciously breathes faster and more deeply than normal, even at rest, to make up for the lack of oxygen. However, hyperventilation also leads to loss of carbon dioxide from the blood, making the blood more alkaline, and in turn depressing ventilation. However, 48 to 72 hours after exposure to high altitude, the kidney comes to the rescue and begins to excrete alkali from the blood to restore a more balanced environment in which hyperventilation can continue unabated.