High Altitude Medical Advice for Travelers

A Brief Review of the Pathophysiology of Altitude Illness

High Altitude Pulmonary Edema

High altitude pulmonary edema was first described as a unique clinical condition associated with altitude by Charles Houston in 1960. Prior to the late 1950’s, pulmonary deaths at altitude were attributed to acute cardiac failure or pneumonia. Houston described a young cross-country skier who had developed pulmonary edema while skiing over a 12,000 pass in Colorado. Subsequent tests ruled out any heart failure, and the pulmonary edema resolved rapidly with descent. The question remained, however, as to how and why the fluid leaked into the alveolar spaces in the first place. One of the mysteries was the speed with which the fluid could accumulate and cause death, and the remarkable reversibility of the fluid leakage once the person had descended. There were no existing medical models to explain this condition.

It has been shown that all visitors to high altitude experience an increase in their pulmonary artery pressure. This finding led to the conclusion that pressure alone was forcing a transudate into the alveolar tissue and air spaces. However, bronchoscopic lavage performed in climbers suffering from HAPE on Mt. McKinley demonstrated that the fluid was an exudate, with relatively large proteins. This forced the hypothesis that major leaks were developing in pulmonary capillaries. A current hypothesis postulates that increased intra-capillary pressure forces the basement membrane cells apart, allowing protein leakage. When the pulmonary artery pressure is reduced, the cells fall together again, sealing off the leak, and accounting for the dramatic recovery associated with descent.

However, pulmonary artery pressures are increased in all persons traveling to high altitude, and not all people get HAPE. Hackett has made the observation that climbers on Mt. McKinley who developed HAPE had a high pulmonary artery pressure. These climbers were evacuated to a lower altitude and recovered enough to ascend a few days later. Upon return to the same altitude where they had previously gotten ill, they remained asymptomatic, even though their pulmonary artery pressure just as high as before. Therefore, other unknown mechanisms must determine which of these people with high pulmonary artery pressures will subsequently develop HAPE.

High Altitude Cerebral Edema

The cerebral symptoms associated with altitude illness have been noted for over 2000 years, with reference to "the great headache mountains" in China. Initially, the symptoms were thought to be due to diffuse hypoxic swelling of cerebral cells. However, other models of hypoxic swelling, such as post-traumatic or post-anoxic, take much longer to reverse than HACE, which improves dramatically and rapidly with descent. Therefore, some researchers postulated that hypoxia triggered a deficiency of neurotransmitters, leading to the symptoms of AMS and HACE. Better understanding of neurotransmitters has fully refuted this theory. Recently, observations made by Hackett et al based on magnetic resonance images of brains in people who had been evacuated for HACE demonstrated the presence of free interstitial water in the area around the circle of Willets. This phenomenon of free water leaking into the brain is unique to HACE, and was previously thought to be impossible due to protective measures associated with the "blood-brain barrier." However, the leakage of free water into the interstitial space can explain the rapid reversibility of HACE with descent. [Personal communication from Peter Hackett].

There is also some evidence that the amount of space around the brain in the skull, and the ability of cerebrospinal fluid to flow down the spinal cord may also determine who gets symptoms of AMS or not. People with the capacity to accommodate small amounts of swelling in the brain appear to tolerate adjustment to altitude better than people with brains tucked more tightly into the skull.

Acclimatization Advice and Schedules: The Acclimatization Line

A person traveling to high altitude can be taught to understand the process of acclimatization and illness through a concept known as the "acclimatization line." A group of people standing at sea level would each have a hypothetical thin line at around 9000 feet, below which they will feel fine, and above which they would experience symptoms of altitude illness. The height of this acclimatization line would vary genetically with each individual. If the person ascends to altitude, but stays below the acclimatization line, there will be no symptoms, and the process of acclimatization can take place. After a night at 9000 feet, one’s acclimatization line will rise, perhaps to 11,500 feet. If one moves up the next day to 11,300 feet, one would remain asymptomatic and continue to acclimatize. However, if the person moves up to 11,800 feet, symptoms of AMS would ensue. It appears that if one’s symptoms begin to occur very near to the acclimatization line, the body can continue to adjust, and a day’s rest at the same height will result in resolution of symptoms. If the symptoms at 11,800 feet are ignored, however, and the person moves up another 1500 feet or so, the symptoms will continue to worsen and further adaptation will not take place. It is then necessary to get below the point where the symptoms began in order to start seeing improvement. This last point illustrates why it is so dangerous to ascend with any symptoms of altitude illness.

Altitude Advice for Travelers

Travelers on prolonged trips to high altitude, such as trekkers in Nepal, should be taught that sensible itineraries are only the first step in avoiding severe altitude illness. Most trekking itineraries are a middle-of-the-road approach, and do not guarantee that all clients will not get altitude illness. The main goal of altitude illness advice is not to avoid getting altitude symptoms at all, but to react appropriately if altitude symptoms do occur. In other words, it’s okay to get altitude illness, but it’s not okay to die from altitude illness.

The main safety points in regard to altitude illness can be summarized in the following three rules:

• Learn the early symptoms of altitude illness and be willing to recognize when you have them.
• Never ascend to sleep at a higher altitude with any symptoms of altitude illness.
• Descend if your symptoms are getting worse while resting at the same altitude.

When we review cases of fatal altitude illness, we almost invariably find that the person ascended with symptoms that could have been recognized as due to altitude illness. In most of these cases, the symptoms were either ignored, minimized, or attributed to another cause. In organized trekking groups, there is a great deal of pressure to keep up with the group schedule or be left behind. Since leaving a client behind is problematic logistically for a trekking group, even the leader can contribute to the denial of altitude symptoms. Trekkers who are traveling with an organized trekking group may have a false sense of security in regard to their risk of dying from altitude illness. A 1991 study showed that trekkers in organized trekking groups had a statistically significant increased risk of dying compared to trekkers who were not in an organized group⁴. This fact emphasizes that group pressure and the reluctance to be left behind if one admits symptoms is a risk factor for dying from altitude illness. Thus, being willing to recognize altitude symptoms when they are present is a key point.

AMS symptoms will invariably worsen with ascent. Occasionally, however, it is necessary to ascend in order to get to a lower altitude, such as crossing a pass. If the symptomatic person appears to have the ability to make it over the pass, and will sleep at a lower altitude that night, this is a risk that can be taken. But no one with any symptoms of altitude illness should ascend to sleep at a higher altitude.

Most symptoms of altitude illness occur after spending the night at a higher altitude. If the rate of ascent has been reasonable, these symptoms usually resolve with a day’s rest at the same altitude. However, if the person’s symptoms continue to worsen during the day, descent is mandatory. Usually this decision should be made by around 3:00 p.m. in a trekking setting so that descent can be made during daylight. However, descent should never be delayed because it is "too late" in the day.

Symptoms can either begin while ascending to a new camp, or after spending the night at the new height. In general, symptoms that begin in the morning after spending the night at a new altitude are more likely to clear up with rest at the same altitude than symptoms that began the day before while ascending to the camp.

Differential Diagnosis of Altitude Illness

The diagnosis of altitude illness at altitude requires a high index of suspicion. Trekkers have been advised for years that: "If you are not doing well at altitude, it’s altitude illness until proven otherwise." This is sound advice, and was formulated to assure that altitude illness is considered in the differential diagnosis of any illness at altitude. However, other illnesses can occur at altitude that mimic altitude sickness, but may have significantly different implications. The key to differentiating between altitude illness and other medical conditions at altitude is the history of the present illness and the presenting symptoms.

Any medical practitioner or traveler confronted with potentially serious altitude illness should begin their evaluation by evaluating the current symptoms. Headache, anorexia, nausea, vomiting, and profound fatigue can all be symptoms of AMS. Diarrhea is not associated with altitude illness. Fever can occur with HACE or HAPE, and can be a confusing finding. If the history and symptoms are compatible with altitude illness, the fever can usually be attributed to the altitude illness. However, fever would only present, in these cases, after the onset of other AMS symptoms. A fever that pre-dates the symptoms of altitude illness should be attributed to other causes.

The headache associated with AMS is not characteristic enough to be pathognomonic altitude illness. The headache often starts at the back of the head and radiates forward, and is constant in nature. But a throbbing frontal headache can also be due to altitude. It is imperative that all headaches at altitude are treated as altitude headaches, and no further ascent is attempted until any headache has disappeared. There is no sense betting one’s life that the current headache is not due to altitude.

The symptoms of altitude illness almost always have a gradual onset, and get worse slowly over several hours. The sudden onset of severe neurologic symptoms should raise suspicion of an intracranial problem. Previously unsuspected brain tumors have been reported to have presented suddenly upon traveling to high altitude. Guillain-Barre syndrome was once mistaken for HACE in a high altitude setting where the patient presented with mild headache and a disturbance in the tandem gait

Lateralizing neurologic findings are almost never due to AMS or HACE alone. One should be concerned about cerebral vascular accident when lateralizing symptoms are present. Additionally, cranial nerve palsies, with the possible exception of 6th cranial nerve palsies, are not associated with altitude illness. Loss of vision has been associated rarely with traveling rapidly to high altitude, and has been attributed to migraine-like spasm. Recently, reports have surfaced that people who have undergone radial keratotomy to correct vision have developed severe short-sightedness at altitude and become functionally blind. This condition reverses readily with descent, but could be a fatal obstacle for a high altitude mountaineer stranded blind on a Himalayan mountain ridge.

HAPE presents with unusual breathlessness upon exertion, and eventually at rest. Cough is usually present, but cough at high altitude is so common from other causes that it is rarely a useful clinical sign of HAPE. Descent is mandatory as soon as HAPE can be suspected, as the symptoms can progress rapidly, and death can occur within hours of recognizing clinical HAPE. Unfortunately, exertion considerably worsens HAPE. Exertion by the sick person should be minimized during descent, but this is not always possible. Occasionally, climbers with apparent HAPE have died a pulmonary death despite several thousand feet of descent. It has been postulated that some of these deaths may have been due to the problem of exerting during descent. However, a case report by Shlim raised the possibility that multiple pulmonary embolism could account for a presentation that mimics HAPE and fails to improve with descent. The diagnosis of pulmonary embolism should be entertained whenever severe pulmonary symptoms occur after acclimatization should have taken place, or when pulmonary symptoms fail to improve completely after a significant descent.

The importance of the history of the present illness cannot be overemphasized in altitude illness. The person taking the history should inquire about the height at which the trip began, and the altitude at which the victim slept at each point up to the present. This information should be written down so that it can be easily referred to. The history of any altitude related symptoms at any of these prior heights should be elicited.

In order for symptoms to be attributed to altitude illness, they must begin as the person is ascending. A person who has been asymptomatic at the high point of a trek cannot develop AMS while descending. In almost all instances of severe altitude illness, the history will elicit symptoms of AMS at a lower height that were ignored or attributed to something else by the patient. Virtually all life-threatening altitude illness is due to ascending with recognizable symptoms. This point can be stressed to travelers as the key point in preventing severe altitude illness.

Evaluating the patient that has already descended from altitude with altitude illness is a slightly different process. One can assume that the descent has definitively treated the altitude problem, so one should now be alert for either complications of altitude illness, or the possibility of a different diagnosis. Persistent neurologic symptoms that don’t show rapid signs of improvement at low altitude should be investigated with a brain scan. In severely comatose patients, the coma can rarely persist for several days, but usually patients regain consciousness fairly rapidly. Altered sensorium clears up first, along with the headache. The gait ataxia can persist for 24-48 hours post descent, and is usually the last symptom to clear up. HAPE is a high risk for a subsequent pulmonary infection, and a low threshold should be used to prescribe appropriate antibiotics if persistent productive cough, or fever, persist. Chest x-ray in HAPE usually shows fluffy infiltrates that are often more prominent on the right side than the left. A dense consolidation should raise the question of pneumonia or pulmonary infarct.