Spring is here and you’re off with your friends to Colorado for as much skiing as you can get in the next nine days. Departing Houston Intercontinental at 8 a.m., arriving in Denver at 11 a.m. and heading for the lodge, you arrive at the summit of Winter Park by 1 p.m. You and your entourage have gone from near sea level to over 12,000 feet in five hours, skied half the day, eaten a hearty dinner, had a couple beers and hit the rack to dream about the next full day of alpine adventuring.
Early the next morning, you awake with a pounding headache, take two aspirin, drink a cup of coffee and head for the slopes. The headache does not abate as you approach the base lodge and by the time you arrive at the summit nausea has befriended your headache. Determined not to let the terrible twosome interfere with a day of skiing, you press on and recognize that you feel better as you ski down from the summit and worse every time you ascend to the top. At the end of the day, you have no appetite, skip dinner, can’t even look at a beer and go immediately to bed. The next morning you wake refreshed, feel great and finish the ski vacation sans headache or nausea, not knowing that what you just experienced was a bout of acute mountain sickness.
High-altitude illness is the general term encompassing the syndromes affecting people traveling to higher elevations. These syndromes are acute mountain sickness (AMS), high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE). AMS occurs most often, with HACE and HAPE having lower incidence rates, but a much higher mortality rate.1
More people are hiking and skiing at altitudes between 6,000 and 9,000 feet worldwide.2 More than 22 million people visit Colorado ski resorts annually.3 Of those traveling to Colorado, altitude illness will affect almost 25% of those arriving from low land areas.4 Globally, from 20–90% of unacclimatized travelers ascending to elevations above 7,500 feet will experience a high altitude headache.3
Risk factors for high altitude illness include the speed of ascent, the elevation attained, previous high altitude illness, the level of exertion, traveler’s age and beginning from an elevation below 2,700 feet above sea level.1,4 Travelers younger than 50 years old are at a higher risk than those over 50.1 Generally speaking, at elevations between 4,500 and 7,500 feet travelers are at some risk, while symptoms will appear more often at elevations above 7,500 feet.1 Some chronic medical conditions affected by altitude exposure are pulmonary hypertension, COPD, CHF, HTN and sickle cell disease.4 Additionally, patients with sickle cell disease are at an increased risk for splenic infarction at altitudes above 4,900 feet.4
Symptoms of AMS and early HACE include a headache and at least one of the following: anorexia, nausea, vomiting, dizziness, lightheadedness, difficulty sleeping, fatigue or weakness.4 The cardinal symptom is a headache similar to a migraine after a recent gain in elevation.1,4 Symptoms begin to appear within six to 12 hours after arrival and are most commonly reported the morning following the first night at elevation.3,4 Mild symptoms will often spontaneously resolve for travelers at destinations below 11,400 feet, while severe symptoms may progress to cerebral edema if untreated.4
The body’s immediate response to an ascent is a rise in intracranial pressure from hypoxia and a corresponding increase in breathing rate. Hyperventilating helps to increase the partial pressure of oxygen as well as decreasing the partial pressure of carbon dioxide producing respiratory alkalosis, reduced renal carbonic acid formation and an elevated pH.3 Additionally, a coincident release of catecholamines increases pulse, blood pressure and pulmonary artery pressure, causing cerebral blood flow to increase by almost 25% in the first 12–24 hours. This increase in cerebral blood flow has the potential to cause increased hydrostatic pressure, increased capillary permeability and vasogenic edema if auto-regulation is impaired or buffer system failure occurs.3 Pulmonary vasoconstriction will initially improve the ventilation/perfusion mismatch, but left uncorrected, pulmonary edema and right heart failure will follow.3 Within 24–48 hours after arriving at your destination elevation, renal bicarbonate dieresis will normalize pH allowing for any necessary increases in breathing rate to continue.3 Final acclimatization and normalization of vital signs normally occurs during the next 4–5 days with hemoglobin and hematocrit values increasing by almost 10%.3