Acute Mountain Sickness

In a 1993 survey involving 3158 respondents, Honigman et al reported that 25% of visitors to an elevation of 2000 to 3200 m developed AMS on arrival. (Table 1 ) ⁶ The following risk factors for developing AMS were identified:

• Living at sea level
• Prior history of AMS
• Age less than 60
• Obesity
• Underlying lung disease

A 2002 study of mountaineers by Schneider et al did not validate the above risk factors. However, it looked at a select group; i.e., fit mountaineers, many of whom had prior altitude experience; plus, there was a election bias, as only those who had made it to 4559 m were included.⁷ The study by Honigan et al is  here fore considered a better representation of individuals at risk for altitude illness. Physical fitness level has not been shown to influence the incidence of AMS.^{8 9}

In a 1976 study of 278 Himalyan trekkers at 4243 m, the incidence of AMS was found to be 53% in unacclimatized individuals.¹⁰ A 1986 study of trekkers at 5400 m had a similar incidence of 49%. Since these two studies were performed, knowledge of altitude illness and its prevention increased; thus, a subsequent  tudy in 2001 reported a decreased incidence of 28%.¹¹ An incidence of 29% was also reported in a 2004  study by Gaillard et al who studied 500 trekkers hiking to 5400 m. The decreased AMS incidence in the 2004 study was probably also due to a slower rate of ascent compared to the 1986 study and increased use of  elf-medication for AMS, from 17 to 56%.¹²
 
Rapid ascent is a risk factor for AMS. (Figure 1)In one study, 14% of racers in an expedition race who ascended rapidly from 3000 to 4500 m developed AMS which required medical treatment (this did not include those with AMS who did not request formal medical treatment).¹³ In another study involving rapid ascent in the Alps, the incidence of AMS was 9% at 2850 m, 13% at 3050 m, 34% at 3650 m, and 53% at 4559 m.¹⁴ In a case series of 459 climbers in Iran, a rapid ascent from 2900 to 4200 m over four hours resulted in a 61% incidence of AMS.¹⁵ A convenience sample of 228 pilgrim trekkers to 4300 m in Nepal found a 68% incidence of AMS, similar to that found on a Mount Rainier ascent.¹⁶



This incidence of AMS in children at altitude is also substantial; 28% of children who ascended to 2835 m from 1600 m developed AMS, as determined by a questionnaire of 558 children age nine to 14.¹⁷

High Altitude Pulmonary Edema

HAPE represents the severe pulmonary syndrome due to progressive AMS. It is responsible for the greatest number of high altitude fatalities (up to 20 annually¹⁸), with a mortality approaching 50% if descent is not undertaken in a timely manner.¹⁹ HAPE occurs two to five days after arrival at a new elevation and is very rare after one week of acclimatization.²⁰ This timing data comes from a European series of 52 patients admitted with HAPE. All had echocardiography, a complete history and exam, and blood  ultures performed to rule out other causes of the symptoms.²¹ All were treated with nasal oxygen, oral nicardipine, and bedrest at a post descent elevation of 500 m. All recovered and were discharged after a mean of four days (+/- 2). In a retrospective study of 47 cases from Vail, Colorado, the mean onset of symptoms was 2.5 ± 0.8 days after arrival at altitude. In all cases, HAPE may come on and progress either insidiously or rapidly over a few hours. Symptoms may develop and worsen at night.²²

The incidence of HAPE varies with the altitude achieved and the rate of ascent. Climbers in the Alps who ascend to 4559 m over two to four days have a reported incidence of less than 0.2%;²³ however, if the same altitude is reached in 22 hours, the incidence increases to 10%.²⁴ In a report of soldiers airlifted rapidly to 5500 m, the incidence of HAPE has been reported to be 15.5%.²⁵ A study from Vail, Colorado 2 reported an incidence of 0.01 to 0.1% amongst skiers at the lower elevations of 2500 to 3000 m.²⁶
 
The incidence of subclinical pulmonary edema may also be significant. In an observational study carried out at 4559 m in the Alps, 15% of climbers were found to have rales or interstitial edema on chest xray; 92% of this group also had decreased pulmonary closing volumes, confirming that these subjects did have HAPE. Seventy-four percent of all other asymptomatic climbers also had decreased closing volumes, suggesting up to three-quarters of all climbers may have some degree of pulmonary overload, though this is of questionable clinical significance.^27,28
 
Individuals found to be susceptible for HAPE have a significant risk of recurrence, with a reported incidence of 66% on subsequent altitude exposures.²⁹ Susceptibility to HAPE may be predictable by testing an individual’s pulmonary pressure response to sea level hypoxic testing or to exercise testing; however the sensitivity (77 to 94%) and specificity (76 to 93%) are not well established.³⁰ The young appear to be at the highest risk of HAPE.^31,32

Conditions which either increase the pulmonary arterial pressure or affect the blood/lung barrier can increase the risk of developing HAPE.^33-35 HAPE incidence is likely higher in children just before or after an upper espiratory infection. This has also been seen in animal studies.^36,37 Vigorous exercise, because it elevates pulmonary artery pressure, may increase HAPE risk in those susceptible and, therefore, should be avoided for the first few days at altitude.38 There has also been an association of patent foramen ovale (PFO) and HAPE, an observational study of 25 HAPE susceptible individuals found that the incidence of PFO was three times higher in HAPE susceptible persons versus those not susceptible.

High Altitude Cerebral Edema

HACE was first described in 1913 by Ravenhill as “Nervous Punta,” a central nervous system (CNS) form of  mountain sickness.⁴⁰ It represents the neurological syndrome of severe AMS and is the least common form of altitude illness. A case series of 1925 soldiers rapidly transported 3350 to 5000 m reported an incidence of  .2%.71 In the Alps, the HACE incidence is reported as 1:588 at 4559 m and 1:4000 at 2795 to 3050 m.⁴¹ A case series in 1976 found a similar incidence of 1.8% out of 278 trekkers at 4243 m.⁵³ The incidence of climbers on Denali is reported at 2 to 3%.⁴² A convenience sample from Nepal reported the highest incidence, with a HACE rate of 31%; this is the only study to show a higher incidence of HACE than HAPE which is a  finding that the authors could not explain. The study was a convenience sample of 228 out of 5000 subjects, and the authors concluded that the high altitude pilgrims sampled may, for some reason, represent a highly susceptible group. HACE typically occurs three to five days after arrival at elevations higher than 3000 m, with a mean altitude onset of 4730 m. The lowest altitude at which HACE has been reported is 2100 m.⁴³  this  same review, the first done on HACE since the 1970s, gives 24 to 36 hours as the typical time of  progression  rom AMS to HACE. Coma may occur as soon as 24 hours after ataxia is noted.⁴  

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