Chapter 9
LOW-PRESSURE and HIGH-ALTITUDE ENVIRONMENTS

Worthe S. Holt*

The discussion of high-pressure environments in Chapter 8 noted that humans function well only within a narrow range of barometric pressures. Ascent to altitude places workers in an adverse environment and exposes them to multiple stressors—decreased barometric pressure, reduced oxygen levels (hypoxia), ionizing and nonionizing radiation, and low temperatures. Most workers are acclimated to sea-level or near-sea-level pressures; reduced barometric pressures and oxygen levels will produce a range of symptoms ranging from mild discomfort to severe disease or even death.

OCCUPATIONAL SETTING

It was estimated that more than 140 million people worldwide permanently resided above 2440 m (8000 ft). Tourism to mountainous regions of the Western United States exposed an estimated 35 000 000 people to the hypobaric environment.1 Occupationally, pilots and flight attendants have the greatest potential exposure, although actual incidents in commercial aviation are infrequent due to cabin pressurization. Inside observers in hypobaric pressure chambers and scientists at research laboratories located at high altitudes routinely perform duties at decreased barometric pressures. Individuals who travel to mountainous regions as employees of the construction or travel industries are also at risk, depending on the altitude reached and the time taken to reach that altitude. Rescue workers and the military may also be at risk.

LOW-PRESSURE ENVIRONMENTS

Measurement issues

Barometric pressure is a measurement of the weight of the atmosphere at any given point. To ensure uniformity in the calibration of altimeters used in the aviation industry, the concept of standard atmosphere was universally accepted in the 1920s.2 Standard atmosphere is defined as a sea-level pressure of 760 mmHg at a temperature of +15°C and a linear decrease in temperature as one ascends of 6.5°C/km (Table 9.1). Equivalent units of standard atmosphere include 1 atmosphere (atm), 29.92 inHg, 14.7 lb/in.2, 760 Torr, and 1013.2 mbar. Atmospheric pressure is denser at the lower altitudes, as the weight of the atmosphere above compresses the air below. On a standard day, 5486 m (18 000 ft) marks the midpoint of atmospheric pressure.

TABLE 9.1 Altitude–pessure–temperature relationships.

Altitude (m) Pressure Temperature (°C)
(mbar) (Torr)
Sea level 1013 760 15.00
100 1001 751 14.35
200 989 742 13.70
300 977 733 13.05
400 966 724 12.40
500 954 716 11.75
1 000 898 674 8.50
2 000 795 596 2.00
3 000 701 525 −4.49
4 000 616 462 −10.98
5 000 540 405 −17.47
10 000 264 198 −49.90
15 000 121 90 −56.50
20 000 55 41 −56.50
25 000 25 19 −51.60
30 000 11 8 −46.64
40 000 2 2 −22.80
50 000 0.8 0.6 −2.5

Exposure guidelines

There are no formal guidelines for hypobaric exposures. As the agency responsible for aviation safety in the United States, the Federal Aviation Administration (FAA) establishes requirements for supplemental oxygen use in both pressurized and unpressurized aircraft as detailed in US Code of Federal Regulations (CFR), Title 14, Part 91.211.

Physiology and the physics of gases

The behavior and impact of gases in the body are largely the result of the three well-described gas laws previously discussed (Chapter 8): Boyle’s law, Dalton’s law, and Henry’s law. Boyle’s law established the inverse relationship of the pressure and volume of a gas in a closed system at a constant temperature. Pressure reduction results in directly proportional expansion of a fixed mass of a gas. Dalton’s law, or the law of partial pressures, states that each gas in a mixture exerts pressure independent of the other gases present. Approximately 80% of the Earth’s atmosphere is composed of nitrogen. Oxygen fills the remaining 20%. Finally, Henry’s law describes the behavior of gases dissolved in a liquid under pressure. If the pressure is increased, the amount of gas dissolved in a liquid will increase; conversely, if the pressure acting on the liquid’s surface is reduced, gases will exit the solution.

Pathophysiology, diagnosis, and treatment

Physiologically, hypoxia is the greatest threat to workers’ survival in low-pressure environments. Hypoxia is covered on its own in the next section of this chapter. This section will focus on the deleterious behavior of gases contained in the body during exposure to reduced pressures.

BAROTRAUMA (TRAPPED GASES)

As an individual ascends to altitude, gases present in the body respond according to Boyle’s law, that is, gases expand inversely to the pressure acting on them. The middle ear, lungs, gastrointestinal tract, and paranasal sinuses are gas-containing cavities and normally vent expanding volumes through physiologic openings such as the Eustachian tubes, mouth or rectum, or paranasal ostia. Preexisting disease may interfere with the passage of expanding gases, creating a trapped gas syndrome. Trapped gases produce a range of symptoms, from mild discomfort to pain of such intensity as to interfere with job performance. Workers usually experience trapped gas symptoms on ascent. Exceptions include ear or sinus blocks, which occur on descent. Gas in the middle ear normally vents through the Eustachian tube on ascent. The same is true for air found in the paranasal sinuses, even in the presence of preexisting disease, for example, an upper respiratory infection. On descent, the volume in the middle-ear space or sinus is recompressed, and unless one is able to equalize the space to ambient conditions, barotrauma may result from the negative pressure in the middle ear/sinus, with actual tearing of the mucosal lining.

Diagnosis 

Most trapped gas symptoms appearing during routine flight resolve on return to the surface, with the exception of ear or sinus blocks associated with descent. Patients presenting with flight-related symptoms should be carefully evaluated for preexisting disease, especially those of the upper respiratory tract. In the case of descent-related ear block, direct visualization of the ear will reveal a retracted tympanic membrane with increased vascular marking in mild cases and middle-ear effusion, hemotympanum, or perforation in more severe cases. Patients experiencing sinus barotrauma will typically complain of sharp localized pain over the affected region, 80% of the time involving the frontal sinuses. Additional findings include epistaxis in 15% of patients.3 A sinus series may reveal clouding or fluid levels in the affected sinus.

Treatment 

Symptomatic treatment of persistent symptoms includes temporary removal from flying duties, oral or nasal decongestants, and analgesics. Otitic barotrauma symptoms usually resolve in a matter of days. Barosinusitis sequelae may persist for weeks. As it is impossible to directly measure the ability to equilibrate sinuses, an acceptable indirect measure of normal function is when the patient can comfortably equalize the ears through the Valsalva maneuver (forced expiration with the lips closed and the nostrils compressed). Until such time, workers should be removed from flying duties.

AVIATION DECOMPRESSION ILLNESS

The mechanisms of altitude- and diving-related decompression illness are identical—nitrogen present in the tissues leaves solution as the ambient pressure acting on the body is reduced on ascent. Decompression illness is more common in aviators operating unpressurized aircraft above 5500 m, although Voge reported a case occurring at 4268 m (14 000 ft).4 Commercial aircraft protect occupants from decompression illness by maintaining cabin pressures at or below 2400 m (8000 ft). Risk factors for aviation-related decompression illness include altitude, duration and rate of exposure, physical exertion, low temperatures, age greater than 40 years, female gender, and recent exposure to increased pressure, for example, SCUBA diving.5,6 Neurological decompression sickness has been documented in the high-altitude aviation environment and effectively addressed by reducing the frequency and duration of exposure as well as increasing the pressure differential in the aircraft. A safe interval between diving and flying may be as short as 2 hours or as long as 48 hours, depending on the number of dives and whether decompression was required. Divers should consult the Navy Dive Tables (discussed in Chapter 8).

Rapid decompression 

Sudden decompression occurs when a pressurized aircraft suffers a structural or mechanical failure that results in loss of internal pressurization. Rapid changes in ambient pressure greatly increase the risk of decompression illnesses. The effect on passengers and crew is dependent on multiple factors, including the length of time of equilibration from the aircraft’s internal pressure to the ambient external pressure and the differential in pressures. Extremely rapid decompression is termed an “explosive” decompression and can produce an instantaneous overexpansion of the lung with resultant pulmonary trauma, leading to a pneumothorax, subcutaneous emphysema, or air emboli entering the vascular system. Fortunately, such decompressions are limited to aircraft with small cockpit spaces flying at higher altitudes and are relatively rare.

Diagnosis and treatment 

Decompression illness symptoms might develop in flight, on descent, shortly after landing or be delayed for several hours.5 All workers experiencing a rapid decompression should be thoroughly evaluated for signs and symptoms of decompression illness. In a study of 447 cases of altitude-related decompression illness, Ryles observed that 83.2% had musculoskeletal involvement, 70% of the time involving the knees. Approximately 3% experienced pulmonary symptoms, 10.8% developed paresthesias, and 0.5% had frank neurologic findings.7 Any person with signs or symptoms suggesting postflight decompression illness should be referred immediately to a hyperbaric chamber, as immediate recompression is the only appropriate therapy. Maintaining the greatest possible ambient pressure during transport is critical to avoid further sequelae. If aeromedical evacuation to a distant recompression chamber is necessary, the flight should be at the lowest possible altitude, preferably in an aircraft pressurized to sea level.

Prevention

Clearly, primary prevention is the method of choice for avoiding decompression sickness. Those exposed to a changing pressure environment should receive education and training. Workers must be aware of the risks associated with exposure to differing atmospheric pressures, as well as the signs and symptoms that are the first manifestations of decompression illness. All workers exposed to changing atmospheric pressure must follow the guidelines established for safe entry, work, egress, and emergencies.

HYPOXIA

Most of the life-threatening effects of altitude are due to hypoxia. The response of humans to hypoxia is complex and is heavily dependent on the severity and rate of exposure. The aviator who experiences sudden loss of cabin pressure at altitude has a different physiologic response from a traveler who has traveled for weeks on the ground to reach the same altitude. Broadly speaking, acute hypoxia occurs over seconds to an hour or two; chronic hypoxia occurs from many hours to days.

Pathophysiology of acute hypoxia

Ascent to altitude reduces both the ambient pressure and the oxygen content available for gas exchange (Table 9.2). At 2438 m, there is a 25% reduction in the partial pressure of oxygen entering the lungs; by 5500 m it is reduced by half. Commercial and military aviators are at increased risk of hypoxia, as jet aircraft routinely operate at altitudes exceeding 7315 m (24 000 ft). Loss of pressurization or failure of personal breathing equipment can result in loss of consciousness in a matter of minutes. In some environments requiring an increase in the work of breathing, reduced tidal volume and resultant hyperventilation may mimic hypoxia.

TABLE 9.2 Atmospheric pressure and oxygen levels at altitude.

Altitude Pressure Ambient
(m) (ft) (PSIA) (mmHg) PO2 (mmHg) PaO2 (mmHg)
Sea level 14.69 759 159 103
610 2 000 13.66 706 148 93.8
1219 4 000 12.69 656 137 85.1
1829 6 000 11.77 609 127 76.8
2438 8 000 10.91 564 118 68.9
3048 10 000 10.10 522 109 61.2
3658 12 000 9.34 483 101 54.3
4267 14 000 8.63 446 93 47.9
4877 16 000 7.96 411 86 42.0
5486 18 000 7.34 379 79 37.8
6096 20 000 6.76 349 73 34.3
6706 22 000 6.21 321 67 32.8
7315 24 000 5.70 294 61 31.2

PSIA, pounds per square inch atmospheric.

As the partial pressure of oxygen decreases, the body’s ability to maintain adequate oxyhemoglobin saturation is impaired. Table 9.3 outlines the impact of hypoxia on oxygen availability to the arterial circulation on ascent to 6706 m (22 000 ft).

TABLE 9.3 Oxyhemoglobin saturation at selected altitudes.

Tissue level Altitude
Sea Level 3048 m (10 000 ft) 5486 m (18 000 ft) 6706 m (22 000 ft)
Alveolus PO2 (mmHg) l00 60 38 30
Arterial PO2 (mmHg) l00 60 38 30
Venous PO2 (mmHg) 40 31 26 22
A–a gradient (mmHg) 60 29 l2 8
Oxyhemoglobin saturation (%) 98 87 72 60

Physiological response to acute hypoxia

Acute hypoxia occurs in a series, of stages, progressively affecting those tissues with the greatest requirement for oxygen, particularly the nervous system.

INDIFFERENT STAGE (SURFACE TO 3000 M)

Early symptoms begin to appear but are frequently unnoticed by the individual. Vision will be mildly impaired, especially night vision and color vision. Cognitive functioning is normal, with slight decrements in novel task performance. Respiratory rate and depth of inspiration and cardiac output begin to increase. Oxygen saturation is maintained at 90–98%.

COMPENSATORY STAGE (3000–4500 M)

Oxygen saturation falls below 90%. Errors in skilled task performance appear along with euphoria and impaired judgment, although workers are frequently unaware of any deficiencies. Prolonged exposure produces a generalized headache.

DISTURBANCE STAGE (4500–6100 M)

Oxygen saturation falls below 80%. Cerebral functions are severely impaired. Mental calculations become unreliable. Headaches increase in severity, and neuromuscular control is greatly diminished. Tunnel vision frequently occurs. Personality and emotional changes appear and range from elation or euphoria to belligerence. Increased respiratory drive leads to hyperventilation and hypocapnia. Paresthesias of the extremities and lips are followed in severe cases by tetany and carpopedal or facial spasms. The chances of recovery are poor, due to serious deficiencies in judgment and loss of muscular coordination.

CRITICAL STAGE (ABOVE 6100 M)

Oxygen saturation is below 70%. Comprehension and mental performance decline rapidly, and unconsciousness occurs within minutes, often without warning (Table 9.4).

TABLE 9.4 Duration of useful consciousness.

Altitude Duration of useful consciousness
(m) (ft)
5 486 18 000 20–30 minutes
6 706 22 000 10 minutes
7 620 25 000 3–5 minutes
9 144 30 000 1–2 minutes
10 668 35 000 30–60 seconds
12 192 40 000 14–20 seconds
13 106 43 000 9–12 seconds

Treatment and prevention of acute hypoxia

Initial management of hypoxia is with the immediate use of 100% oxygen. Aircraft lacking an oxygen system or experiencing a depressurization should begin an immediate emergency descent. Recovery usually occurs within seconds of supplemental oxygen use, although a transient worsening of symptoms may occur for 15–60 seconds.

Hypoxia prevention requires adequate oxygen during flight, through either individual oxygen systems or aircraft pressurization. In commercial aircraft, the high-flying passenger jet provides a pressurized cabin that rarely exceeds an altitude of 2400 m (8000 ft). In unpressurized aircraft, supplemental oxygen is required for the pilot at a cabin altitude of 14 000 ft or higher. If flight is maintained for >30 minutes at altitudes between 12 500 and 14 000 ft, the pilot must use oxygen. When flying above 15 000 ft, all occupants must have supplemental oxygen.8 At an altitude of 10 363 m (34 000 ft), 100% oxygen is required in order to maintain adequate oxygenation, equivalent to sea level. In some aircraft, particularly in the military high-altitude environment, regulators to increase the partial pressure of oxygen and/or provide positive pressure ventilation are necessary. Sustained flight at ambient altitudes of 13 700 m (45 000 ft) or higher requires use of pressure suits. Prolonged elevated partial pressures of oxygen can introduce a new set of challenges, including alveolar atelectasis and chronic cough.

MEDICAL SURVEILLANCE AND EDUCATION

Commercial airline transport pilots are required to undergo FAA-approved physical examinations every 6 months to maintain their medical certification.9 Annual flight physicals are mandatory for military aviators, who receive excellent medical surveillance, given the high ratio of flight surgeons to aircrew and robust prevention programs in place throughout the armed services. Preemployment and periodic examinations pay great attention to otorhinolaryngeal conditions that might predispose aircrew to otitic or sinus barotrauma.

Primary prevention is the goal. Aircrews receive extensive training in the physiology of operating in hypobaric environments. The US Code of Federal Regulations (CFR), Title 14, Part 61.31 (g)(2)(i) indicates that “no person may act as pilot in command of a pressurized airplane that has a service ceiling or maximum operating altitude, whichever is lower, above 25 000 ft MSL unless that person has completed ground training that includes instruction on respiration; effects, symptoms, and causes of hypoxia and any other high altitude sicknesses; duration of consciousness without supplemental oxygen; effects of prolonged usage of supplemental oxygen; causes and effects of gas expansion and gas bubble formations; preventive measures for eliminating gas expansion, gas bubble formations, and high altitude sicknesses; physical phenomena and incidents of decompression; and any other physiological aspects of high altitude flight.”

The FAA coordinates low-pressure chamber “flights” at US Air Force bases to allow civilian aviators to experience hypoxia in a controlled environment—information for such courses is available on the World Wide Web at hhttps://www.faa.gov/pilots/training/airman_education/aerospace_physiology/cami_enrollment/. The US armed services maintain a large network of hypobaric chambers, as military aviators are required to complete low-pressure training every 3–4 years. Aviators learn early in their career to refrain from flying when congested. Foods that cause excessive intestinal gas—beans, cabbage, cauliflower, carbonated beverages, or peas—are also soon avoided.

The risk of decompression illness in flight can be minimized through several strategies. Use of 100% oxygen for 30 minutes before flight will reduce the body’s nitrogen load, as will use of oxygen throughout a flight. Limiting the altitude and duration of exposure will significantly reduce the incidence. SCUBA divers should allow a sufficient interval between diving and flight. A minimum of 12 hours should elapse following a no-compression dive with less than 2 hours total bottom time; 24–48 hours is recommended after more complex dive profiles.5

HIGH-ALTITUDE ACCLIMATIZATION AND ILLNESS

Acute exposure to high altitude is fatal to unprotected workers in a matter of minutes (Table 9.4), yet men have climbed the tallest peaks in the world with nothing more than thermal protection. The difference lies in a man’s ability to adapt to severely hypoxic conditions through progressive acclimatization over extended time periods (days to months).

Acute mountain sickness (AMS)

Acute mountain sickness is the most common altitude-related illness affecting travelers to high altitude. Chinese authors first described AMS in 32 BC. Jose de Acosta, a Jesuit priest living in Peru in the sixteenth century, provided a more complete description based on his experiences in the Andes.10 AMS consists of a group of symptoms occurring 6–48 hours after rapid ascent. At elevations over 3000 m, 25% of travelers will have mild symptoms, including headache, fatigue, nausea, malaise, loss of appetite, and disturbed sleep.11 Symptoms are so nonspecific that patients often fail to recognize their condition. The most important reason to diagnosis AMS is that it is often unrecognized; it may progress to high-altitude cerebral edema (HACE) or high-altitude pulmonary edema (HAPE) (see below) if there is further increase in altitude without adequate time for acclimatization. A greater incidence has been reported in individuals in their early 20s.12

PATHOPHYSIOLOGY OF AMS

No etiology has been firmly established for AMS. There is evidence of cerebral vasodilation with increased blood flow and leakage of proteins and fluid across the blood–brain barrier, but the exact mechanism remains elusive.13

DIAGNOSIS AND THERAPY

Complete history and physical examination are usually adequate to rule out conditions with similar symptoms such as viral illnesses, exhaustion, dehydration, or hangover. Mild AMS is limited to the symptoms described above and is best treated with arrest of ascent or a slight descent to allow time for acclimatization—usually 1–3 days is sufficient. Acetazolamide (Diamox) 125–250 mg twice a day has been effective in reducing symptoms14 but may result in diffuse paresthesias. Acetaminophen or nonsteroidal anti-inflammatory drugs are indicated to manage headaches. Theophylline reduced AMS symptoms in 14 subjects given 375 mg oral slow-release theophylline twice a day at simulated altitudes of 3454 m.15

Symptoms of moderate AMS include severe headache not relieved by medication, nausea and vomiting, progressive weakness and fatigue, shortness of breath, and loss of coordination. Moderate AMS should be treated with descent. When descent is delayed, oxygen and acetazolamide should be considered.

High-altitude cerebral edema (HACE)

PATHOPHYSIOLOGY

HACE is a potentially fatal metabolic encephalopathy believed to be of vasogenic etiology, with leaking of protein and water across the blood–brain barrier.16

DIAGNOSIS

HACE occurs in 2–3% of trekkers at altitudes of 5500 m, although HACE can appear in individuals above 2500 m.14 Symptoms include severe headache, nausea, vomiting, ataxia, disorientation, hallucinations, seizures, stupor, and coma. Mild AMS can progress to HACE in 12–72 hours.

TREATMENT

HACE is life-threatening—definitive therapy is immediate descent with close supervision as symptoms may worsen while descending. When descent is delayed due to the situation or patient’s condition, oxygen and dexamethasone, 10 mg intravenously and then 4 mg intramuscularly every 6 hours, are indicated.11 Prognosis is poor once the patient becomes comatose.

High-altitude pulmonary edema (HAPE)

PATHOPHYSIOLOGY

HAPE is the most frequent cause of death of the altitude illnesses. It frequently develops on the second night of exposure at altitudes above 2500 m. In Colorado, 1 in 10 000 skiers will develop HAPE, with a higher incidence in younger men. HAPE victims develop substantial increases in pulmonary artery pressures, with increased vascular permeability. Fluid increases in the lungs, reducing oxygen exchange. Respiratory alkalosis and severe hypoxemia follow, with mean oxygen saturations of 56%.14

DIAGNOSIS

Early symptoms include dyspnea on exertion, fatigue, weakness, and dry cough. Signs typically are tachycardia, tachypnea, rales, pink-tinged frothy sputum, and cyanosis. Radiographs show patchy peripheral infiltrates, which may be unilateral or bilateral.14

TREATMENT

Immediate descent to lower altitudes with close monitoring is required. Patients should be kept warm and minimize exertions. If descent is impossible due to conditions, nifedipine (10 mg every 4 hours)17 and oxygen (4–6 L/min) have been shown to improve patients. Descent remains the key to therapy.

Prevention of altitude illnesses

The rate of ascent and individual susceptibility are the primary determinants of altitude illnesses. Physical fitness is not protective. The key to prevention is a gradual ascent, when feasible. Workers traveling from altitudes below 1200 m to altitudes above 2500 m should spend at least one night at 1500–2200 m or alternatively 2 or 3 nights at 2800–3000 m before proceeding higher.18

There is a diversity of recommendations regarding further ascents and only two prospective studies to support the guidance.19,20 The Himalayan Rescue Association recommends ascending no more than 300 m/day with a rest day (no ascent in sleeping altitude) for every additional 600–900 m and no single day gain greater than 800 m.21 The Wilderness Medical Society recommends limiting ascent to 500 m/day with a rest day every 3–4 days.22

Returning to lower altitudes at night to sleep enhances acclimatization, possibly because of the relative hypoxemia during sleep.18 Sleep hypnotics and alcohol should be avoided, as they suppress breathing during sleep, worsening cerebral oxygenation. High-carbohydrate diets and avoidance of dehydration or overexertion have also been widely reported as helping to prevent high-altitude illnesses, although precise mechanisms are unknown.23

Acetazolamide is the drug of choice to prevent or limit the severity of AMS and HACE and accelerates the rate of acclimatization. Acetazolamide 125 mg should be given twice a day beginning the day before ascent and continued until 2 days at the highest sleeping altitude or until descent begins.18 Acetazolamide is a nonantibiotic sulfonamide with low cross-reactivity with sulfa antibiotics, but patients with a history of drug allergy should be assessed before receiving acetazolamide. While the most common allergic reaction is a rash, anaphylaxis has been reported.18

Dexamethasone can mask symptoms and can be started on the day of ascent. The recommended dose is 4 mg every 12 hours for passive (sedentary) ascent and 4 mg every 6 hours for active ascent.18 It can be stopped after 2–3 days at the highest sleeping altitude or when starting descent, but should not be taken for more than 10 days to prevent adrenal suppression.18

In military or rescue operations requiring rapid ascent above 3500 m without time for acclimatization, acetazolamide and dexamethasone can be used together.18

For workers with a history of HAPE, nifedipine is recommended to prevent recurrence.24 Salmeterol may be a helpful addition for those at the highest risk.22

Workers with underlying medical conditions that can be worsened by hypoxia (including lung disease, heart disease, sickle cell disease, and others) should be evaluated to determine whether work restrictions, additional medications, or additional oxygen is needed.

OTHER ALTITUDE-RELATED CONDITIONS

Vision

Beck Weathers’ experience on an ill-fated Mt Everest expedition in 1996 heightened the public’s awareness of high-altitude effects on patients who have undergone eye surgery. Weathers, a Texas pathologist, suffered severe hyperopia at altitude following his radial keratotomy (RK), effectively disabling him.24 Ng et al. experimentally demonstrated reversible hyperopic changes in RK subjects exposed to altitudes of 4300 m.25 Studies of postphotorefractive keractomy (PRK) and laser in situ keratomileusis (LASIK) patients revealed no change in PRK patients and a small but statistically significant myopic change in LASIK patients.26 The mechanism in all cases appears to be hypoxia-induced corneal hydration.27

Extreme altitudes have also been implicated in high-altitude retinopathy (HAR). Weidman and Tabor examined 40 climbers climbing Mt Everest. Fourteen of 19 climbers who ascended to altitudes between 4880 and 7620 m developed HAR, and 19 of the 21 who exceeded 7620 m (25 000 ft) developed HAR.28 Most patients were asymptomatic; descent was not required.

Pregnancy

Altitude has been implicated in a number of complications of pregnancy. Ali et al. and Niermeyer have suggested in independent studies that there is an increased incidence in preterm labor among pregnant high-altitude travelers.29,30 Palmer et al. reported a 16% incidence of preeclampsia at 3100 m compared to a 3% rate at 1260 m at high and low altitudes in Colorado. Birth weight averaged 285 g less in those deliveries at 3100 m.31

Radiation exposure

It has long been known that high altitude exposes workers to elevated levels of cosmic radiation, especially in higher latitudes.32 Aircrews on polar routes have significantly higher exposures than those flying equatorial routes, but the long-term impact on health is currently unknown. Gundestrup and Storm reported increased acute myeloid leukemia, malignant melanoma, and skin cancer rates in Danish male jet cockpit crew members. The melanomas and skin cancers were attributed to sun exposure during vacations rather than occupational exposure at altitude.33 Other studies have shown individual exposures to be well within current international recommended exposures,34–38 although a pregnant flight attendant would have to change routes to remain under the exposure limits.38

References

  1. 1. Hultgren HN. High altitude medicine. Stanford: Hultgren Publications, 1997:10–1.
  2. 2. Ward MP, Milledge JS, West JB. High altitude medicine and physiology. London: Chapman & Hall Medical, 1995:32–7.
  3. 3. O’Reilly BJ. Otorhinolaryngology. In: Ernsting J, Nicholson AN, Rainford DJ, eds. Aviation medicine. 3rd edn. Oxford: Butterworth-Heinemann, 1999:319–36.
  4. 4. Voge VM. Probable bends at 14,000 feet: a case report. Aviat Space Environ Med 1989; 60(11):1102–3.
  5. 5. Heimbach RD, Sheffield PJ. Decompression sickness and pulmonary overpressure accidents. In: DeHart RL, ed. Fundamentals of aerospace medicine. 2nd edn. Baltimore: Williams & Wilkins, 1996:131–61.
  6. 6. Weien RW, Baumgartner N. Altitude decompression sickness: hyperbaric results in 528 cases. Aviat Space Environ Med 1990; 61(9):833–6.
  7. 7. Ryles MT, Pilmanis AA. The initial signs and symptoms of altitude decompression sickness. Aviat Space Environ Med 1996; 67(10):983–9.
  8. 8. Code of Federal Regulations 14, part 91, subpart C, section 91.211 Supplemental oxygen. April 25, 2000. Government Printing Office, Washington, DC.
  9. 9. Code of Federal Regulations 14, part 61, subpart A, section 61.23 Medical certification and duration. October 10, 2000. Government Printing Office, Washington, DC.
  10. 10. Hultgren HN. High altitude medicine. Stanford: Hultgren Publications, 1997:213–4.
  11. 11. Hultgren HN. High altitude medicine. Stanford: Hultgren Publications, 1997:212–48.
  12. 12. Hackett PH, Rennle D. The incidence, importance, and prophylaxis of acute mountain sickness. Lancet 1976; 2:1149–55.
  13. 13. Hackett PH. The cerebral etiology of high-altitude cerebral edema and acute mountain sickness. Wilderness Environ Med 1999; 10(2):97–109.
  14. 14. Kloche DL, Decker WW, Stepanek J. Altitude-related illnesses. Mayo Clin Proc 1998; 73(10):988–93.
  15. 15. Fischer R, Lang SM, Steiner U, et al. Theophylline improves acute mountain sickness. Eur Respir J 2000; 15(1):123–7.
  16. 16. Hackett PH. High altitude cerebral edema and acute mountain sickness. A pathophysiology update. Adv Exp Med Biol 1999; 474:23–45.
  17. 17. Oelz O, Maggiorini M, Ritter M, et al. Nifedipine for high altitude pulmonary oedema. Lancet 1989; 2(8674):1241–4.
  18. 18. Zafren K. Prevention of high altitude illness. Travel Med Infect Dis 2014; 12(1):29–39.
  19. 19. Bloch KE, Turk AJ, Maggiorini M, et al. Effect of ascent protocol on acute mountain sickness and success at Muztagh Ata, 7546 m. High Alt Med Biol 2009; 10(1):25e32.
  20. 20. Beidleman BA, Fulco CS, Muza SR, et al. Effect of six days of staging on physiologic adjustments and acute mountain sickness during ascent to 4300 meters. High Alt Med Biol 2009; 10(3):253e60.
  21. 21. Zafren K, Honigman B. High-altitude medicine. Emerg Med Clin North Am 1997; 15(1):191e222.
  22. 22. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med 2010; 21(2):146e55.
  23. 23. Bartsch P, Maggiorini M, Ritter M, et al. Prevention of high-altitude pulmonary edema by nifedipine. N Engl J Med 1991; 325(18):1284e9.
  24. 24. Krakauer J. Into thin air. New York: Anchor Books, 1997:246–9.
  25. 25. Ng JD, White LJ, Parmley VC, et al. Effects of simulated high altitude on patients who have had radical keratotomy. Ophthalmology 1996; 103(3):452–7.
  26. 26. White LJ, Mader TH. Refractive changes at high altitude after LASIK. Ophthalmology 2000; 107(12):2118.
  27. 27. Mader TH, Blanton CL, Gilbert BN, et al. Refractive changes during 72-hour exposure to high altitude after refractive surgery. Ophthalmology 1996; 103(8):1188–95.
  28. 28. Wiedman M, Tabin GC. High-altitude retinopathy and altitude illness. Ophthalmology 1999; 106(10):1924–6; discussion 1927.
  29. 29. Ali KZ, Ali ME, Khalid ME. High altitude and spontaneous preterm birth. Int J Gynaecol Obstet 1996; 54(1):11–5.
  30. 30. Niermeyer S. The pregnant altitude visitor. Adv Exp Med Biol 1999; 474:65–77.
  31. 31. Palmer SK, Moore LG, Young D, et al. Altered blood pressure during normal pregnancy and increased preeclampsia at high altitude (3100 meters) in Colorado. Am J Obstet Gynecol 1999; 180(5):1161–8.
  32. 32. Mohr G. The future perspective. In: DeHart RL, ed. Fundamentals of aerospace medicine. 2nd edn. Baltimore: Williams & Wilkins, 1996:37–55.
  33. 33. Gundestrup M, Storm HH. Radiation-induced acute myeloid leukaemia and other cancers in commercial jet cockpit crew: a population-based cohort study. Lancet 1999; 354(9195):2029–31.
  34. 34. Bagshaw M, Irvine D, Davies DM. Exposure to cosmic radiation of British Airways flying crew on ultra-longhaul routes. Occup Environ Med 1996; 53(7):495–8.
  35. 35. Oksanen PJ. Estimated individual annual cosmic radiation doses for flight crews. Aviat Space Environ Med 1998; 69(7):621–5.
  36. 36. Tume P, Lewis BJ, Bennett LG, et al. Assessment of cosmic radiation exposure on Canadian-based routes. Health Phys 2000; 79(5):568–75.
  37. 37. Bagshaw M. Cosmic radiation in commercial aviation. Travel Med Infect Dis 2008; 6(3):125–7.
  38. 38. Waters M, Bloom TF, Grajewski B. The NIOSH/FAA Working Women’s Health Study: evaluation of the cosmic-radiation exposures of flight attendants. Health Phys 2000; 79(5):553–9.

Note

..................Content has been hidden....................

You can't read the all page of ebook, please click here login for view all page.
Reset
18.191.236.174