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1     Altitude Sickness/ (1625)
2     Altitude Sickness/pc, dt, th [Prevention & Control, Drug Therapy, Therapy]
(480)
3     *Altitude Sickness/pc, dt, th (263)
4     exp sports/ or exp exertion/ (111424)
5     1 and 4 (455)
6     *Altitude Sickness/ and 5 (353)
7     high altitude.tw. and 6 (179)
8     limit 7 to (human and english language) (151)
9     limit 8 to yr=1996-2004 (82)
10     limit 9 to ovid full text available (1)
11     limit 9 to local holdings (24)
12     10 or 11 (25)
13     9 not 12 (57)
14     from 13 keep 5,14-15,23,38,41-42,51,55 (9)
15     12 or 14 (34)
16     from 15 keep 1-34 (34)
17     from 16 keep 1-34 (34)

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<1>
Unique Identifier
  10902930
Authors
  Bonnon M. Noel-Jorand MC. Therme P.
Institution
  Universite de la Mediterranee Aix-Marseille II, Faculte des Sciences du Sport,
La Timone, Marseille, France.
Title
  Effects of different stay durations on attentional performance during two
mountain expeditions.
Source
  Aviation Space & Environmental Medicine. 71(7):678-84, 2000 Jul.
Abstract
  BACKGROUND: Hypoxia-induced deficits in intellectual performance are linked to
the altitude level reached, the speed of the ascent and the time spent at high
altitude. This study analyzes attentional changes during adaptation to two
different types of stay at high altitude on two different expeditions: one
involving a 16-d trip between 2,000 m and 5,600 m, followed by a 2-d ascent to
6,440 m and back again; the other, a 21-d stay at 6,542 m. We tested the
hypothesis that, at similar high altitudes, decrements in attentional
performance would only occur during a long duration stay. METHODS: Indexes for
attentional performance were calculated for two experimental groups under
normoxia before the climb, under acute and chronic hypoxia during the climb, and
under normoxia after the climb. They were compared for two control groups tested
only under normoxia. RESULTS: The altitude stay was found to have an effect on
the 6,542 m group when compared with the controls. Group performance differed at
2 d and 21 d after their arrival at 6,542 m and after their return to normoxia.
When all the test administrations were pooled together for this expedition we
noted an interaction between the level of difficulty of the task and the
experimental and control groups: namely the difference between the groups was
greater for the difficult task than it was for the easy task. No effect was
found for the other expedition (at 5,600 m) when the group tested was compared
with the controls. CONCLUSION: For a 21-d stay at an altitude of 6,542 m with
the same ascent protocol as a group climbing to a lower altitude (16 d between
2,000 m and 5,600 m followed by a 2 d ascent to 6,440 m and back again),
subjects appeared to suffer from attentional performance deficits which
persisted for several days after the subjects returned to normoxic conditions.
<2>
Unique Identifier
  12498553
Authors
  Cauchy E. Larmignat P. Boussuges A. Le Roux G. Charniot JC. Dumas JL.
Richalet JP.
Institution
  Departement de Medecine de Montagne de l'Hopital de Chamonix, Chamonix,
France. m.cauchy@ch-sallanches-chamonix.fr
Title
  Transient neurological disorders during a simulated ascent of Mount Everest.
Source
  Aviation Space & Environmental Medicine. 73(12):1224-9, 2002 Dec.
Abstract
  BACKGROUND: Transient neurological disorders are often observed at high
altitude but are poorly documented under field conditions. The mechanism usually
invoked is a hypocapnic vasoconstriction due to severe hypoxic hyperventilation.
During a simulated ascent of Mount Everest in a hypobaric chamber by eight
volunteer alpinists (Operation Everest III, Comex '97), three subjects presented
neurological symptoms. We report here on the clinical observations and testing
to detect mechanisms in addition to hypocapnic vasoconstriction. METHODS: The
experiment was designed to investigate factors limiting physiological
performance at altitude and the pathophysiology of acute mountain sickness. A
retrospective analysis was made comparing the three cases of transient
neurological disorder at high altitude (TNDHA) with the five subjects who had no
neurological symptoms. RESULTS: Analysis of clinical and blood parameters showed
no difference between cases and controls. The cases showed no neurological
sequelae following the experiment and were normal on cardiac imaging. However,
one case had a history of migraine in his youth, leading us to hypothesize that
segmental vasoconstriction was a factor. In another case, gas bubbles were
detected in the pulmonary artery by transthoracic echocardiography when he was
symptomatic, suggesting that gas emboli may have played a role. All three cases
shared a possible triggering factor in that each experienced hyperventilation
alternating with straining against a closed glottis shortly before the onset of
symptoms. CONCLUSION: Mechanisms other than hypocapnic vasoconstriction in
hypoxia may be causal factors of TNDHA. The existence of triggering factors and
evidence of a possible embolic mechanism should be further explored.


<3>
Unique Identifier
  10902931
Authors
  Purkayastha SS. Bhaumik G. Sharma RP. Arora BS. Selvamurthy W.
Institution
  Defence Institute of Physiology & Allied Sciences, Timarpur, Dehli, India.
Title
  Effects of mountaineering training at high altitude (4,350 m) on physical work
performance of women.
Source
  Aviation Space & Environmental Medicine. 71(7):685-91, 2000 Jul.
Abstract
  BACKGROUND: Little is known about work performance of women in hypobaric
hypoxia. Moreover, whether native women of moderate altitude (2,000-2,100 m)
differ from their lowland counterparts in their ability to adjust to hypobaric
hypoxia is also not known. Hence, physiological alterations on work performance
due to mountaineering training with altitude adaptation was evaluated in two
groups of women and compared to the differences in the responses of the native
women of moderate altitudes (Highlanders-HL) with those of the plains
(Lowlanders-LL). METHODS: Pre-training tests were conducted at 2,100 m, then
during sojourn to 4,350 m and re-tested again after return to 2,100 m. Physical
work performance was assessed following standard step-test-exercise on a 30 cm
stool with 24 cycles x min(-1) for 5 min. Heart rate, BP, ventilation, oxygen
consumption and oxygen saturation were monitored at rest and during exercise
followed by 5 min recovery in all three situations. RESULTS: During initial
assessment, HL showed higher cardiovascular efficiency with faster recovery of
exercise heart rate. Both groups showed significant improvement in physical
performance due to mountaineering training at high altitude (HA). The difference
in performance between two groups narrowed down at 4,350 m and further reduced
during re-test with maintenance of initial superiority of the HL. CONCLUSIONS:
a) Native women of moderate altitude (HL) are more fit compared with their
plains counterparts (LL); b) All women achieved marked improvement in
cardiovascular and respiratory efficiency as well as the step-test score due to
intense mountaineering training at HA, and the rate of improvement in physical
performance was higher in LL; c) Further, induction by trekking under
progressive hypoxia coupled with rigorous mountaineering activity at HA merits
in understanding better acclimatization and improved physical performance.


<4>
Unique Identifier
  11086670
Authors
  Hendricks DM. Pollock NW. Natoli MJ. Vann RD.
Institution
  Center for Hyperbaric Medicine and Environmental Physiology, Duke University
Medical Center, Durham, NC 27710, USA.
Title
  Mountaineering oxygen mask performance at 4572 m.
Source
  Aviation Space & Environmental Medicine. 71(11):1142-7, 2000 Nov.
Abstract
  BACKGROUND: Supplemental oxygen delivered by mask at high altitude is used to
increase arterial oxygen saturation (SaO2) thereby mitigating physiological and
cognitive dysfunction secondary to hypoxemia. Historically, mask performance has
not been well documented although it may be a critical factor in determining the
success of an expedition. METHODS: Three mountaineering masks were used by ten
healthy, nonaltitude-acclimatized participants (eight males, two females) to
compare ventilatory responses, SaO2, heart rate, and end-tidal gases. Masks
tested were: Life Support Engineering Ltd. (LSEL); Zvezda Enterprise (ZE); and a
prototype of our own design (Duke). Test conditions were as follows: simulated
altitude at 0 and 4572 m (15,000 ft); rest and cycle exercise at 75 W; and
supplemental oxygen flow at 0, 1.1 +/- 0.05, and 1.7 +/- 0.06 L x min(-1) (mean
+/- SD). Statistical analysis was completed using GLM (SAS software). RESULTS:
As there were no differences between the 1.1 and 1.7 L x min(-1) flow rates, the
data were pooled. All three masks improved SaO2 with the ZE and Duke masks being
more effective during exercise, maintaining mean SaO2 >90%. CONCLUSIONS: All
three masks provided at least partial protection of physiological norms during
rest and exercise at 4572 m. The ZE and Duke systems offered the best
performance. The need for performance evaluation as part of system design is
evident as subtle differences in design can significantly affect performance.


<5>
Unique Identifier
  10807827
Authors
  Bartsch P. Eichenberger U.   Ballmer PE.   Gibbs JS.   Schirlo C.   Oelz O.
Mayatepek E.
Institution
  Institute of Sportsmedicine, University Hospital, Heidelberg, Germany.
peter_bartsch@med.uni-heidelberg.de
Title
  Urinary leukotriene E(4) levels are not increased prior to high-altitude
pulmonary edema.
Source
  Chest. 117(5):1393-8, 2000 May.
Abstract
  STUDY OBJECTIVE: To examine whether increased urinary cysteinyl-leukotriene
E(4) (LTE(4)) excretion, which has been found to be elevated in patients
presenting with high-altitude pulmonary edema (HAPE), precedes edema formation.
DESIGN: Prospective studies in a total of 12 subjects with susceptibility to
HAPE. SETTING: In a chamber study, seven subjects susceptible to HAPE and five
nonsusceptible control subjects were exposed for 24 h to an altitude of 450 m
(control day), and exposed for 20 h to 4,000 m after slow decompression over 4
h. In a field study, prospective measurements at low and high altitude were
performed in five subjects developing HAPE at 4,559 m. PARTICIPANTS:
Mountaineers with a radiographically documented history of HAPE and control
subjects who did not develop HAPE with identical high-altitude exposure.
INTERVENTIONS: 24-h urine collections. MEASUREMENTS AND RESULTS: In the
hypobaric chamber, none of the subjects developed HAPE. The 24-h urinary LTE(4)
did not differ between HAPE susceptible and control subjects, nor between
hypoxia and normoxic control day. In the field study, urinary LTE(4) was not
increased in subjects with HAPE compared to values obtained prior to HAPE at
high altitude and during 2 control days at low altitude. CONCLUSIONS: These data
do not provide evidence that cysteinyl-leukotriene-mediated inflammatory
response is associated with HAPE susceptibility or the development of HAPE
within the context of our studies.


<6>
Unique Identifier
  9596338
Authors
  Toepfer M. Hartmann G. Schlosshauer M. Hautmann H.     Tschop M.   Fischer R.
Huber RM.
Title
  Adrenomedullin: a player at high altitude?.
Source
  Chest. 113(5):1428, 1998 May.


<7>
Unique Identifier
  9404756
Authors
  Grissom CK. Zimmerman GA. Whatley RE.
Institution
  Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and
Training Institute, University of Utah, Salt Lake City, USA. ldcgriss@ihc.com
Title
  Endothelial selectins in acute mountain sickness and high-altitude pulmonary
edema.
Source
  Chest. 112(6):1572-8, 1997 Dec.
Abstract
  STUDY OBJECTIVES: Mechanical or inflammatory injury to pulmonary endothelial
cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS)
and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This
study was designed to determine whether markers of endothelial cell activation
or injury, plasma E- and P-selectin, were increased after ascent to high
altitude, in AMS or in HAPE. DESIGN: We collected clinical data and plasma
specimens in control subjects at sea level and after ascent to 4,200 m, and in
climbers with AMS or HAPE at 4,200 m. Data analysis was performed using standard
nonparametric statistical methods, and results reported as mean+/-SD. SETTING:
National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska.
PATIENTS: Blood samples and clinical data were collected from 17 healthy
climbers at sea level and again after ascent to 4,200 m, and from a different
group of 13 climbers with AMS and 8 climbers with HAPE at 4,200 m. Climbers with
AMS were divided into normoxic (n=7) and hypoxemic (n=6) groups. MEASUREMENTS
AND RESULTS: Using an enzyme immunoassay technique, plasma E-selectin
concentrations were found to be increased in the 17 control subjects after
ascent to 4,200 m (17.2+/-8.2 ng/mL) as compared to sea level (12.9+/-8.2 ng/mL)
(p=0.001). Plasma E-selectin concentrations were also increased in subjects with
hypoxemic AMS (30.6+/-13.4 ng/mL) and HAPE (23.3+/-9.1 ng/mL) compared to
control subjects at sea level (p=0.009). Increased plasma E-selectin
concentration significantly correlated with hypoxemia (p=0.006). Plasma P-
selectin concentrations were unchanged after ascent to 4,200 m and in subjects
with AMS and HAPE. CONCLUSION: Because E-selectin is produced only by
endothelial cells, increased plasma E-selectin after ascent to high altitude and
in hypoxemic climbers with AMS and HAPE provides evidence that endothelial cell
activation or injury is a component of hypoxic altitude illness.


<8>
Unique Identifier
  12793625
Authors
  Kuo DC. Jerrard DA.
Institution
  Division of Emergency Medicine, University of Maryland School of Medicine. 419
West Redwood Street, Suite 280, Baltimore, MD 21201, USA. dkuo@umaryland.edu
Title
  Environmental insults: smoke inhalation, submersion, diving, and high
altitude. [Review] [127 refs]
Source
  Emergency Medicine Clinics of North America. 21(2):475-97, x, 2003 May.
Abstract
  In the expanding search for recreation, we spend more and more of our time in
various environments. Whether the air is thin or compressed or smoke-filled or
there is no air at all, emergency physicians continue to meet and treat the
various pulmonary emergencies that the environment may create. The authors
present the background, diagnosis, and management of a few of the more common
pulmonary emergencies that the environment may produce. [References: 127]


<9>
Unique Identifier
  9056576
Authors
  Zafren K. Honigman B.
Institution
  Columbia Alaska Regional Hospital and Providence Alaska Medical Center,
Anchorage, USA.
Title
  High-altitude medicine. [Review] [201 refs]
Source
  Emergency Medicine Clinics of North America. 15(1):191-222, 1997 Feb.
Abstract
  This article discusses prevention, recognition, and treatment of altitude
illnesses, especially acute mountain sickness, high-altitude pulmonary edema,
and high-altitude cerebral edema. Physicians advising travelers and trekkers who
will be visiting high-altitude areas will find an organized approach to giving
pretravel advice. Physicians practicing in or visiting high-altitude areas will
find guidelines for diagnosis and treatment. This article also addresses the
issue of patients with underlying diseases who wish to travel to high-altitude
destinations. [References: 201]


<10>
Unique Identifier
  11513303
Authors
  Walter R. Maggiorini M. Scherrer U. Contesse J. Reinhart WH.
Institution
  Department Innere Medizin, Kantonsspital, Chur, Switzerland.
roland.walter@dim.usz.ch
Title
  Effects of high-altitude exposure on vascular endothelial growth factor levels
in man.
Source
  European Journal of Applied Physiology. 85(1-2):113-7, 2001 Jul.
Abstract
  Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and
permeability factor that is inducible by hypoxia. Its contribution to high-
altitude illness in man is unknown. We measured VEGF levels in 14 mountaineers
at low altitude (490 m) and 24 h after their arrival at high altitude (4,559 m).
At high altitude, VEGF increased from [mean (SEM)] 32.5 (9.2) to 60.9 (18.5)
pg.ml(-1) (P < 0.004) in the arterial blood, and from 15.9 (2.9) to 49.3 (15.9)
pg.ml(-1) (P= 0.0001) in the mixed venous blood. Whereas at low altitude venous
and arterial VEGF levels were not statistically different from each other (P=
0.065), the VEGF concentration was significantly lower in venous than in
arterial blood samples at high altitude (P=0.004). The pulmonary capillary VEGF
concentration remained unchanged at high altitude [14.8 (2.5) vs 17.1 (5.4)
pg.ml(-1), P=0.85]. VEGF levels in the nine mountaineers who developed symptoms
of acute mountain sickness (AMS), and in the six subjects who had radiographic
evidence of high-altitude pulmonary edema were similar to those in subjects
without symptoms. VEGF was not correlated with either AMS scores, mean pulmonary
arterial pressures, arterial partial pressure of O2, or alveolar-arterial O2
gradients. We conclude that VEGF release is stimulated at high altitude, but
that VEGF is probably not related to high-altitude illness.


<11>
Unique Identifier
  8880116
Authors
  Droma Y. Hayano T. Takabayashi Y. Koizumi T. Kubo K. Kobayashi T.
Sekiguchi M.
Institution
  First Department of Internal Medicine, Shinshu University School of Medicine,
Matsumoto, Japan.
Title
  Endothelin-1 and interleukin-8 in high altitude pulmonary oedema.
Source
  European Respiratory Journal. 9(9):1947-9, 1996 Sep.
Abstract
  We present a case of high altitude pulmonary oedema (HAPE) with pulmonary
hypertension and polymorphonuclear leucocyte (PMN) accumulation in
bronchoalveolar lavage fluid (BALF), which occurred in a 21 year old man. Plasma
endothelin-1 (ET-1) and interleukin-8 (IL-8) concentration in BALF were elevated
on admission, and returned to normal level at recovery, when the pulmonary
artery pressure and the PMN counts in BALF were normal. In addition, E-selectin
and intercellular adhesion molecule-1 (ICAM-1) in BALF were also slightly
increased on admission. These findings suggest that endothelin-1 is a
vasoconstrictor which contributes to the pulmonary hypertension in high altitude
pulmonary oedema, and that some of the inflammatory mediators play an important
role in chemotaxis and accumulation of polymorphonuclear leucocytes in the
development of high altitude pulmonary oedema.


<12>
Unique Identifier
  9630030
Authors
  Litch JA. Tuggy M.
Institution
  Himalayan Rescue Association, Kathmandu, Nepal.
Title
  Cough induced stress fracture and arthropathy of the ribs at extreme altitude.
Source
  International Journal of Sports Medicine. 19(3):220-2, 1998 Apr.
Abstract
  Cough and chest wall pain at high altitude have only received passing mention
in the medical literature. Increased minute ventilation of cold dry air at very
high altitude is likely to cause airway irritation. This in turn may result in
airway drying, mucus production, postnasal drip from vasomotor rhinitis, and
bronchospasm acting individually or in combination to stimulate the vagal cough
reflex. The cough is exacerbated further at extreme altitudes above 5500 m, and
may result in intercostal muscle strain and single or multiple rib fractures. We
present a case of multiple cough induced stress fractures and arthropathy
documented by technetium-99 bone scan in a high altitude climber and suggest the
addition of the term High Altitude Cough Syndrome (HACS) to the medical syntax
to identify this discrete medical problem of exposure to very high altitude.


<13>
Unique Identifier
  12165883
Authors
  Tannheimer M. Thomas A. Gerngross H.
Institution
  Bundeswehrkrankenhaus Ulm Department of Surgery, Ulm, Germany.
arkus.tannheimer@arcormail.de
Title
  Oxygen saturation course and altitude symptomatology during an expedition to
broad peak (8047 m).
Source
  International Journal of Sports Medicine. 23(5):329-35, 2002 Jul.
Abstract
  Thirteen healthy European mountaineers (11 male, 2 female) participated in the
62-day German-Pakistani Research Expedition to Broad Peak (8047 m) in the
Karakorum, Pakistan. During ascent, base camp stay and approach to the summit,
oxygen saturation was measured by pulse oximetry at rest, during exercise and
during sleep; in addition, questionnaires on high altitude symptomatic had to be
answered. We found a dramatic decrease in oxygen saturation especially at
extreme altitudes (7100 m: Median 63%, Min 59%, Max 65%) and a long time
required for real acclimatization. The lowest figures at 4850 m were found
during maximal exercise, 77.5% (69 - 85%) and during sleep, 81% (73 - 88%), the
highest ones at rest, 86.5% (77 - 89%). There was a significant correlation
(Spearman rank correlation coefficient with ties) between measured oxygen
saturation during the ascent to/stay at base camp and high altitude illness (p =
0.005 - 0.05), as well as with high altitude performance (p = 0.025 - 0.01). The
limiting values of "no high altitude symptomatic", "high altitude discomfort",
AMS and the malignant forms could be estimated for acclimatized
(>90%/>80%/>70%/<70%) and unacclimatized (>80%/>70%/>65%/<65%) condition. Pulse
oximetry is an objective non-invasive method of measurement that is easy to
handle. It is a suitable device besides clinical examination and questionnaire-
test in the diagnosis of high altitude illness even in the hands of non-
professionals. The measurement at sleep can possibly explain present high
altitude symptomatic despite of (nearly) normal oxygen saturation values at
rest.


<14>
Unique Identifier
  8872664
Authors
  Podolsky A. Eldridge MW. Richardson RS. Knight DR. Johnson EC. Hopkins
SR. Johnson DH. Michimata H. Grassi B. Feiner J. Kurdak SS. Bickler PE.
Severinghaus JW. Wagner PD.
Institution
  Department of Medicine, University of California, San Diego, La Jolla 92093-
0623, USA.
Title
  Exercise-induced VA/Q inequality in subjects with prior high-altitude
pulmonary edema.
Source
  Journal of Applied Physiology. 81(2):922-32, 1996 Aug.
Abstract
  Ventilation-perfusion (VA/Q) mismatch has been shown to increase during
exercise, especially in hypoxia. A possible explanation is subclinical
interstitial edema due to high pulmonary capillary pressures. We hypothesized
that this may be pathogenetically similar to high-altitude pulmonary edema
(HAPE) so that HAPE-susceptible people with higher vascular pressures would
develop more exercise-induced VA/Q mismatch. To examine this, seven healthy
people with a history of HAPE and nine with similar altitude exposure but no
HAPE history (control) were studied at rest and during exercise at 35, 65, and
85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m)
breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91
Torr) gas at both locations. We measured cardiac output and respiratory and
inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard
deviation of the perfusion distribution) increased with exercise. At sea level,
log standard deviation of the perfusion distribution was slightly higher in the
HAPE-susceptible group than in the control group during heavy exercise. At
altitude, these differences disappeared. Because a history of HAPE was
associated with greater exercise-induced VA/Q mismatch and higher pulmonary
capillary pressures, our findings are consistent with the hypothesis that
exercise-induced mismatch is due to a temporary extravascular fluid
accumulation.


<15>
Unique Identifier
  10658026
Authors
  Roach RC. Maes D. Sandoval D. Robergs RA. Icenogle M. Hinghofer-Szalkay
H. Lium D. Loeppky JA.
 Investigator: Loeppky JA.
Institution
  Division of Physiology, Department of Life Sciences, New Mexico Highlands
University, Las Vegas 87701-9000, New Mexico, USA. rroach@hypoxia.net
 Investigator Affiliation: Lovelace Resp Res Inst, Albuquerque, NM
Title
  Exercise exacerbates acute mountain sickness at simulated high altitude.
Source
  Journal of Applied Physiology. 88(2):581-5, 2000 Feb.
Abstract
  We hypothesized that exercise would cause greater severity and incidence of
acute mountain sickness (AMS) in the early hours of exposure to altitude. After
passive ascent to simulated high altitude in a decompression chamber [barometric
pressure = 429 Torr, approximately 4,800 m (J. B. West, J. Appl. Physiol. 81:
1850-1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific
maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On
another day they completed the same protocol but were sedentary (Sed).
Measurements included an AMS symptom score, resting minute ventilation (VE),
pulmonary function, arterial oxygen saturation (Sa(O(2))), fluid input, and
urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of
4.4 +/- 1.0 and 1.3 +/- 0.4 in Ex and Sed, respectively (P < 0.01); but resting
VE and Sa(O(2)) were not different between trials. However, Sa(O(2)) during the
exercise bouts in Ex was at 76.3 +/- 1.7%, lower than during either Sed or at
rest in Ex (81.4 +/- 1.8 and 82.2 +/- 2.6%, respectively, P < 0.01). Fluid
intake-urine volume shifted to slightly positive values in Ex at 3-6 h (P =
0.06). The mechanism(s) responsible for the rise in severity and incidence of
AMS in Ex may be sought in the observed exercise-induced exaggeration of
arterial hypoxemia, in the minor fluid shift, or in a combination of these
factors.


<16>
Unique Identifier
  8872663
Authors
  Eldridge MW. Podolsky A. Richardson RS. Johnson DH. Knight DR. Johnson
EC. Hopkins SR. Michimata H. Grassi B. Feiner J. Kurdak SS. Bickler PE.
Wagner PD. Severinghaus JW.
Institution
  Cardiovascular Research Institute, University of California, San Francisco
94143-0542, USA. mweldridge@ucdavis.edu
Title
  Pulmonary hemodynamic response to exercise in subjects with prior high-
altitude pulmonary edema.
Source
  Journal of Applied Physiology. 81(2):911-21, 1996 Aug.
Abstract
  Individuals with a prior history of (susceptible to high altitude pulmonary
edema (HAPE-S) have high resting pulmonary arterial pressures, but little data
are available on their vascular response to exercise. We studied the pulmonary
vascular response to exercise in seven HAPE-S and nine control subjects at sea
level and at 3,810 m altitude. At each location, both normoxic (inspired PO2 =
148 Torr) and hypoxic (inspired PO2 = 91 Torr) studies were conducted. Pulmonary
hemodynamic measurements included pulmonary arterial and pulmonary arterial
occlusion pressures. A multiple regression analysis demonstrated that the
pulmonary arterial pressure reactivity to exercise was significantly greater in
the HAPE-S group. This reactivity was not influenced by altitude or oxygenation,
implying that the response was intrinsic to the pulmonary circulation. Pulmonary
arterial occlusion pressure reactivity to exercise was also greater in the HAPE-
S group, increasing with altitude but independent of oxygenation. These findings
suggest an augmented flow-dependent pulmonary vasoconstriction and/or a reduced
vascular cross-sectional area in HAPE-S subjects.


<17>
Unique Identifier
  8872664
Authors
  Podolsky A. Eldridge MW. Richardson RS. Knight DR. Johnson EC. Hopkins
SR. Johnson DH. Michimata H. Grassi B. Feiner J. Kurdak SS. Bickler PE.
Severinghaus JW. Wagner PD.
Institution
  Department of Medicine, University of California, San Diego, La Jolla 92093-
0623, USA.
Title
  Exercise-induced VA/Q inequality in subjects with prior high-altitude
pulmonary edema.
Source
  Journal of Applied Physiology. 81(2):922-32, 1996 Aug.
Abstract
  Ventilation-perfusion (VA/Q) mismatch has been shown to increase during
exercise, especially in hypoxia. A possible explanation is subclinical
interstitial edema due to high pulmonary capillary pressures. We hypothesized
that this may be pathogenetically similar to high-altitude pulmonary edema
(HAPE) so that HAPE-susceptible people with higher vascular pressures would
develop more exercise-induced VA/Q mismatch. To examine this, seven healthy
people with a history of HAPE and nine with similar altitude exposure but no
HAPE history (control) were studied at rest and during exercise at 35, 65, and
85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m)
breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91
Torr) gas at both locations. We measured cardiac output and respiratory and
inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard
deviation of the perfusion distribution) increased with exercise. At sea level,
log standard deviation of the perfusion distribution was slightly higher in the
HAPE-susceptible group than in the control group during heavy exercise. At
altitude, these differences disappeared. Because a history of HAPE was
associated with greater exercise-induced VA/Q mismatch and higher pulmonary
capillary pressures, our findings are consistent with the hypothesis that
exercise-induced mismatch is due to a temporary extravascular fluid
accumulation.


<18>
Unique Identifier
  8872663
Authors
  Eldridge MW. Podolsky A. Richardson RS. Johnson DH. Knight DR. Johnson
EC. Hopkins SR. Michimata H. Grassi B. Feiner J. Kurdak SS. Bickler PE.
Wagner PD. Severinghaus JW.
Institution
  Cardiovascular Research Institute, University of California, San Francisco
94143-0542, USA. mweldridge@ucdavis.edu
Title
  Pulmonary hemodynamic response to exercise in subjects with prior high-
altitude pulmonary edema.
Source
  Journal of Applied Physiology. 81(2):911-21, 1996 Aug.
Abstract
  Individuals with a prior history of (susceptible to high altitude pulmonary
edema (HAPE-S) have high resting pulmonary arterial pressures, but little data
are available on their vascular response to exercise. We studied the pulmonary
vascular response to exercise in seven HAPE-S and nine control subjects at sea
level and at 3,810 m altitude. At each location, both normoxic (inspired PO2 =
148 Torr) and hypoxic (inspired PO2 = 91 Torr) studies were conducted. Pulmonary
hemodynamic measurements included pulmonary arterial and pulmonary arterial
occlusion pressures. A multiple regression analysis demonstrated that the
pulmonary arterial pressure reactivity to exercise was significantly greater in
the HAPE-S group. This reactivity was not influenced by altitude or oxygenation,
implying that the response was intrinsic to the pulmonary circulation. Pulmonary
arterial occlusion pressure reactivity to exercise was also greater in the HAPE-
S group, increasing with altitude but independent of oxygenation. These findings
suggest an augmented flow-dependent pulmonary vasoconstriction and/or a reduced
vascular cross-sectional area in HAPE-S subjects.


<19>
Unique Identifier
  10904032
Authors
  Robach P. Dechaux M. Jarrot S. Vaysse J. Schneider JC. Mason NP. Herry
JP. Gardette B. Richalet JP.
Institution
  Ecole Nationale de Ski et d'alpinisme, 74401 Chamonix, France.
med@ensa.jeunesse-sports.fr
Title
  Operation Everest III: role of plasma volume expansion on VO(2)(max) during
prolonged high-altitude exposure.
Source
  Journal of Applied Physiology. 89(1):29-37, 2000 Jul.
Abstract
  We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude
(HA) exposure and intense exercise is involved in the limitation of maximal O(2)
uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in
a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m).
Maximal exercise was performed with and without plasma volume expansion (PVX,
219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to
6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume
(PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was
decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL.
Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared
with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively.
VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The
more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05).
At exhaustion, plasma renin and aldosterone were not modified at HA compared
with SL but were higher at RSL, whereas plasma atrial natriuretic factor was
lower at HA. The present results suggest that PV contributes to the limitation
of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to
increased activity of the renin-aldosterone system, could also influence the
recovery of VO(2)(max).


<20>
Unique Identifier
  11160051
Authors
  Imoberdorf R. Garlick PJ. McNurlan MA. Casella GA. Peheim E. Turgay M.
Bartsch P. Ballmer PE.
Institution
  Department of Internal Medicine, University of Berne, CH-3010 Berne,
Switzerland. R.Imoberdorf@ksw.ch
Title
  Enhanced synthesis of albumin and fibrinogen at high altitude.
Source
  Journal of Applied Physiology. 90(2):528-37, 2001 Feb.
Abstract
  The acute effects of active and passive ascent to high altitude on plasma
volume (PV) and rates of synthesis of albumin and fibrinogen have been examined.
Measurements were made in two groups of healthy volunteers, initially at low
altitude (550 m) and again on the day after ascent to high altitude (4,559 m).
One group ascended by helicopter (air group, n = 8), whereas the other group
climbed (foot group, n = 9), so that the separate contribution of physical
exertion to the response could be delineated. PV was measured by dilution of
(125)I-labeled albumin, whereas synthesis rates of albumin and fibrinogen were
determined from the incorporation of isotope into protein after injection of
[ring-(2)H(5)]phenylalanine. In the air group, there was no change in PV at high
altitude, whereas, in the foot group, there was a 10% increase in PV (P < 0.01).
Albumin synthesis (mg. kg(-1). day(-1)) increased by 13% in the air group (P =
0.058) and by 32% in the foot group (P < 0.001). Fibrinogen synthesis (mg. kg(-
1). day(-1)) increased by 40% in the air group (P = 0.068) and by 100% in the
foot group (P < 0.001). Hypoxia and alkalosis at high altitude did not differ
between the groups. Plasma interleukin-6 was increased modestly in both groups
but C-reactive protein was not changed in either group. It is concluded that
increases in PV and plasma protein synthesis at high altitude result mainly from
the physical exercise associated with climbing. However, a small stimulation of
albumin and fibrinogen synthesis may be attributable to hypobaric hypoxia alone.


<21>
Unique Identifier
  11543191
Authors
  Nicolas M. Thullier-Lestienne F. Bouquet C. Gardette B. Gortan C. Joulia
F. Bonnon M. Richalet JP. Therme P. Abraini JH.
Institution
  Laboratoire de Neurosciences Integratives, Universite Henri Poincare Nancy 1,
Vandoeuvre-les-Nancy, France.
Title
  An anxiety, personality and altitude symptomatology study during a 31-day
period of hypoxia in a hypobaric chamber (experiment 'Everest-Comex 1997').
Source
  Journal of Environmental Psychology. 19(4):407-14, 1999 Dec.
Abstract
  Extreme environmental situations are useful tools for the investigation of the
general processes of adaptation. Among such situations, high altitude of more
than 3000 m produces a set of pathological disorders that includes both cerebral
(cAS) and respiratory (RAS) altitude symptoms. High altitude exposure further
induces anxiety responses and behavioural disturbances. The authors report an
investigation on anxiety responses, personality traits, and altitude symptoms
(AS) in climbers participating in a 31-day period of confinement and gradual
decompression in a hypobaric chamber equivalent to a climb from sea-level to
Mount Everest (8848 m altitude). Personality traits, state-trait anxiety, and AS
were assessed, using the Cattell 16 Personality Factor questionnaire (16PF), the
Spielberger's State-Trait Anxiety Inventory (STAI), and the Lake Louise
concensus questionnaire. Results show significant group effect for state-anxiety
and AS; state-anxiety and AS increased as altitude increased. They also show
that state-type anxiety shows a similar time-course to cAS, but not RAS.
Alternatively, our results demonstrate a significant negative correlation
between Factor M of the 16PF questionnaire, which is a personality trait that
ranges from praxernia to autia. In contrast, no significant correlation was
found between personality traits and AS. This suggests that AS could not be
predicted using personality traits and further support that personality traits,
such as praxernia (happening sensitivity), could play a major role in the
occurrence of state-type anxiety responses in extreme environments. In addition,
the general processes of coping and adaptation in individuals participating in
extreme environmental experiments are discussed.


<22>
Unique Identifier
  9509829
Authors
  Fiorenzano G. Papalia MA. Parravicini M. Rastelli V. Bigi R. Dottorini M.
Institution
  Department of Pulmonary Medicine, E. Morelli Hospital, Sondalo (Sondrio),
Italy.
Title
  Prolonged ECG abnormalities in a subject with high altitude pulmonary edema
(HAPE).
Source
  Journal of Sports Medicine & Physical Fitness. 37(4):292-6, 1997 Dec.
Abstract
  High Altitude Pulmonary Edema (HAPE) is an uncommon type of non-cardiogenic
pulmonary edema. Few data are available regarding ECG abnormalities in patients
with HAPE. They are usually slight and related to acute pulmonary hypertension.
This paper describes a case of prolonged ECG abnormalities in a subject with
HAPE, with no proven cardiac diseases. The Authors discuss the pathopysiological
aspects of this kind of hypoxic-induced right ventricular overload with
extensive T-wave negativity in precordial leads.


<23>
Unique Identifier
  10732898
Authors
  Grunig E. Mereles D. Hildebrandt W. Swenson ER. Kubler W. Kuecherer H.
Bartsch P.
Institution
  Department of Cardiology, University of Heidelberg, Germany.
ekkehard_gruenig@med.uni-heidelberg.de
Title
  Stress Doppler echocardiography for identification of susceptibility to high
altitude pulmonary edema.
Source
  Journal of the American College of Cardiology. 35(4):980-7, 2000 Mar 15.
Abstract
  OBJECTIVE: This prospective single-blinded study was performed to quantitate
noninvasive pulmonary artery systolic pressure (PASP) responses to prolonged
acute hypoxia and normoxic exercise. BACKGROUND: Hypoxia-induced excessive rise
in pulmonary artery pressure is a key factor in high-altitude pulmonary edema
(HAPE). We hypothesized that subjects susceptible to HAPE (HAPE-S) have
increased pulmonary artery pressure response not only to hypoxia but also to
exercise. METHODS: PASP was estimated at 45, 90 and 240 min of hypoxia (FiO2 =
12%) and during supine bicycle exercise in normoxia using Doppler-
echocardiography in nine HAPE-S and in 11 control subjects. RESULTS: In the
control group, mean PASP increased from 26+/-2 to 37+/-4 mm Hg (deltaPASP
10.3+/-2 mm Hg) after 90 min of hypoxia and from 27+/-4 to 36+/-3 mm Hg
(deltaPASP 8+/-2 mm Hg) during exercise. In contrast, all HAPE-S subjects
revealed significantly greater increases (p = 0.002 vs. controls) in mean PASP
both during hypoxia (from 28+/-4 to 57+/-10 mm Hg, deltaPASP 28.7+/-6 mm Hg) and
during exercise (from 28+/-4 to 55+/-11 mm Hg, deltaPASP 27+/-8 mm Hg) than did
control subjects. Stress echocardiography allowed discrimination between groups
without overlap using a cut off PASP value of 45 mm Hg at work rates less than
150 W. CONCLUSIONS: These data indicate that HAPE-S subjects may have abnormal
pulmonary vascular responses not only to hypoxia but also to supine bicycle
exercise under normoxic conditions. Thus, Doppler echocardiography during supine
bicycle exercise or after 90 min of hypoxia may be useful noninvasive screening
methods to identify subjects susceptible to HAPE.


<24>
Unique Identifier
  10192076
Authors
  Clarke CR.
Institution
  National Hospital for Neurology, London.
Title
  Three journeys to high altitude: medicine, Tibetan thangkas, and Sepu Kangri.
Source
  Journal of the Royal College of Physicians of London. 33(1):78-84, 1999 Jan-
Feb.
Abstract
  This article begins by highlighting the work of several pioneers of altitude
medicine, and their achievements in physiology and clinical observation. Tibetan
medicine of the 17th century is then introduced, particularly the medical
paintings (thangkas) and the conduct of traditional physicians. Finally, I
mention recent British mountain exploration in central Tibet during 1996, 1997
and 1998 and the challenge of Sepu Kangri which, at 6,995m, is the highest peak
of the eastern Nyangla Qen Tangla Shan.


<25>
Unique Identifier
  11989137
Authors
  Brundrett G.
Institution
  geoffbrundrett@waitrose.com
Title
  Sickness at high altitude: a literature review. [Review] [67 refs]
Source
  Journal of the Royal Society of Health. 122(1):14-20, 2002 Mar.
Abstract
  When some individuals spend just a few hours at low atmospheric pressure above
1,500 m (5,000 ft)--such as when climbing a mountain or flying in a plane at
high altitude--they become ill. Altitude sickness studies originally
concentrated on life-threatening illnesses which beset determined and athletic
climbers at extreme altitudes. In recent years, however, research attention is
moving towards milder forms of sickness reported by a significant proportion of
the growing number of visitors to mountain and ski resorts at more moderate
altitude. Some of this research is also relevant in understanding the problems
experienced by passengers in newer planes that fly at a significantly higher
equivalent cabin altitude, i.e. 2,440 m (8,000 ft), than earlier designs.
Engineering solutions--such as enriched oxygen in enclosed spaces at altitude,
or in the case of aircraft, lower cabin altitudes--are possible, but for an
economic assessment to be realistic an engineer needs to identify the scale of
the problem and to understand the factors determining susceptibility. This
review concentrates on the problems of mountain sickness in the ordinary
population at altitudes of around 3,000 m (10,000 ft); this is a problem of
growing concern as ski resorts develop, mountain trekking increases in
popularity, and as higher altitude cabin pressures are achieved in aircraft.
[References: 67]


<26>
Unique Identifier
  11830197
Authors
  Cremona G. Asnaghi R. Baderna P. Brunetto A. Brutsaert T. Cavallaro C.
Clark TM. Cogo A. Donis R. Lanfranchi P. Luks A. Novello N. Panzetta S.
Perini L. Putnam M. Spagnolatti L. Wagner H. Wagner PD.
Institution
  Unit of Respiratory Medicine, San Raffaele University Scientific Institute,
Via Olgettina 60, 20132 Milano, Italy. george.cremona@hsr.it
Title
  Pulmonary extravascular fluid accumulation in recreational climbers: a
prospective study.[see comment].
Comments
  Comment in: Lancet. 2002 Aug 17;360(9332):570-1; author reply 571-2; PMID:
12241684, Comment in: Lancet. 2002 Aug 17;360(9332):570; author reply 571-2;
PMID: 12241683, Comment in: Lancet. 2002 Aug 17;360(9332):571; author reply 571-
2; PMID: 12241685, Comment in: Lancet. 2002 Jan 26;359(9303):276-7; PMID:
11830190
Source
  Lancet. 359(9303):303-9, 2002 Jan 26.
Abstract
  BACKGROUND: High altitude pulmonary oedema (HAPE) that is severe enough to
require urgent medical care is infrequent. We hypothesised that subclinical HAPE
is far more frequent than suspected during even modest climbs of average effort.
METHODS: We assessed 262 consecutive climbers of Monte Rosa (4559 m), before
ascent and about 24 h later on the summit 1 h after arriving, by clinical
examination, electrocardiography, oximetry, spirometry, carbon monoxide
transfer, and closing volume. A chest radiograph was taken at altitude.
FINDINGS: Only one climber was evacuated for HAPE, but 40 (15%) of 262 climbers
had chest rales or interstitial oedema on radiograph after ascent. Of 37 of
these climbers, 34 (92%) showed increased closing volume. Of the 197 climbers
without oedema, 146 (74%) had an increase in closing volume at altitude. With no
change in vital capacity, forced expiratory volume in 1 s and forced expiratory
flow at 25-75% of forced vital capacity increased slightly at altitude, without
evidence of oedema. If we assume that an increased closing volume at altitude
indicates increased pulmonary extravascular fluid, our data suggest that three
of every four healthy, recreational climbers have mild subclinical HAPE shortly
after a modest climb. INTERPRETATION: The risk of HAPE might not be confined to
a small group of genetically susceptible people, but likely exists for most
climbers if the rate of ascent and degree of physical effort are great enough,
especially if lung size is normal or low.


<27>
Unique Identifier
  9690443
Authors
  Zafren K.
Title
  Gamow bag for high-altitude cerebral oedema.[comment].
Comments
  Comment on: Lancet. 1998 Jun 13;351(9118):1815; PMID: 9635981
Source
  Lancet. 352(9124):325-6, 1998 Jul 25.


<28>
Unique Identifier
  9798594
Authors
  Tschop M. Strasburger CJ. Hartmann G. Biollaz J. Bartsch P.
Title
  Raised leptin concentrations at high altitude associated with loss of
appetite.
Source
  Lancet. 352(9134):1119-20, 1998 Oct 3.
<29>
Unique Identifier
  10416557
Authors
  Anooshiravani M. Dumont L. Mardirosoff C. Soto-Debeuf G. Delavelle J.
Institution
  Department of Radiology, Hopital des Enfants Reine Fabiola, Brussels, Belgium.
alpamayo@usa.net
Title
  Brain magnetic resonance imaging (MRI) and neurological changes after a single
high altitude climb.
Source
  Medicine & Science in Sports & Exercise. 31(7):969-72, 1999 Jul.
Abstract
  PURPOSE: Neurological impairment, mental dysfunction, and brain imaging
changes caused by severe hypoxia have been described by several authors.
However, the occurrence of transitory, long lasting, or permanent brain damage
has been debated. Although climbing to 8000 m is reserved to a small number of
climbers, there are hundreds of lowlanders spending relatively short holidays
climbing peaks up to 6000 m in the Andes or in the Himalayas. They are usually
not well acclimated and often suffer from acute mountain sickness (AMS). The aim
of this study was to examine the effect of a single high altitude exposure on
the changes in brain MRI and neuropsychological testing in climbers. METHODS:
Brain MRI, medical history, and a battery of neuropsychological tests were
obtained in eight male climbers between 31 and 48 yr of age a few days before
and between 5 and 10 d after returning to sea level following ascent to
altitudes of over 6000 m without oxygen. RESULTS: The mean AMS symptom score
recorded at 5500 m was three in all climbers, headache being the predominant
symptom. CONCLUSION: We did not observe the changes in brain imaging and in
neuropsychological testing observed by other authors. The residual central
nervous system impairment following return from high altitude was not observed
in our study, and the good results in neuropsychological testing were well
correlated with the unchanged brain MRI imaging.


<30>
Unique Identifier
  11143435
Authors
  Sonna LA. Kain JE. Hoyt RW. Muza SR. Sawka MN.
Institution
  Thermal and Mountain Medicine Division, U.S. Army Research Institute of
Environmental Medicine, Natick, MA 01760, USA.
Title
  Ambulatory physiological status monitoring during a mountaineering expedition.
Source
  Military Medicine. 165(11):860-6, 2000 Nov.
Abstract
  OBJECTIVE: To evaluate an ambulatory physiological monitoring system during a
mountaineering expedition. We hypothesized that the Environmental Symptoms
Questionnaire, combined with frequent measurement of oxygen saturation and core
temperature, would accurately identify cases of environmental illness. METHODS:
Twelve military mountaineers took a daily Environmental Symptoms Questionnaire,
monitored fingertip oxygen saturations, and recorded core temperatures while
climbing a 4,949-m peak. Illnesses identified by the system were compared with
those identified by spontaneous reports. RESULTS: The system correctly
identified one case of high-altitude pulmonary edema and two illnesses that were
not reported to the physician (one case of acute mountain sickness and one of
self-limited symptomatic desaturation). However, it did not identify two
illnesses that were severe enough to preclude further climbing (one case of
sinus headache and one of generalized fatigue). CONCLUSIONS: Our monitoring
system may complement, but cannot replace, on-site medical personnel during
mountaineering expeditions.


<31>
Unique Identifier
  10519586
Authors
  Wiedman M. Tabin GC.
Institution
  Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114,
USA.
Title
  High-altitude retinopathy and altitude illness.[see comment].
Comments
  Comment in: Ophthalmology. 2000 Jul;107(7):1212; PMID: 10889073
Source
  Ophthalmology. 106(10):1924-6; discussion 1927, 1999 Oct.
Abstract
  OBJECTIVE: To determine the relationship between high-altitude retinopathy
(HAR) and other altitude-related illnesses and establish a classification system
for HAR. DESIGN: Observational case series. PARTICIPANTS: All 40 climbers among
3 Himalayan expeditions who ascended to altitudes between 16,000 and 29,028 feet
above sea level (summit of Mt. Everest) were examined for signs of HAR and
altitude illness (AI). METHODS: All subjects had dilated fundus examinations
before the ascent, intermittent fundus, and medical examinations during the
climb and a dilated fundus and medical examination within 2 days after attaining
their highest altitude. MAIN OUTCOME MEASURES: Careful fundus drawings or fundus
photography or both were obtained for all participants. All subjects gave a
subjective assessment of their symptoms of acute mountain sickness (AMS) and
were assessed clinically for signs of high-altitude cerebral edema (HACE).
RESULTS: Nineteen of 21 climbers who ascended above 25,000 feet developed HAR.
Fourteen of 19 climbers who attained altitudes between 16,000 and 25,000 feet
were found to have retinopathy. A grading system for HAR describing the severity
of the retinopathy was developed. Correlation of the retinopathy with other AI
showed that AMS was endemic and that a statistically significant correlation
exists between HAR and HACE (P = 0.0240). CONCLUSION: Recognizing advancing
grades of HAR may allow physicians to recommend initiating empiric treatment
with oxygen, steroids, diuretics and immediate descent to prevent HAR
progression, macular involvement, or potentially fatal HACE. High-altitude
retinopathy is both a significant component of and a predictor of progressive
AI.


<32>
Unique Identifier
  10889073
Authors
  Murdoch DR.
Title
  High-altitude illness.[comment].
Comments
  Comment on: Ophthalmology. 1999 Oct;106(10):1924-6; discussion 1927; PMID:
10519586
Source
  Ophthalmology. 107(7):1212, 2000 Jul.


<33>
Unique Identifier
  10946741
Authors
  Yarnell PR. Heit J. Hackett PH.
Institution
  Department of Neurology, University of Colorado School of Medicine, St.
Anthony's Hospital Denver, USA.
Title
  High-altitude cerebral edema (HACE): the Denver/Front Range experience.
[Review] [22 refs]
Source
  Seminars in Neurology. 20(2):209-17, 2000.
Abstract
  High-altitude cerebral edema (HACE) is a potentially fatal metabolic
encephalopathy associated with a time-dependent exposure to the hypobaric
hypoxia of altitude. Symptoms commonly are headache, ataxia, and confusion
progressing to stupor and coma. HACE is often preceded by symptoms of acute
mountain sickness and coupled, in its severe form, with high-altitude pulmonary
edema. Although HACE is mostly seen at altitudes above that of the Denver/Front
Range visitor-skier locations, we report our observations over a 13-year period
of skier-visitor HACE patients. It is believed that this is a form of vasogenic
edema, and it is responsive to expeditious treatment with a successful outcome.
[References: 22]


<34>
Unique Identifier
  11858498
Authors
  Mannucci PM. Gringeri A. Peyvandi F. Di Paolantonio T. Mariani G.
Title
  Short-term exposure to high altitude causes coagulation activation and
inhibits fibrinolysis.
Source
  Thrombosis & Haemostasis. 87(2):342-3, 2002 Feb.

				
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