Intracranial Pressure at High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Raised Intracranial Pressure ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Pressure Changes ◽  
Serial Measurements

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

Intracranial Pressure, High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 88 (s32) ◽  
pp. 26P-26P
Author(s):  
AD Wright ◽  
CHE Imray ◽  
MSC Morrissey ◽  
RJ Marchbanks ◽  
AR Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

scholarly journals Acute mountain sickness (AMS) in a Nepali pilgrim after rapid ascent to a sacred lake (4380 m) in the Himalayas

2018 ◽  
Vol 11 (1) ◽  
pp. bcr-2017-222888
Author(s):  
Simant Singh Thapa ◽  
Buddha Basnyat
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Severe Headache ◽  
Vulnerable Group ◽  
High Incidence ◽  
The Usa ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Supportive Management ◽  
Temporary Health

A 55-year-old female Nepali pilgrim presented to the Himalayan Rescue Association Temporary Health Camp near the sacred Gosainkund Lake (4380 m) north of Kathmandu, Nepal, with a complaint of severe headache, vomiting and light-headedness. She was diagnosed with severe acute mountain sickness. Intramuscular dexamethasone was administered. Paracetamol (acetaminophen in the USA and Canada) and ondansetron were given as supportive management for headache and nausea. Arrangements were made to have her carried down by a porter immediately. After the descent, all her symptoms resolved. High-altitude pilgrims are a more vulnerable group than trekkers and mountaineers. Pilgrims generally have a rapid ascent profile, have low awareness of altitude illness and are strongly motivated to gain religious merit by completing the pilgrimage. As a result, there is a high incidence of altitude illness among pilgrims travelling to high-altitude pilgrimage sites.

scholarly journals Analysis of High-altitude Syndrome and the Underlying Gene Polymorphisms Associated with Acute Mountain Sickness after a Rapid Ascent to High-altitude

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jie Yu ◽  
Ying Zeng ◽  
Guozhu Chen ◽  
Shizhu Bian ◽  
Youzhu Qiu ◽  
...  
Keyword(s):  
High Altitude ◽  
Gene Polymorphisms ◽  
Acute Mountain Sickness ◽  
Rapid Ascent ◽  
Mountain Sickness

scholarly journals The cerebral venous system and hypoxia

2016 ◽  
Vol 120 (2) ◽  
pp. 244-250 ◽  
Author(s):  
Mark H. Wilson ◽  
Christopher H. E. Imray
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Venous Outflow ◽  
Edema Formation ◽  
Care Environment ◽  
Fluid Production ◽  
High Altitude Cerebral Edema ◽  
Blood Inflow ◽  
Mountain Sickness

Most hypobaric hypoxia studies have focused on oxygen delivery and therefore cerebral blood inflow. Few have studied venous outflow. However, the volume of blood entering and leaving the skull (∼700 ml/min) is considerably greater than cerebrospinal fluid production (0.35 ml/min) or edema formation rates and slight imbalances of in- and outflow have considerable effects on intracranial pressure. This dynamic phenomenon is not necessarily appreciated in the currently taught static “Monro-Kellie” doctrine, which forms the basis of the “Tight-Fit” hypothesis thought to underlie high altitude headache, acute mountain sickness, and high altitude cerebral edema. Investigating both sides of the cerebral circulation was an integral part of the 2007 Xtreme Everest Expedition. The results of the relevant studies performed as part of and subsequent to this expedition are reviewed here. The evidence from recent studies suggests a relative venous outflow insufficiency is an early step in the pathogenesis of high altitude headache. Translation of knowledge gained from high altitude studies is important. Many patients in a critical care environment develop hypoxemia akin to that of high altitude exposure. An inability to drain the hypoxemic induced increase in cerebral blood flow could be an underappreciated regulatory mechanism of intracranial pressure.

Intermittent Hypoxic Exposure Reduces Acute Mountain Sickness Upon Subsequent Rapid Ascent to High Altitude

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S170-S171
Author(s):  
Ken Kambis ◽  
Julie Barnes ◽  
Michio Yasukawa ◽  
Reina Chamberlain ◽  
Tiffanie Tsui ◽  
...  
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Hypoxic Exposure ◽  
Rapid Ascent ◽  
Mountain Sickness

scholarly journals Remote ischemic preconditioning does not prevent acute mountain sickness after rapid ascent to 3,450 m

2017 ◽  
Vol 123 (5) ◽  
pp. 1228-1234 ◽  
Author(s):  
Marc M. Berger ◽  
Franziska Macholz ◽  
Lukas Lehmann ◽  
Daniel Dankl ◽  
Marcel Hochreiter ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Ischemic Preconditioning ◽  
Acute Mountain Sickness ◽  
Remote Ischemic Preconditioning ◽  
Systolic Pulmonary Artery Pressure ◽  
Transthoracic Doppler Echocardiography ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
The Brain

Remote ischemic preconditioning (RIPC) has been shown to protect remote organs, such as the brain and the lung, from damage induced by subsequent hypoxia or ischemia. Acute mountain sickness (AMS) is a syndrome of nonspecific neurologic symptoms and in high-altitude pulmonary edema excessive hypoxic pulmonary vasoconstriction (HPV) plays a pivotal role. We hypothesized that RIPC protects the brain from AMS and attenuates the magnitude of HPV after rapid ascent to 3,450 m. Forty nonacclimatized volunteers were randomized into two groups. At low altitude (750 m) the RIPC group ( n = 20) underwent 4 × 5 min of lower-limb ischemia (induced by inflation of bilateral thigh cuffs to 200 mmHg) followed by 5 min of reperfusion. The control group ( n = 20) underwent a sham protocol (4 × 5 min of bilateral thigh cuff inflation to 20 mmHg). Thereafter, participants ascended to 3,450 m by train over 2 h and stayed there for 48 h. AMS was evaluated by the Lake Louise score (LLS) and the AMS-C score. Systolic pulmonary artery pressure (SPAP) was assessed by transthoracic Doppler echocardiography. RIPC had no effect on the overall incidence (RIPC: 35%, control: 35%, P = 1.0) and severity (RIPC vs. control: P = 0.496 for LLS; P = 0.320 for AMS-C score) of AMS. RIPC also had no significant effect on SPAP [maximum after 10 h at high altitude; RIPC: 33 (SD 8) mmHg; controls: 37 (SD 7) mmHg; P = 0.19]. This study indicates that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate AMS and the magnitude of high-altitude pulmonary hypertension. NEW & NOTEWORTHY Remote ischemic preconditioning (RIPC) has been reported to improve neurologic and pulmonary outcome following an acute ischemic or hypoxic insult, yet the effect of RIPC for protecting from high-altitude diseases remains to be determined. The present study shows that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate acute mountain sickness and the degree of high-altitude pulmonary hypertension. Therefore, RIPC cannot be recommended for prevention of high-altitude diseases.

Autonomic cardiovascular regulation in subjects with acute mountain sickness

2005 ◽  
Vol 289 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Paola A. Lanfranchi ◽  
Roberto Colombo ◽  
George Cremona ◽  
Paolo Baderna ◽  
Liliana Spagnolatti ◽  
...  
Keyword(s):  
High Altitude ◽  
Potential Role ◽  
Acute Mountain Sickness ◽  
Low Frequency ◽  
Short Term ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Normalized Units ◽  
Hypoxic Gas Mixture

The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS ( P < 0.01). At high altitude, the low-frequency (LF) component of systolic BP variability (LFSBP) was higher ( P = 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower ( P = 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude ( P < 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP ( P < 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.

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