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Hra articles

Himalayan Rescue Association Nepal
Buddha Basnyat, David R Murdoch
High- altitude illness is the collective term for acute mountain sickness (AMS),high altitude cerebral oedema (HACE), & high altitude pulmonary oedema(HAPE).the pathophysiology of these syndromes is not completely understood,although studies have substantially contributed to the current understanding ofseveral areas. These areas include the role & potential mechanishms of brainswelling in AMS & HACE mechanisms accounting for exaggerated pulmonaryhypertention in HAPE, & the role of inflammation & alveolar-fluid clearance inHAPE. Only limited information is available about the genetic basis of high-altitudeillness, & no clear associations between gene polymorphisms & susceptibility havebeen discovered. Gradual ascents will always be the best strategy for preventinghigh altitude illness, although chemoprophylaxis may be useful in some situations.
Despite investigation of other agents, acetazolamide remains the preferred drugfor preventing AMS. the next few years are likely to see many advances in theunderstanding of the causes & management of high- altitude illness.
In may ,2003, fell the anniversaries of two important high altitude achievements.
May 29 was the 50th anniversary of the first ascent of Mount Everest by EdmundHillary & Tenzing Norgey. May 8 was the 25th anniversary of first ascent ofMt.Everest without the use of supplementary use of oxygen by Reinhold messner &Peter Habeler. Both achievements were once thought to be beyond humancapabilities. The fact that these target were achieved, & have been repeated manytimes since, is the testimony to the ability of the human beings, with the rightpreparation , to tolerate hypoxia.
Human beings go to high altitude for many reasons. Around 140 people livepermanently at altitude higher than 2500m. some ,such as minors in southAmerica, commute to altitude up to 6000m for work. Large number of peopletravel to high altitude for recreational pursuits, such as mountaineering, trekking,& skiing. The deployment of military personnel to high altitude areas in Asia aspart of regional conflict in Kashmir & Afganisthan has also become a focus ofattention.
High- altitude illness is the collective term for the syndromes that can affectunacclimatised traveller shortly after ascent to high altitude. The termencompasses the mainly cerebral syndromes of acute mountain sickness (AMS) &the high altitude cerebral oedema (HACE),& the pulmonary syndrome high altitudepulmonary oedema (HAPE). HACE & HAPE occur much less frequently than AMS,but are potentially fatal.
We provide an update on high altitude illness, with particular emphasis on thecurrent understanding of pathophysiology, prevention, & treatment.
The most important risk factor for the development of high altitude illness are rateof ascent , altitude reached (especially the sleeping altitude), & individualsusceptibility. The rate of AMS among conference delegates to moderate Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
altitudes(1920-2957m)in Colorado,USA, was 25%. In the mount region ofNepal,about 50%of trekker who walk to altitude higher than 4000m over 5 or moredays develop AMS,&84%of people who fly directly to 3860m are affected. Highaltitude illness is much more likely to occur at altitude higher than 2500m than atlower altitudes,but is being increasingly recognised altitude between 1500m to2500m.the incident of HACE & HAPE is much lower than for AMS< with astimatesin the range 0.1-4.0%Other risk factor for high altitude illness include a history of high altitude illness &permanent residence lower than 900m.exertion is risk factor for AMS,but lack ofphysical fitness is not.children & adult are seem to be equally affected, but peopleolder than 50 years may be less suceptible to AMS than younger people. Althoughthere is thought to be no difference between the sexes in suceptibility to AMS, insome studies rate of illness have been higher among women than men. nEckirradiation or surgery & respiratory tract infection are potential risk factor for highaltitude illness that warrant further study. Although an association between AMS& dehydration has been noted. it is unclear whether dehydration is an independentrisk factor for AMS. The vulnerability of porters & pilgrims to high altitude illnesshas been highlighted.
Search stategy & selection criteriaWe undertook a computer- aided search of pubmed, & used the key words altitude, acute mountains sickness, high altitude pulmonary edema,high altitudepulmonary oedema, high altitude cerebral edema, high altitude cerebral oedema,hypoxia & mountaineering. We also reviewed journal reference lists & abstractfrom international scientific meetings, & used for existing knowledge of primarypublication in the field. Priority was given to recent reports covering topical issues& report that, in our understanding, have contributed substantially to the currentknowledge about high altitude illness.
Clinical presentation
AMS is characterised by non specific symptoms & a paucity findings. The main
symptoms are headache, anorexia, nausea, vomiting, fatigue, dizziness, and sleep
disturbance, but not all need to be present. Headache is deemed the cardinal
symptom, but the characteristics are not sufficiently distinctive to differentiate it
from other causes of headache. Symptoms of AMS typically appear 6-12h after
arrival at high altitude. Diagnostic signs are absent, and the presence of abnormal
neurological or respiratory signs can show progression to or development of HACE
or HAPE. The non specific symptoms & signs of AMS can result in diagnostic
confusions with other disorders, such as exhaustion, dehydration, hypothermia,
alcohol hangover, and migraine.
HACE is widely viewed as the stage of AMS, & is normally preceded by symptoms
of AMS. HACE is characterised by ataxia & altered consciousness, which may
progress to coma & death due to brain herniation. People with concomitant HAPE
may progress very rapidly from AMS to HACE. Clinical examination may reveal
papilloedema, ataxia, retinal haemorrhages, and,occasionally, focal neurological
The pathophysiology of AMS & HACE has been the subject of several reviews. The
exact mechanism causing these syndromes is unknown , although evidence point
Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
to the process in the central nervous system. Characterstics of established AMSinclude relative hypoventilation, impaired gas exchange, increased sympatheticactivity, fluid retention & redistribution, & in moderate to severe AMS,raisedintracranial pressure.
Hackett & Roach have proposed a model explain the pathophysiology of AMS &HACE (fig1). In this model, hypoxaemia elicits various neurohumoral &haemodynamic responces that that ultimately leads to raised cerebral blood flow,altered permeability of the blood brain barrier, & cerebral oedema.These changesresult in brain swelling & intracranial pressure. According to the model, AMSoccur in the people who have inadequate cerebrospinal capacity to buffer the brainswellings; those with the greater ratio of cranial cerebrospinal fluid to brainvolume are better able to compensate for swelling through displacement ofcerebrospinal fluid, & are less likely to develop AMS than people with the lowerratio. This hypothesis is attractive, but remains speculative.
Mechanisms that cause brain swelling at high altitude
Fluid accumulation in the brain may be caused by cytotoxic oedema (cell swelling
due to increased intracellular osmolarity), vasogenic oedema ( lead of blood brain
barrier with extravasation of proteins & fluid into the interstinal space), or both.
Cytotoxic oedema may occur in the later stages of HACE because of increased
cerebrospinal fluid pressure, decreased perfusion,& focal ischaenia, but it does not
explain AMS or early HACE, it is unkindly that AMS is associoted with hypoxiaemia
suffering enough to impair cell-ion homoeostasis & cause swelling, by contrast,
HACE may be associated with vasogenic oedema MRIfindings among patients with
HACE show changes consistent with vasogenic oedema. Further support for the
presence of vasogenic oedema include the time course of onset & resolution of
simptoms & signs, findings from AMS & HACE in sleep,& the response to
corticosteroids(only vasogenic oedema is steroid responsive.),vasogenic oedema at
high altitude probably occurs is a consequence of a combination of factor, is of
which cannot on its own explain the process . those factor may include raised
cerebral capillary pressure resulting in a mechanical vascular leak, impaired
cerebral autoregulation in the presence of hypoxia cerebral vasodilatation, &
altertation in premeability of the blood –brain barrier because of hypoxia-induced
chemical mediators such as bradykinin, histamina, nitric oxide, arachidonic, &
vascular endothelial growth factor. The angiogenic cytokine, vascular endothelian
growth factor, has received particular attention. Gene expression & production of
vasular endothelial growth factor, a potent promoter of capillary leakage, is
upregulated by hypoxia & may play apart in the development of AMS &
HACE.vascular endothelial growth factor caused hypoxia-induced increase of
vascular leakage in the brains of mice. However, prelimimary studies of plasma
vascular endotheliak growth factor centrations in climbers have inconsistent & so
no association with high altitude illness. Indirect evidence for the role for vascular
endothellial growth factor in high altitude illness comes for the observation that
dexamethsone, used in the prevention & treatment of AMS, blocks hypoxia
up-regulation of this cytokine.
Mild cerebral oedema as a cause of AMS
Little objective evidence supports the presence of cerebral oedema in
AMS.cerebral oedema was present in a sheep model of AMS & HACE among
animals that had the equivalent of moderate to severe AMS, but it is unclear
Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
whether those peoples also had HACE. In MRI studies, reduced cerebrospinal fluidvolume, increased T2-weighed signal in the corpus callosum, increased brainvolume occurred with ascent to high altitude. These changes suggest the presenceof brain swelling, but it is unclear weather it is due to cerebral oedema.
Furthermore this changes are not limited with the people who had AMS & provideevidence that all people have some degrees of brain swellings on ascents to highaltitude.reports of space occupying lesions first becoming symptomatic at highaltitude support the concept of brain swelling at high altitude.
High altitude headache
Headache is most common & most prominent symptoms of AMS, although its
cause remain unclear. Sanchez del rio & moskowitz that the cause of high altitude
headache is multifactoral, with various chemical & mechanical factor activating a
final common pain pathway, the trigeminovascular system. Triggering factor
associated with high altitude hypoxia may include nitric oxide , arachidonic-acid
metabolites, serotinin, & histamine, which sensitise small unmyelinated fibre
conveying pain & accumulate in proximity to trigominovascular fibres , thereby
causing headache. The response to non steroidal antiinflammatory drugs &
steroids provides indirect evidence for the involvement of the arachidonic-acid
pathway & inflammation in the genesis of high altitude headache. Although high
altitude headache & AMS in general, shares many characterstics with migraine, it
is unknown whether similar pathogenic are involved in two disorders. Of note
response of high altitude headache to the 5 hydroxytryptamine agonist
sumatriptan have been inconsistent.
Individual susceptibility
Some people are more susceptible to AMS than others. This fact has promoted
substantial efforts by researchers to explain difference in susceptibility & to
develop method of predicting the risk. The role of hypoxia ventilatory response has
been a particular area of interest ;the hypothesis that the people who are
susceptible to AMS have a decreased ventilatory response of hypoxia.
Collectively,the result from high altitude & hyperbaric chamber studies show a
weak association between hypoxia ventilatory response of AMS suspetible
individual at low altitude being slightly lower than those not susceptible to AMS.
ventilatory response of carbon-dioxide & the presence of perodic nocturnal
breathing do not seem to be associated with suceptibilty of AMS.
Ross suggested that suceptibility to AMS may be explained by anatomical
difference in intracranial & intraspinal cerebrospinal fluid capacity. people with
small ratio cranial cerebrospinal fluid to brain volume are less ableto tolerate brain
swellings through displacement of cerebrospinal fluid than people with high ratios.
These people consequently become more symtomatic from mild brain swelling &
are more likely to develop AMS. Preliminary data from neuroimaging
measurements supports that the tight brain brain is associated with severity of
AMS. If this hypothesis is correct elderly people should be less suceptible to AMS
because of their ability to accommodate brain swelling due to immature cranial
sutures open fontanelles.
Prevention & treatment :
Gradual ascent, allowing time for acclimatisation, is the best strategy for
preventing high altitude illness. Determining an idea ascent rate, however is
Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
difficult & varies from person to person . one rule of thumb is that at higher than3000m, each night should average not more than 300m above the previous, with arest day every 2-3 days. For many people this ascent rate is too slow, &recommendation now take ascent speed into account & state that the heightdifference between the consecutive sleeping sites should average not more than600m per day. Each formula emphasises sleeping altitudes, which means that ispermissible to ascend more than the recommended daily rate, as long as descent ismade before sleeping(climb high sleep low) . a night spent at intermediate altitude(1500-2500) before ascent to high altitude will also aid acclimatisation. Forexample skiers who are resident at sea level will benefit from a night spent inDenver before sky vacation in Aspen (base altitude2400).traveller should befamiliar with the symptoms of high altitude illness and be encouragerd not toascend further if they have these symptoms. It is also helpful to have flexible travelitenerary so that additional rest days can be incorporated if required. In somesituation, pharmacological prophylaxis may be warranted. These situation includerapid ascent to altitudes higher than 3000m (eg,flying to LA PAZ, BOLIVIA,at3625m)& for people increased suceptibility to AMS. Acetezolamide is the preferreddrug , although the ideal dose is undecided. The standard recommendation is 250mg twice daily, from one day before ascent; the drug is widely administered at 250mg twice daily , but only limited data support the efficacy of this dose regimen. Inone systematic review acetazolamide was judged ineffective as a prophylactic atdaily doses lower than 750mg. This claim runs contrary to clinical experience, &probably reflects the strict criteria for the inclusion of studies in the review, & thefact that studies with different ascent rates are compared. Trial directly comparingdifferent doses of acetazolamide in people at similar rate of ascent are needed toclarify this issue. Dexamethasone is also effective for AMS prophylaxis (normaldose 8mg daily is divided doses),& is frequently the alternative if acetazolamidecannot be prescribed. Acetazolamide is probably slightly more effective thandexamethasone, & the combination of both drug is more effective than eitheralone.
Preliminary evidence shows that GINGKO BILOBA has more prophylactic activityagainst AMS. During an ascent from 1800m-5200m over 10 days, no person takingGINGKO extract as the dose of 80mg twice daily experienced AMS, compared with40% of people taking placebo. GINGKO 120 mg twice daily taken for 5 days beforeexposure reduced the incident & severity of AMS during ascent from1400m-4300m over 2hr in the third study gingko 60mg three times daily, startedone day before rapid ascend from sea level to 4205m, compared with placebo inpreventing AMS in trekkers ascending from 4248m (BB unpublished data).gingko’seffect may be due to its antioxidant activity. This concept is supported by datasuggesting that ingestion of antioxidant vitamins may reduce the incidence &severity of AMS.
The principles of treatment of AMS are to avoid further ascend until symptomshave resolved, to descend if there is no improvement or if symptoms worsen, & todescend immediately is the first signs of cerebral or pulmonary oedema. Rest aloneis frequently sufficient for mild AMS; analgesis & antiemetics may affordsymtomatic relief. Descent & oxygen are the treatment of choice for moderate tosevere AMS. even a small descent to 400-500m may be sufficient to relievesymptoms. Additional phamacotherapy may be used in conjunction with the Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
treatment already mentioned, especially if descent is impossible & oxygen isunavilable. Acetazolamide 250mg twice or three times daily & dexamethasone 4mgevery 6h to help lessen the severity of symptoms of AMS. stimulated descent in aportable hyperbaric chamber is also effective , & may be particularly useful whendescend is impossible. The treatment of HACE is immediate desent in conjunctionwith oxygen if available, & dexamethsone.
Clinical presentation
HAPE typically occur in the first 2-4 days after arrival at altitude higher than
2500m, & is not necessarily preceded by AMS. Risk factors for HAPE are the same
as for AMS & HACE. In addition HAPE may be over represented in men compared
with women, & cold is a risk factor. People with abnormalities of the
cardiopulmonary circulation that are associated with increased pulmonary blood
flow pressure such as unilateral absence of a pulmonary artery or primary
pulmonary hypertension, or both are at increased risk of HAPE,even a moderate
The first symptoms of HAPE are generally dysponea on exertion & reduced
exercise tolerance greater than expected for the altitude. Cough, dry & annoying
at first, becomes later in the illness with blood stained sputum. Physical findings
may be initially subtle. Tachypnoea & tachycardia are present at rest as the illness
progresses, & fever is common, although rarely exceeding 38.3 celsius. Crakles
are evedient on chest auscultation. HAPE is frequently accompanied by signs of
HACE. There is no radiographic features specific to HAPE, & electrocardiography
may show evidence of right-ventricular strain.
The existence of a subclinical form of HAPE was addressed by cremona &collagues. Among a group of climbers to Monte Rosa(4559m), 77%had indirectevidence of pulmonary extavascular fluid accumulation based on increased closingvolumes. Exercise at sea level is also associated with increased pulmonary arterypressure & transvascular fluid flux, & the contribution of exercise & hypoxia to thefindings from this study are uncertain. If these findings are related to subclinicalpulmonary oedema,it is also unclear weather this is a prognostic factor for thedevelopment of clinically relevant HAPE.
HAPE is a non cardiogenic pulmonary oedema charaterised by exaggerated
pulmonary hypertention leading to vascular leakage through overperfusion, stress
failure or both. The exact mechanism that causes the accentuated hypoxia
pulmonary vasoconstriction is unclear. Undoubtedly, several factor combine to
render an individual susceptible to HAPE.
Mechanisms accounting for exaggerated pulmonary hypertention
Pulmonary artery pressure & pulmonary vascular resistence are high in HAPE, but
HAPE is not due to left ventricular failure. Furthermore, individuals susceptible to
HAPE have an exxaggerated rise in pulmonary artery pressure in response to
hypoxia & exercise & drugs that lower pulmonary artery pressure are effective for
the treatment & prevention of HAPE. Evidence shows that the abnormal rise in
pulmonary artery pressure is accompanied by an increase in capillary pressure at
onset of HAPE, with a threshold of 19mmhg for the development o f clinical HAPE.
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There are possible causes of pulmonary hypertension seen in HAPE. Hultgrenproposed that uneven hypoxic pulmonary vosocontriction may cause regionaloverperfusion of capillaries in the area of least arterial vasoconstriction, leading toincreased capillary pressure & leakage. Support for this concept is provided byradio-isotope perfusion studies, & by the increased susceptibility to HAPE amongpeople with pulmonary circulation abnormalities associated with overperfusion ofrestricted pulmonary vascular beds.
Endothelial dysfunction may also play a part in causing the excessive pulmonaryhypertension of HAPE through impaired release of relaxing factor & augmentedrelease of relaxing factor & augmented release of vosoconstrictors. Inhalation ofnitric acid endothelium- derived relaxing factor decreases systolic pulmonaryvaso-constriction is associated with impaired nitric oxide synthesis, possibly due tonitric oxide synthase activity. The endothelium also synthesises vasoconstrictorfactors . Endothelin-1 is one such factor thought to play an important part inregulation of pulmonary vascular tone. At high altitude,endothelial-1 concentrationare higher in mountaineers prone to HAPE than those resistant to HAPE.
Moreover, there is the direct relation between altitude- induced increase in plasmaendothelin-1 concentration & systolic pulmonary artery pressure, as well as theendothelin-1 plasma concentration & pulmonary pressure measure at high altitude.
People susceptible to HAPE exihibit exaggerated sympathetic activation duringshort term hypoxia breathing at low altitude & during high altitude exposure.
These findings leads to speculation that increased sympathetic activity maycontribute to exaggerated pulmonary hypertension in HAPE. Consistent with thisconcept, in HAPE -adrenergic blockage leads to improved haemodynamics &oxygenetion compared with other vasodilators.
Exercise & cold lead to increased pulmonary intravascular pressure , may becontributing factor to the development of HAPE. High intensity exercise mayinduce high protein pulmonary oedema in human beings & animals, presumablythrough stress on the pulmonary vasculature. Cold probably increases pulmonaryartery pressure through sympathetic stimulation, & has been noted as a risk factorof HAPE in Colorado.
Role of inflammation
Weather the alveolar capillary leak in HAPE is caused by an inflammatory process ,
much like in acute respiratory distress syndrome, or by high microvascular
pressures is unclear. Evidence for the presence of inflammation in people with
HAPE has come from several sources. Many patients with HAPE & fever,
peripheral leukocytosis & raised erythrocyte sedimentation rates. Examination of
bronchoalveolar lavage fluid from two groups of patients of HAPE(climber of
Mount Mckinley & patients admitted to hospital in Japan) have shown a striking
cellular response, with raised concentration of proinflammatory mediators &
cytokines, that results to normal after recovery from HAPE. Further evidence for
an inflammatory component of HAPE is provided by the high rate of preceding
respiratory-tract infection in children who develop HAPE, the association between
certain major HLA-immuno modulating alleles with susceptibility to HAPE, &
raised plasma E selectin concentrations in hypoxaemic climber of AMS & HAPE.
One study has provided evidence that inflammation is not the primary event in the Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
pathogenesis of HAPE. Swenson & colleagues collected bronchoalveolar fluid froma small group of climbers at4559m in the Swiss Alps. Analysis of this fluid showedno rise in neutrophils or inflammatory mediators. The difference between theMount Mckinley & Japanese studies might be explained by the timing of lavages.
In the earlier studies bronchoalveolar lavage was done after HAPE was wellestablished, generally 1-2 days after onset . Swenson & colleagues didbronchoscopy very early in the course of illness, mostly within 3-5 h.they reasonthat the inflammation associated in HAPE is a secondary event that occur as a theconsequence of alveolar flooding. Support for this argument comes fromprospective studies measuring inflammatory markers showing no evidence ofinflammation before or at the onset of HAPE.
Although inflammation may not be a primary event in the HAPE-susceptibleindividuals, people who are constitutionally resistant to HAPE may develop thedisorder if factor favouring increased permeability, such as inflammation, arepresent. Such a situation may arise after a viral lower respiratory-tract infection.
Alveolar-Fluid clearance
The alveolar epithelium has an important role in fluid balance of the lung. Sodium
is taken up by the alveolar cells at the apical surface & is transported out of the
cell across the basolateral membrane by sodium, potassium ATPase. Blunting of
this process may impair clearance of alveolar fluid & peridispose individual to
pulmonary oedema.
In one study, impaired alveolar fluid clearance was thought to have a role in thedevelopment of HAPE. In a double blind, randomised, placebo-controlled study ofHAPE susceptible mountaineers, prophylactic inhalationof the -adrenergic agonistsalmeterol reduced the incidence of HAPE by 50%. -adrenergic agonistup-regulate the clearance of alveolar fluid & lesson pulmonary oedema in animalmodes, although salmeterol may have additional haemodynamic action that alsoprevent HAPE. In the same study at low altitude , the nasal transepithelialpotential difference, a marker of transepithelial sodium & water transport in thedistal airways, was more than 30%lower in HAPE susceptible than in nonesusceptible people. These finding suggest that sodium dependent absorption offluid from the airways may be defective in people susceptible to HAPE & supportthe concept that alveolar fluid clearance may have a pathogenic role in pulmonaryoedema.
Characterstics of extravasation in HAPE
Stess failure of pulmonary capillaries due to high micro- vascular pressure has
been postulated as the final process in HAPE that leads to extravasation of blood
cell & plasma. Disruption of alveolar epithelium & endothelium has been noted in
the lungs of rabbit perfused under high pressure & in rats exposed to high
altitude. This concept would account for the mild alveolar haemorrhage seen
among patient with HAPE, but weather this mechanism entirely account for the
high permeability leak in HAPE is unclear. The lack of increased
bronchoalveolar-lavage fluid leukotriene b4& lack of activated intravascular
cogulation due to exposure of basement membranes in early HAPE mitigate
against early capillary stress failure. The leak might initally be due to a
non-traumatic alternation in the normal selectivity of the alveolar capillary barrier
Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
to high-molecular weight molecules, that capillary stress failure is a latephenomenon. The possibility that the leak is sited more proximally in thepulmonary vasculature has not been discounted.
Role in genetic factor
Gene polymorphism that confer difference in the activities of key enzymes may
play a part in the pathogenesis of HAPE. At present, only limited data are
available. Endothelial nitric oxide synthase gene polymorphisms were associated
with susceptibility to HAPE in Japan,but not in Europe. Although
angiotensin-converting enzymes gene polymorphism may confer a performance
advantage at high altitude, there is no clear association with susceptibility to
HAPE. Susceptibility to HAPE & susceptibility to primary pulmonary hypertension
share some physiological similarities, but preliminary data suggest that the two
disorders have different genetic backgrounds.
Prevention & treatment
As for AMS & HACE, the best way to prevent HAPE is to ascend gradually to allow
sufficient time for acclimatisation. In people with the history of HAPE, 20 mg slow-
release nifedipine every 8 hr prevented HAPE after rapid ascent to 4559m. inhaled
B-adrenergic agonist may also be useful in the prevention of HAPE.
Early recognition is the first key statement in the treatment of HAPE. Therefore,
descent & supplementary oxygenare the most important therapies. Exertion should
be kept at minimum. If oxygen is unavailable & decent is impossible, treatment in
the portable hyperbaric chamber may be life saving, although the recumbent
position necessary for operation may not be tolerated by the patient. Continuous
airways pressure may also be useful in the treatment of HAPE; a portable device
has been developed that can be can be used in mountains. 10 mg nifedipine,
followed by 20-30 mg slow release every 12-24h may be useful as an adjunct to
descent & oxygen.
Future directions
Although the epidemiology of high altitude illness has been extensively
investigated, there are several unresolved issues. What are the precise role of age
sex exercise & respiratory tract infection in susceptibility to AMS & HAPE ?
research should continue to search for the genetic basis of high altitude illness.
The effort will aid the understanding of the pathophysiology of AMS, HACE, &
HAPE, & may provide marker of susceptibility of high altitude illness.
Studies investigating the pathophysiology of high altitude illness should focus onthe time period immediately after exposure to high altitude to observe thecomplete time sequence of changes that occur in response to hyperbaric hypoxia.
High- resolution scanning such as MRI, posistron emission tomography, & single–photon CT techniques will allow investigators to characterised changes in thelungs in HAPE & in brain in AMS & HACE. An animal model of HAPE will resolvemany issues, including the sequence of events that leads to a permeability leak, thetime course for the appearance of inflammatory markers, the role of sodium &water re-absorption, & the efficacy of various agent for the prophylaxis &treatment. Experiment with selective stimulants of alveolar sodium transport willclarify the role of this process in the development of HAPE. For AMS &HACE,better characterisation of the substances that alter permeability of blood brain Copyright 1973-2012 Himalayan Rescue Association Nepal Himalayan Rescue Association Nepal
barrier is needed, & may identify new potential therapeutic targets.
We need to improve our ability to advice travellers about their individual risk inAMS & ideal ascent ratesto prevent this disorder. Reseach may involve theidentification of markers of susceptibility & incorporation of these markers intomathematical model to predict the likelihood that AMS will develop. This goal canbe achieved only by establishing comprehensive database of individual ascentprofiles linked to demographicdata & measurement of AMS, similar to project DiveExploration underwater diving. Drugs with activities that may help prevent or treathigh altitude illness, such as gingko, sidenafil, & garlic, need further assessment.
________________________________________________________________Fig2:proposed pathophysiology of high-altitude pulmonary oedema Fig 1.Proposed pathophysiology of AMS & HACE Copyright 1973-2012 Himalayan Rescue Association Nepal


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