Annals of Neurosciences, Vol 12, No 3 (2005)
Annals of Neurosciences, Volume 12, Issue 3 (July), 2005
HIGH ALTITUDE NEUROLOGICAL SYNDROMES PART 1.
Corresponding Author Prof. (Dr.) PVS Rana
Prof of Neurology Department of Medicine
Manipal Teaching Hospital
Phulbari – 11, Pokhara, Nepal
Phone: +97761 520416 ext 117
Fax:+977 61 527862
Email:
Abstract
Induction to high altitude exposes the individual to increasingly severe hypoxia resulting in high altitude illnesses. Neurological symptoms constitute an important aspect of these illnesses. The high altitude headache is the commonest and is reported in as high as 83% of the members of an expedition over 7000 feet. Among various studies incidence of acute mountain sickness varied from 8.3% to 67%. While incidence of life threatening high altitude cerebral edema is reported as less than 0.001% in people traveling to 2500 meters to 1% for those traveling to 4000–5000 meters, the incidence of high altitude pulmonary edema varied from 0.4 to 15.5%. While 20–8% of acute mountain sickness case develop cerebral edema, 50% cases of high altitude pulmonary edema have acute mountain sickness another 14% have high altitude cerebral edema. High altitude pulmonary edema and high altitude cerebral edema, if unrecognized or left untreated, are associated with a high mortality rate of 44% and 60% respectively. Early recognition, prompt treatment and evacuation to low altitude result in complete recovery. Strict adherence to acclimatization schedule and physical checkup before induction to high altitude can prevent these complications. The areas where high altitude activities are common should have a well equipped hospital with trained staff and an evacuation plan There is a need of evolving a method of predicting the illness before induction to high altitude. This article summarizes the present knowledge regarding clinical manifestations, pathogenesis and management of neurological syndrome and high altitude with reference to high altitude illnesses.
Key Words: High altitude, Acute mountain sickness (AMS), High altitude cerebral edema (HACE), High altitude pulmonary edema (HAPE), Cerebral form of high altitude pulmonary edema, Acclimatization, Hypoxia,
Introduction
The term “High altitude” was earlier used arbitrarily to cover height of 3000 meters and above as majority of subjects ascending above this altitude develops signs and symptoms of acclimatization (1). Barry & Pollard, 2003 (2) graded various altitudes as intermediate altitude (1500–2500 meters), high altitude (2500–3000 meters), very high altitude (3500–5800 meters) and extremely high altitude when the height is more than 5800 meters respectively. The illnesses predominantly manifesting with cerebral and pulmonary symptoms, in an un-acclimatized person, immediately after ascent to a high altitude and are grouped under the term “High Altitude Illnesses”. Though hypoxia at high altitude affects all the systems but the main brunt is on central nervous system and is responsible for associated mortality in these disorders. The various neurological syndromes (Table-1) manifesting at high altitude (3) have gained importance because of increasing mountaineering expeditions, trekking and other adventure sports activities at high altitudes (4). The illnesses at high altitude are a major health problem at places where mountaineering expeditions are an industry in itself. High altitude illnesses have gained further importance due compulsion of maintaining Army at high altitudes. While a low fatality of 0.0036% is reported in trekkers in Nepal (5), a higher death rate of 1.9% was reported in soldiers posted at high altitude (6). A figure of 17% was reported in British mountaineers attempting climbing peaks over 7000 meters (7). If left untreated, a high mortality rate of 44% to 60% is reported in high altitude pulmonary edema (8) and high altitude cerebral edema (9) respectively. The most important aspect is that these potentially fatal illnesses can be prevented. High altitude medicine has received an academic boost with a spate of excellent reviews in the medical literature (2, 3, 8, 10–12). In this review the commonly occurring high altitude illnesses (AMS, HACE and HAPE), where CNS symptoms predominates, will be discussed.
Neurological Syndromes at High Altitude
1. High Altitude Headache
High altitude Headache (HAH) is the most common symptom developing in fresh inductee to high altitude areas. The HAH is usually bi frontal and is mild to moderate in intensity but with passage of time it increases in severity and may be accompanied with giddiness. In a prospective study during expedition to Kanchenjunga base camp (i.e. height 5100 meters) in Nepal, Silber et al., 2003 (13) reported this symptom in 83% members of the expedition. The HAH was more severe in women and in those who had prior history of headache. Older age appears to offer some protection. These, patients should be examined thoroughly and observed closely as development of headache may herald the onset of AMS or life threatening HACE or HAPE. In addition, head ache is an important symptom of sub acute mountain sickness and chronic mountain sickness. While sub acute mountain sickness manifest in low landers during their prolong stay (over 3 months) at an altitude of more than 5000 meters as congestive cardiac failure and severe pulmonary hypertension (14), the chronic mountain sickness is seen in natives permanently residing at high altitudes (15). In initial stages the headache may respond to oxygen, rest and analgesics. Both paracetamol and ibuprofren are equally effective (16).
2. Acute Mountain sickness
Acute mountain sickness (AMS) is the next commonest illness at high altitude. The earliest description of AMS is of To Kan, between 37–32 B.C, in a man crossing the Kilak pass (17). A similar illness (balloon sickness) was reported during ascent to 29,000 feet in an open hot-air balloon in 1862 (18). The term "acute form of mountain sickness" was first used by Hepburn in 1895 (19). Though rare cases have been described at lower attitudes (i.e. at 2000 meters), AMS usually develops above the height of 2500 meters with incidence increasing from 22% at 1850–2750 meters (20) to 42% at the altitude of 3000 meters (21) respectively. In various studies its incidence is reported to vary from 8.3% to 67% (6,22). The illness develops with in 6–10 hours of ascent but some time it may develop even earlier.
1. Illnesses affecting the central nervous system (CNS)
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2. Illnesses affecting the peripheral nervous system (PNS)
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3. Miscellaneous syndromes**
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Schoene et al. 2003 (3) modified: ** some related to acclimatization
The symptoms of AMS are non specific. Hackett et al., 1976 (22) reported clinical presentation in 178 cases of AMS. Headache was the commonest symptoms reported in 76% cases. Headache was throbbing, type, localized to bi temporal or occipital regions, worse at night or early in the morning and increased on bending or on Valsalva maneuver. It was not relieved by analgesics in 26% cases. Other symptoms reported were insomnia in 70%, anorexia in 38%, nausea in 35%, dizziness in 27%, breathlessness in l9%, oliguria in l4%, vomiting in l4%, lassitude in 13%, and in coordination in 11% cases respectively. Mild fever (38.30C), fitful sleep with arousal, tachycardia and hypotension are also reported in case of AMS (23). The prognosis depends upon the severity of illness. In milder form the symptoms regresses completely within few days to week time. Highest numbers of AMS cases are reported from India in troops deployed at the height of 3500 to 5500 meters (6). Severe symptoms in 840 soldiers lasted for 2–5 days.
While 40% were still ill after 7 days, in 13% symptom lasted for more than 30 days. Complete recovery was seen in 38% within 3 days and in 59.6% cases within seven days respectively. In some symptoms persisted up to 5–6 months. Only 3 patients expired where symptoms were severe.
As there are no physical findings, the diagnosis of acute mountain sickness is based on development'of headache in a fresh inductee arriving at the height (above 2500 meters), not responding to analgesics and rest and when it is followed by one or more of other symptoms i.e. gastrointestinal symptoms (anorexia, nausea or vomiting), insomnia, dizziness, lassitude or fatigue (24).
Treatment (2,3,6,12) of milder form of AMS includes rest, analgesics, anti emetics and oxygen inhalation to maintain a SpO2 of more than 90%. Severe cases of AMS (i.e. headache with marked nausea, dizziness, lassitude, fatigue, insomnia and fluid retention) and stay at high altitude of more than 12 hours should be treated as emergency with descent to a lower altitude (i.e. 500 meters or more) and use of analgesics or anti emetics or both to relieve the symptom of headache. In mild cases rest and acclimatization at a lower altitude may suffice. Acclimatization may be hastened by using acetazolamide (125 to 250 mg twice a day). When decent is not possible the patients should be treated with use of a portable hyperbaric chamber, oxygen inhalation (i.e. 1–2 liters/minute) and drug therapy i.e. acetazolamide 750–1000 mg/d or dexamethasone 4 mg every 6 hourly or both till symptoms resolve. The acetazolamide produces its beneficial effects by decreasing CSF production, inducing diuresis and metabolic acidosis, compensatory hyperventilation and improving oxygenation while steroids produce beneficial effects by reducing cerebral edema. A few randomized control trials have tried to study the role of short term use of hyperbaric chambers in treatment of AMS. It was found that hyperbaric therapy (25) is equally efficacious as oxygen therapy and superior to bed rest but benefit after 12 hours could not be established in these studies.
Portable pressure chambers are now an essential requirement of any high altitude expedition for providing emergency treatment by simulating descent when evacuation of patient is not possible or delayed. Many prototypes (i.e. Gamow's bag, Certag bag, Portable altitude chamber) are available. They are light weighing about 4.8 Kg (Certag bag) to 7kg (Gamow's bag) and require continuous inflation to flush out carbon dioxide. Slow compression and decompression and continuous evaluation of patient at hourly intervals is essential. With a mechanical pump the pressure is raised. If raised by 2 psi (110 mms of Hg) result in simulated descent by 2000 meters (i.e. 4800 m or 14000 feet will be 2100m Or 7000 feet). These bags are provided with altimeters. Advantage of Certag bag is that it has 2 layers and is provided with 2 inflation and 2 opening preset valves as an addition safety measure. Portable Altitude chamber is of different shape with more space at head end, has rounded zip and the altimeter is inside the bag. The static pressure chamber is the life line of any hospital at high altitude. More patients can be treated simultaneously depending upon their size and the descent to sea level can be simulated with in an hour or so.
3. High altitude cerebral edema
High altitude cerebral edema (HACE) is the most serious and the life threatening complication noted in inductee to high altitude. Like AMS, the development of high altitude cerebral edema depends on the speed of ascent and the altitude reached with incidence of less than 0.001 % for people traveling to 2500 meters and approximately 1% for low landers traveling to 4000–5000 meters respectively (2). It is considered as an end spectrum of AMS or of high altitude pulmonary edema (HAPE) where severe hypoxemia causes rapid development of AMS and cerebral edema. About 2–8% of cases of AMS develops HACE or HAPE (3). Clinical features include a pro dromal stage characterized by behavioral or mental changes (2) followed by rapidly developing features of encephalopathy. Any. headache of increasing severity developing after a time lag and not responding to analgesics should alert the individual as it herald the onset of HACE. If untreated, it is followed by nausea, vomiting, dizziness, vertigo, ataxia, hallucinations, disorientation, confusion and alteration in sensorium leading to coma and death. Early development of disabling truncal ataxia (rarely limb ataxia), is considered as the most sensitive indicator of HACE. (26). Other manifestations include seizures, altered speech, urinary incontinence, cranial nerve palsies, visual field defects, dysarthria, motor deficits, retinal hemorrhages and papilledema (2,12,26). Focal deficits though described are rare and should raise possibilities of other neurological disorders especially when symptoms of HACE are lacking and when there is no improvement with descent to a lower altitude or with oxygen and dexamethasone (12). In severe cases features of high altitude pulmonary edema may also be present. Autopsy studies (27,28) revealed edematous brain with flattening of gyri and obliteration of sulci with evidence of uncal and tonsilar herniation commonly associated with peticheal hemorrhages. In some cases intracerebral hemorrhage and subarachnoid hemorrhage are also reported. According to Lake Luis scoring system (24), HACE can be diagnosed when patient of AMS develops change in mental status and or ataxia.
Treatment (12,26–27) involves immediate descent or evacuation to a lower altitude at least by 610 meters (2000 feet) or more. If descent is delayed, treatment involve use of portable hyperbaric chambers (discussed above), administration of oxygen (4–6 1/min), steroids (dexamethasone 4 mg every 6 hourly) and acetazolamide (250mg twice daily).
4. Cerebral form of high altitude pulmonary edema
High altitude pulmonary edema (HAPE) is another life threatening complication at high altitude with reported incidence of 0.4 to 15.5% (26–27,29–30) and a mortality of 44% in untreated cases (8). It accounts for. most of the death at high altitude illness (12). There is a time lag before HAPE develops. In 50% cases HAPE develop it within 3 days and another 26% in 4–10 days of induction to high altitude (27). However, Hackett & Roach, 2001(12) observed that the development of HAPE is rare after 4 days at a given altitude owing to adoptive capability of pulmonary vasculature. Like AMS and HACE, it rarely occurs below 2500 meters and it incidence increasing with altitude and the speed of ascent. Though pulmonary signs and symptoms (i.e. cough, haemoptysis progressing dyspnoea, tachycardia, tachypnoea, evidence of pulmonary edema and dependant edema) dominate the clinical picture, its presentation as AMS or with predominant cerebral symptoms (Cerebral form of HAPE) have been reported (27, 30). Cerebral form of HAPE manifests with giddiness, headache, hallucinations, lack of interest in surrounding and altered sensorium leading to coma. These symptoms are due to development of cerebral edema in these cases. Symptoms of AMS and HACE are reported in 50% and 14% cases of HAPE respectively (31). Investigation reveals right ventricular strain .in ECG, patchy infiltrate localized (right middle and lower zone) in mild cases and bilateral in severe cases respectively X ray chest, severe arterial hypoxemia and respiratory alkalosis (27, 32). According to Lake Luis scoring system (24), HAPE can be diagnosed when on induction to high altitude (a) at least two of four symptoms (dyspnoea at rest, cough, weakness or decreased exercise performance, chest tightness or congestion) and (b) two of four signs (crackles or wheezing in at least one lung field, central cyanosis, tachypnoea, or tachycardia) are present.
Treatment (12,27,29) of choice is immediate descent of at least 610 meters (2000 feet) until asymptomatic. If patient cannot be evacuated, the treatment should include oxygen inhalation at a rate of 4–6 1/min, oral nifedipine 10 mg followed by 30 mg (sustained release) every 12 hourly. Nifedipine is only necessary when oxygen is not available and descent is not possible. It reduces pulmonary arterial pressure by 30% but barely increases the partial pressure of arterial oxygen (33,34). If available portable hyperbaric bag (discussed above) can be used before evacuation to a lower altitude is achieved. Supplemental oxygen and descent reduce pulmonary arterial pressure by 30–40% (33–35) and increases arterial oxygen pressure thereby reversing the effect of illness. Both measures are the key to successful therapy. Failure to improve arterial oxygen saturation to more than 90% with in 5 minutes of starting oxygen therapy and those with associated cerebral edema should be moved to lower altitude and hospitalized. There is no role of bronchodilators and antibiotics. The cases reported by Singh et al., 1969 (6) were treated with IV frusemide and morphine and in pressure chamber till evacuated to plains. Even most severe and moribund cases could be saved with this treatment schedule. Both these drugs divert blood from pulmonary to systemic circulation. While frusemide causes diuresis and decreased CSF secretion, morphine decreases the anxiety (23). Recently role of Beta agonists in treatment is suggested considering their usefulness for prevention of HAPE and their role in increasing clearance of fluid from alveolar space (36).
Pathophysiology of high altitude illnesses
The hypoxic insult is the main cause of harmful effects at high altitude. With increase in altitude there is progressive decrease in atmospheric pressure and partial pressure of oxygen (PaO2) which decreases progressively from 90–95% at sea level to 60% and 35% at 2800 meters (9200 feet) and 6100 meters (20140 feet) respectively (37). This decrease in PaO2 produces (a) hyperventilation through stimulation of carotid body chemoreceptor (38) leading to rise in PaO2, fall in PaCO2 and respiratory alkalosis. Fluctuating levels of PaO2 & PaCO2 is responsible for nocturnal periodic breathing (Cheyenne Stokes breathing). However, the alkalosis is transient and within 24–48 hours it is counterbalanced by increased bicarbonate excretion through kidneys. The net effect of this increase in alveolar oxygen pressure; (b) Hematological changes includes hemo concentration, new RBC production secondary to increased erythropoietin production favoring increased oxygen carrying capacity of blood (37); (c) Increased 2,3 diphosphoglycerate production resulting in shift of oxygen dissociation curve to right which facilitate release of oxygen to the tissues (39); (d) Release of catecholamine causing tachycardia and increase in blood pressure, venous tone and cardiac out put (e) Increased cerebral blood flow .which is partly counterbalanced by hypocapnea.. These acute changes occurs within hours and along with chronic changes help one to acclimatize and ascend to and to live in high altitude. Failure of this acute acclimatization process result in high altitude illness (HAH, AMS, HACE & HAPE).
The facts to be remembered are that (a) high altitude illnesses (AMS, HACE and HAPE) develops some time after the induction to high altitude and this "Time Lag" is an essential diagnostic feature of these illnesses, (b) The risk factors are common and include rapid ascent, actual altitude reached, length of stay, a history of high altitude illness (6,22,40), altitude at which travelers sleep (40), residence at altitude below 990 meters (20) and exercise (41); (c) a marked individual susceptibility in development of AMS, HACE or HAPE and may be genetically influenced (40); (d) Age and sex of the inductee i.e. while younger persons are more susceptible (22), the incidence in children and in adults is same (42) and women are less susceptible to acute pulmonary edema but have similar incidence of AMS (43), (d) Physical fitness is not protective against high altitude illnesses, (e) There is no adverse effect of hypertension, diabetes, coronary artery disease and pregnancy (32,41).Although, no information exist how prior of coexisting illnesses contribute to susceptibility to altitude illnesses but any condition which results in hypoventilation, hypoxemia, pulmonary hypertension or raised intracranial tension or fluid retention may exacerbate or induce altitude illnesses (3). Some reports even suggest that neck irradiation and surgery predispose to a risk of developing severe AMS or HACE (44).
Presence of pulmonary and cerebral edema was noted in fatal AMS cases by Singh et al., 1969 (6). However, Fisher et al., 2004 (45) found no evidence of cerebral edema in severe acute mountain sickness. AMS is now considered to be primarily due to the body's response to modest hypoxia resulting in release of vasogenic mediators, impaired cerebral autoregulation (46), elevated cerebral capillary pressure (47), alteration in blood brain barrier and vasodilatation (48) producing predominantly vasogenic cerebral edema. (2, 49–50). Important mediators adversely affecting BBB include vascular endothelial growth factor, inducible nitrous oxide synthetase and bradykinins (51–53). Vascular endothelial growth factor (VFGF) is also suggested to have a role in the production of AMS and HACE. It is a protein produce due to hypoxia and causes increase in vascular permeability (54). Soluble VEGF receptor, sFlt-1 was found to be low at sea level and a significant rise in free VEGF after induction to high altitude was noted in those developing AMS (54). The "tight fit" hypothesis proposes that individual anatomy of the craniospinal axis determines tolerance to mild brain edema and may help explaining the individual susceptibility for developing AMS (50, 55). Those with a greater ratio of cranial cerebrospinal fluid to brain volume are better able to compensate for brain swelling through displacement of CSF and less likely to develop AMS. Severity of AMS depends upon the degree of cerebral edema. As 2–8% cases of AMS progresses to develop HACE or HAPE where cerebral symptoms dominates, a similar mechanism seems responsible for these illnesses as well. The HACE is now considered an end stage of AMS.
The pathophysiology of HAPE is still unclear. Cardiac functions, including wedge pressure and atrial pressure, are normal. Many factors may be operating i.e. (a) development of patchy pulmonary hypertension due to exaggerated hypoxic pulmonary vasoconstriction (56), (b) increase in pulmonary blood volume, which in initial stage is induced by hypoxia and later it is centrally mediated, (c) increased capillary wedge pressure secondary to increased pulmonary blood volume and vasoconstriction and (c) damage to pulmonary capillaries. Some pulmonary capillary beds are closed due hypoxic vasoconstriction or by capillary wall edema causing pulmonary ventilation perfusion mismatch which further aggravates hypoxia and causes diversion of whole flow through remaining widely dilated and already damaged capillaries with capillary leakage (57). Over perfusion of damaged and dilated pulmonary capillaries due to increased pulmonary blood volume further increases the capillary pressure and leakage. Radioisotope perfusion studies (58) and high incidence of HAPE in persons with congenital or acquired pulmonary vasculature abnormalities support this view (31, 57, 59–60). There is no role of inflammations in HACE. Susceptible persons have (a) previous history of HAPE where recurrence rate as high as 60% is noted on induction to high altitude of 4550 meters (61), (b) reduced ventilatory response to hypoxia and exercise (50,56), (c) impaired endothelial functions (i.e. under expression of vasodilators – nitric oxide or over expression of constrictors -endothelin-1) (62–63), (d) impaired clearance of sodium and water from alveolar space due to genetic difference in the ameloride sensitive sodium channels (62) and (e) high incidence of HLA DR-6 and HLA DQ-4 antigens suggesting a immunogenetic basis for susceptibility for HAPE (64). Another view postulate HAPE is a type neurogenic pulmonary edema because of presence of RBC, and spectrum of serum proteins in pulmonary lavage fluid (65) Maron, 1987), increased plasma and urinary catecholamine (66), sympathetically mediated vasoconstriction (66) and the association of HAPE with HACE.
Preventive measures:
Preventive measures are the same as for AMS, HACE and HAPE and include
- Avoiding overexertion, exposure to cold and dehydration by liberal fluid intake. The latter is due to increased water loss resulting from hypoxia induced hyperventilation drive, increased physical exertion, decreased thirst, increased insensible loss and breathing through dry air at high altitude is common. Further ultraviolet (UV) light also add to this loss by increasing the temperature .A temperature as high as 40–420C (102–1040 F) can be produced by UV light in a closed space so common in tents used by the mountaineers.
- Strict compliance of acclimatization instructions: Slow and gradual ascent and spending the night at an intermediate altitude and avoiding direct transport to altitudes of more than 2750 meters. Attempt should be made to achieve best acclimatization with slow rate of ascent. Recommended rate (2) of ascent above 3000 meters are to rest for a day for every 1000 meters of elevation and increasing the sleeping altitude by only 300–600 meters per day (i.e. climb high and sleep at lower altitude). One should rest for 24 hours if ascent is by plane. This acclimatization require at least 1–3 days at a given altitude. Full acclimatization may take even longer. Close watch of tachycardiac response at high altitude is suggested to roughly estimate the level of acclimatization (26).
- Pharmacological prophylaxis: Pharmacological prophylaxis with carbonic anhydrase inhibitor acetazolamide has been found effective. It is given at a dose of 250 to 500 mg twice a starting one day prior to ascent and continuing till full acclimatization is achieved. A lower dose of 125 mg twice a day is also found beneficial with fewer side effects (40). A similar drug methazolamide (67), 150 mg once a day starting one week prior to ascent, has also been found promising with fewer incidences of paraesthesias in comparison with acetazolamide. These drugs probably act by decreasing CSF production and by abolishing apnoec spells by causing intracellular acidosis in the respiratory center. Pharmacological prophylaxis of HAPE with nifedipine (20–30 mg of extended release preparation every 12 hourly and salmeterol (68) have been tried and found effective.
- Detection of person prone for high altitude illnesses: It is difficult to detect person prone for high altitude illness. Normally a person's pulse rises by 20% or more on awakening in the morning on induction and subsiding after a week of stay at high altitude (8) .
A decreased tachycardic response is noted in person developing high altitude illness. Observation of tachycardic response may be one method. (68). Austin & Sleigh, 1995 (69) evaluated two groups of climbers before and twice during the ascent to a maximum height of 5640 meters. Using a scoring system consisting of questionnaire on illnesses related to AMS and measurement breath holding time, gag reflex and hyperventilation response Breath holding was measured in seconds with subjects seated after a maximal inspiration. The gag reflex was assessed by touching the posterior pharynx with a wooden spatula and scoring the response as 0 if there was no response, 1 if the response was mild, 2 if it was moderate, and 3 if it was severe. The subjects also hyperventilated maximally for one minute and assessed their own response on this four point scale. Subjects scoring 15 and under were classed as being well, those scoring 16–30 as having mild, and those scoring over 30 as having severe AMS. Nineteen people developed AMS, nine of them severely. All 10 of those with a severe gag reflex (score of 2 or 3) developed AMS but only nine of the 30 subjects with scores of 0 or 1 for the gag reflex developed the AMS. All six subjects with severe dizziness on hyperventilation (score of 3) developed AMS compared with only nine of the 26 who did not become dizzy on hyperventilation or only mildly so. With Fisher's exact test for independence the highest predictors of AMS were gag reflex.(P=0.002), breath holding (P=0.041), and hyperventilation (P=0.083). Using these univariate predictors the acute mountain sickness could be predicted correctly in 78% of cases by the gag reflex ((10+21)/40), 63% by hyperventilation ((9+16)/40), 63% by breath holding ((6+19)/40), and 85% by combining these in a multivariate model ((15+19)/40). It does appear possible to distinguish those at risk of developing AMS. If a hypersensitive gag reflex, extreme dizziness on hyperventilation, or short breath holding time is found, these people should avoid ascent to or should be observed closely. However, this study is not confirmed by larger trial. Other workers have found that level of physical fitness, pulmonary function tests and vascular and pulmonary responses are inconsistent in predicting individual's susceptibility to altitude illness (2). However the people with respiratory diseases should avoid induction to high altitude.
Conclusions
Many medical problems are encountered at high altitude but they are preventable by health education, prior physical checkup and allowing induction of only healthy individuals to high altitude and strict compliance of acclimatization schedule. A high index of suspicion and a thorough knowledge of high altitude physiology is essential for early detection and prompt treatment of potentially fatal medical problems at high altitude. A thumb rule is the close monitoring of fresh inductee who develops any fresh symptoms. Beside this a well planned rescue operation with trained medics and paramedics to provide on the spot emergency care and evacuation to lower altitude are an inescapable requirement. The requirement of well equipped hospital especially with pressure chamber can not be over emphasized.
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