Children are probably no more susceptible to high-altitude illnesses than individuals of other ages. However, altitude illness may be difficult to identify because young children do not report the very subjective symptoms of these syndromes, resulting in the possibility of a delay in recognition and treatment. An international consensus statement concerning ascent to high altitude with children has considered this issue in detail (Pollard et al., 2001).
There is some suggestion that there may be an increased risk of sudden infant death syndrome (SIDS) in communities living at altitude. Furthermore, more prolonged exposure to high altitude ( > 1 month) in infancy risks the development of subacute infantile mountain sickness (SIMS). SIMS is right heart failure secondary to pulmonary hypertension (caused by hypoxia) and occurs in up to 1% of infants residing over 3000 m for more than 1 month (Sui et al., 1988).
Ascent to high altitude is associated with activation of the sympathetic nervous system and an increase in heart rate, cardiac output and blood pressure, which return to sea-level values by 3 months. In addition, hypoxic pulmonary vasoconstriction results in pulmonary hypertension. The physiological stress of hypoxia and cold has important implications for patients with coronary artery disease, who may experience new or worse angina, hypertension which may be harder to control, and heart failure and pulmonary vascular disease which may deteriorate. Risks can be minimised with appropriate medical advice.
Uncontrolled hypertension is a contraindication to ascent to high altitude as it will be exacerbated by hypoxia. Hypertension must be controlled prior to travel, the ideal level being below 140/85.
In myocardial ischaemia the balance between myocardial oxygen supply and demand is disturbed. Hypoxaemia in the presence of coronary stenoses would be expected to reduce oxygen supply to the myocardium and worsen ischaemia. Sympathetic activation also worsens myocar-dial ischaemia as a consequence of increased cardiac work and coronary vasoconstriction in regions of abnormal endothelial vasomotor control (Hultgren, 1997; Levine et al., 1997). The increased work of breathing probably has a minor effect but respiratory alkalosis produced by hyperventilation may also cause coronary vasoconstriction.
Patients with coronary artery disease may experience an increase in symptoms. Nevertheless, neither acute ECG changes of myocardial ischaemia at rest (Yaron et al., 1995; Levine et al., 1997) nor symptomatic deterioration (Yaron et al., 1995) have been reported in patients aged over 65 years with coronary artery disease who visited 2500 m for 5 days.
Exercise studies in patients with coronary artery disease have shown decreased exercise tolerance and earlier appearance of angina and ST segment changes on the ECG. Acute exposure to 2500 m is associated with a small but significant reduction in the work required to provoke myocardial ischaemia (Levine et al., 1997). This is induced at a lower level of myocardial oxygen demand than at sea level. These studies suggest that the acute effects of hy-poxia are due mainly to increased cardiac work and do not appear to be directly related to myocardial hypoxia
Patients with uncomplicated chronic stable angina in Canadian Cardiovascular Society (CCS) classes I and II are at low risk. Patients with more severe, but stable, angina (CCS III and IV) require review by their physician and, if they ascend to altitude, may require an increase in medications to control symptoms. Unstable angina and recent myocardial infarction are contraindications to ascent. Old myocardial infarction is only a problem when there is significant angina, left ventricular dysfunction or arrhythmias. These patients should undergo medical examination prior to travel.
Patients ascending above 2500 m should be warned to expect an increase in their anginal symptoms and to minimise exercise during the first 4 days on arrival at high altitude. They should plan for a slower rate of ascent than normal. They should take a fresh supply of glyceryl trinitrate with them. It has been suggested that if a patient can reach stage 3 of the Bruce treadmill protocol ( > 6 min) without discomfort, that patient will be able to tolerate an altitude of 4270 m without discomfort (Hultgren, 1997). The predictive value of pretravel exercise testing in acute hypoxia is not established.
ease may deteriorate significantly above 2500 m. Some patients with right ventricular disease are intolerant of the extra load placed on the ventricle by the pulmonary hypertensive response to hypoxia. Anomalies of the pulmonary circulation may precipitate HAPE (see above, High-altitude Pulmonary Oedema). Coarctation of the aorta may cause cerebral hypertension and precipitate HACE. Patients with coarctation of the aorta should not ascend to altitude unless their coarctation has been repaired and shown to be relieved, and hypertension is well controlled below 140/85. Particular care should be taken to avoid dehydration in cyanosed patients because of the risk of thrombosis. Many patients with congenital heart disease will require a specialist opinion prior to ascent.
Normal myocardial performance is not affected by altitudes up to the summit of Mount Everest. Patients with coronary artery disease with mild to moderately impaired left ventricular function without residual ischaemia have good tolerance to exposure to an altitude of 2500 m (Erdmann et al., 1998). Acute or decompensated heart failure is a contraindication to ascent. Patients in New York Heart Association (NYHA) class I and II may travel provided they are medically stable and their baseline Pao2 is > 70 mm Hg. Patients in NYHA class III or IV must be medically stable and should be discouraged from ascent above 2500 m.
Arrhythmias may be precipitated by sympathetic activation, and respiratory alkalosis which may reduce serum potassium. No change has been detected in arrhythmic substrate in hypoxia as detected by signal averaged ECGs (Levine et al., 1997). Single premature ventricular complexes during exercise do increase modestly with acute exposure to 2500 m without an increase in repetitive forms and it is unlikely that moderate altitude exposure substantially alters the risk of life-threatening arrhythmias in patients with coronary disease.
Patients with uncontrolled ventricular or supraven-tricular arrhythmias should not ascend to high altitude. Frequent or high-grade ventricular ectopy is also a contraindication to ascent above 2500 m.
Congenital heart disease encompasses a wide range of conditions whose natural history and response to hy-poxia may be altered by surgery. In general, conditions associated with cyanosis and/or pulmonary vascular dis
Although theoretically the cold, dry, hypoxic mountain environment should worsen bronchoconstriction, there is little evidence of deterioration in practice. Asthmatics often find that they have less trouble at high altitude and this is likely to be related to the absence of allergens in the air and the reduced air density. They may also be helped by the increased sympathetic drive and production of corticosteroids at altitude.
Patients should not ascend to altitude unless their asthma is stable. Travellers to remote places should take an emergency supply of steroids with them in case of deterioration.
A small fall in Pao2 results in a large fall in arterial oxygen saturation in these patients because their Pao2 falls on the steep slope of the oxygen dissociation curve. These patients will notice significant deterioration in their breath-lessness on ascent to altitude. AMS prophylaxis with acetazolamide may worsen breathlessness by increasing ventilation.
Lung function should be optimised and stable prior to ascent to altitude. Administration of gas mixtures containing oxygen levels the patient will encounter in the field may be used to assess gas exchange and risk in the lung function laboratory. A chest infection is more serious at high altitude than at sea level and patients should carry an emergency supply of steroids and antibiotics.
Patients with sleep apnoea, kyphoscoliosis and disorders of the chest wall including the respiratory muscles may be unable to increase ventilation in response to hypoxia.
This problem will worsen ventilatory failure particularly at night. A specialist opinion may be required.
People with sickle cell disease or sickle thalassaemia are at risk for sickle crises at altitudes over 2000 m and, consequently, should avoid ascent to high altitude. The risk for those with sickle cell trait is less, although splenic infarction has been reported in this group while exercising at altitude.
The major challenges to diabetic control at high altitude are the increased energy expenditure compared with sea-level activity, and the risk of intercurrent illnesses. Close attention to glucose level is essential, although this may be complicated by inaccurate and inconsistent performance of some blood glucose meters above 2000 m.
Few data exist on the risks to pregnant women and their fetuses from brief visits to high altitude. Intrauterine growth retardation, pregnancy-induced hypertension, and neonatal hyperbilirubinaemia are complications associated with permanent high-altitude residents. Until further data are available, it is prudent to advise pregnant women to avoid prolonged exposures to altitudes over 3000 m.
Exposure of the cornea to hypoxia causes swelling and changes in corneal topography. For persons who have had radial keratotomy, the swelling ofthe hypoxic cornea is not uniform, and this results in significant visual changes. In contrast, significant refractive changes are not noted in people who have had LASIK surgery (laserassisted in situ keratomileusis) following corneal hypoxia.
There has been concern about the risk of thrombosis while taking the oral contraceptive pill at high altitude, especially given the presence of other prothrombotic factors at altitude, such as polycythaemia and dehydration. There is currently no evidence to support an increased risk.
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