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Altitude sickness
Last reviewed: 23.04.2024
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The altitude sickness includes several associated syndromes caused by a reduction in available O2 in the air at high altitudes. Acute mountain sickness (OHS), the easiest form, manifests itself as a headache along with one or more systemic manifestations. High-altitude cerebral edema (VOGM) is manifested by encephalopathy in people with acute mountain sickness.
High-altitude pulmonary edema (VOL) is a form of non-cardiogenic pulmonary edema that causes severe dyspnoea and hypoxemia. Light forms of acute mountain sickness can occur in travelers and skiers. Diagnosis is based on clinical signs. Treatment of a mild degree of acute mountain sickness includes analgesics and acetazolamide. In severe cases it is necessary to lower the victim as soon as possible and, if possible, give him an additional O2. In addition, dexamethasone can be effective in high-altitude cerebral edema, and nifedipine with high-grade pulmonary edema.
With increasing altitude, atmospheric pressure decreases, while the percentage of O2 content in the air remains constant; Thus, the partial pressure of O2 decreases with altitude and at 5800 m (19,000 ft) it is about 1/2 of the pressure at sea level.
Most people can climb to a height of 1500-2000 m (5000-6500 ft) during the day without problems, but approximately 20% climbing 2500 m (8000 ft) and 40% reaching a height of 3000 m (10 000 ft) ), this or that form of altitude sickness (WB) develops. The likelihood of developing altitude sickness is affected by the rate of ascent, the maximum height reached and sleep at altitude.
[Risk factors for altitude sickness
High altitude has a different effect on people. However, in general, the risk increases the physical load and, possibly, the cold, the risk is higher for people already suffering altitude sickness, and for those who live at low altitude [<900 m (<3000 ft)]. Little children and young people, apparently, are more susceptible. Diseases such as diabetes mellitus, IHD and moderate COPD (chronic obstructive pulmonary disease) do not serve as risk factors for high altitude disease, but hypoxia can adversely affect their course. Physical training does not protect against altitude sickness.
Pathophysiology of altitude sickness
Acute hypoxia (as happens, for example, with a rapid rise to a high altitude in an unsealed airplane) changes the functional state of the central nervous system within minutes. Altitude disease occurs as a result of a neurohumoral and hemodynamic response to hypoxia and develops within hours or days.
In the first place, the central nervous system and the lungs suffer. In both systems, capillary pressure and capillary leakage are increased, with possible development of edema.
In the lungs, hypoxia-induced increase in pulmonary artery pressure causes interstitial and alveolar edema, which worsens oxygenation. Focal hypoxic vasoconstriction of small vessels causes hyperperfusion with increased pressure, damage to the capillary wall and capillary leakage in areas of less vasoconstriction. There are assumptions about various additional mechanisms of altitude sickness; an increase in sympathetic activity, dysfunction of the endothelium, a decrease in the concentration of nitric oxide in the alveoli (possibly due to a decrease in the activity of nitric oxide synthase), and an amyloride-sensitive sodium channel defect. Some of these factors may have a genetic component.
Pathophysiological mechanisms in the central nervous system are less clear, but may include a combination of hypoxic vasodilation of the brain, a violation of the blood-brain barrier and brain edema caused by water retention and Na +. There is a suggestion that patients with a low ratio of CSF volume to brain volume are less tolerant of its edema (i.e. CSF displacement), and they are more likely to develop altitude sickness. The role of atrial natriuretic peptide, aldosterone, renin and angiotensin in the development of altitude sickness is not clear.
Acclimatization. Acclimatization is a complex of reactions that gradually restore tissue oxygenation to normal in people under high-altitude conditions. However, despite acclimatization, at high altitude hypoxia appears in all. Most people acclimatize to a height of up to 3000 m (10,000 feet) in a few days. The higher the altitude, the longer the adaptation time. However, no one can fully acclimate to a long stay at an altitude of> 5100 m (> 17,000 feet).
Acclimatization is characterized by constant hyperventilation, which increases oxygenation of tissues, but also causes respiratory alkalosis. Alkalosis is normalized during the day, as HC0 3 "is excreted in the urine.As the pH normalizes, the volume of ventilation can increase further.The cardiac output initially grows, the quantity and functional capacity of red blood cells increases. For many generations, the living different ethnic groups adapt to her several other ways.
Symptoms and Diagnosis of Altitude Disease
Different clinical forms of altitude sickness do not represent separate manifestations of altitude sickness, but create a spectrum in which one form or more can be present in varying degrees.
Acute mountain sickness
The most common form, its development is possible at low altitudes, such as 2000 m (6500 ft). Probably, acute mountain sickness is a consequence of moderate cerebral edema, it manifests itself as a headache and at least one of the following symptoms: fatigue, symptoms of a digestive tract disorder (anorexia, nausea, vomiting), dizziness and sleep disorder. Physical stress worsens the condition. Symptoms usually appear 6-10 hours after lifting and subside after 24-48 hours, but sometimes they develop into high-altitude cerebral edema and lungs, or both. Diagnosis is based on clinical data; Laboratory tests give nonspecific results, and in most cases are not needed. The development of acute mountain sickness is typical for ski resorts, and some victims mistakenly mistaken it for the consequences of excessive alcohol consumption (hangover) or for acute viral infection.
High-altitude cerebral edema
High-altitude cerebral edema is manifested by headache and diffuse encephalopathy with stunning, drowsiness, stupor and coma. Ataxic gait is a reliable early warning sign. Seizures and neurological deficits (eg, cranial nerve palsy, hemiplegia) are less common. Edema of the optic nerve disk and hemorrhage in the retina are possible, but for diagnosis it is not necessary. Within a few hours, coma and death may occur. High-altitude cerebral edema is usually differentiated from a coma of another etiologic genesis (eg, infection, ketoacidosis). At the same time, fever and rigidity of the occipital muscles are absent, blood and CSF analyzes without pathology.
High-altitude pulmonary edema
High-altitude pulmonary edema usually develops within 24-96 h after a rapid ascent to a height of> 2500 m (> 8000 ft) and leads to death more often than other forms of high altitude sickness. Infectious respiratory diseases, even minor ones, increase the risk of high-altitude pulmonary edema. High-altitude pulmonary edema is more common in men (unlike other forms of high altitude sickness). At permanently living at altitude high-altitude pulmonary edema can develop after a brief stay at low altitude upon return home.
Initially, patients experience shortness of breath, reduced exercise tolerance and dry cough. Later, pink or bloody sputum, respiratory distress syndrome, are added. The examination is characterized by cyanosis, tachycardia, tachypnea and a moderate increase in body temperature (<38.5 ° C). With the same frequency, local or diffuse wheezing is detected (sometimes audible without a stethoscope). Hypoxemia, often extremely severe, with a saturation of 40 to 70% according to pulse oximetry. When chest radiography, if it is possible, the borders of the heart are not dilated, the focal edema of the lungs (often middle or lower lobes) is determined, which is usually not present in heart failure. High-altitude pulmonary edema can quickly progress; coma and death are possible within a few hours.
Other violations
At high altitude, the appearance of peripheral edema and edema of the face. Headache without other symptoms of acute mountain sickness occurs quite often.
Hemorrhages in the retina are possible even at a low altitude of 2,700 m (9,000 ft), but most often they occur when ascending> 5000 m (> 16,000 ft). Usually, hemorrhages in the retina are not accompanied by any symptomatology, if they do not occur in the visual spot area; pass quickly and without complications.
In people who have previously suffered radial keratotomy, severe visual disturbances at elevations> 5000 m (> 16,000 ft) and even below [3000 m (10,000 ft)] are possible. These alarming symptoms disappear quickly, right after the descent.
Chronic mountain sickness (the disease Monge) is rare, affects long-lived people at altitude. It is manifested by fatigue, shortness of breath, pains, pronounced polycythemia and, sometimes, thromboembolism. The disease is often accompanied by alveolar hypoventilation. Patients should be lowered; recovery is slow, and a return to height can cause a relapse. Repeated phlebotomy can reduce the severity of polycythemia, but relapse is possible.
Treatment of altitude sickness
Acute mountain sickness. Climbing must be stopped and physical exertion reduced until symptoms disappear. Other treatments include fluids, analgesics for headaches, an easy diet. With severe symptoms, a rapid descent of 500-1000 m (1650-3200 ft) is usually effective. Acetazolamide 250 mg twice a day inside can reduce symptoms and improve sleep.
High-altitude cerebral edema and high-altitude pulmonary edema. The patient must be evacuated from the height immediately. If the descent is delayed, complete rest and inhalation of O2 is necessary. If descent is not possible, O2 inhalations, preparations and sealing in a portable hyperbaric bag allow you to gain time, but can not replace the therapeutic effect of descent.
With high-altitude cerebral edema nifedipine 20 mg per tongue, then long-acting tablets of 30 mg reduce the pressure in the pulmonary artery. Diuretics (eg, furosemide) are contraindicated. The heart with high-altitude edema of the brain is not affected, and the appointment of digitalis preparations is impractical. With a rapid descent, high-altitude cerebral edema is usually resolved within 24-48 hours. In the presence of high-altitude edema of the brain in history, most likely there will be a relapse and this should be known.
With high-altitude pulmonary edema (and severe acute mountain sickness), dexamethasone helps, first 4-8 mg, and then 4 mg every 6 hours. It can be administered orally, subcutaneously, intramuscularly or intravenously. You can add acetazolamide 250 mg twice a day.
Prevention of altitude sickness
It is important to consume a lot of fluids, since inhaling large volumes of dry air at a height greatly increases water loss, and dehydration with a slight hypovolemia intensifies the symptoms. It is better to avoid adding salt. Alcohol exacerbates acute mountain sickness, worsens breathing in sleep, enhancing breathing disorders. In the first few days, frequent intake of small portions of food containing many easily digestible carbohydrates (for example, fruits, jams, starches) is recommended. Although physical preparation increases resistance to load at height, this does not protect against the development of any form of altitude sickness.
Climb. The gradualness of the ascent is extremely important when at an altitude of> 2500 m (> 8000 ft). The first night should be at an altitude of 2500-3000 m (8000-10 000 feet), if further spending the night at a higher altitude, then at the site of the first night, climbers should spend 2-3 more nights. On each day thereafter, the height of the lodging can be increased to about 300 m (1000 ft), although higher rises during the day are permissible, but with a mandatory descent for sleep. The ability to rise without the appearance of symptoms of altitude sickness in humans varies, usually the group is guided by the slowest participant.
Acclimatization ends quickly. After staying at a lower altitude for several days, acclimatized climbers should again rise gradually.
Medications. Acetazolamide 125 mg every 8 hours reduces the likelihood of acute mountain sickness. The drug is available in the form of capsules with a prolonged action (500 mg once a day). Acetazolamide can be taken on the day of ascent; its action inhibits carbonic anhydrase and, thus, increases ventilation of the lungs. Acetazolamide 125 mg orally before bedtime reduces the respiratory rate (almost universal sleep remedy at high altitude), thus preventing acute drops in the partial pressure of O2 in the blood. The drug is contraindicated in cases of allergy to sulfanilamide preparations. Analogs of acetazolamide have no advantages. Acetazolamide can cause numbness and paresthesia of the fingers; these symptoms are benign, but may bother the affected person. For patients taking acetazolamide, carbonated beverages can be tasteless.
The flow of low O2 during sleep at altitude is effective, but inconvenient, due to the cumbersome equipment.
Patients with an episode of high-altitude cerebral edema in a history should prophylactically take nifedipine prolonged action of 20-30 mg orally 2 times a day. Inhalational beta-adrenomimetics may be effective.
Analgesics can prevent altitude headache. Prophylactic use of dexamethasone is not recommended.