Acute mountain sickness

Introduction to acute high altitude disease Acute altitude sickness (acutealtitudesickness) is a variety of pathological reactions that occur after rapid exposure to hypoxia. It is a common disease in the highlands. At present, the naming and classification of acute high altitude diseases are basically unified at home and abroad. According to the clinical symptoms and conditions of the disease, the International High Altitude Disease Conference has divided it into light, moderate and severe acute altitude sickness. Light (I degree): Although there are symptoms but normal activities, you can continue climbing; medium (II degree): severe symptoms, decreased mobility, can not continue climbing, need to rest in bed; heavy (III degree): progressive development And serious symptoms such as confusion, need first aid and escort the plain or low altitude. basic knowledge The proportion of illness: 0.021% Susceptible people: no special people Mode of infection: non-infectious Complications: pulmonary edema

Cause of acute high altitude disease

Environmental factors (45%):

The incidence of acute high altitude disease is related to the speed of the mountain, altitude, living time and physical fitness. Generally speaking, when the plain people quickly enter the plateau above 3000m above sea level, about 50% to 75% of people have acute altitude sickness, but after 3~ After 10 days of attendance, the symptoms gradually disappeared.

Self-factor (35%):

Most authors believe that the incidence of this disease is lower than that of young people, and that women are lower than men; the incidence of acute high altitude disease is positively correlated with male body mass index (weight/height 2) (p<0.05), and female body mass index Irrelevant, indicating that obese men are more susceptible.

Pathogenesis

Hypobaric hypoxia is the basic cause of this disease, but its pathophysiology and pathogenesis are still unclear. The current research suggests that it is related to the following factors.

1. Insufficient alveolar ventilation

Lung ventilation is the first step in the oxygen transport process. Plateau hypoxia can stimulate the peripheral chemoreceptors of the carotid body, increase lung ventilation, increase alveolar oxygen partial pressure, and increase arterial oxygen saturation, thus making the body more ingested. Oxygen, however, some people, especially those with high altitude sickness, have no significant increase in lung ventilation after hypoxic stimulation, and there is relative hypoventilation. Hackett believes that relative lung insufficiency may be due to primary Sexual respiratory drive is weakened (hypoxic ventilatory response), or due to secondary ventilation depression (Ventilatory Depression), Moore et al. performed hypoxia on 8 patients with symptoms of acute high altitude disease (susceptible) and 4 asymptomatic patients. A controlled study of ventilation response (HVR) found that the HVR of the former was significantly lower than that of the latter. When the 4800 m plateau was simulated, compared with the control group, the lung ventilation of the susceptible person was reduced, the end-tidal PCO2 was increased, and the arterial oxygen saturation was observed. The degree of decline, and the symptoms of acute high altitude sickness, suggesting that people with low ventilatory response in the plains are prone to acute high altitude sickness after entering the plateau. Therefore, the hypoxic ventilatory response is considered to be One of the good indicators for predicting acute altitude sickness.

2. Fluid retention and body fluid redistribution

Singh et al. observed that when the plains quickly reached the 4500m plateau, most people experienced facial and ankle edema, polyuria and weight loss, but generally returned to normal after 2 to 3 days of altitude training. However, a few people recovered time. Prolonged, and there is less urine, weight gain, etc., weight gain is positively correlated with the severity of altitude sickness. Diuretics and corticosteroids can prevent and treat acute altitude sickness. These data prove that fluid retention or body fluid transfer from intracellular to extracellular Related to the occurrence of acute high altitude disease, the mechanism of fluid retention is complicated, and there are many factors involved. The acute altitude sickness, including the elevation of plasma or urine antidiuretic hormone (ADH) in patients with high altitude pulmonary edema, increased the secretion of ADH. The reabsorption of water in the distal renal tubules and collecting ducts increases, resulting in edema and oliguria. However, some people believe that vasopressin only increases in high altitude pulmonary edema, but acute altitude sickness does not increase significantly. Bartsch et al found acute plateau. The levels of renin and aldosterone were significantly higher in patients with susceptibility to the 4559m plateau than in the control group. Synthesis and secretion, angiotensin I (Angiotensin I), which is formed in the liver, decomposes angiotensin I (Angiotensin I), which forms angiotensin II, angiotensin under the action of angiotensin converting enzyme II can cause peripheral vasoconstriction, and acts on the adrenal cortex hormone to promote the secretion of aldosterone, thereby increasing the reabsorption of sodium ions in the renal tubules and retention of sodium water. In addition, the content of norepinephrine in the blood is also increased, indicating that hypoxia is also It can stimulate the release of catecholamines from sympathetic nerves, cause renal vasoconstriction, reduce renal blood flow, thereby reducing glomerular filtration rate and reducing urination. Therefore, the patient's oliguria is also associated with decreased glomerular filtration rate.

3. Increased intracranial pressure

Patients with acute high altitude sickness often have symptoms of nervous system such as nausea, vomiting, headache and nighttime periodic breathing. These symptoms are related to elevated intracranial pressure. Mastsuzawa et al. performed brain magnetics on 10 healthy people after simulated hypoxia for 8 hours. Resonance (MRI) examination results in cerebral white matter edema in patients with severe acute high altitude disease. Recently, (1998) Hackett et al observed 9 MRI of brain edema in the brain, including 7 cases of white matter, especially corpus callosum edema. However, no abnormalities were found in the gray matter. It is currently believed that most of the moderate and severe acute altitude sickness have interstitial edema, but whether the cerebral edema is also unclear in the mild type, the mechanism of interstitial edema is still controversial, according to the traditional theory. Hypoxia directly inhibits Na-K-ATPase, inactivates the sodium pump, accumulates sodium ions in the cells, and then causes cerebral edema. However, it has recently been found that the oxygen transmission of the brain tissue remains normal in the plateau due to increased cerebral blood flow. Therefore, hypoxia or even severe hypoxia does not affect the ion channel.

Hackett believes that high altitude cerebral edema is caused by changes in cerebral hemodynamics, or vascular (angio) or interstitial cerebral edema caused by dysregulation of the oxygen-sensory pathway of the blood-brain barrier. Vasodilatation, increased cerebral blood flow, abnormal increase in capillary pressure, resulting in increased vascular permeability, blood in the blood from the blood vessels into the stroma, interstitial edema, animal models found, awake sheep inhaled hypoxic mixture At 96h, the capillary pressure of the brain increased from 20mmHg to 50mmHg, the permeability of the blood-brain barrier increased significantly, the water content of the brain tissue increased, and the dry-humidity ratio decreased significantly, which caused the increase of blood-brain barrier permeability. There are mechanical damage to the vessel wall, and biochemical factors, such as hypoxic cerebral vasodilation, increased cerebral blood flow and pressure, resulting in vasodilation, shear stress in the wall, resulting in increased capillary permeability. Acute hypoxia increases certain metabolites in the blood, such as bradykinin, histamine, arachidonic acid, etc., and causes cerebral vasodilation and increased permeability.

4. Lung gas exchange disorder

There is no significant change in lung function in early or mild acute high altitude sickness, but in severe cases, pulmonary function may be abnormal, including decreased lung capacity, increased residual volume and closed volume, and weakened lung impedance. Kronenberg et al. report that normal people are from sea level. When the rapid arrival reached the 3800m area for 72h, the static lung compliance decreased by 20%, and the alveolar-arterial oxygen pressure difference (A-aDO2) increased. Selland et al., who were susceptible to high altitude pulmonary edema in the low-pressure chamber, simulated 4400m, the lung capacity decreased, and the residual The gas volume increased, and the maximum expiratory mid-flow rate decreased significantly. Some scholars found that the altitude of patients with acute high altitude disease was significantly lower than that of acute altitude sickness, and it was negatively correlated with the score of acute high altitude sickness, abnormal lung function and hypoxia. Pulmonary interstitial edema or subclinical edema, such as pulmonary vasoconstriction caused by hypoxia, increased pulmonary arteriolar resistance, and hypoxic stress response, promote pulmonary capillary and The alveolar epithelial cells have increased permeability, and the intravascular fluid overflows into the interstitium, and pulmonary interstitial edema occurs. The result is that the area is reduced and the lungs are reduced. Measuring, so that an increase in lung water content is reduced lung elasticity, oppression around the bronchial tubes, causing small airway obstruction.

Acute high altitude disease prevention

1. Strengthen the adaptive exercise on the plateau, including the limit of the speed of climbing; stay at the middle height (2000~3000m) for about two weeks for adaptive exercise; after entering the plateau, the physical activity is gradual and so on.

2. Adjunctive medication. For those who need to enter the plateau quickly (such as by plane), you can use compound Codonopsis tablets or acetazolamide before departure.

3. To educate people who have just entered the plateau self-protection knowledge, ask for more water, rest more, and avoid high-intensity exercise within 3 days. Give high-vitamin, high-protein, high-calorie light diet, keep warm, prevent colds and frostbite.

4. The average person enters the plateau from the plain, and both physical and psychological needs to make some adaptive changes. Due to lack of oxygen, headache, dizziness, difficulty in breathing and other clinical syndromes, preventive measures are not appropriate, prone to acute altitude sickness, and even further develop into high altitude pulmonary edema and high altitude cerebral edema, which is acute, sick and rapid. Oxygen therapy for acute high altitude disease has certain effects, but the use and supply of oxygen is very inconvenient, and the effect of using oxygen alone is not obvious for preventing altitude sickness.

Acute high altitude disease complications Complications pulmonary edema

Pulmonary edema with left heart failure.

Symptoms of acute high altitude sickness Common symptoms Breathing difficulties Heartbeat speeding Tinnitus Appetite diminished Chestiness Vision disorder Appetite is not vibrating Short hair vertigo

Symptom

Common symptoms are headache, insomnia, loss of appetite, fatigue, difficulty breathing, etc.

Headache is the most common symptom. It is often forehead and double ankle pain. When you wake up at night or in the morning, the pain is aggravated. If the lung ventilation increases, such as mouth breathing, mild activity, etc., the headache can be alleviated. If the headache is severe, there may be visual impairment. However, the fundus examination is normal. In addition, symptoms of nervous system such as insomnia, dreams, tinnitus, dizziness, lack of concentration, and decreased judgment often occur. The symptoms of the gastrointestinal tract are indigestion, loss of appetite, abdominal distension, and severe nausea. , vomiting, and even abdominal pain, a scholar has quickly reached the altitude of 5100m when the sudden abdominal cramps, abdominal distension and pressure, nausea, have no intention but no diarrhea; when quickly withdrew back to 4000m, the symptoms gradually disappeared, the breathing deepened, chest tightness Shortness of breath, difficulty in breathing is often laborious. If breathing difficulties occur at rest, it is a harbinger of high altitude pulmonary edema. Individuals have periodic breathing at night and frequent wakefulness.

2. Signs

There are no special signs of acute high altitude disease. Usually, the lips are delicious, the nails are in bed, the heart rate can be slowed down, the heart beats faster or there is paroxysmal tachycardia, and occasionally there is pre-contraction. Singh checked 1975 patients with acute mountain disease. Two to three people were found to have bradycardia and normal blood pressure, but transient hypotension or hypertension may occur. The apical area may smell I-II systolic murmur, and the second sound of pulmonary valve area is enhanced. Or hyperthyroidism, occasionally in the side of the lungs and localized dry snoring, which may be caused by pulmonary vasoconstriction, but the breath sounds clear and no wet voice, severe facial and lower extremity edema.

Acute altitude sickness examination

1. Contact with the plateau: It is the first time you enter the plateau or return to the plains to return to the plateau for a period of time, or from the plateau to another higher.

2. The altitude of the affected area.

3. The time from entering the plateau to the onset of the disease.

4. Whether there are obvious incentives for the onset, such as excessive speed, physical activity, cold or climate change, hunger, fatigue, insomnia, motion sickness, emotional stress, upper respiratory tract infection and other factors.

5. After the illness, there is no history of oxygenation or transfer to a low place (below 3000m).

6. There are no similar symptoms before entering the plateau or before the onset.

Diagnosis and identification of acute high altitude disease

diagnosis

At present, the international diagnosis of acute high altitude disease is based on the acute high altitude sickness clinical symptom score method (AMS-score) developed by the International High Altitude Disease Conference. However, the scoring method has not been widely applied in China, so as to facilitate communication with the international community, The content of the AMS-score scoring method is briefly described as follows: The scoring method is to self-reported each symptom according to the patient's clinical manifestations:

1. Headache: no headache 0, mild headache 1, moderate headache 2, severe 3.

2. Gastrointestinal symptoms: asymptomatic 0, poor appetite or nausea 1, moderate nausea or vomiting 2, severe nausea and vomiting 3 .

3. Fatigue and/or weakness: no fatigue 0, slight fatigue or weakness 1, moderate fatigue or weakness 2, severe fatigue or weakness 3 .

4. Dizziness: no dizziness 0, mild dizziness 1, moderate dizziness 2, severe dizziness 3.

5. Sleep disorders: sleep is the same as usual 0, sleep is not as normal 1, easy to wake up, poor sleep 2, can not sleep at night 3 .

6. Changes in mental status: no change 0, lethargy/burnout 1, depression/blur 2, lethargy/light coma 3, coma 4.

7. Ataxia: no ataxia 0, can maintain balance 1, gait instability 2, walking easily fall 3, can not stand 4.

8. Peripheral edema: no edema 0, local edema 1, systemic edema 2 .

According to the above self-symptom score, each person's physical activity is evaluated as: 0 activity is normal; 1 is mildly decreased; 2 is moderately decreased; 3 is severely reduced, that is, bedridden. Symptom scores > 4 points can be considered as acute altitude sickness.

Differential diagnosis

Acute high altitude disease is mainly differentiated from viral diseases such as influenza. The flu often has sore throat, sneezing, stuffy nose, runny nose, fever, headache, and systemic muscle pain. Acute altitude sickness generally does not have fever, no upper respiratory tract. Symptoms, no muscle pain, in addition, excessive drinking, strenuous exercise, dehydration can lead to severe headache, nausea, vomiting, oliguria and other symptoms similar to acute high altitude disease, should be identified.

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