Contents 1 Pinyin 2 English reference 3 Overview 4 Disease name 5 English name 6 Alias ??of high altitude polycythemia 7 Classification 8 ICD number 9 Epidemiology 10 Cause 11 Pathogenesis 11.1 Reduced respiratory drive 11.2 Erythropoietin Role of hemoglobin oxygen affinity 12 Clinical manifestations of high altitude polycythemia 12.1 Symptoms 12.2 Signs 13 Complications of high altitude polycythemia 14 Laboratory tests 15 Auxiliary tests 16 Diagnosis 17 Differential diagnosis 18 Treatment of high altitude polycythemia 18.1 Improving hypoxia 18.2 Bloodletting therapy 18.3 Anticoagulation and antithrombosis 18.4 Traditional Chinese medicine 18.5 Other treatments 19 Prognosis 20 Prevention of high altitude polycythemia 21 Related drugs 22 Related examinations attached: 1 Acupoints for the treatment of high altitude polycythemia 1 Pinyin
gāo yuán hóng xì bāo zēng duō zhèng 2 English reference
altitude erythrocytosis 3 Overview
High altitude polycythemia (high altitude polycythemia) refers to people who have lived at high altitudes for a long time. Excessive red blood cell proliferation caused by acclimation to a hypoxic environment. It is the most common clinical type of chronic mountain sickness. Most people develop it in areas above an altitude of 3200m, but a few people who are susceptible to hypoxia may develop it in areas below an altitude of 3200m. Compared with healthy people at the same altitude, due to chronic hypoxia, patients with plateau polycythemia have significantly higher red blood cells, hemoglobin, and red blood cell volumes, lower arterial oxygen saturation, and are accompanied by clinical symptoms and signs of polyemia; Pathological changes include congestion, blood flow stasis and hypoxic damage in various organs and tissues. Common symptoms are: dizziness, headache, shortness of breath, chest tightness, fatigue, joint pain, anorexia, weight loss, memory loss, and insomnia. In addition, there are irregular menstruation in women, impotence in men, decreased sexual intercourse, etc.
Chronic hypobaric hypoxia is the root cause of high altitude polycythemia. Smoking heavily for a long time at plateau will hinder the transmission of oxygen, reduce tissue oxygen uptake, aggravate hypoxemia, and lead to the occurrence of hypererythema. Obesity and nocturnal sleep breathing disorder in plateau areas can also easily induce excessive red blood cell hyperplasia.
High altitude polycythemia can be complicated by cerebral hemorrhage and high altitude heart disease.
The fundamental cause of plateau polycythemia is excessive red blood cell proliferation caused by tissue hypoxia; therefore, the most effective treatment is to remove the hypoxic environment. Over the years, although a lot of exploration has been carried out on drugs or other treatments, and a lot of progress has been made, there have yet to be reports on methods that are truly effective in clinical application or recognized by domestic and foreign scholars.
Although high-altitude polycythemia is a systemic multi-system disease, there are very few cases of direct death from high-altitude polycythemia. However, the damage in cases of plateau polycythemia is very extensive and involves multiple systemic changes. Those with heart, lung, and brain involvement have a poor prognosis.
For patients with severe plateau polycythemia who have particularly high three hematological indicators and have comorbidities, or whose condition gradually worsens each time they return to the plateau, they should be removed from the hypoxic environment as soon as possible and transferred to the plains. or lower altitudes. 4 Disease name
High altitude polycythemia 5 English name
high altitude polycythemia 6 Alias ??of high altitude polycythemia
plateau erythrocythemia; high altitude polycythemia; high altitude polycythemia; Hypererythrocytosis 7 Classification
Respiratory Medicine> Plateau and Mountain Sickness> Chronic Mountain Sickness 8 ICD Number
J98.8 9 Epidemiology
High altitude erythrocytosis The incidence of the disease is closely related to altitude, gender and race.
Generally speaking, the incidence of plateau polycythemia is highest in immigrants, but it can also occur in people who have lived for a long time, and is higher in men than in women. There seems to be no direct relationship with age. Altitude is the basic factor for plateau polycythemia, which generally occurs in areas above 3500m, and as the altitude increases, the prevalence increases linearly.
According to domestic diagnostic standards, hemoglobin >200g/L and hematocrit >65%.
Epidemiological surveys of immigrants in Qinghai Province at altitudes of 3200m, 4500m and 5300m found that the prevalence rates were 4.5%, 20% and 69.5% respectively; data from Tibet at altitudes of 3000m, 4045m and 4800m were 1.7%, 31.5% and 69.5% respectively. 70%. The disease rate among Tibetans who have lived for a long time is about 10 times lower than that among immigrants.
Foreign standards are different from domestic ones. For example, Peruvian scholars proposed that hemoglobin should be greater than 210g/L, and Bolivia proposed that hemoglobin should be >220g/U. According to this standard, Tuftsd et al. surveyed 600 long-term residents in La Paz (3883m), Bolivia. Among them, 42 (7%) had hemoglobin >220g/L. These people were older and most of them were obese.
The incidence rate in men is significantly higher than that in women. For example, Chinese scholars conducted a survey in the 3780m area and found that the prevalence rate in men was 15.9% and that in women was only 1.5%. Among a group of 98 patients with hypererythema, 79 (80.6%) were male and 19 (18.4%) were female. Nath reported 27 cases of hypererythema in India (3965m), all in males. The factors that cause men to be more ill are: men have poorer sleep quality than women, so they are prone to nocturnal hypoxemia; women suffer from iron deficiency due to menstrual blood loss, which can prevent the abnormal proliferation of red blood cells; more men smoke than women; in addition, Differences in sex hormones also play a role.
The relationship between age and this disease is still controversial. Valarde reported 72 cases of hypererythema in Peru, with an average age of 62 years, and the prevalence increased with age. However, Chinese scholars believe that this disease has nothing to do with age.
Existing data confirm that smoking is a factor that cannot be ignored in promoting the increase of red blood cells. Someone investigated the relationship between smoking and hyperthermia and found that the prevalence of smokers is as high as three times that of non-smokers; and the higher the altitude, the greater the amount of smoking, and the easier it is to develop the disease. A scholar compared the arterial blood gas changes of 308 smokers and 260 non-smokers in Xining (2260m) area and found that the blood oxygen saturation of smokers was significantly lower than that of non-smokers (P<0.05), while the hemoglobin concentration Higher than non-smokers (P<0.01), and 2 cases of hypererythema were detected in the smoking group, while there was no case in the non-smoking group. 10 Causes
Chronic hypobaric hypoxia is the fundamental cause of high altitude polycythemia. Smoking heavily for a long time at plateau will hinder the transmission of oxygen, reduce tissue oxygen uptake, aggravate hypoxemia, and lead to the occurrence of hypererythemia. Obesity and nocturnal sleep breathing disorder in plateau areas can also easily induce excessive red blood cell hyperplasia. 11 Pathogenesis
Chronic hypobaric hypoxia is the fundamental cause of plateau polycythemia. Although many theories and hypotheses have been put forward through which pathways and mechanisms it causes polycythemia, there is a relatively centralized view. Yes: 11.1 Respiratory drive is weakened
Previous studies have suggested that people who have lived on the plateau for a long time or for a long time have a reduced hypoxia ventilatory response (HVR), which is considered to be the best adaptation (acclimation) of the human body to the plateau environment. performance. The blunting of ventilatory response is related to the length of time living on the plateau. Weil et al. found that when people from the plains lived on the plateau for 25 to 30 years, their HVR was similar to that of people who lived on the plateau, but some people have questioned this. However, after a few people from the plains arrived on the plateau and lived for several months to several years, their HVR weakened, and they developed excessive red blood cell proliferation, hypoxemia, and an increase in the carbon partial pressure of carbon dioxide differentiation. Cruz found that at the same altitude, the PaCO2 of hypererythrocythemia was significantly higher than that of non-altitude polycythemia patients, 38.1mmHg and 32.5mmHg respectively (P<0.01); scholars studied the blood gas and blood gas levels of 21 cases of plateau polycythemia in an area of ??4300m. Pulmonary function, it was found that the patient's resting pulmonary ventilation was about 70% to 80% of that of healthy people, the tidal volume was 60% to 75%, and there was mild small airway obstruction; blood gas analysis showed that the patient's pH was lower than that of normal people, and An increase in PaCO2 indicates that plateau polycythemia manifests as alveolar hypoventilation. Severinghaus proposed that when lung function is basically normal, the cause of alveolar hypoventilation may be related to the weakening of respiratory drive, that is, the weakened response of peripheral or (and) central chemoreceptors to hypoxia. Sun et al. studied the HVR of plateau people in Lhasa (3685m). The results showed that the slopes of HVR in plateau polycythemia and normal people were A17±8mmHg/(L·min) and 114±22mmHg/(L·min) (P <0.05), end-tidal PCO2 were 36.6±1.0mmHg and 31.5±0.5 mmHg respectively (P<0.05). This further suggests that insufficient pulmonary ventilation in plateau polycythemia may be related to the inactivation of HVR. However, Kryger et al (3100m) compared the HVR of patients with plateau polycythemia and plateau residents and found that there was no significant difference in HVR between the two groups, that is, both groups showed blunting of HVR. However, the tidal volume decreased and the dead space to tidal ratio increased in the patient group. What's more interesting is that when pure oxygen (100%) is inhaled, the patient's lung ventilation increases and the end-tidal PCO2 decreases, while there is no significant change in normal people.
Therefore, the inactivation of HVR is not the only cause of high altitude polycythemia. There may be other factors, which leads to the hypothesis that hypoxia inhibits the respiratory center, that is, hypoxic ventilatory depression. Current studies indicate that reduced respiratory drive, whether peripheral or central, is a major factor leading to significant hypoxemia and relative hypercapnia in patients. However, the causal relationship between them is still unclear. Whether, like patients with high altitude pulmonary edema, the weakening of ventilatory drive occurs before high altitude polycythemia, that is, whether it is related to genetics, is a new topic worthy of in-depth exploration. Some people believe that the occurrence of plateau polycythemia is not a single factor. In addition to respiratory-driven factors, heavy smoking, chronic respiratory infections, nocturnal sleep-disordered breathing, and obesity-hypopnea syndrome can all cause the reduction of arterial oxygen saturation. 11.2 The role of erythropoietin
Erythropoietin (EPO) is a glycoprotein hormone with a molecular weight of approximately 39,000. It mainly acts on the erythropoietin receptor on the membrane of erythroid committed progenitor cells, promoting the proliferation and differentiation of these committed progenitor cells, accelerating the maturation of red blood cells, and preventing apoptosis (Apoptosis). EPO is secreted by hepatocytes during fetal and neonatal periods, while in adulthood it is mainly secreted by renal tubulointerstitial fibroblasts, but the liver still retains the ability to produce EPO. In addition, small amounts of EPO were also found in the brain, lung and thymus tissues of mice. Regarding the regulation of EPO, the recognized factor is tissue hypoxia, but there may be other factors as well. Hypoxia, whether hypotensive (plateau) or hematogenous (anemia), can inhibit the production of EPO. When animals are exposed to 7% hypoxia, erythropoietin mRNA increases 150-fold, and can increase 300-fold in severe anemia. Klause measured serum EPO on 9 mountaineers. The average sea level was 6 units. When entering an altitude of 4350m, it increased to 58 units in 42 hours and dropped to 31 units after 88 hours. However, it was still higher than the plain value, and the concentration of EPO was consistent with SaO2 There was a significant negative correlation (r=0.6). EPO begins to increase after animals are exposed to hypoxia for 30 minutes in a hypobaric chamber, reaching a peak at 48 hours, and then gradually decreases. These data suggest that regardless of simulated hypoxia or plateau conditions, EPO initially increases and can decrease after 2 to 4 days of hypoxia acclimation, but will not drop to the plain value. This shows that the kidney has a feedback regulation effect on EPO. However, how the kidneys regulate EPO and how EPO regulates red blood cell production remains controversial. Generally speaking, when the renal oxygen receptors are attacked by hypoxia, the renal tubulointerstitial fibroblasts secrete EPO and secrete EPO and secrete the original cells of the bone marrow to promote the division of nuclear red blood cells and accelerate the maturation of red blood cells. Therefore, the number of red blood cells in the blood increases. increase. As a result, on the one hand, it increases the oxygen-carrying capacity of hemoglobin, improves oxygen delivery, and improves tissue hypoxia; on the other hand, if the hematocrit exceeds 60%, the blood viscosity will significantly increase, the blood flow will be slow, and the blood will stagnate in the microcirculation. , and even thrombosis occurs, which blocks the transmission of oxygen, thus aggravating tissue hypoxia. Therefore, Winslow proposed that in hypoxic environment, excessive secretion of EPO may be an important factor in the formation of high altitude polycythemia. However, some researchers have found that the EPO of patients with hypererythema is not significantly higher than that of normal people. Leon Velarde studied the EPO of normal people and hypererythematous people who lived on the plateau in Peru (4300m) and compared it with normal people on the plains. It was found that the EPO of the plateau group (whether normal or hypererythematous) was significantly higher than that of the plain group. There were no significant differences between normal subjects and hypererythematous individuals. Therefore, although EPO is the main regulator of erythrocyte production rate, it is difficult to use changes in EPO to explain the entire formation mechanism of high altitude polycythemia.
Modern research on the molecular biology of EPO has shown that EPO gene expression is related to hypoxia inducible factor (HIF). HIF is a heteromeric protein composed of HIF1α and HIF1β. Some people believe that HIF1 is an oxygen sensor that can activate the gene transcription of proteins (or enzymes) related to hypoxia, such as EPO, vascular endothelial growth factor (VEGF), endothelin 1 (ET1) and glycolytic enzymes (glycolytic enzymes). enzyme), etc., but the relationship between EPO and HIF is currently more studied. HIF1, also known as EPO gene expression induction or enhancement factor, acts on the 3’ side region of the EPO gene. When cells were cultured in 1% hypoxia, the RNA level of HIF1 increased significantly, but decreased when cultured in 20% oxygen, indicating that the production of HIF is closely related to the oxygen tension of the cells. The increase of HIF1 can promote the transcription of EPO gene and accelerate the secretion of EPO and the formation of red blood cells. Recently, Yu et al. (1999) compared mice with congenital partial defective HIF1 (HIFl±) and non-deficient HIF1 (HIFl±) mice after being exposed to 10% oxygen for 1 to 6 weeks. It was found that HIFl± mice developed erythrocytosis, right ventricular hypertrophy, pulmonary hypertension and pulmonary vascular muscularization significantly later than those in the control group.
It is suggested that HIF1 not only acts on the formation of EPO, but also has an effect on other tissues, such as pulmonary artery pressure, cardiac hypertrophy, etc. This will provide new ideas for the study of the pathogenesis of chronic mountain sickness. 11.3 Decreased oxygen affinity of hemoglobin
About 97% of the oxygen transported by blood is combined with Hb and is present in red blood cells. The combination and dissociation of oxygen and Hb is a reversible reaction, namely Hb O2óHbO2. During the oxygenation or oxygen dissociation process, due to the different conformations of Hb, an S-shaped curve can be formed, which is the oxygen dissociation curve. The oxygen dissociation curve has important physiological significance. It is affected by pH, PCO2, temperature and 2,3 diphosphoglycerate (2,3DPG), of which 2,3DPG is particularly important. 2,3DPG is a product of the glycolysis branch of red blood cells. The increased level of 2,3DPG in the blood can combine with Hb, thus reducing the affinity between Hb and oxygen. The oxygen dissociation curve shifts to the right and oxygen release increases. After the human body rapidly enters the plateau, the concentration of 2,3DPG increases significantly, which is the body's compensatory manifestation of adapting to hypoxia. However, the relationship between changes in 2,3DPG and hypererythema is not entirely clear. Eaton found that the 2,3DPG of patients with plateau polycythemia was 23% higher than that of normal people at the same altitude. The author found in the 4300m area that the 2,3DPG in the whole blood and red blood cells of patients with plateau polycythemia was significantly higher than that of local healthy people. It is negatively correlated with PaO2 and positively correlated with P50 (PO2 when SaO2 is equal to 50%). Therefore, at plateau 2, although the increased concentration of 3DPG improves oxygen delivery and increases tissue oxygen uptake, its abnormal increase can cause a decrease in free hemoglobin in the lungs and a significant decrease in blood oxygen affinity, causing the blood to take up oxygen from the alveoli. Difficulty, thus SaO2 decreases; as a result, it promotes the synthesis of 2,3DPG, causing SaO2 to further decrease, thus forming a vicious cycle and developing into more serious erythrocytosis. Therefore, excessive 2,3DPG concentration is one of the manifestations of human body's maladaptation to plateau.
Although high-altitude polycythemia is a systemic multi-system disease, there are very few cases of direct death from high-altitude polycythemia. AriasStellar reported 3 autopsies, and Wolverine reported 12 cases. The pathological damage of high-altitude polycythemia is very extensive, with multi-system changes. The heart, brain and lungs are most commonly affected, and the degree of damage is also serious. Brain manifestations include shallowing of the grooves on the surface of the brain parenchyma, dilation and congestion of blood vessels at the base of the brain and leptomeninges, or rupture of blood vessels, and spot or patchy bleeding in the brain; swelling of brain cells and interstitial edema. Nerve cells undergo necrosis and localized or widespread softening occurs. People with pure high altitude polycythemia do not develop cardiac enlargement. If there are obvious pathological changes in the heart, it is regarded as high altitude heart disease (see the next section for details). The surface of the lungs is dark red and has a solid texture; the alveolar walls are thickened, the alveolar cavities are enlarged, or the interstitial pulmonary edema is present. Pulmonary capillaries are highly dilated and congested, the muscular layer of pulmonary arterioles is thickened, and intraluminal thrombosis forms. Other organs, such as the adrenal glands, digestive tract, kidneys and spleen, may also suffer from bleeding, thrombosis and tissue necrosis. 12 Clinical manifestations of high-altitude polycythemia 12.1 Symptoms
High-altitude polycythemia is mostly chronic and has no clear onset time. It usually occurs one year after moving to the plateau, or the original acute mountain sickness persists and does not heal. To. High-altitude polycythemia is anoxic damage to various organs throughout the body caused by increased blood viscosity and slow blood flow. Depending on the degree of damage to each organ, its clinical symptoms vary in severity and are very complex. The most common symptoms are headache, dizziness, shortness of breath, fatigue, and memory loss. The severity of clinical symptoms is related to the degree of tissue hypoxia caused by hematological changes. After leaving the hypoxic environment and returning to the plains, the symptoms gradually disappear as the hemoglobin and hematocrit return to normal, but they may relapse when returning to the plateau. Peruvian scholars summarized the common symptoms and signs of high altitude polycythemia as follows: headache, shortness of breath, fatigue, lethargy, palpitations, sleep disorders, tinnitus, poor appetite, cyanosis, conjunctival capillary congestion and dilation, muscle and/or joint pain, Clubbing of fingers (toes), numbness of fingers and toes, and abnormal sensation. Domestic scholars have counted 360 cases, and the common symptoms are: dizziness, headache, shortness of breath, chest tightness, fatigue, joint pain, anorexia, weight loss, memory loss, and insomnia. In addition, irregular menstruation in women, impotence in men, and decreased sexual intercourse have also been reported. 12.2 Signs
Cyanosis is the main sign of high altitude polycythemia, and more than 95% of patients have varying degrees of cyanosis. The lips, cheeks, edges of the auricles, fingernail beds, and other parts of the body are bluish-purple, and the facial telangiectasia is purple-red stripes, forming a face typical of plateau polycythemia, that is, the "plateau blood-rich face." The conjunctival membrane of the eyes is highly congested, the tongue is purple, the tongue coating is thick and cracked, and the glossopharyngeal mucosa is black or blue-purple. About 17.7% of patients had clubbing fingers, and 12.8% had nail depression. Some patients have facial and lower limb edema, and the liver and spleen may be enlarged. The heart rhythm is generally regular, but a few people have bradycardia or sinus arrhythmia. In about 20% of cases, grade I and II murmurs can be heard in the apex area and pulmonary valve area, and the pulmonary artery II sound is hyperactive or split. The blood pressure can be high or low, and the pulse pressure difference is small. 13 Complications of high altitude polycythemia
High altitude polycythemia can be complicated by cerebral hemorrhage and high altitude heart disease. 14 Laboratory tests
Abnormally increased number of red blood cells in the blood.
Hemoglobin concentration is also abnormally elevated. Velarde reported 72 cases of high altitude polycythemia in Peru (3850m), with a mean hemoglobin of 235 g/L and a hematocrit of 71%. The diagnostic criteria for plateau polycythemia in my country are: red blood protein >200g/L, hematocrit >65% and red blood cell count >6.5×1012/L. The total number and classification of white blood cells were within the normal range, and the platelets were the same as those of healthy people at the same altitude. The main characteristic of the bone marrow granulocyte system is the vigorous proliferation of the erythroid system, which accounts for 33.3% of the nucleated cells, especially the middle and late immature erythrocytes. There were no obvious changes in the granulocyte and megakaryocyte systems. Patients with plateau polycythemia have reduced pH. Blood gas analysis showed significant hypoxemia (Table 1). PaO2 decreases. PaCO2 increases. AaDO2 increases. Relative hypercapnia. Except for mild abnormalities in small airway function, there were no significant changes in lung function. Small airway function is manifested in the patient's increased closed volume and reduced flow in the middle of forced expiration. 15 Auxiliary examination
Due to the increased blood viscosity and slow blood flow during gastroscopy, it not only directly affects the microcirculation of the gastric mucosa, but also causes thrombosis in the capillaries due to the hypercoagulable state of the blood, leading to severe ischemia of the gastric mucosa. Hypoxia can easily cause mucosal bleeding, erosion and necrosis. Chu reported the gastroscopic and pathological changes of 21 cases of plateau polycythemia. The main manifestations were chronic erosive gastritis, chronic superficial gastritis and linear ulcers in the gastric antrum. Under the microscope, about 90% of gastric mucosal bleeding or hemorrhagic spots can be seen, showing edema-like changes, and about 81% have mucosal erosion and necrosis. A few people have mild intestinal metaplasia and proliferative changes histologically.
Simple high-altitude polycythemia generally does not cause electrocardiographic changes, or mild changes, such as low QRS voltage, incomplete right bundle branch block or localized right ventricular block.
X-ray examination shows that patients with plateau polycythemia often have a history of smoking, so the lung texture is generally increased and thickened, and some are reticular. If there are no heart or blood pressure abnormalities, the heart shadow may be normal. If pulmonary hypertension and plateau heart disease occur, the right ventricle will enlarge, the pulmonary artery segment will bulge, and the diameter of the right lower pulmonary artery will increase. 16 Diagnosis
1. Immigrants living on plateaus above 3000m above sea level, or a small number of long-term residents.
2. Headache, dizziness, shortness of breath, fatigue, sleep disorders, cyanosis, congestion of the conjunctival membrane of the eyeball, etc.
3. Hemoglobin＞200g/L, hematocrit＞65% and red blood cell count＞6.5×1012/L.
4. Symptoms and signs disappear after leaving the hypoxic environment, but relapse when returning to the plateau.
5. Exclude polycythemia caused by other diseases. 17 Differential diagnosis
1. Secondary polycythemia: Polycythemia mainly caused by chronic bronchitis, emphysema, cyanotic congenital heart disease, thoracic deformity, etc. These diseases have typical symptoms and signs, such as chronic cough, heart murmur, etc., so they are not difficult to identify.
2. Polycythemia vera: This disease mostly affects people over 50 years old. No primary disease or cause can be found. It cannot be recovered after moving to the plains. Blood oxygen saturation is normal and there is no bloody face. ; The bone marrow changes to hyperplasia of all hematopoietic systems and spleen enlargement. 18 Treatment of high-altitude polycythemia
The root cause of high-altitude polycythemia is excessive red blood cell proliferation caused by tissue hypoxia; therefore, the most effective treatment is to escape from the hypoxic environment. Over the years, although a lot of exploration has been carried out on drugs or other treatments, and a lot of progress has been made, there have yet to be reports on methods that are truly effective in clinical application or recognized by domestic and foreign scholars. Based on its pathogenesis, the basic treatment principles are: Human body surface area calculator, BMI index calculation and evaluation, female safe period calculator, due date calculator, normal weight gain during pregnancy, drug safety classification during pregnancy (FDA), five elements and eight characters, adult blood pressure evaluation, body temperature level evaluation, diabetes Dietary recommendations: Clinical biochemistry common units conversion basal metabolic rate calculation Sodium supplementation calculator Iron supplementation calculator Prescription common Latin abbreviations Quick check Common symbols for pharmacokinetics Quick check Effective plasma osmotic pressure calculator Ethanol intake calculator
Medical Encyclopedia, calculate now! 18.1 Improve hypoxia
(1) Intermittent oxygen inhalation: nasal cannula or mask can be used to inhale low-flow oxygen, generally 1 to 2L/min is appropriate, 2 hours each time, 2 times/d. Oxygen inhalation can significantly reduce the symptoms of mild patients, but for severe patients, since the body's oxygen transport capacity is severely damaged, oxygen inhalation alone cannot improve symptoms, and drug treatment is required along with oxygen inhalation.
(2) Hyperbaric oxygen chamber (or hyperbaric oxygen bag): There are few clinical data on using hyperbaric oxygen chamber to treat hypererythema. Generally speaking, hyperbaric oxygen chambers (bags) increase the oxygen content of arterial blood, increase blood oxygen saturation, improve clinical symptoms, and reduce the number of red blood cells. However, experts believe that although the symptoms of patients with high-altitude polycythemia improved significantly in the hyperbaric oxygen chamber, their symptoms recurred a few hours after leaving the cabin or the next day, and the hemodynamic indicators did not improve. Therefore, the efficacy of hyperbaric oxygen chamber in patients with plateau polycythemia, whether in the short or long term, needs further observation.
18.2 Bloodletting therapy
If the hemoglobin is >250 g/L, the hematocrit is >70%, and there are signs of vascular embolism or cerebral ischemia, bloodletting therapy may be considered. Generally, 300m1 of venous blood is taken each time, once a week, and 4 times is a course of treatment. Phlebotomy should be followed by infusion of normal saline, dextran or plasma. This therapy only improves symptoms in the short term and is effective in preventing various secondary diseases, so it is only used for patients with severe altitude polycythemia. 18.3 Anticoagulation and antithrombosis
Patients with severe plateau polycythemia have excessive red blood cell proliferation and a hypercoagulable state of blood, which can easily lead to thrombosis or intravascular coagulation. Therefore, anticoagulation treatment is appropriate: dicoumarol 100 mg, 3 times/d orally; sodium alginate diester 50 to 100 mg, intravenously, or 50 mg orally, 3 times/d; Viper defibrination 1 to 2 U/kg, Still dripping. Heparin 0.5~1mg/kg, diluted in glucose saline for intravenous infusion. 18.4 Traditional Chinese Medicine
Traditional Chinese medicine is my country’s unique advantage in treating various chronic altitude sickness. Traditional Chinese medicine has also achieved good results in treating high altitude polycythemia. According to TCM syndrome differentiation, the main symptom of plateau polycythemia is blood stasis and qi stagnation, and the treatment is to activate blood circulation and remove stasis, especially to promote qi and activate collaterals. Commonly used prescriptions from Tibet People's Hospital:
Duoxue No. 0 prescription: Salvia miltiorrhiza, paeonol bark, Ligusticum chuanxiong, Panax notoginseng, turmeric, safflower, tangerine peel, and citrus aurantium.
Prescription No. 1 for Duoxue: Cortex Phellodendron, Gypsum, Poria, Alisma, Gardenia, Yiren, and White Hair Root.
Duoxue No. Ⅱ Recipe: Scutellaria baicalensis, Anemarrhena, Ophiopogon japonicus, Keel, Schisandra chinensis, Radix Rehmanniae, Mulberry.
Qinghai Provincial Hospital of Traditional Chinese Medicine has achieved good results by applying Rhodiola rosea to treat high altitude polycythemia. Usage: Rhodiola rosea 600mg orally, 2 times/d, 15 days as a course of treatment. 18.5 Other treatments
Diethylstilbestrol is widely used abroad. It can inhibit EPO, reduce hemoglobin, and has a certain effect on high altitude polycythemia. However, long-term use of large doses can lead to side effects such as penis enlargement, sexual dysfunction, and bone and joint pain. Commonly used dosage: 2mg/d, oral or intramuscular injection.
(1) Rest: Reduce labor intensity, avoid strenuous physical activities, ensure rest time, especially sleep time at night, improve the sleep environment, and improve sleep quality.
(2) Adjust your diet: eat more fruits and fresh vegetables, supplement various vitamins, and prohibit smoking and drinking.
(3) Specific care: High altitude polycythemia is due to long-term chronic hypoxia, compensatory increase in red blood cells, resulting in increased blood viscosity, arterial oxygen partial pressure, blood oxygen saturation, Blood oxygen content decreases and arterial blood carbon dioxide partial pressure increases; early complications are mainly the formation of small thrombus in the extremities. In the late stage, due to the activation of a large number of procoagulant factors, secondary hyperfibrinolysis occurs, and the main complications are thrombosis and DIC.
Proactive preventive measures should be taken for patients who have experienced thromboembolism: oral administration of small doses of enteric-coated aspirin, 25% magnesium sulfate hot compress on the embolized area, etc., in order to activate blood circulation and remove blood stasis, control the development of the disease, and promote The purpose of patient recovery. For patients with heart failure, vasodilator, cardiotonic, diuretic and other drugs should be used appropriately according to the patient's condition. For comatose patients with cerebral vascular embolism, coma care should be provided; when suctioning sputum, the movements should be gentle to prevent damage to the oral mucosa and tracheal mucosa. The suction time should not be too long and the pressure should not be too high to avoid pulmonary insufficiency. Zhang, tracheospasm injury, increased intracranial pressure, etc.
(4) Psychological care: High-altitude polycythemia is an absolute increase in red blood cells and total blood volume, and an increase in blood viscosity; patients have no obvious discomfort in the early stage and do not attract attention. Once discovered, psychological and mental health problems The burden increases. Nursing staff should take the initiative to care, be considerate, and comfort patients, and explain to them and their families the characteristics of such diseases, the benefits of early treatment, and matters that should be paid attention to; nurses and patients should maintain close contact so that nursing staff can gain the trust of patients; and make patients familiar with the hospital environment. , be hospitalized with peace of mind, and actively cooperate with diagnosis and treatment in order to achieve early physical and mental health. 19 Prognosis
Although high altitude polycythemia is a systemic multisystem disease, there are very few cases of death directly from high altitude polycythemia. However, the damage in cases of plateau polycythemia is very extensive and involves multiple systemic changes. Those with heart, lung, and brain involvement have a poor prognosis. 20 Prevention of high-altitude polycythemia
Patients with severe high-altitude polycythemia who have particularly high three hematological indicators and have comorbidities, or whose condition gradually worsens each time they return to the plateau, should leave the hospital as soon as possible Low oxygen environment, move to plains or lower altitudes. 21 Related drugs
Oxygen, carbon dioxide, glycerin, dicoumarol, sodium alginate diester, heparin, glucose, salvia miltiorrhiza, skullcap, diethylstilbestrol 22 Related tests
Hemoglobin, blood oxygen Saturation, hematocrit, partial pressure of carbon dioxide, erythropoietin, endothelin, bone marrow granulocyte system, blood oxygen content. Acupoint Qigen for treating high altitude polycythemia
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