High altitude cerebral edema

Introduction to high altitude cerebral edema High altitude cerebral edema (highaltitudecerebraledema) is a severe disorder of the central nervous system caused by acute hypoxia. It is characterized by acute onset, clinical manifestations characterized by severe headache, vomiting, ataxia, and progressive disturbance of consciousness. Pathological changes mainly include brain tissue ischemia or hypoxia injury, cerebral circulatory disorders, resulting in cerebral edema and increased intracranial pressure. If not treated properly, it is often life-threatening. In the past, it was often called alpine (original) coma, cerebral alpine disease, acute high altitude sickness encephalopathy and high altitude cerebral hypoxia syndrome. basic knowledge The proportion of illness: 0.0035% Susceptible people: no specific population Mode of infection: non-infectious Complications: cerebral hemorrhage, high altitude pulmonary edema

Causes of high altitude cerebral edema

(1) Causes of the disease

The incidence of high altitude cerebral edema 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~ Symptoms disappeared after 10 days of attendance. Most authors believe that the incidence of this disease is lower in younger people than in younger women than in men; the incidence of acute high altitude sickness is positively correlated with male body mass index (weight/height 2). p<0.05), regardless of the female body mass index, indicating that obese men are more susceptible.

(two) pathogenesis

Among all organs of the body, the brain is the most active oxygen-consuming person. The oxygen consumption per minute of 100g brain tissue is 3.5ml, which is almost 20-25 times of the muscle requirement. When the human body is exposed to low oxygen environment, although The partial pressure of inhaled oxygen is significantly reduced, but the body's internal regulation of hypoxia is increased, so that cerebral blood flow is increased, oxygen transmission and oxygen utilization rate of brain tissue are still maintained at normal levels, and brain tissue generally does not suffer from hypoxic injury. Under hypoxia, the changes of cerebral circulation are related to the partial pressure of oxygen in the blood, the partial pressure of carbon dioxide and the level of tissue metabolism. Siesjo pointed out that when the arterial oxygen partial pressure drops to 30mmHg, the cerebral circulation begins to be disordered, and the brain tissue is disordered. The pathogenesis of high altitude cerebral edema is very complicated. The main changes are brain interstitial edema and brain cell swelling caused by hypoxia.

1. cytotoxic edema Cytotoxic edema refers to intracerebral edema caused by ischemic and/or hypoxic injury of brain tissue, resulting in severe brain function disorder, patients may experience coma, increased intracranial pressure The amount of cerebrospinal fluid increased sharply; brain CT and MRI showed cerebral gray matter edema, cytotoxic edema is mainly caused by insufficient energy of brain cells caused by severe hypoxia, resulting in weakened ion pump function, sodium retention in cells, recently, Green (2000) found that when the human body enters the 6200m plateau, the Na-K-ATPase of the muscle cells is down-regulated. It is also reported that when the animal inhales 15% hypoxic gas mixture, the cerebral blood flow and blood lactic acid No obvious change, while inhaling 6% oxygen for 8min, cerebral blood flow increased significantly, blood lactic acid content increased to 40mg/ml, indicating that severe hypoxia leads to brain cell energy metabolism disorder, high energy oxidative phosphorylation process is weakened, the result can be reduced Ion transport of cell membrane can enhance anaerobic glycolysis, increase lactic acid production, cause cerebral vasodilation, increase blood flow, hypoxia can also directly act on vascular endothelial cells, release vasodilator Factors, smooth muscle relaxation of small arteries, increased blood flow and blood volume, increased vascular permeability, due to increased osmotic pressure of brain capillary, plasma colloidal substances, ions, water from the outside of the cell into the cell, the emergence of brain cell permeability swelling (osmotic swelling), brain tissue swelling and increased brain volume, on the one hand can oppress the surrounding small blood vessels, so that local blood circulation is insufficient, on the other hand due to increased vascular pressure, capillary mechanical damage and local blood supply deficiency, focal cerebral deficiency Focal ischemia, according to MRI examination, cytotoxic cerebral edema is often developed from the basis of acute high altitude disease, so some people refer to moderate and severe acute altitude sickness as mild cerebral edema, ie vascular cerebral edema, but It is difficult to distinguish clearly in clinical practice.

2. Angioedema (angioedema) is caused by mechanical damage to the blood-brain barrier caused by elevated capillary pressure, resulting in increased permeability of the blood vessel wall, causing fluid to seep out of the blood vessel wall and into the brain interstitial, resulting in the brain The quality of the edema, the patient's brain pressure can be elevated, brain MRI examination showed white matter edema of the brain.

3. Modern research on angiogenesis shows that when tissue is hypoxic and/or ischemic, there are many new vascular growths in the injured area, also known as angiogenesis, and angiogenesis is in the field of modern medical research. It is of great concern, especially in the pathogenesis of tumors, burns, cardiomyopathy and pulmonary hypertension. Angiogenesis is caused by stimulation or chemotaxis of various peptide angiogenic factors, including transforming growth factors. ( (transforming growth factor-), tumor angiogenesis factor, platelet-derived growth factor, interleukin-8 and vascular endothelial growth factor (VEGF) VEGF), etc., among which VEGF is more abundantly secreted by macrophages, which can promote mitosis of vascular endothelial cells and increase vascular permeability, so it is also called vascular permeability factor. VEGF is known. It has a strong lysis effect on the capillary basement membrane, and can destroy vascular endothelial cells, expand the intercellular space, and blood vessels Increased permeability, previous studies have confirmed that brain tumor tissue, especially tissue ischemic or necrotic areas, VEGF-mRNA gene expression is most obvious, recently, Xu (1998) and other rats exposed to 9% to 6% low Oxygen gas 3h, VEGF-mRNA of brain tissue began to increase, reaching a peak at 12h, indicating that hypoxia can promote the increase of VEGF in brain tissue. Therefore, Severinghaus suggested that the lysis of VEGF on the basement membrane of brain capillary caused by acute hypoxia is a plateau. An important factor in brain edema.

According to the literature, the autopsy report of patients who died of high altitude cerebral edema is about 25 cases. The common features are: cerebral surface and cerebral vasodilatation, congestion and edema, brain surface, brain parenchyma such as gray matter, white matter, corpus callosum and cerebellum Point-like hemorrhage, microscopic nerve cell swelling, unclear margin, blurred staining, cerebral vascular wall calcification, Fuhgren summarized 11 autopsy data, including cerebral edema in 9 cases (81.8%), cerebral hemorrhage in 7 cases (63.6%), Cerebral venous sinus embolization in 3 cases (27.3%), pulmonary vascular embolism in 6 cases (54.5%), pulmonary infection in 5 cases (45.5%), bronchial pneumonia in 8 cases (72.7%), pulmonary edema in 7 cases (63.6%), Tibet Autonomous hospitals reported 7 autopsy cases, including 7 cases of brain edema (100%), 6 cases of cerebral hemorrhage (86%), 2 cases of cerebral embolism (28.6%), 4 cases of pulmonary edema (57.1%), and 1 case of pulmonary embolism (14.4 %), Kobayashi reported 4 cases, all found cerebral edema and scattered cerebral hemorrhage, nerve cell swelling and deformation.

Plateau cerebral edema prevention

Prevention: Although a lot of explorations have been made on the prediction of susceptibility, no ideal method has been found. The author believes that hypoxic ventilatory response, pulmonary impedance differential wave, lung diffusion capacity, and changes in oxygen saturation after maximal exercise have certain value for predicting altitude sickness. Before entering the mountain, you should adapt to your mental and physical fitness. If you have the conditions, you should perform intermittent hypoxia stimulation and exercise in the low-pressure chamber, so that the body can change to a certain extent from the plain to the plateau anoxic environment. Physiological adjustment. It is currently considered that in addition to being particularly susceptible to hypoxia, stepped uphill is the safest and safest way to prevent acute high altitude disease. The author suggests that if you are entering the high altitude, you should stay at 2500~3000m for 2~3 days, and then the daily rising speed should not exceed 600~900m. After reaching the plateau, avoid drinking alcohol and taking sedative hypnotics for the first two days. Do not do heavy physical activity, but mild activities can promote habits. Avoid cold, pay attention to heat preservation, and advocate using a high-carbohydrate diet. The use of acetazolamide, dexamethasone, acanthopanax, compound Codonopsis, and sulpiride before the mountain may be effective in preventing and alleviating the symptoms of acute high altitude disease.

Most of the disease occurs in extra-high altitude areas, where traffic and medical conditions are poor. Therefore, it is very important to conduct early diagnosis and rescue. Of course, if there are conditions, it should be appropriate to transfer the case to a low altitude.

Plateau cerebral edema complications Complications cerebral hemorrhage

Plateau cerebral edema often associated with pulmonary edema, scattered cerebral hemorrhage.

Plateau cerebral edema symptoms common symptoms dyspnea consciousness loss heart rate increased coma complexion pale shock response dull heart failure expression indifference

Symptom

The pathological essence of high altitude cerebral edema is cerebral edema. The clinical manifestations are a series of neuropsychiatric symptoms. The most common symptoms are headache, vomiting, lethargy or weakness, ataxia and coma. According to the occurrence and development of this disease, some people have the brain Edema is divided into pre-coma (light brain edema) and coma (heavy brain edema).

Pre-coma performance: Most patients have severe symptoms of acute high altitude disease before coma, such as severe headache, progressive aggravation, frequent vomiting, decreased urine output, difficulty breathing, listlessness, apathy, lethargy, unresponsiveness, and then turn into a coma There are very few patients who go straight into the coma without the above symptoms. During the coma period: if they are not diagnosed and treated in time before the coma, the patient turns into a coma within a few hours; pale, cold limbs, loss of consciousness, cyanosis Obvious, severe vomiting, incontinence, convulsions in severe cases, meningeal irritation and pathological reflexes, severe coma, cerebral hemorrhage, heart failure, shock, pulmonary edema and serious infection, etc., if not rescued, the prognosis bad.

2. Signs

Patients often have lip cyanosis, increased heart rate, no special signs of nervous system in the early stage, most of the sputum reflexes are normal, pupils have light reflection, severe patients may have abnormal limb tension, unilateral or bilateral extensor toe reflex positive, neck stiffness The pupils are not equal, the response to light is slow or disappeared, and the fundus examination often shows vein dilatation, retinal edema, hemorrhage and optic disc edema.

Examination of high altitude cerebral edema

Cerebrospinal fluid examination of lumbar puncture confirmed that most patients with elevated cerebrospinal fluid pressure, such as 11 cases of lumbar puncture in the cerebrospinal fluid pressure of 90 ~ 340mmHg, cerebrospinal fluid in 8 cases, bloody 1 case, increased protein 2 cases.

Fundus examination Approximately 85% of patients have varying degrees of fundus changes, manifested in venous dilatation, increased arteriovenous ratio, punctate, flaky or flaming hemorrhage, retinal edema, hemorrhage and optic disc edema.

CT scan of the brain, Kobayashi reported 9 cases of high altitude pulmonary edema with cerebral edema CT findings, found that 8 cases of ventricular volume decreased, brain parenchyma density increased, showing white matter edema (Figure 1); after a few weeks of healing, all returned to normal .

Brain MRI examination of Hackett examined MRI of 9 cases of high altitude cerebral edema, of which 7 cases of white matter edema, especially the corpus callosum.

At the time of admission, the cerebral ventricle was filled with edema fluid, and the density of brain tissue was reduced. After one week of treatment, the edema fluid was clearly absorbed, the ventricle was clear, and the density was normal.

Diagnosis and differential diagnosis of high altitude cerebral edema

diagnosis

Any clinical manifestations of cerebral edema caused by acute hypoxia, severe headache, vomiting, lethargy, ataxia and coma can be diagnosed, early diagnosis is very important, and the symptoms of acute mountain sickness are alleviated. And progressive increase, should be alert to the occurrence of high altitude cerebral edema.

Differential diagnosis

The disease should be differentiated from intracranial infectious diseases, carbon monoxide poisoning, cerebral hemorrhage, and epilepsy.

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