What Is Acute Hypoxia?

Onset is usually more acute. The mild person may have irritability, euphoria, excitement, slow response, poor perception and orientation, and have breathing, increased heart rate, increased blood pressure, and hypertenoid reflexes. Serious people can have different degrees of will

Diphosphocholine

Acute hypoxic encephalopathy

Acute hypoxic encephalopathy A syndrome caused by a series of neuropsychiatric disorders caused by acute hypoxia. It can be caused by acute massive blood loss, severe heart failure or emphysema, heartbeat, respiratory arrest, and hypoxemia.

Introduction to Acute Hypoxic Encephalopathy

Diphosphocholine Cognitive disorders, generalized or localized seizures. If the coma deepens, the limbs are cold, sweating, blood pressure is further reduced, heart sounds are weak, eyeballs are fixed or swimming, shallow and deep reflexes disappear, muscle tone is reduced, positive pathological reflexes or diaphragmatic reflexes are neutral, and often accompanied by de-braining Tonicity; if the condition worsens, it often dies from breathing and cardiac arrest. After rescue, the mild person can gradually wake up, leaving no or only some minor sequelae; in the severe case, they are left with varying degrees of mental retardation and neurological signs, or have been in a state of de-cortex or de-brainy for a long time. It can often be diagnosed based on the above clinical manifestations and clear etiology.

If a heart attack or respiratory arrest occurs, resuscitation and related medications should be performed as soon as possible, and rapid recovery and consolidation of breathing and circulation functions should be sought. At the same time, the cause should be treated to improve and correct cerebral hypoxia as soon as possible; strengthen the prevention and treatment of complications such as cerebral edema, secondary infection, acidosis and epilepsy; give necessary neurotrophic drugs such as citicoline (250mg), coenzyme Q10 (10mg), coenzyme A (50U), ATP (20mg) and cibilin (5mg), etc., to create conditions for the future recovery of neural function.

Causes of Acute Hypoxic Encephalopathy

Common causes, such as:

1.Buried by sand, chest trauma, nerve gas, status epilepticus

Nitrite Respiratory dysfunction and insufficient oxygen inhalation caused by respiratory muscle paralysis and anesthesia accident.

2. Laryngeal edema or convulsions caused by various reasons, severe pulmonary edema, accidental entry of foreign bodies into the respiratory tract, and severe stagnation of the tongue in patients with coma.

3. Oxygen-carrying dysfunction caused by carbon monoxide or nitrite poisoning.

4. The oxygen content in the inhalation is too low.

Pathogenesis of acute hypoxic encephalopathy

The pathogenesis is very complicated, many links are unknown, but mainly related to the following aspects:

(I) Changes in cerebral blood flow: When asphyxia and hypoxia are incomplete, the blood flow of various organs in the body is redistributed to ensure blood flow to the heart, brain, and adrenal glands. If hypoxia continues to exist, this compensation mechanism fails and the brain Blood perfusion decreased, and there was a second redistribution of blood flow, that is, the blood flow to the cerebral hemisphere was reduced to ensure blood perfusion in the thalamus, brain stem, and cerebellum. At this time, the sagittal region of the cerebral cortex and the white matter below it (the marginal regions of anterior, middle, and posterior cerebral perfusion) are most vulnerable. If asphyxia and hypoxia are acute completeness, the above compensation mechanisms are ineffective, and brain damage Occurs in the most vigorous parts of the metabolism (thalamus, brain stem nucleus), but the cerebral cortex is not affected.

(2) Impaired energy metabolism: It is considered to be its main mechanism. The energy required by the brain comes from glucose oxidation. Anaerobic glycolysis during hypoxia causes sugar consumption , lactic acid increases, leading to hypoglycemia and metabolic acidosis; ATP Insufficient functions of the cell membrane sodium pump and calcium pump, so that sodium and calcium ions enter the cell, causing cytogenic brain edema, calcium ions can also activate the enzymes regulated by them, causing the decomposition of phospholipid components in the cytoplasmic membrane to produce a large amount of peanuts. Enoic acid; further produces thromboxane, prostacyclin ATP cAMP affects synaptic transmitter transmission; affects the structure and function of nerve cells; the function of many vasoactive substances that depend on cAMP decreases cerebral vasospasm brain Tissue damage.

(3) Neurotoxic substances: When the brain is hypoxic excitatory AA, oxygen free radicals increase block mitochondrial phosphorylation and oxidation, destroy cell structure and enzymes.

(4) Nerve cell apoptosis: It is a form of cell death, which is necessary for the development and maturity of an individual and to maintain normal physiological processes. If excessive apoptosis occurs, it will become a pathological state. Recent studies have confirmed that HIE can induce neuronal apoptosis and a variety of pathological mechanisms

Respiratory failure As a result of the interaction, at the same time that acute necrosis of the nerve cells occurs, apoptosis has already occurred. Can be as early as 1 hour after hypoxic-ischemic, until 1 to 2 weeks later.

Clinical manifestations of acute hypoxic encephalopathy

The neurological symptoms of HIE gradually progress after birth, and some cases can turn from excitement to suppression or even coma, reaching the most severe level at 72 hours, and gradually improve and recover after 72 hours. Clinicians should make detailed dynamic observations of neurological symptoms within 3 days after birth, and give indexing.

HIE Clinical Grading

Item mild to moderate

Excessive consciousness, lethargy, dull coma

Normal decrease in muscle tone disappears

The original reflection hugs slightly active and weakens and disappears

Congenital malformation

Sucking normally weakens and disappears

Convulsions are not usually accompanied by commonness or persistence

Central respiratory failure

Pupil changes without or without asymmetry or enlargement, light reflection disappears

Normal frontal tension is normal or slightly full and full of tension

The course and prognosis are most obvious in 24 hours, and gradually disappear within 3 days. Most of the good prognosis symptoms are anti-inflammatory at the end of 1 week. Those who do not disappear after 10 days may have a high sequelae mortality rate. Most of them die within 1 week. The symptoms of survivors may be For several weeks, the sequelae are more likely.

diagnosis

The history and clinical manifestations of acute hypoxic encephalopathy are often non-specific and easily confused with other diseases in the neonatal period. The main reasons are:

Clinical evidence of acute hypoxic encephalopathy

1. Have a clear history of abnormal obstetrics that can lead to intrauterine hypoxia and severe manifestations of intrauterine distress: if fetal movement is significantly reduced, fetal heart <100 beats / second, meconium opacity above °.

2. Asphyxia at birth, especially severe asphyxia, such as Apgar score 1 minute 3 & acute ;, 5 minutes 6 & acute ;, rescue for more than 10 minutes, need positive intubation for more than 2 minutes to breathe.

3 Within 12h after birth: disorders of consciousness such as excessive excitement (tremor tremors, long eye opening time

Hemoglobin , Gaze, etc.), drowsiness, lethargy, and even coma; changes in limb muscle tone (weakness, softness), abnormal primary reflexes, such as hug reflexes being too active, weakening or disappearing, sucking reflexes being too active or disappearing, sucking reflexes weakening or disappearing.

4 In severe cases, convulsions or frequent convulsions, and increased cardia tension.

5. In severe cases, brainstem symptoms can occur, such as respiratory rhythm irregularity, reduced breathing, pauses and other central respiratory failure, pupils shrink or expand, slow response to light, or even disappear, some children with nystagmus.

6. HIE should pay attention to the difference between intracranial hemorrhage and intrauterine infectious encephalitis and congenital malformations.

Auxiliary examination of acute hypoxic encephalopathy

1. Laboratory examination of blood gas analysis to understand hypoxia and acidosis; blood glucose, blood electrolytes, myocardial enzymes, liver and kidney function can determine metabolic disorders and multiple organ damage; phosphocreatine kinase brain isoenzyme (CK-BB), neurone Alcoholase (NSE) can determine the severity of brain damage.

2. Film degree exam

The purpose is to further clarify the location and extent of HIE lesions, determine whether to incorporate intracranial hemorrhage and types of bleeding, and dynamic serial examinations have certain significance for assessing prognosis. Cerebral edema is usually the main thing within 3 days after birth, and you can also check for intracranial hemorrhage; if you want to check

Brain edema Hypoxic-ischemic damage to the cerebral parenchyma and intraventricular hemorrhage are appropriate to be examined 4 to 10 days after birth, and there are still lesions to be examined after 3 to 4 weeks, which is closely related to the prognosis.

2.1CT sees:

(1) The bilateral cerebral hemispheres showed diffuse low-density shadows, and the ventricles narrowed or even disappeared, suggesting cerebral edema.

(2) The symmetrical density of bilateral basal ganglia and thalamus increased, suggesting the existence of basal ganglia and thalamus injury, which needs to coexist with cerebral edema.

(3) A decrease in the density of the brain tissue was found in the distribution area of the aorta of the brain, indicating that there is an infarction of the aorta and its branches.

(4) A symmetrical low-density area around the ventricle, especially above the anterior horn of the lateral ventricle, suggests that the white matter around the ventricle is softened, often accompanied by intraventricular hemorrhage, and more common in preterm infants.

(5) According to CT, the low-density distribution of white matter in the brain can be divided into light, medium, and heavy 3 degrees, and the CT index is not completely consistent with the clinical index. Mild: scattered in the focal low-density shadows in 2 brain lobes. . Moderate: Low density shadows more than 2 brain lobes, white

cell Contrast of gray matter. Severe: diffuse low-density shadow, gray matter and white matter boundaries disappear, but the basal ganglia and cerebellum still have normal density, moderate and severe often accompanied by subarachnoid hemorrhage, intraventricular hemorrhage into cerebral hemorrhage.

2.2B Ultrasound findings

(1) Widely and evenly distributed mild echo enhancement in the parenchyma of the brain, accompanied by narrowing or disappearing of ventricles, sulci and hemisphere fissures, and weakening of cerebral arterial pulse, suggesting the presence of cerebral edema.

(2) The bilateral basal ganglia and thalamus exhibit bilaterally symmetric strong echo reflexes, suggesting the presence of basal N ganglia and thalamus damage.

(3) A localized strong echo reflex is seen in the cerebral arterial distribution area, suggesting the presence of infarcts of the cerebral aorta and its branches.

(4) In the coronal section, an inverted triangle bilaterally strong echo area is seen above the anterior horn of the lateral ventricle; in the sagittal section, there is an irregularly distributed strong echo area along the lateral ventricle, suggesting the presence of softening of white matter around the ventricle.

2.3 brain function status check

2.3.1 EEG examination

EEG can reflect changes in brain dysfunction during the disease and play a role in the early diagnosis and prognosis of HIE.

(1) The EEG performance of HIE is dominated by abnormal background activity, with low voltage, isopotential and

Brain atrophy Outbreak suppression is more common.

(2) The degree of abnormal EEG examination within 1 week after birth is basically the same as the clinical grade, and EEG still does not improve significantly after 2-3 weeks, which is of certain significance for judging the prognosis.

(3) If it can do 24-hour dynamic EEG, it will increase the value of clinical application.

2.3.2 Cerebral hemodynamic examination The application of color Doppler ultrasound can effectively measure the blood flow velocity and vascular resistance of the anterior, middle, and posterior arteries of the brain, and evaluate changes in cerebral hemodynamics.

2.3.3 Magnetic resonance spectrum (MRS) of brain metabolism examination is a non-invasive method for detecting chemical constituents in the brain (ATP, creatine phosphate, lactin); in recent years, a non-invasive diagnostic method-near infrared spectroscopy Technology (NIRS) receives attention. Using oxygenated hemoglobin, deoxyhemoglobin, and other substances to absorb near-infrared light in different light regions in different principles, real-time monitoring of brain oxygenation and cell metabolism.

Treatment of Acute Hypoxic Encephalopathy

Principles of treatment of acute hypoxic encephalopathy

1. Strive for early treatment as soon as possible: Treatment of neurological symptoms after resuscitation should start treatment, it is best to start treatment within 24 hours, up to 48 hours.

2. Comprehensive measures should be taken to ensure the stability of the internal environment and the normal operation of various organ functions, followed by symptomatic treatment and restoration of energy metabolism of nerve cells, and promotion of repair and regeneration of damaged nerve cells.

3. The treatment should be timely and careful, and each treatment measure should be carefully operated within the prescribed time.

4. There should be enough courses of treatment, 10 to 14 days for moderate HIE, 20 to 28 days for severe HIE, and even after the neonatal period, the course of treatment is too short, affecting the effect, without requiring excessive intervention for mild HIE.

5. Medical staff must have confidence in the treatment, actively strive for parents' trust and cooperation, and believe that the prognosis after treatment will be improved, and even severe severe HIE after active treatment can reduce or avoid neurological sequelae.

3 Treatment within 3 days after birth of acute hypoxic encephalopathy

Treatment at this stage is mainly aimed at multiple organ damage caused by asphyxia and hypoxia to ensure the stability of the internal environment of the body; actively control various neurological symptoms, and the focus of treatment is three-support and three-symptoms.

1. Three support

(1) Maintain good ventilation and ventilation functions to keep blood gas and PH values in the normal range. Low-flow oxygen inhalation for 6 hours after asphyxia resuscitation. Those with cyanosis who have difficulty breathing can increase the inhaled oxygen concentration and prolong the oxygen inhalation time; those with acid replacement should give a small dose of NaHCO3; those with mild exhaled acid (PaCO29.33Kpa) can be mechanically ventilated Reduce brain edema.

(2) Eliminate symptoms of brainstem: severe HIE deep coma, shallow breathing, irregular rhythm or apnea, pupil shrinkage or enlargement, disappearance of light response; eyeball fixation or tremor; pale skin, cold extremities, heart sounds Low bluntness, prolonged refilling time of skin capillaries; or frequent seizures and difficult to control medication, naloxone should be used early, the dose is 0.05-0.10mg / kg, intravenous injection, and then changed 0.03--0.05mg / (kg .h) intravenous drip for 4-6h, 2-3 days.

2. Other free radicals can be removed with viTC (0.5g / dldrip) or vitE10-50mg / dim or orally, vitk15 ~ 10mg / d or im × 2-3 days, and N-cell metabolism drugs can be applied early after 24h.

410 Treatment of 4-10 days after birth of acute hypoxic encephalopathy

Application of drugs that promote N cell metabolism or drugs that improve cerebral blood flow can eliminate energy metabolism disorders caused by hypoxia and ischemia, and gradually restore damaged nerve cells to their functions. One of the following drugs can be selected.

1. CDPC: 100-125mg / d or Livzon Sele (2 ~ 5ml / d + 50ml solution × 10 ~ 14 days) can be used within 24 hours after birth. One of the above two drugs can be selected.

2. Compound Danshen injection: it can be applied 24 hours after birth, 6 ~ 10ml / dldrip × 10-14 days.

3 After treatment, the condition of children with moderate HIE and some severe HIE can start to improve from the 4th to the 5th day, such as crying, sucking, muscle tension recovery, and convulsions; by the 7th day to the 9th day, the condition improves significantly. . Such children can continue to be discharged until 10 to 14 days without sequelae.

4 After the 10th day of severe HIE treatment, no obvious improvement was seen, such as unconsciousness or coma, low muscle tone, no original reflex, and no sucking, convulsions, and intracranial pressure. Intensive treatment.

5. During this stage of treatment, attention should be paid to the observation of neurological symptoms and signs, and it is best to use NBNA scores and EEG monitoring.

10 Treatment after acute hypoxic encephalopathy 10 days after birth

It is mainly aimed at those who are not satisfied with the above treatments for severe HIE to prevent neurological sequelae. The key points are:

1. Lizhu Saile , compound Danshen injection can be used repeatedly for 2 to 3 courses.

2. Those with conditions can add brain cell growth peptide.

3 Strengthen neonatal interventions, such as touching and passive limb movements.

4 Maintain water and electrolyte balance, and provide sufficient milk and calories.

5. Intervention during the neonatal period. (1) Visual stimulation method: bright red balls hanging on the bedside to tease or look at the human face every day;

(2) Auditory stimulation method: low-pitched and melodious music, 3 times a day, 15 minutes each time;

(3) Tactile stimulation: passively flex the limbs, touch and massage;

(4) Vestibular motor stimulation: Shake and shake.

Postnatal neonatal treatment of acute hypoxic encephalopathy

1. You need to continue treatment if

(1) After 28 days of treatment, the symptoms of the nervous system have not disappeared, the NBNA score is less than 36 points, and the EEG is abnormal.

(2) In the second and third months of review, CT, B ultrasound or MRI showed brain softening, ventricular enlargement, brain atrophy, softening of white matter around the ventricle, or basal ganglia lesions.

(3) In the second and third months, you cannot raise your head, have inflexible hands, cannot pick up objects, land on your toes, have abnormal muscle tension, and have hyperknee reflexes.

2. treatment method:

(1) 5ml of Livzon Sele or 1600 ~ 4000U of brain cell growth factor or 6-10ml of Fufang Danshen:

(2) 1 to 10 times a day for a total of 2 to 3 or up to 6 months, at the same time, functional training according to age and pronunciation defects, and early intervention based on psychosomatic, behavioral, emotional, feeding, and comprehensive treatment.

Prognosis

The timely and objective evaluation of the long-term prognosis of children who have developed HIE is the basis of rescue decisions and should be comprehensively evaluated.

1. Evaluation time and content: There are different evaluation contents in different stages.

(1) Within 24 hours after birth: whether HIE occurs;

(2) Around 72 hours: the severity of brain injury, preliminary assessment of prognosis;

(3) 10 to 14 days: evaluation of the possibility and severity of sequelae of the nervous system;

(4) 28 days: comprehensive recovery and formulation of intervention treatment plan.

2. Reference value of clinical and auxiliary examinations:

(1) NBNA score: The score at 14 days after birth is still 35, and the sensitivity to the poor prognosis is 96.3%.

(2) Imaging examination: abnormal changes in mild and moderate HIE images usually return to normal within 1 week, and in some moderate and severe cases, if the image changes do not recover after 10-14 days, that is no longer cerebral edema It is the late pathological changes of neuronal degeneration and necrosis. Brain cavities and atrophic changes appear in imaging after 3 to 4 weeks, indicating a poor prognosis and clinical neurological sequelae.

(3) Electrophysiological examination: HIE is accompanied by EEG changes, and those who have completely recovered to normal within 2 weeks have a good prognosis. However, EEG showed severe changes such as "outbreak suppression", "low voltage", and "electric rest", especially those with a longer duration, indicating that the prognosis is dangerous and the sequelae serious.

Clinical data of acute hypoxic encephalopathy

1.1 General Information

The patients were all male fishermen from fishing and loading and unloading Ti fish, aged 18 to 42 years, with an average age of 27 years. The shortest time from onset to arrival was 1 hour for the elderly and 24 hours for the elderly, with an average of 3.5 hours.

1.2 clinical manifestations

They were divided into two groups A and B according to the existence of conscious disturbance. Twelve patients in group A were conscious and had dizziness, headache, nausea, chest tightness, palpitations, and weakness in the limbs; 4 patients had blurred vision, tearing, and conjunctival congestion; ECG showed sinus arrhythmia; blood routine Leukocytes and neutrophils increased in 4 cases. Group B had 72 cases with varying degrees of disturbance of consciousness; irritability and struggling in 13 cases; 35 cases of shallow coma and 24 cases of deep coma, all had urinary incontinence, dull pupillary light reflection, irregular breathing, and irregular heart rhythm. There were 22 cases of tears and conjunctival hyperemia; 16 cases of conjunctival hemorrhage. 45 cases of bilateral Babinski (+). The electrocardiogram showed 16 cases of sinus bradycardia, 2 cases of first-degree AVB, 38 cases of sinus speed, and 32 cases of ST-T shift down. 13 cases of blurred vision and 4 cases of blindness showed no obvious changes in fundus after treatment consciousness cleared. Leukocytes and neutrophils increased in 53 cases, and liver function was normal.

1.3 treatment

Quickly treat symptoms after admission: Take off the clothes contaminated by Ti fish, wash them with warm water at 28 32 , and wash the skin with a towel dipped in 2% 3% sodium bicarbonate until there is no odor; unstable to breathing Those who received respiratory stimulants colamin and lobelin were given one static push; those with a slow heart rate were given atropine 1 mg; and those who were restless and struggling were given a stable push of 10-20 mg; After the above treatment, the patient's condition was allowed At that time, he was quickly sent to the hyperbaric oxygen chamber for treatment. After the treatment, in addition to symptomatic treatment, 20% mannitol, flumesonone, fructose 1.6 diphosphate, cytochrome C, VitC, VitB6, and citicoline are given intravenously to improve the tissue metabolism of important organs such as the heart and brain. Reduce intracranial pressure. Those with ocular symptoms should be treated with ofloxacin eye drops and sugolide eye ointment. After that, light patients will be treated once a day, and severe patients will be treated twice a day with hyperbaric oxygen. And closely observe vital signs and heart, brain, and kidney functions.

1.4 Results

Of the 86 patients, 83 were cured; 2 patients had mild dizziness and decreased memory; 1 patient had palpitations; blindness and blurred vision all recovered after 3 to 6 days. The length of hospital stay was 6 days for the short and 42 days for the elderly.

Introduction

2.1 Ti fish is also called "sunny chaos". It has been verified by the "Aquatic Marine Fisheries Research Institute" that in summer, Ti fish can decompose and release harmful gases such as hydrogen sulfide, sulfur dioxide, ammonia and some harmful gases of unknown nature after leaving the sea for 5 minutes. Oxygen is consumed during this process, resulting in a high concentration of harmful gases in the fish tank and a low oxygen content. If you do not pay attention to preparations for ventilation and ventilation during loading and unloading, you will quickly get sick due to hypoxia and poisoning when entering the warehouse. If you are short, the elderly will be in a coma or even "lightning-like death" within a few minutes. The key to treatment is to quickly leave the working environment, clean the skin as soon as possible, and quickly correct hypoxia (the most effective treatment method is hyperbaric oxygen therapy), to eliminate poison gas, thereby reducing the brain edema caused by it and the damage to other organs.

2.2 The "Aquatic Marine Fisheries Research Institute" has verified that the harmful gases decomposed by Ti fish are mainly hydrogen sulfide and sulfur dioxide. Although the patient was out of the working environment, the clothes and skin were covered with rotten Ti fish. Due to the body temperature, he continued to release harmful gases. When he was admitted to the hospital, it was still full of spicy and egg smell. Both hydrogen sulfide and sulfur dioxide are weakly acidic gases, with a larger specific gravity than air, which is easy to deposit and adhere. Before clarifying the harmful gas composition, we simply cleaned the patient's skin. In the later period, we selected 2% to 4% sodium bicarbonate according to this characteristic, which improved the cleaning effect. It can be seen from the conclusion of the scientific research titled "Nursing and Rescue of Ti Fish Corrupted Gas Poisoning" in our hospital that the recovery time of patients washed with sodium bicarbonate is significantly better than that of patients washed with water.

2.3 The brain is an important organ for life activities. It consumes a large amount of oxygen and lacks oxygen reserves in the brain tissue. Therefore, it is extremely poorly tolerant to hypoxia. Once the blood oxygen supply is interrupted, the brain tissue will suffer the effects of hypoxia first. Correcting hypoxia can often lead to serious consequences. In the treatment of patients with Ti fish spoiled gas poisoning, hyperbaric oxygen has a positive effect and a unique effect. It mainly plays a role in the following aspects: increasing the partial pressure of blood oxygen and the amount of physical dissolved oxygen in the plasma, quickly reducing or eliminating tissue hypoxia; the nucleotide activity is enhanced under hyperbaric oxygen, the cytochrome oxidase is activated, and the sugar is broken down The reaction is inhibited, and the formation of high-energy phosphate bonds is increased. Enzyme synthesis in mitochondria and organelles is also enhanced. In addition, it can inhibit the process of lipid peroxidation, promote the function of natural amino antioxidants, and stabilize the formation of lipid peroxidation hydrolysate in the brain. Through these effects, the cerebral dysfunction caused by hypoxia in the brain can be improved and the brain function can be restored; increase the blood oxygen diffusion and distance; reduce cerebral edema, reduce intracranial pressure, and improve the permeability of the blood-brain barrier, so that The drug easily enters the brain tissue and enhances the effect of chemotherapy. In this group of patients, the vital signs tended to stabilize after the first hyperbaric oxygen treatment, and 40% of the patients became clear of consciousness. Most of the other patients became clear within 12 hours of leaving the warehouse. Only one patient received the second treatment (interval 12). Hours). The patients treated outside the hospital were gradually cleared after 24 to 48 hours, and some patients died. In our work, we found that in the process of hyperbaric oxygen treatment, we cannot be satisfied with the consciousness clearing, and if we terminate the hyperbaric oxygen therapy prematurely, we should continue the treatment to prevent complications. The two patients with residual dizziness in this group were those who were anxious to be discharged from hospital and terminated premature hyperbaric oxygen therapy. After the patient's consciousness cleared, he continued to apply mannitol, flumetasone, fructose 1.6-bisphosphate, and oxygen inhalation to correct cerebral edema and heart damage caused by hypoxia.

2.4 Some patients are irritable and struggling at the time of consultation, and cannot perform hyperbaric oxygen therapy. For these patients, while applying mannitol and other treatments, they should be given a stable and quiet push to quickly enter the hyperbaric oxygen chamber after sedation. Such symptoms can be satisfactorily controlled. The stability half-life is short, the respiratory depression is light, and the onset of the effect is rapid, which can make the patient quickly sedated. The stable dosage varies from 10 to 20 mg / time. Generally, patients can be basically controlled after 50 to 70 mg. A few patients can control the dosage up to 200 mg.

2.5 Some patients in this group have transient vision blurring and blindness. The reasons for the analysis are as follows: sulfur dioxide can directly stimulate the cornea and cause ocular conjunctivitis; hypoxia and toxic gases. The two together act on the optic nerve and the optic cortex center, stop aerobic metabolism in the brain, mutate the neural axis, and interfere with brain cell metabolism to reduce ATP production, which cause metabolic disturbances and conduction disorders in the visual center of the brain, leading to visual central reaction disorders. Hyperbaric oxygen corrects central hypoxia in time and eliminates harmful gases to promote its functional recovery. Sucotherapy is a blood extract of calf. It contains no proteins and antigens, and is non-toxic. It can improve the utilization of oxygen in the tissues of the body and promote the absorption of major metabolites. It has a particularly significant recovery and regeneration function. The application of flaxine together can effectively protect the cornea and conjunctiva and restore their functions quickly.