Brain edema: A “water crisis” in the skull

In the complex physical structure of the human body, the brain is like a sophisticated command centre, which regulates all the functions of the body. And brain edema, which involves an abnormal accumulation of liquids in the brain tissue, is like a sudden “water crisis” that seriously threatens the normal functioning of the brain and the health of the patient. Brain edema refers to a pathological phenomenon of increased brain moisture, resulting in increased brain capacity. The causes are diverse and, first, brain damage is one of the common causes. Serious head traumas, such as car accidents, crashes, etc., can lead to direct damage to the brain tissue, as well as to cerebrovascular fractures and haemorrhage, which in turn trigger local inflammation and blood circulation disorders. These changes can undermine the integrity of the blood and brain barriers, and allow components in the veins, such as liquids and proteins, to seep into the cracks of brain tissue, thus creating brain edema. For example, when a construction worker accidentally fell from a high ground during the construction process, suffered a severe head injury and was taken to a hospital on an emergency basis, he was examined and found to have not only a fractured skull and internal hemorrhage, but also to have a significant brain oedema. Cerebrovascular disease is also an important contributing factor to brain oedema, which, when brain infarction occurs, causes the death of local brain tissues as a result of ischaemic oxygen, followed by a range of pathological processes, including cytotoxic oedema and vascular oedema. Anemic blood causes neurocytoenergy metabolic disorders, ion-pump disorders in the membrane, and large numbers of sodium ions and water molecules enter the cell, causing cell swelling, i.e. cyllprima. Over time, the extent of vascular oedema is further exacerbated by the damage to the blood-brain barrier caused by the vascular internal cell in the ischaemic zone, as well as by the permeability of the vascular fluids in the cell gap, which creates vascular edema. Brain haemorrhage is due to the direct entry of blood into the brain tissue and the formation of haematoma, which is subject to oppression and irritation, as well as to the destruction of the blood-brain barrier and brain oedema. Among the causes that cannot be overlooked are intracranial infections, where pathogens such as bacteria, viruses, fungi, etc. enter the skull and induce encephalitis or meningitis. In the course of the infection, pathogens and their toxins stimulate inflammatory responses to the brain, resulting in increased cerebrovascular permeability and increased seepage of liquids, resulting in brain oedema. In the case of summer mosquito bites, the type B encephalitis virus can attack the nerve centre, causing encephalitis, oedema, high fever, headaches, vomiting, convulsions, etc., and unconsciousness in serious cases. In addition, certain systemic diseases, such as liver and urinary-toxic cerebral diseases, may be associated with cerebral oedema. These diseases lead to metabolic disorders in the body, the accumulation of toxins in the blood, and affect the metabolism of brain tissues and the stability of the internal environment, which in turn leads to brain edema. There are also brain tumours, the growth of which constrains the surrounding brain tissue and hinders the circulation of blood, while the tumour tissue itself may cause vascular permeability change and promote brain edema. Clinical manifestations of cerebral oedema are strongly related to the extent of the oedema, its location, its rate of development, etc. At an early stage, patients may display symptoms such as mild headaches, dizziness, nausea, vomiting, which can easily be ignored or misdiagnosed as other diseases. With the increase in brain oedema and the gradual increase in the internal pressure of the skull, the patient has a more visible headache, which tends to be severe and of a continuing nature. The vomiting is mostly ejective, irritant to the vomiting centre due to increased internal pressure. Visual impairment may also occur in the form of blurred vision, re-vision, etc., because of the oppression of the optic nerve by high skull pressure. When brain edema is further developed, which leads to the formation of a herring, the patient ‘ s condition is rapidly reversed and repeated. The gill is a brain tumult in which the brain is moved with poor intracircle stress, and if the patient is not treated in a timely manner, the patient falls into a coma as a result of respiratory failure and is likely to die. For the diagnosis of brain edema, there is a need for a comprehensive and multi-faceted information. First, detailed medical history inquiries and medical examinations are the basis. Doctors are asked whether the patient has a head injury, a history of cerebrovascular diseases, a history of infection, etc., and at the same time assess the patient ‘ s nervous system, examining the state of consciousness, the size of the pupils and the reflection of light, physical activity, etc. Images play a key role in the diagnosis of brain edema. The skull C.T. is a common test method, where brain edema is represented on CT images as a low-density reflection of the brain ‘ s substance, which clearly shows the extent, extent and extent of the brain edema, and whether it is accompanied by other pathologies, such as brain bleeding, tumors, etc. The MRI is more sensitive to early diagnosis of cerebral oedema, and can more accurately show nuanced changes in brain tissues and oedema types, such as the high signal images visible on the T2 weighted image. In addition, vertebrae vertebrae examination detects brain vertebral fluid pressure and understanding of intracranial pressure, but is handled with caution to prevent the induction of encephalus. Tests such as blood routines, blood biochemicals and condensation can help to identify the causes of the disease if it is to be judged whether there are infectious and metabolic disorders. Reducing internal stress, improving brain tissue infusion, protecting brain tissue function, and treating congenital diseases are the main objectives of the treatment of brain edema. First, dehydration is one of the more common methods. The glyphol is a powerful dehydration agent, which reduces brain oedema by increasing plasma permeation pressure, so that the moisture in the brain tissue enters the blood vessels and is excreted through the kidney. However, the use of glyphol requires dose and speed attention to avoid complications such as electrolyte disorders due to excessive dehydration and loss of kidney function. For some patients with unsatisfied glycerine, glycerine nut sugar is also a common dehydration option, with mild dehydration and less effect on kidney function. In addition, diuretics such as fur sermi can be used in conjunction with dehydration to enhance dehydration. The reduction of intracranial stress also needs to be accompanied by a proactive response to primary diseases. In the case of patients with cerebral brain damage, the removal of haematoma and the repair of a skull fracture require timely surgical treatment, while in the case of cerebrovascular diseases, treatment is required through ablution, condensation, blood stoppage, etc., depending on the condition; in the case of patients with intracral infections, the choice of highly sensitive antiviral or antimony drugs should be made; in the case of patients with brain tumours, surgery is required for tumour removal, leaching or chemotherapy. Sub-temperature therapy is also an effective complementary treatment. The brain edema is protected by reducing body temperature, the metabolic rate of the brain tissue and the need for oxygen and energy in the brain tissue. Physical or pharmaceutical cooling can generally be used to keep body temperature between 32 and 35 °C, but life signs such as the patient ‘ s temperature, heart rate, blood pressure, etc., need to be closely monitored in the course of implementation to prevent complications such as poor heart and coagulation. The prognosis of cerebral oedema depends on a number of factors, such as the timely removal of the cause of the disease, the severity of the haematoma, and the timeliness and effectiveness of the treatment. For patients with mild cerebral oedema and with a primary disease that can be effectively controlled, the prognosis is relatively good, the brain function may gradually recover and the symptoms of the patient may be reduced. However, serious neurological after-effects, such as severe brain oedema, formation of encephalus, late treatment, and severe patient mortality. As a serious intracranial pathology, the brain edema is like a sword of Damocles hanging over the patient’s head. Understanding their causes, clinical performance, diagnostic methods and treatment strategies is essential for the timely detection and effective treatment of cerebral edema, for protecting the brain function of the patient and for saving his or her life. Today, as medicine evolves, we look forward to more effective treatments to respond to the “water crisis” in this skull, bringing more life and hope to patients.