The beauty of life lies in seeing. People, before the end of their lives, actually have many tissues and organs that are difficult to function. For example: teeth, ears, eyes, etc., etc. The most unacceptable is the eyes. Many eye diseases can end a person’s vision before life. Glaucoma, is one such disease. It, may creep up on us and take away my vision without knowing it. Do not think that glaucoma is still far away from us. In fact, many problems have been quietly coming since childhood, and at every stage of our lives, it may be waiting for an opportunity to make trouble, and if we don’t pay attention, there may be problems. When problems appear and then remedy them, it is already too late. Glaucoma, a common eye disease characterized by high eye pressure and damage to the optic nerve. The causes of glaucoma are complex, and it can be said that high eye pressure is the direct cause of damage to the eye. There are also many causes of high intraocular pressure. Simply put, the eye is out of balance between the inside and outside of the eye. The rest of the eye, except for the vitreous humor and the lens, is water, known as atrial fluid. The inside of the eye needs to remain clear and not have blood vessels. The transport of nutrients and the drainage of metabolites from the lens and vitreous humor depend on the atrial fluid. Poor reflux of atrial fluid raises intraocular pressure, and to a lesser extent, because of excessive production. Persistent elevated IOP can cause damage to the eye. The most important area of damage is the optic nerve. The optic nerve is the pathway through which the eye’s photoreceptor cells convert light signals into electrical signals to the visual center. It is concentrated in the posterior pole of the eye at a point the size of 2mm in diameter that penetrates the eye. This point is visible under the fundoscope as a rounded bulge with a somewhat concave center and is called the optic papilla. The damage from high intraocular pressure is mainly in this area. Early changes are only changes in the shape of the optic nerve papilla and do not affect visual function. The shape change becomes more pronounced over time. When the pressure in the eye remains elevated or is maintained for an extended period of time, the optic nerve papilla becomes significantly subluxated. When the majority of the optic papillae (more than 60%) are sunken, impairment of visual function may occur. The first sign of functional impairment is a change in the visual field. Glaucoma can be diagnosed when the visual field changes show glaucomatous features. In fact, the damage begins long before the diagnosis of glaucoma is confirmed. In addition to changes in the shape of the optic papilla, there are gradual changes in visual function. The earliest change is in color vision, and later on some abnormalities are shown from visual electrophysiology. Many of the reported early changes in glaucoma indicate that the damage has begun, but the specificity is not obvious enough to use this as a basis for diagnosis yet. However, one thing is certain, it indicates that the damage has already occurred. Therefore, the American Glaucoma Society proposes that the first stage of glaucoma staging is the injury stage. This is followed by the preclinical, clinical, and absolute stages in that order. Why is the injury stage placed before clinical symptoms appear? Because the damage is the earliest to start, at this time the doctor does not know, and the patient does not know. By the preclinical stage, some test indicators have been suggested, but the patient does not know yet. By the time the patient comes to the doctor in the preclinical stage, he or she may have missed the opportunity for prevention and simple treatment. In the absolute stage, there is no longer any vision, and the only way to cope is to respond passively or give up treatment. When symptoms cannot be relieved, extreme measures may have to be taken to alleviate or stop the pain, which every ophthalmologist does not want to see. Glaucoma eventually goes to this stage, only some people go slower and do not come out of the damage stage for life. Some go faster and finish the process before they are old enough to do so. Most patients, through various treatments, do not make it to the end in his lifetime. As human life expectancy continues to increase, this threat is increasingly becoming visible. The majority of patients diagnosed with glaucoma are already in the clinical phase. Only a small percentage are problems found during various examinations, and even if they are found, the only medical advice is to observe and wait for real evidence before dealing with them. By this time, prevention has lost its chance and treatment is not yet the time. Only the damage phase or before the damage phase has a chance for prevention. This leads to some questions: How to determine the damage stage of glaucoma? Is there a way to stop the damage? When is it necessary to take action? Who can accept that a person should be protected from glaucoma in a good eye? To face these questions, let’s first look at what causes high IOP. The main reason for high IOP is the lack of atrial fluid flow. There are many reasons that affect the flow of atrial fluid, and there is one type of open-angle glaucoma whose cause is still unknown. The main cause is that the outflow of atrial fluid is blocked by the trabecular meshwork-Schlemm’s canal system; some patients have a genetic predisposition to the disease, such as the TIGR gene and OPTN gene; and some patients have a family history of glaucoma. One type of closed-angle glaucoma is caused by an acute increase in IOP due to atrial angle closure. The vast majority of patients with acute closed-angle glaucoma are pupillary block type, and a few patients are non-pupillary block type. Open-angle glaucoma is more likely to be myopic and closed-angle glaucoma is more likely to be hyperopic. Based on these patterns, we can narrow down some active prevention. For myopic patients and those with a family history of glaucoma, start by paying attention to eye use, monitoring changes in intraocular pressure, paying attention to fundus changes, and minimizing visual fatigue. For patients with hyperopia, reasonable prescription lenses are used to reduce the burden and avoid abnormally developed ciliary muscles that take up the atrial aqueous pathway. For these potential patients, some other prevalent problems to be aware of are mood swings and excessive eye use. Controlling emotions requires lifelong attention; excessive eye use or continued eye use after visual fatigue is an external cause of creating a poor internal environment of the eye. Taking appropriate breaks or identifying the triggers of visual fatigue and dealing with them properly is the key to prevention. In recent years, there is a popular research – binocular vision. It remains to be proven that binocular vision abnormalities are the causative factor of visual fatigue and may be the causative factor of increasing myopia, and whether it could also be the causative factor of high intraocular pressure. It can be inferred that perfecting binocular vision should be helpful in preventing high IOP. For diagnosed glaucoma, long-term treatment can only be given as prescribed by the doctor. There is a large sample of statistics to refer to. This is a long-term observation from the United States. The report found that by setting the target IOP below 20 mmHg, for every 2 mmHg reduction, 20% of glaucoma patients would avoid losing their vision during their lifetime. It is recommended that a target IOP of 16 mmHg or less for glaucoma may prevent 60% of patients from losing their vision during their lifetime. Some normal pressure glaucoma requires an even lower target IOP, even below 10 mmHg. Failure to control this with medication requires surgery. Lowering IOP plays a pivotal role in preserving vision in patients with glaucoma. Although, modern medicine can effectively control IOP, after all, it requires long-term medication ordering or continued control after surgery. Preventive measures early in the damage period and before can not only effectively prevent the occurrence of high IOP and delay the glaucoma process, but may also effectively counteract damage to the eye from high IOP by improving the internal environment of the eye. By perfecting binocular vision early, it is possible to avoid going to this step. We hope that all of you who have hidden glaucoma will not let our vision end before our lives through active prevention and persistent treatment.