In clinical work and on the Internet, we often encounter some questions from patients and friends about glaucoma medication, and this article provides brief answers to these questions for your reference only. 1. Is the purpose of glaucoma medication to lower IOP? Yes, at present, the purpose of glaucoma medication is only to lower IOP, ideally to achieve the target IOP, that is, the IOP state when the damage to the patient’s optic nerve and visual field no longer progresses. In the future, it is possible to develop drugs with other mechanisms of action besides IOP reduction, such as optic nerve protection agents or even gene therapy drugs. 2. Should I use IOP-lowering drugs even for glaucoma without high IOP? Newly diagnosed glaucoma patients with repeated 24-hour IOP curves confirming that the IOP is indeed not high can be diagnosed as normal IOP glaucoma. Such patients should also be treated with IOP-lowering drugs, because research has confirmed that reducing the baseline IOP by 25% to 30% in patients with normal IOP glaucoma can help stop the progression of the disease. 3.What are the most commonly used drugs for primary open-angle glaucoma? The most commonly used drugs for primary open-angle glaucoma are topical prostaglandin derivatives (such as latanoprost, travoprost, bemiprost), beta-blockers (such as timolol, carteolol, levobunolol, betaxolol), alpha agonists (such as brimonidine), and carbonic anhydrase inhibitors (brinzolamide). Local eye drops of pupil constrictors (such as maurozoline) and systemic application of carbonic anhydrase inhibitors (such as vinpocetine) and hypertonic agents (such as isosorbide, glycerol combination, mannitol) are less commonly used, and they are only applied short-term in some special cases such as high intraocular pressure (such as more than 35 mm Hg) and urgent reduction of intraocular pressure before surgical treatment. 4.What is the drug of choice for primary open-angle glaucoma? How to choose several drugs? Prostaglandin derivatives have become the drug of choice for primary open-angle glaucoma in most places because of their strong IOP-lowering effect and the low number of doses (only once a day). This is clearly stated in a number of clinical guidelines both nationally and internationally. However, this class of drugs is more expensive, and in some considerable areas of mainland China, these drugs are still the first choice for primary open-angle glaucoma pharmacotherapy due to the lack of inclusion in the medical insurance list and the lack of such drugs in some areas. The three prostaglandin derivatives latanoprost, travoprost, and bemiprost have similar IOP-lowering effects, and the side effect is mainly conjunctival congestion at the early stage of dropping, but the IOP-lowering effect and degree of conjunctival congestion of the three drugs may vary from patient to patient, and how to choose can be decided by the doctor with the help of local drug availability, health insurance coverage, and the degree of side effects. beta-blockers in However, their IOP-lowering effect is significantly lower than that of prostaglandin-derived agents, and most beta-blockers cannot be used in patients with bronchial asthma and sinus bradycardia. 5.When do two or three drugs need to be used in combination? How to match? When one drug alone cannot control IOP to the target IOP (usually the patient’s IOP is high), a combination of two or three drugs is needed. The principle of combination is to use drugs with different mechanisms of action, such as prostaglandin derivatives with beta-blockers, or alpha agonists, or carbonic anhydrase inhibitors, and there are many options, depending on the local availability of drugs, the effect of lowering IOP, and the side effects that occur after use. However, drugs with the same mechanism of action should not be combined (such as latanoprost with travoprost, timolol with carteolol), which not only cannot increase the effect of lowering IOP, but can make the side effects increase. 6.What additional medication is needed if the pupil of the affected eye is found to be enlarged? In glaucoma patients, the pupil of the affected eye may become larger due to (1) acute or post-acute attacks of closed-angle glaucoma; (2) advanced or absolute glaucoma; (3) misuse of pupil dilators; (4) blunt eye injuries; and (5) combined optic nerve diseases such as ischemic optic disc lesions and optic neuritis. The first four cases can be considered for the application of pupil constricting agents such as trichothecene drops, especially in acute attacks of closed-angle glaucoma, but the duration and effect of the application of trichothecene varies. If the pupil dilator is used by mistake, it may induce an acute attack in untreated closed-angle glaucoma, while no special treatment is necessary for closed-angle glaucoma and open-angle glaucoma after filtration surgery; traumatic pupil dilatation after blunt eye injury is caused by damage to the pupillary sphincter, and maurozanthine does not restore its function. 7. Is it okay to control IOP below the upper limit of normal 21mmHg after medication? Or should it be lower? To what extent is it safe to lower it? The IOP can only be controlled at the target IOP after medication. The target IOP is the upper limit of IOP at which the optic nerve and visual field damage no longer progresses, so it needs to be adjusted after several fundus and visual field examinations under treatment. However, in general, IOP control below 21 mmHg in glaucoma patients should be the basic requirement. The target IOP is related to various factors such as the degree of glaucoma damage and the patient’s life expectancy, etc. The more severe the glaucoma damage and the longer the life expectancy, the lower the required target IOP. 8.How long does it take for the IOP to drop to the target value after the medication is normally administered? This depends on the type and amount of medication used and the patient’s condition. Patients with acute glaucoma usually have high IOP and are asked to check IOP after 1 day or even a few hours of medication to see if their IOP drops to normal (below 21mmHg); patients with chronic glaucoma usually do not have high IOP and are usually asked to check IOP after 1~2 weeks of medication, but of course whether the target IOP has been reached cannot yet be determined based on one or two IOP results alone, as mentioned earlier, it is required to be checked based on The patient’s multiple fundus changes are compared with the visual field examination to determine. 9.When do I need to take oral medications (e.g., vincristine, acetazolamide)? What is the effect? Do I need to use it for a long time? Are the side effects significant? When the IOP is high in glaucoma patients, if the IOP cannot be reduced to the normal range within a short period of time by simply applying several local IOP-lowering drugs, additional oral IOP-lowering drugs, including carbonic anhydrase inhibitors and hyperosmolar agents, can be used for a short period of time. These drugs should not be used for a long time, because long-term application may cause blood electrolyte disorders, and even liver and kidney function, hematopoietic dysfunction, etc. 10.Who needs to use neurotrophic drugs? Which of these drugs are more effective? Do they need to be used for a long time? Are there any side effects? There is a lack of definitive and effective optic nerve nutrition drugs that have been proven in multicenter clinical trials. Most of the drugs that have been tried lack convincing and objective evaluation indicators. 11.Will my vision improve after using the medication? Can visual field damage be gradually repaired? Glaucoma is the first irreversible blindness in the world. The so-called irreversible blindness means that the vision loss, optic nerve damage and visual field loss caused by glaucoma cannot be recovered under the existing medical technology, because the target organs damaged by glaucoma are the retinal ganglion cells and their axons C optic nerve, and there is no definite and effective method to reverse the optic nerve damage so far. Therefore, it is very important for glaucoma to emphasize early detection and reasonable treatment. The early stage of chronic glaucoma does not cause vision loss, so patients with vision loss should first undergo an optometric examination to exclude vision loss due to refractive error.