Glaucoma is a worldwide leading cause of irreversible vision loss. This is because patients who have glaucoma tends to observe no sign or symptoms of the disease till a relatively late stage. Glaucomas are a group of progressive eye nerves damage characterized by degeneration of retinal major output cells and resulting changes in the eye nerve head. Loss of the major output cells is related to the level of intraocular pressure, but other factors may also play a role. Reduction of intraocular pressure is the only proven method to treat the disease. Although treatment is usually initiated with ocular  drops that lowers the blood pressure to the eyes, plastic surgery of the bundle of eye fibers usually using a laser may also be used to slow disease progression. Diagnosis is frequently delayed. A general understanding of how the disease is contacted, the diagnosis, and treatment may assist primary care physicians in referring high-risk patients for comprehensive eye examination and in more actively participating in the care of patients affected by this condition.
There is considerable evidence suggesting that compromise of the vessels that conduct blood-tissue exchange of the eye nerve(Microvasculature) may have a role in glaucomatous optic nerve damage. Improvement of ocular blood flow in patients with open-angle glaucoma following intraocular pressure reduction may be possible. Since vascular theory is based on the idea of abnormal perfusion due to either increased Intraocular pressure or other factors leading to breakdown of autoregulation and optic nerve head ischemia, improvement of ocular blood flow following Intraocular pressure reduction is possible.
Although elevated intraocular pressure is a very consistent risk factor for the presence of glaucoma, several population-based studies found intraocular pressure was lower than 22 mm Hg in 25% to 50% of individuals with glaucoma. Despite the strong association between elevated intraocular pressure and glaucoma, substantial numbers of people with elevated intraocular pressure never develop glaucoma even during lengthy follow-up. Glaucoma progresses without causing symptoms until the disease is advanced with substantial amounts of neural damage. When symptoms do occur, the disease results in vision loss with concomitant reduction in quality of life and the ability to perform daily activities, such as driving. Early intervention is essential to slow the progression of the disease. Seeing an eye care practitioner should is paramount for patients at risk of glaucoma. 
With retinal ganglion cell death and optic nerve fiber loss in glaucoma, characteristic changes in the appearance of the optic nerve head and retinal nerve fiber layer occur. These changes are the most important aspect of a glaucoma diagnosis and can be identified during ophthalmoscopic examination of the optic nerve head. The importance of conducting an appropriate ophthalmologic examination of the eye cannot be overstated with respect to early detection of glaucoma. Retinal ganglion cell loss causes progressive deterioration of visual fields, which usually begins in the midperiphery and may progress in a centripetal manner until there remains only a central or peripheral island of vision. 

Treatment
Slowing disease progression and preservation of quality of life are the main goals for glaucoma treatment. The decrease in quality of life associated with glaucoma may occur earlier than previously thought, underscoring the importance of early diagnosis and treatment. Reduction of intraocular pressure is the only proven method to treat glaucoma. Results from several multicenter clinical trials have demonstrated the benefit of lowering intraocular pressure in preventing the development and slowing the disease’s progression.

The target intraocular pressure should be achieved with the fewest medications and minimum adverse effects. Several different classes of pressure-lowering medications are available. Medication choice may be affected by cost, adverse effects, and dosing schedules. In general, prostaglandin analogues are the first-line of medical therapy. These drugs reduce intraocular pressure by reducing outflow resistance resulting in increased aqueous humor flow through the uveoscleral pathway. These drugs are administered once nightly and have few, if any, systemic adverse effects. However, they can cause local adverse effects such as conjunctival hyperemia, elongation and darkening of eyelashes, loss of orbital fat (so-called prostaglandin-associated periorbitopathy), induced iris darkening, and periocular skin pigmentation.
Laser trabeculoplasty and incisional surgery are further methods that can be used to lower intraocular pressure for patients who do not respond to antiglaucoma medications. The results of clinical trials have reaffirmed the utility of antiglaucoma medications in slowing the progression of the disease.
Surgical management is mostly indicated when there is inadequate intraocular pressure lowering or is indicated for those with progression of optic nerve or visual field damage despite medical and laser treatment. Trabeculectomy, either alone or in combination with lens extraction should be considered if the pressure control remains too high despite laser and medical treatment, especially in more advanced cases of open-angle glaucoma. Lens extraction is also performed when lens-related mechanisms predominate, especially in cases in which a significant cataract impairs vision. Finally, glaucoma drainage implants may be used in patients with chronic angle closure similarly to open-angle glaucoma when trabeculectomy has failed to control pressure, or in eyes that are deemed to be at high risk of failure with trabeculectomy.
Are you a patient suffering glaucoma, or have you been around someone diagnosed of Glaucoma, kindly comment your experiences to help others identify symptoms of glaucoma early enough and make better choices in managing it. 

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