Older persons are most frequently affected by glaucoma, which is the second most common factor in irreversible blindness in the US. Primary open-angle and angle-closure, as well as secondary open and angle-closure glaucoma, are the two main forms of adult glaucoma. Primary open-angle glaucoma is the most typical kind in the United States (POAG).
The condition known as glaucoma is characterized by an acquired loss of retinal ganglion cells and axons inside the optic nerve or by an optic neuropathy that causes a distinctive look of the optic nerve head and a gradual loss of vision as a result. Unless early glaucoma symptoms are noticed during a normal eye exam, patients with POAG can go unnoticed until substantial optic nerve damage has occurred. In contrast, acute angle-closure glaucoma can appear unexpectedly, cause a more rapid loss of vision, and be accompanied by eye discomfort, headaches, nausea, and emesis. It can also cause corneal edema.
Elevated intraocular pressure (IOP) and associated optic neuropathym are symptoms of secondary glaucoma, which is typically associated with a past eye injury or disease condition. The last kind of glaucoma, known as normal or low-tension glaucoma, manifests in people who have the same pattern of vision loss as POAG but normal intraocular pressure measurements.

DIFFERENTIAL-DIAGNOSIS

Although the precise cause of glaucoma is still unclear, higher ocular pressures are correlated with the condition in the majority of POAG patients. Common symptoms of open-angle glaucoma include delayed, painless damage to the optic nerve, which is considered to be caused by the eye’s drainage system failing. The optic nerve ganglion cell nerve fiber layer experiences a distinctive damage pattern as a result of the diminished outflow capability or increased resistance to aqueous outflow.
Peripheral vision slowly declines in both eyes as the condition worsens, eventually impairing central vision if undiagnosed or untreated. The reason why affected individuals don’t detect a change in their vision until their loss is advanced and impacting the center vision is due to this pattern of loss.
With increasing intraocular pressure and consequent optic nerve damage, secondary open-angle type glaucoma is caused by injury, eye illness, and very rarely eye surgery. Neovascularization-causing illnesses are the most frequent mechanism for the secondary open-angle kind.

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EPIDEMIOLOGY

Globally, glaucoma affects more than 70 million people, and 10% of those affected are bilaterally blind, making it the main cause of permanent blindness. It is quite likely that many more people are affected than are known to have glaucoma since the condition can go unnoticed until it is severe.
Even though several genes, such as myocilin (MYOC, GLC1A) (CCDS1297.1), optineurin (OPTN, GLC1E) (CCDS7094.1), and WD repeat domain 36 (GLC1G) (CCDS4102.1) are linked to a monogenic, autosomal dominant phenotype, they only cause fewer than 10% of all instances of glaucoma. In particular, those of African descent have an incidence of glaucoma that is 2.8 times greater than that of Europeans, and Asians are more likely to suffer angle-closure glaucoma and normal-pressure glaucoma than Europeans. Japanese people are most likely to have normal-tension glaucoma. Age is a significant risk factor for the ongoing loss of retinal ganglion cells across all kinds.

PATHOPHYSIOLOGY

The retinal ganglion cells are central nervous system neurons that receive signals from photoreceptors, analyze them, and send them down axons through the optic nerve to other brain regions. The ganglion cell nuclei in the retina send axons together with the retinal arteries via the lamina cribrosa, a collagen-based structure like a sieve, to the optic disc. The axons and myelin sheath that make up the optic nerve continue behind the lamina cribrosa.
For instance, open-angle glaucoma causes the holes in the lamina crib rosa’s anterior area to enlarge. Progressive visual field deterioration brought on by the loss of retinal ganglion cells often starts in the mid-periphery and progresses until only a central or peripheral island of intact vision is left. Unknown processes underlie the degeneration of retinal ganglion cells. The various glaucoma subtypes are categorized based on the corresponding structural alterations in the eye’s anterior region.

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EVALUATION

A fundoscopic examination, visual field tests, tonometry, optical coherence tomography, and gonioscopy are used to evaluate the patient. The visual acuity test, pachymetry to measure corneal thickness, and retinal scans to track developing alterations in the retinal nerve fiber layer are other important examinations. The above-mentioned testing modalities are used to identify glaucoma based on the typical clinical signs of progressive optic neuropathy or visual field abnormalities. Glaucoma cannot be diagnosed with a single gold-standard test.
The American Academy of Ophthalmology currently advises routine thorough eye exams for people with glaucoma risk factors, with a frequency established on an individual basis, taking age, risk factors, race, and family history into consideration.

MANAGEMENT/TREATMENT OF GLAUCOMA

The basic objectives of glaucoma treatment are to slow disease progression and maintain quality of life. The need for early identification and treatment is highlighted by the possibility that the reduction in quality of life associated with glaucoma would emerge earlier than previously believed. The only known approach to treat glaucoma is to lower intraocular pressure.
Patients in the Ocular Hypertension Treatment Study were randomly assigned to receive treatment or no treatment if they had ocular hypertension (high intraocular pressure without clinical symptoms of glaucomatous damage to the optic nerve or visual field). In the pharmaceutical group, 4.4% of patients showed indications of glaucoma at the end of the 5-year follow-up period, compared to 9.5% in the untreated group. Patients in the Early Manifest Glaucoma Trial were likewise randomly assigned to receive therapy or no treatment, but at the baseline appointment, glaucoma was diagnosed in each patient.
The degree and kind of glaucoma are taken into consideration when managing it. Therapy can only assist to stop more damage and vision loss at this stage; it cannot reverse any of the visual loss that has already happened. Monitoring the development of the disease is made easier by visual field testing and mapping of vision loss. The groups of pharmaceuticals include prostaglandin analogs, beta-blockers, carbonic anhydrase inhibitors, an alpha-2 agonist, miotic agents, and more recently, rho-kinase inhibitors and nitric-oxide donating drugs. In some situations, laser trabeculoplasty is employed as the main form of therapy.

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PROGNOSIS/COMPLICATIONS

If neglected, glaucoma is not a benign condition and can cause lifelong visual loss. The likelihood of harming the optic nerve increases as pressure rises. The prognosis is positive for the majority of individuals with therapy, nevertheless. Low intraocular pressures can stop the evolution of this condition and stop further loss of the visual field.
Loss of the visual field is one of glaucoma’s side effects, which progresses to no longer being able to see light in the damaged eye and eventually causing total blindness.

DETERRENCE

IjijEvery comprehensive eye exam includes routine test of both eyes’ intraocular pressure. These are crucial screening tests to find glaucoma suspects early in the disease process, combined with a fundoscopic examination paying close attention to the optic nerve. Those who are highly suspicious of having glaucoma require further testing to confirm the diagnosis. The causes, risk factors, and course of therapy for glaucoma should be explained to patients.