This patient has primary open angle glaucoma (POAG). Patients with POAG present with bilateral peripheral visual loss that occurs gradually and painlessly. Findings on examination are increased cup:disc ratio, vertical extension of the central cup, and disc hemorrhages. Testing shows an elevation of intraocular pressure (generally considered >22 mm Hg) and loss of peripheral visual field depth. The primary treatment for POAG is lowering the intraocular pressure with medications. β-Blockers have traditionally been used as first-line therapy, although prostaglandins are increasingly being used for this purpose. Other medication options include α-adrenergic agonists, cholinergic agents, and topical carbonic anhydrase inhibitors, and although effective, they are associated with more ocular side effects than β-blockers or prostaglandins. Other interventions include laser therapy and surgical therapy, such as iridectomy or trabeculectomy.

Ophthalmic or posterior ciliary artery occlusion (sometimes referred to as arteritic anterior ischemic optic neuropathy) is the most common cause of permanent vision loss in patients with giant cell arteritis, as the ophthalmic artery and the posterior ciliary artery (a branch of the ophthalmic artery from the internal carotid artery) serve as the main arterial supply to the optic nerve. Giant cell arteritis is unlikely in this patient due to his younger age, chronic symptoms, bilateral involvement, and the absence of systemic symptoms such as fatigue, fever, or weight loss.

Optic neuritis is an inflammatory, demyelinating condition, most commonly occurring in the setting of multiple sclerosis, which typically presents with rapid onset (hours to days) of eye pain (particularly with movement) and monocular visual loss. This diagnosis is not supported by this patient's clinical setting or presentation.

Papilledema, or swelling of the optic disc, results from increased intracranial pressure. Papilledema may be seen with any entity that causes increased intracranial pressure, including intracranial mass lesions, cerebral edema, and cerebrospinal fluid production or resorption abnormalities. Findings on funduscopic examination include venous engorgement, blurring of the optic margins, and elevation of the optic disc, none of which are seen in this patient.