Papilledema represents optic disc edema secondary to elevated intracranial pressure, requiring urgent diagnostic workup to identify the underlying etiology. The pathophysiology involves impaired axoplasmic transport at the lamina cribrosa where elevated CSF pressure compresses retinal ganglion cell axons, causing axonal swelling, mitochondrial dysfunction, and if sustained, Wallerian degeneration with irreversible optic atrophy. The optic nerve is anatomically surrounded by the subarachnoid space containing CSF—elevated ICP is directly transmitted to the optic nerve sheath. Fundoscopic progression follows a predictable pattern: Stage 1 (early)—obscured nasal disc margin, C-shaped halo, preserved temporal margin; Stage 2 (established)—circumferential disc elevation, obscured major vessels, peripapillary hemorrhages; Stage 3 (chronic)—disc pallor, narrowed vessels, optociliary shunts; Stage 4 (atrophic)—flat, pale disc with permanent vision loss. The differential for bilateral disc edema includes papilledema (elevated ICP), malignant hypertension, bilateral optic neuritis, infiltrative optic neuropathy, and diabetic papillopathy. For unilateral disc edema: anterior ischemic optic neuropathy (AION), optic neuritis, compressive lesion, central retinal vein occlusion, and pseudopapilledema (optic disc drusen). The clinician must order and interpret appropriate diagnostics, initiate treatment for the underlying cause, manage ICP reduction, and determine surgical...