Acute angle-closure glaucoma (AACG) is an ophthalmic emergency caused by sudden obstruction of aqueous humor outflow from the anterior chamber. Aqueous humor is continuously produced by the ciliary body epithelium at approximately 2-3 μL/minute and flows from the posterior chamber through the pupil into the anterior chamber, draining through the trabecular meshwork and Schlemm canal at the iridocorneal angle. In angle closure, the peripheral iris physically occludes the trabecular meshwork, preventing aqueous outflow. This most commonly occurs when the lens pushes the iris forward (pupillary block), which is precipitated by mid-dilation of the pupil (dim lighting, anticholinergic medications, sympathomimetic agents). Intraocular pressure (IOP) rapidly rises from the normal range of 10-21 mmHg to 40-80+ mmHg. The elevated pressure compresses the optic nerve head and retinal ganglion cell axons at the lamina cribrosa, causing ischemic damage. Corneal endothelial cell dysfunction from elevated IOP results in corneal edema, producing the characteristic halo effect around lights. Without emergent treatment, permanent optic nerve damage and blindness occur within hours.