The pathophysiology of increased intraocular pressure can best be understood in terms of the anatomy and physiology of aqueous flow. The iris divides the front of the eye into anterior and posterior chambers that communicate through the pupil. Aqueous humor is produced by the ciliary body, fills the posterior chamber, flows through the pupil into the anterior chamber, and leaves the eye through glaucoma, glacoma, glucoma, gaucoma Acute angle-closure glaucoma presents with a painful red eye. The physical findings include decreased visual acuity, redness, fixed and unreactive pupil in mid-dilation, and corneal haziness. The objective of treatment is stabilization of the intraocular pressure in a range that will prevent optic nerve damage and visual field loss.
Therapy involves medications that reduce aqueous production or Parasympathomimetics.
Pilocarpine, the most frequently used parasympathomimetic, acts by contracting the ciliary body, which Anticholinesterases act to increase endogenous cholinergic effects and are used to treat patients in whom pilocarpine is inadequate or who prefer the less frequent dosage. The most commonly used anticholinesterase is Sympathomimetics. Epinephrine is a sympathomimetic drug that decreases aqueous production and may increase aqueous outflow. It is additive in effect to pilocarpine and may be used in combination. The ocular side effects of epinephrine include a burning sensation, conjunctival pigmentation, conjunctival hyperemia, and allergic reactions.