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Pathophys and Cause

Cause:Genetic predisposition, hyperopia (farsightedness)

Pathophys:Normally, aqueous humor is secreted in posterior chamber by the ciliary body, then goes through the pupil to the anterior chamber and out the trabecular meshwork at the scleral–iris junction. Congenital predisposition of a smaller eye and shallow anterior chamber w close apposition of iris and lens so that fluid is trapped where it is made behind the iris, which bows forward to cover the trabecular meshwork blocking outflow. Secretion of aqueous humor then causes pressure to build, compressing first the optic nerve where the scleral cribosa is the weak point, leading to cupping and atrophy when chronic.

Epidemiology

~0.2% of population; esp in middle-aged and elderly

Signs and Symptoms

Sx:Onset usually age >50 yr. Precipitated by mydriatics, antacids, anesthesia, darkness. Rainbow halos often first sx, due to corneal edema; eye pain, sudden, often bilateral; headache, nausea and vomiting, scotomas in nasal fields causing blindness

Si:

Red eye, esp circumcorneal; partially dilated fixed pupil. Corneal edema, blistered and hazy; corneal pressure >30 mm Hg, pressures >18 mm Hg have a 65% sens/specif (Nejm 1993;328:1097).

If chronic or recurrent attacks, optic disc is pale and cupped

Tonometry: 8-22 = normal; 20-30 = probably normal (only 3.5% will go on to glaucoma in 5 yr); >30 mm Hg much higher % go on to glaucoma

Complications

Blindness; other eye affected within 5-10 yr in 40-80%, and use of pilocarpine does not protect

Treatment

Rx:Surgical laser iridotomy under local; may need pilocarpine 1-2% gtts q 5-10 min until relieved + systemic carbonic anhydrase inhibitor (acetazolamide 1 gm iv or 0.5 gm po stat) to lower pressure enough to allow laser rx