In primary closed-angle glaucoma, enlargement or forward movement of the lens causes obstruction of normal aqueous flow through the pupil. Often, this occurs in people with shallow anterior chambers of the eye.
As the lens has blocked off pupillary flow of aqeous humor, fluid begins to build up behind the iris.
Increased pressure from aqeous fluid behind the iris leads to the iris bowing forward, mechanically obstructing the trabecular mesh. As this meshwork is unaccessible, the canal of Schlemm cannot resorb aqueous fluid. This leads to increased fluid buildup in the posterior chamber of the eye.
In secondary closed-angle glaucoma, an inciting event, such as hypoxia, causes neovascular proliferation within the eye. This typically takes place on the anterior surface of the iris.
The neovascular proliferation of the iris leads to tissue contraction and mechanical obstruction of the trabecular mesh. The tissue contraction causes the angle in the anterior eye (where the trabecular meshwork is), to be conformationally changed.
Chronic disease develops over time and is usually asymptomatic. Patients complain of progressive peripheral vision loss and on exam will have increased intraocular pressure and possible optic nerve damage.
Acute cases of closed-angle glaucoma are usually from primary lens obstruction of pupillary flow. It is described as sudden, severe eye pain, along with blindness.
Upon inspection, patients will have a "rock hard" eye, due to increased intraocular pressure.
Another associated symptom that patients complain of is frontal headache.
Acute situations of closed-angle glaucoma are a true opthalmologic emergency and need immediate care.
Due to its mydriatic effects, epinephrine is contraindicated and can severely worsen symptoms.
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