Acute episodic increase in intraocular pressure to several times the normal value (10-20 mm Hg) due to sudden blockage of drainage. Production of aqueous humor and trabecular resistance are normal.
Epidemiology: The incidence among persons over the age of 60 is one per thousand. Women are three times as likely to be affected as men. Inuit are more frequently affected than other ethnic groups, whereas the disorder is rare in blacks.
Etiology: (See also physiology and pathophysiology of aqueous humor circulation): Anatomically predisposed eyes with shallow anterior chambers (see Fig. 10.1) pose a relative impediment to the flow of aqueous humor through the pupil. This pupillary block increases the pressure in the posterior chamber (Fig. 10.18a). The pressure displaces the iris anteriorly toward the trabecular meshwork, suddenly blocking the outflow of aqueous humor (angle closure). A typical glaucoma attack occurs unilaterally due to widening of the pupil either in dark surroundings and/or under emotional stress (dismay or fear). A typical situation is the evening mystery movie on television. Iatrogenic pharmacologic mydriasis and systemic psychotropic drugs can also trigger a glaucoma attack.
H Bear in mind that mydriatic agents entail a risk of triggering a glaucoma attack by widening the pupil. Therefore, it is important to evaluate the depth of the anterior chamber in every patient even prior to a routine fundus examination.
Symptoms: Acute onset of intense pain. The elevated intraocular pressure acts on the corneal nerves (the ophthalmic nerve or first branch of the trigeminal nerve) to cause dull pain. This pain may be referred to the temples, back of the head, and jaws via the three branches of the trigeminal nerve, which can mask its ocular origin.
Nausea and vomiting occur due to irritation of the vagus nerve and can simulate abdominal disorders. The generalized symptoms such as headache, vomiting, and nausea may dominate to the extent that the patient fails to notice local symptoms.
Diminished visual acuity. Patients notice obscured vision and colored halos around lights in the affected eye. These symptoms are caused by the corneal epithelial edema precipitated by the enormous increase in pressure.
Prodromal symptoms. Patients report transitory episodes of blurred vision or the appearance of colored halos around lights prior to the attack. These prodromal symptoms may go unnoticed or may be dismissed as unimportant by the patient in mild episodes where the eye returns to normal. Early identification of those risk patients with shallow anterior chambers and gonio-scopic findings is important as damage to the structures of the angle may be well advanced before clinical symptoms appear.
The full clinical syndrome of acute glaucoma will not always be present. The diminished visual acuity may go unnoticed if the other eye has normal vision. Patients' subjective perception of pain intensity can vary greatly.
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