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Acute angle-closure glaucoma (AACG) is an ocular emergency and receives distinction due to its acute presentation, need for immediate treatment, and well-established anatomic pathology. Rapid diagnosis, immediate intervention, and referral can have profound effects on patient outcome and morbidity.
Acute angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP >21 mm Hg, conjunctival injection, corneal epithelial edema, mid- dilated nonreactive pupil, and shallower chamber in the presence of occlusion.
AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle.
Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, and a shorter axial eye length. Of the many predisposing anatomical variations, a narrow angle and a thin, floppy iris have the most devastating consequences.
In AACG, the eye’s natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. This term articulates the obstruction and blockage of aqueous flow from the posterior chamber to the anterior chamber. When pupillary block occurs in conjunction with a floppy thin iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage thus increasing IOP.
AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity. Outcome after AACG is dependent on duration from onset to treatment, underlying ocular disease, and ethnicity. The degree of IOP elevation has been shown to have less impact on future visual acuity. Studies report that as many as two thirds of individuals with AACG had no visual field loss. However, Asians appear to be more refractory to the initial medical management, and, even after definitive treatment, they experience a progressive increase in IOP and deterioration in visual acuity.
Classically, patients are elderly, suffer from hyperopia, and have no history of glaucoma. Most commonly, they present with periorbital pain and visual deficits. The pain is boring in nature and associated with an ipsilateral headache. Patients note blurry vision and describe the phenomenon of, “seeing halos around objects.” Careful investigation may elucidate a precipitating factor (i.e.: dim light, anticholinergic, sympathomimetic medications). In a large percentage of patients, extraocular symptoms and systemic manifestations are the chief complaint. Patients present with headache and may receive medications for migraines or an evaluation for a subarachnoid hemorrhage. Several case reports discuss patients presenting with vomiting and abdominal pain that were misdiagnosed with gastroenteritis.
The evaluation of the eye includes visual acuity, the external eye, visual fields, a funduscopic examination, pupils, ocular motility, and IOP. All of which tend to be affected in AACG. Patients complain of blurred vision, and testing reveals the ability only to detect hand movements. They are unable to identify numbers and letters on distance charts or near cards. Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea obscures the funduscopic examination. Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed.
Shallower anterior chambers, anteriorly situated lens, shorter axial eye length, a thin, floppy iris, and a narrow angle lead to a higher propensity for development of AACG. Precipitating factors include drugs (i.e.: sympathomimetics, anticholinergics, antidepressants), dim light, and rapid correction of hyperglycemia.
The diagnosis of AACG is predicated upon the clinical presentation of painful vision loss and a physical examination revealing a fixed mid-dilated pupil. No definitive laboratory or imaging studies are available. However, tonometry must be performed and must demonstrate increased IOP as described above.
The initial first aid is very important. The patient should be brought to the hospital in an expeditious manner to have IOP reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any cosmetic benefit.
The treatment of AACG consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta- blocker, and a topical steroid. Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg PO. A dose of a topical beta-blocker (i.e.: carteolol, timolol) will also aid in lowering IOP. Both beta-blockers and acetazolamide are thought to decrease aqueous humor production and enhance opening of the angle. An alpha-agonist can be added for a further decrease in IOP. Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids.
Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that while supine, the lens falls away from the iris decreasing pupillary block.
Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block.
If the IOP is not reduced 30 minutes after a second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol. Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should not be administered in cardiovascular and renal patients.
Laser peripheral iridotomy (LPI) performed 24-48 hours after IOP is controlled is the definitive treatment for AACG. An ophthalmologist must evaluate all patients for LPI via gonioscopy and complete inspection of the angle. At institutions where an ophthalmologist is immediately available on staff, initial treatment should be performed in conjunction with the specialist.
These include permanent decrease in visual acuity, repeat episodes, malignant glaucoma, and central retinal artery or vein occlusion. Fortunately, for most patients with adequate treatment, vision is recovered.
The greatest problem here is misdiagnosis and delayed diagnosis. Timely intervention is crucial for a favorable outcome and to avoid visual loss. Maintaining a working knowledge of the condition and its myriad presentations is essential to considering the diagnosis. Physicians should have a low threshold for checking intraocular pressure. Rechecking the patient after treatment and referring the patient urgently to an ophthalmologist is critical for a good outcome.
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