Background
Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased intraocular pressure (IOP) and decreased visual acuity. 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.
The acute angle closure literature has been plagued by the lack of a uniform definition and specific diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the various forms of angle closure disease. Primary angle closure, primary angle-closure glaucoma, acute angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, 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.
Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, lens opacities, excessive trabecular pigmentation deposits). The term glaucoma is added if glaucomatous optic neuropathy is present.
Pathophysiology
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.
Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP.
Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can be seen in pan-retinal photocoagulation, scleral buckles, and uveitis.
Frequency
United States
AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity.
Mortality/Morbidity
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.
Race
AACG occurs in 1 of 1000 Caucasians, about 1 in 100 Asians, and as many as 2-4 of 100 Eskimos.
Sex
AACG predominately affects females because of their shallower anterior chamber.
Age
Elderly patients in their sixth and seventh decades of life are at greatest risk.
History
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 (ie, 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.
Physical
- The emergency department 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.
Causes
- 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.
DIFFERENTIAL DIAGNOSIS
Acute Orbital Compartment Syndrome
Conjunctivitis
Corneal Abrasion
Corneal Laceration
Corneal Ulceration and Ulcerative Keratitis
Endophthalmitis
Herpes Zoster Ophthalmicus
Iritis and Uveitis
Orbital Infections
Periorbital Infections
Ultraviolet Keratitis
Vitreous Hemorrhage
Other Problems to be Considered
Anterior uveitis
Glaucoma, malignant
Glaucoma, neovascular
Plateau iris syndrome
Lab Studies
- 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.
Prehospital Care
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.
Emergency Department Care
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
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 which can drastically increase IOP beyond its already elevated level. 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.
After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, adjunct drops, and considering the need for further intervention such as osmotic agents and immediate iridotomy.
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.
Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent.
No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP.1 If the IOP is not reduced 30 minutes after the 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. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP.1 Repeat doses may be necessary if no effect is seen and if tolerated by the patient.
Laser peripheral iridotomy (LPI) performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. While LPI is the current definitive treatment, there is evidence to suggest that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG.
In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy. Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.
The choice of which therapy to use will be made by an ophthalmologist who will evaluate all patients via gonioscopy with 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.
If there is a delayed interval between the initial presentation and definitive ophthalmologic care, the emergency department physician should begin treatment as described above. After an appropriate reduction in IOP, immediate ophthalmologic evaluation must be ensured. If the IOP is unchanged or increased from the time of treatment, further treatment should be discontinued and the attack most likely will terminate only with LPI. Ocular massage through a closed eyelid may be preformed while waiting for ophthalmology if no other treatment reduces IOP.
Consultations
- Ophthalmologic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmologic emergency.
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