AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.
• Precipitating factors include drugs (ie, sympathomimetics, anticholinergics, antidepressants), dim light, and rapid correction of hyperglycemia.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Anterior uveitis
Glaucoma, malignant
Glaucoma, neovascular
Plateau iris syndrome

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 PO. A dose of a topical beta-blocker (ie, carteolol, timolol) will also aid in lowering IOP. Studies have not conclusively demonstrated the superior neuronal or visual field protectiveness of one beta-blocker over another. 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 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.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goal in treatment of AACG is to reduce IOP. Medical management is the first step. A prompt reduction in IOP using topical and systemic medication decreases the duration of elevated IOP and the potential for visual field loss. IOP reduction is accomplished via suppression of aqueous humor production, eliminating pupillary block, and reversing inflammation. As with any medical intervention, intimate knowledge of the drugs, their indications, contraindications, and potential side effects can aid the physician in providing the best treatment and a favorable outcome.

Drug Category: Carbonic anhydrase inhibitors

These are first-line agents that should be used immediately during the initial intervention. They reduce bicarbonate production in the ciliary epithelium and therefore decrease aqueous formation.

Drug Name	Methazolamide (Neptazane)
Description	Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Adult Dose	50-100 mg PO bid/tid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; renal impairment
Interactions	May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alter excretion of other drugs by alkalinizing urine
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur

Drug Category: Beta-adrenergic blockers

These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.

Drug Name	Carteolol (Ocupress)
Description	Nonselective beta-adrenergic receptor. Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation.
Adult Dose	1 gtt in affected eye(s) bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; congestive heart failure; asthma; cardiac conduction defects; breastfeeding
Interactions	May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Drug Name	Levobetaxolol (Betaxon)
Description	Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
Adult Dose	1 gtt in affected eye(s) bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
Interactions	May have additive systemic effects if patient is already on systemic beta-blockers
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons

Drug Name	Levobunolol (AKBeta, Betagan)
Description	Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and may increase outflow of aqueous humor. Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If IOP not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously.
Adult Dose	0.5% solution: 1-2 gtt in affected eye(s) qd 0.25% solution: 1-2 gtt in affected eye(s) bid Severe or uncontrolled glaucoma: 0.5% solution bid; closely monitor patient >1 gtt (0.5% levobunolol) bid not shown to be more effective; if IOP not at satisfactory level on this regimen, concomitant therapy can be instituted; do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
Interactions	May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Drug Category: Alpha-adrenergic agonists

These agents are used as adjunct agents to further decrease IOP secondary to their affect on aqueous humor production.

Drug Name	Brimonidine (Alphagan, Alphagan-P)
Description	Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow.
Adult Dose	1 gtt in affected eye tid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; patients receiving MAO inhibitor therapy
Interactions	Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants such as barbiturates, opiates, and sedatives may potentiate effects of brimonidine
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy

Drug Category: Corticosteroids

These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.

Drug Category: Ophthalmic agents, miotic

These agents pull the peripheral iris tissue away from the trabecular meshwork helping to eliminate obstructed aqueous humor flow. They are ineffective during the initial period due to the ischemic paralysis of the iris. Miotics should be used after the immediate management and initial reduction of IOP.

Drug Category: Hyperosmotics

Hyperosmotic agents increase serum osmolarity and cause a fluid shift from the eye into the vascular space. The subsequent osmotic diuresis reduces IOP.

Drug Name	Isosorbide (Ismotic)
Description	In the eyes, creates an osmotic gradient between plasma and ocular fluids. Induces diuresis by elevating osmolarity of glomerular filtrate, thereby hindering tubular reabsorption of water. May be used to interrupt an acute attack of glaucoma. Use when less risk of nausea and vomiting, compared with other oral hyperosmotic agents, is needed.
Adult Dose	1.5 g/kg PO initially, followed by 1-3 g/kg PO bid/qid prn
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; anuria, severe dehydration, frank or impending acute pulmonary edema, and severe cardiac decompensation
Interactions	None reported
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Use repetitive doses with caution, particularly in patients with diseases associated with salt retention

Drug Name	Mannitol (Osmitrol)
Description	Reduces elevated IOP when pressure cannot be lowered by other means. Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.
Adult Dose	1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
Interactions	May decrease serum lithium levels
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• A low threshold for admission should be used with AACG patients. Patients who received osmotic agents may require electrolyte and volume status monitoring. Immediate ophthalmologic follow up must be scheduled and, at certain institutions, admission will help to facilitate this.

Further Outpatient Care

• Patients will remain on oral acetazolamide, pilocarpine, and beta-blockers or alpha-agonists until definitive treatment. After LPI, 33% will require topical medication to maintain lower IOP.

Deterrence/Prevention

• Fellow eye surgery

Complications

• Permanent decrease in visual acuity
• Repeat episode
• Malignant glaucoma
• Fellow eye attack
• Central retinal artery or vein occlusion

Prognosis

• Several studies evaluated patients after treatment for AACG and demonstrated favorable outcomes. With adequate treatment, most patients recover their lost vision. In Caucasians, IOP was controlled with LPI alone in 65-76%. Asians more often have medically refractory initial attacks and require medications after LPI. They also have higher rates of visual field loss and subsequent increases in IOP. It has been hypothesized that the initial attack is often more severe in Asians resulting in greater trabecular damage. Another possibility is the formation of peripheral synechiae (adhesions) causing a creeping angle reclosure.

Patient Education

• For excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see eMedicine's patient education articles Acute Angle-Closure Glaucoma, Glaucoma FAQs, Glaucoma Overview, and Understanding Glaucoma Medications.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• To reduce the risk of lawsuits, emergency physicians should make the diagnosis and obtain an ophthalmologic consult as soon as possible.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Choong YF, Irfan S, Menage MJ. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye. Oct 1999;13 (Pt 5):613-6. [Medline].
2. Ang LP, Aung T, Chua WH. Visual field loss from primary angle-closure glaucoma: a comparative study of symptomatic and asymptomatic disease. Ophthalmology. Sep 2004;111(9):1636-40. [Medline].
3. Aung T, Friedman DS, Chew PT. Long-term outcomes in asians after acute primary angle closure. Ophthalmology. Aug 2004;111(8):1464-9. [Medline].
4. Aung T, Oen FT, Wong HT. Randomised controlled trial comparing the effect of brimonidine and timolol on visual field loss after acute primary angle closure. Br J Ophthalmol. Jan 2004;88(1):88-94. [Medline].
5. Berkoff DJ, Sanchez LD. An uncommon presentation of acute angle closure glaucoma. J Emerg Med. Jul 2005;29(1):43-4. [Medline].
6. Blake DR, Nathan DM. Acute angle closure glaucoma following rapid correction of hyperglycemia. Diabetes Care. Nov 2003;26(11):3197-8. [Medline].
7. Bonomi L, Marchini G, Marraffa M. Epidemiology of angle-closure glaucoma: prevalence, clinical types, and association with peripheral anterior chamber depth in the Egna-Neumarket Glaucoma Study. Ophthalmology. May 2000;107(5):998-1003. [Medline].
8. Croos R, Thirumalai S, Hassan S. Citalopram associated with acute angle-closure glaucoma: case report. BMC Ophthalmol. Oct 4 2005;5:23. [Medline].
9. Fourman S. Diagnosing acute angle-closure glaucoma: a flowchart. Surv Ophthalmol. May-Jun 1989;33(6):491-4. [Medline].
10. Fricke TR, Mantzioros N, Vingrys AJ. Management of patients with narrow angles and acute angle-closure glaucoma. Clin Exp Optom. Nov-Dec 1998;81(6):255-266. [Medline].
11. Gohdo T, Tsumura T, Iijima H. Ultrasound biomicroscopic study of ciliary body thickness in eyes with narrow angles. Am J Ophthalmol. Mar 2000;129(3):342-6. [Medline].
12. Kramer P, Ritch R. The treatment of acute angle-closure glaucoma revisited. Ann Ophthalmol. Dec 1984;16(12):1101-3. [Medline].
13. Lam D, Tham C, Lai J, et al. Current approaches to management of acute primary angle closure. Curr Opinion Ophthalmol. 2001;18:146-151.
14. Lim LS, Aung T, Husain R. Acute primary angle closure: configuration of the drainage angle in the first year after laser peripheral iridotomy. Ophthalmology. Aug 2004;111(8):1470-4. [Medline].
15. Lowe RF. Aetiology of the anatomical basis for primary angle-closure glaucoma. Biometrical comparisons between normal eyes and eyes with primary angle-closure glaucoma. Br J Ophthalmol. Mar 1970;54(3):161-9. [Medline].
16. MacCumber M. Management of Ocular Injuries and Emergencies. 1998:237-240.
17. Markowitz SN, Morin JD. Angle-closure glaucoma: relation between lens thickness, anterior chamber depth and age. Can J Ophthalmol. Dec 1984;19(7):300-2. [Medline].
18. Rahim SA, Sahlas DJ, Shadowitz S. Blinded by pressure and pain. Lancet. Jun 25-Jul 1 2005;365(9478):2244. [Medline].
19. Ritch R. Assessing the treatment of angle closure. Ophthalmology. Oct 2003;110(10):1867-8. [Medline].
20. Salmon JF. The management of acute angle-closure glaucoma. Eye. Oct 1999;13 (Pt 5):609-10. [Medline].
21. Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology. Oct 2003;110(10):1869-78; quiz 1878-9, 1930. [Medline].
22. Yip LW, Aquino MC, Chew PT. Measurement of anterior lens growth after acute primary angle-closure glaucoma. Can J Ophthalmol. Apr 2007;42(2):321-2. [Medline].

Article Last Updated: Oct 3, 2007