Bilateral Acute Angle-Closure Glaucoma

Resident & Staff Physician®March 2008 Vol 54 No 3
Volume 0
Issue 0

Bilateral disease is rare but may be caused by several drug classes. Physicians need to consider these medications and other etiologies in their differential diagnosis to ensure prompt and appropriate treatment.

Thomas Matz, MD

Assistant Professor

Department of Emergency Medicine

University Medical Center of Southern Nevada

Las Vegas, NV

Lincoln Abbott, MD, FACEP

Assistant Professor

University of Connecticut

Director of Informatics for Emergency Medicine

Department of Traumatology and Emergency Medicine

Hartford Hospital

Hartford, CT

Glaucoma is a medical illness associated with considerable morbidity and requires immediate attention. Delayed or inappropriate treatment can lead to optic-nerve damage and vision loss. Although acute angle-closure glaucoma usually presents unilaterally, bilateral cases have been reported. A previously unreported case of bilateral disease is presented in this article. This condition, whether unilateral or bilateral, is an ocular emergency that must be appropriately treated to prevent progression to permanent vision loss. Physicians need to familiarize themselves with this entity to ensure immediate diagnosis and proper treatment. Several drug classes have been implicated in this condition and must be considered in the differential diagnosis. Many systemic diseases also have been implicated in bilateral cases. If acute angle-closure glaucoma is recognized early, initial treatment can be provided in the primary care setting, although progressed cases should be referred to an ophthalmologist.

Figure 1—Gross view of AACG.

Glaucoma is a medical illness associated with increased intraocular pressure. Left untreated, it can lead to optic-nerve damage and vision loss. It is usually classified as open-angle or closed-angle, based on the precipitating pathophysiology. Angle-closure glaucoma is characterized by narrowing of the angle formed by the lateral edge of the iris and the cornea, typically not found in "open-angle" glaucoma. Acute angle-closure glaucoma (AACG) is an ocular emergency (Figure 1) that can be reversed if treated immediately and appropriately.1 Although the majority of patients with AACG present with unilateral disease, several cases of bilateral disease have been reported. Another case of bilateral AACG is presented in this article.


Nearly 90% of unilateral AACG cases result from a mechanism called pupillary block.2 Pupillary block commonly arises following a limitation of the aqueous flow from the posterior chamber to the anterior chamber of the eye. The resultant accumulation of fluid in the posterior chamber forces the iris anteriorly in a bowing fashion, obliterating the angle between the cornea and the iris, thereby obstructing the trabecular meshwork.2 As intraocular pressures increase, the pressure gradient across the iris grows and the problem worsens.

Unlike unilateral AACG caused by pupillary block, bilateral AACG typically results from ciliochoroidal effusion syndrome, first described in 2002.3 Certain medications can cause an excessive amount of aqueous fluid production (Table) as well as edema of the ciliary body, which leads to anterior rotation of the ciliary body and the ciliary processes. Subsequently, anterior displacement of the iris occurs, leading to obstruction of the trabecular meshwork, as in pupillary block.


Although AACG is an uncommon disease, risk factors have been identified. Women are more likely to develop AACG than men. Persons older than 50 years are at slightly increased risk, as are individuals with hyperopia. Those with a personal or family history of angle-closure glaucoma are at increased risk for the disease. Finally, people of Eskimo or Asian descent have higher rates of AACG.2


AACG classically presents as a unilateral illness characterized by deep, penetrating eye pain, fogging of vision, and associated halos surrounding light sources. Symptoms include unilateral headache, nausea, vomiting, and loss of visual acuity (the degree of visual loss varies).

The eye examination may reveal a mid-dilated, sluggishly reactive pupil, with loss of corneal clarity and a hazy appearance (Figure 1).4 The globe may feel firm on palpation through closed eyelids and should be compared with the unaffected eye. Slit-lamp examination may reveal perilimbal injection, as well as "cell and flare" in the anterior chamber. Often, narrowing of the angles of the anterior chamber can be discerned. Tonometry will typically reveal a globe pressure of more than 40 mm Hg in patients who are symptomatic.

Bilateral AACG is a much rarer entity than unilateral disease. Bilateral AACG is more likely to present with global (rather than the typical unilateral) headache, and nearly all patients present once vision loss ensues. Findings on physical examination in patients with bilateral AACG frequently follow the same progression as with unilateral disease. Early on, a sluggishly reactive pupil can be found, with little else noted on gross examination. As the disease progresses, the cornea may develop a hazy appearance in conjunction with scleral injection. Slit-lamp examination and tonometry findings typically follow the same pattern as in unilateral AACG, but with both eyes affected.


Systemic disease

Familiarity with the systemic illnesses and medications known to cause bilateral AACG will facilitate early diagnosis and treatment, preventing potentially serious and even irreversible sequelae, such as vision loss. Illnesses such as human immunodeficiency virus,5 herpes zoster,6 immunoglobulin A nephropathy,7 certain congenital anomalies,2 acquired syphilis,2 systemic lupus erythematosus,8 and even snakebites9 have been implicated in bilateral AACG cases.

Drug-induced bilateral AACG

The antiepileptic drug topiramate (Topamax) has been reported in association with bilateral AACG in several cases.10-15 Many other types of medications and modes of drug delivery also have been linked to bilateral AACG, including sulfa derivatives, antiepileptics, anticoagulants, antidepressants, drugs used for general anesthesia, and some weight loss agents (Table).10-27 Adrenergic agents given in nebulized form or systemically have been noted as sources of bilateral AACG. Finally, anticholinergic agents have also been linked to bilateral AACG.28 Of the five cases of bilateral AACG reported in non-English language journals to have occurred following general anesthesia, two abstracts have been translated into English.26,27 Because patients undergoing general anesthesia receive so many medications, it is unclear whether a specific drug is at fault.



Medications implicated in AACG

Sulfa derivatives

  • Sulfonamide
  • Acetazolamide
  • Hydrochlorothiazide


  • Venlafaxine
  • Paroxetine
  • Fluvoxamine
  • Maprotiline
  • Imipramine
  • Amitriptyline

Nebulized agents

  • Ipratropium
  • Beta agonists


  • Topiramate


  • Warfarin

General anesthesia

Weight loss

  • Dexfenfluramine (removed from the market in 1997)


  • Tropicamide
  • Atropine
  • Tricyclic and tetracyclic antidepressants
  • Pilocarpine
  • Botulinum toxin

A 38-year-old woman presented to the emergency department reporting 3 hours of rapidly progressing visual loss in both eyes and a simultaneous onset of periorbital headache. She reported no recent fever, chills, nausea, vomiting, neck pain, trauma, hearing loss, or problems with balance. The patient denied ingesting any toxic agents and noted no recent changes in medications. Her medical history was notable for hepatitis C, depression, migraine headaches, and substance abuse. Her medications included sertraline (Zoloft), fluoxetine (Prozac), ibuprofen, trazodone (eg, Desyrel, Molipan, Trittico), buspirone (BuSpar), and quetiapine (Seroquel). When questioned, she specifically denied using topiramate.

Physical examination demonstrated visual acuity worse than 20/200, from a baseline of nearly 20/20 vision in each eye. Gross inspection of the eyes was unremarkable, with no scleral injection or injury found. Extraocular muscle testing revealed normal function. The pupils were 3 mm each and reactive to light, with no afferent pupillary defect. Fundoscopic examination revealed normal anatomy with no evidence of papilledema or hemorrhage. On slit-lamp examination, the cornea appeared normal and the anterior chamber was shallow and showed no sign of cell or flare. Intraocular pressures, which were measured using Schiotz tonometry, were 35 mm Hg OS and 40 mm Hg OD. The remainder of the physical examination was normal.

A diagnosis of bilateral AACG was made, and the patient was given timolol eye drops and intravenous (IV) acetazolamide (Diamox). She was discharged with a prescription for pilocarpine (eg, Pilocar, Akarpine) eye drops and was told to stop all the medications she had been taking until after visiting the ophthalmologist in the office early the next morning.

During the patient's first follow-up appointment, her headache had improved slightly, but her visual acuity allowed counting fingers at 5 feet bilaterally, with intraocular pressures of 32 mm Hg OD and 26 mm Hg OS. Her angles were still narrowed. For this visit, the patient brought all the medications she had taken in the past month; it was revealed that she had taken a short course of topiramate approximately 1 week before her initial presentation. Discontinuing topiramate therapy was emphasized, and the patient was started on dorzolamide/timolol maleate (Cosopt) and bimatoprost (Lumigan), while pilocarpine was also discontinued.

A follow-up visit 48 hours later found the patient's headache resolved and her visual acuity at 20/40 bilaterally, with intraocular pressures of 8 mm Hg OD and 10 mm Hg OS. Bimatoprost was discontinued, but she continued to take dorzolamide/timolol maleate for 1 week and experienced complete resolution of symptoms and a return to normal visual acuity after 2 weeks.


The treatment algorithm in Figure 2 is applicable to all causes of AACG and can be followed by non-ophthalmologists. Regardless of whether treating unilateral AACG from pupillary block or bilateral AACG secondary to ciliochoroidal effusion, initial treatment is the same. Ophthalmic preparations of beta blockers, carbonic anhydrase inhibitors, and sympathomimetics are given to decrease aqueous production, which decreases the pressure gradient from the posterior chamber to the anterior chamber and thus relieves the closure of the angle between the iris and cornea. Ophthalmic steroid drops decrease the amount of inflammation and improve the flow between the chambers of the eye, while topical miotics improve aqueous drainage through the trabecular meshwork.

Figure 2 gives examples of each class of medication and provides appropriate dosing strategies for initial management in the office or emergency department and suggested treatment strategies upon hospital discharge. Patients who do not respond to treatment with the above regimen should receive IV mannitol, acetazolamide, or both. Admission to the hospital should be considered for patients with severe cases. Whether patients are admitted or discharged, ophthalmology consultation and follow-up are recommended for all patients with acute glaucoma.

Figure 2—Management of acute angle-closure glaucoma in primary care.

In cases of refractory disease unresponsive to medications, the definitive treatment is iridectomy, performed by an ophthalmologist. By removing a portion of the iris, a new communication is opened between the anterior and posterior chambers. This should reestablish the aqueous flow, and the pressure gradient between the anterior and posterior chambers should resolve. Without excess pressure in the posterior chambers, the iris returns to its more planar configuration, the angle of the iris and cornea opens, and normal drainage through the trabecular meshwork resumes.2 Iridectomy is most effective in cases of AACG caused by pupillary block, the most common etiology in unilateral cases. Unfortunately, it is not so effective for cases caused by ciliochoroidal effusion, which is more common in bilateral disease.


AACG is uncommon, and bilateral presentation is even more unusual. Any case of AACG constitutes an ocular emergency and requires immediate diagnosis and treatment. Familiarity with the etiologies and various cases of AACG will help ensure immediate and appropriate treatment. As more medications enter the market, it is likely that physicians will encounter more cases of AACG.


  • Acute angle-closure glaucoma is an ocular emergency. This condition usually presents unilaterally, but it can occur bilaterally; correct diagnosis is crucial.
  • Characteristic symptoms include deep eye pain, fogging of vision, and a global headache, but patients tend to present only after vision loss ensues.
  • Eye examination may reveal a mid-dilated, sluggishly reactive pupil, with loss of corneal clarity and a hazy appearance.
  • Physicians should familiarize themselves with the type of medications that can induce this condition; several cases of bilateral disease have been linked to topiramate (Topamax).


  1. All of the following statements about AACG are correct, except:Pupillary block is the most common mechanism in unilateral AACG.Bilateral AACG usually results from ciliochoroidal effusion syndrome.Beta blockers should not be used in patients withAACG.Both unilateral and bilateral AACG can lead tovision loss.
  2. All of the following factors are associated with increased risk of AACG, except:Age older than 50 yearsMale genderHyperopiaEskimo or Asian ethnicity
  3. Which of the following conditions has been implicated in AACG?HypertensionDiabetesDog biteHerpes zoster
  4. All of the following drug classes have been associated with the onset of AACG, except:Antiepileptic agentsAnticoagulantsAntihistaminesAntidepressants
  5. Which of the following agents has been implicated in AACG?IbuprofenTopiramateWarfarinFluvoxamine

(Answers at end of references list)


  1. Bekoff DJ, Sanchez LD. An uncommon presentation of acute angle-closure glaucoma. J Emerg Med. 2005;29:43-44.
  2. Tello C, Rothman R, Ishikawa H, et al. Differential diagnosis of the angle-closure glaucomas. Ophthalmol Clin North Am. 2000;13:443-453.
  3. Ikeda N, Ikeda T, Nagata M, et al. Ciliochoroidal effusion syndrome induced by sulfa-derivatives. Arch Ophthalmol. 2002; 120:1775.
  4. Morgan A, Hemphill RR. Acute visual change. Emerg Med Clin North Am. 1998;16:825-843, vii.
  5. Zambarakji HJ, Simcock PR. Bilateral angle-closure glaucoma in HIV infection. J R Soc Med. 1996;89:581-582.
  6. al Halel A, Hirsh A, Melamed S, et al. Bilateral simultaneous spontaneous acute angle-closure glaucoma in a herpes zoster patient. Br J Ophthalmol. 1991;75:510.
  7. Pavlin CJ, Easterbrook M, Harasiewicz K, et al. An ultrasound biomicroscopic analysis of angle-closure glaucoma secondary to ciliochoroidal effusion in IgA nephropathy. Am J Ophthalmol. 1993;116:341-345.
  8. Wisotsky BJ, Magat-Gordon CB, Puklin JE. Angle-closure glaucoma as an initial presentation of systemic lupus erythematosus. Ophthalmology. 1998;105:1170-1172.
  9. Srinivasan R, Kaliaperumal S, Dutta TK. Bilateral angle closure glaucoma following snake bite. J Assoc Physicians India. 2005;53:46-48.
  10. Medeiros FA, Zhang XY, Bernd AS, et al. Angle-closure glaucoma associated with ciliary body detachment in patients using topiramate. Arch Ophthalmol. 2003;121:282-285.
  11. Thambi L, Kapcala LP, Chambers W, et al. Topiramate-associated secondary angle-closure glaucoma: a case series. Arch Ophthalmol. 2002;120:1108.
  12. Rhee DJ, Goldberg MJ, Parrish RK. Bilateral angle-closure glaucoma and ciliary body swelling from topiramate. Arch Ophthalmol. 2001;119:1721-1723.
  13. Sankar PS, Pasquale LR, Grosskreutz CL. Uveal effusion and secondary angle-closure glaucoma associated with topiramate use. Arch Ophthalmol. 2001;119:1210-1211.
  14. Banta JT, Hoffman K, Budenz DL, et al. Presumed topiramate-induced bilateral acute angle-closure glaucoma. Am J Ophthalmol. 2001;132:112-114.
  15. Craig JE, Ong TJ, Louis DL, et al. Mechanism of topiramate-induced acute-onset myopia and angle-closure glaucoma. Am J Ophthalmol. 2004;137:193-195.
  16. Kadoi C, Hayasaka S, Tsukamoto E, et al. Bilateral angle-closure glaucoma and visual loss precipitated by antidepressant and antianxiety agents in a patient with depression. Ophthalmologica. 2000;214:360-361.
  17. Ritch R, Krupin T, Henry C, et al. Oral imipramine and acute angle-closure glaucoma. Arch Ophthalmol. 1994;112:67-68.
  18. Jimenez-Jimenez FJ, Orti-Pareja M, Zurdo JM. Aggravation of glaucoma with fluvoxamine. Ann Pharmacother. 2001;35:1565-1566.
  19. Ng B, Sanbrook GM, Malouf AJ, et al. Venlafaxine and bilateral acute angle-closure glaucoma. Med J Aust. 2002;176:241.
  20. Kirwan JF, Subak-Sharpe I, Teimory M. Bilateral acute angle-closure glaucoma after administration of paroxetine. Br J Ophthalmol. 1997;81:252.
  21. Hall SK. Acute angle-closure glaucoma as a complication of combined beta-agonist and ipratropium bromide therapy in the emergency department. Ann Emerg Med. 1994;23:884-887.
  22. Geanon JD, Perkins TW. Bilateral acute angle-closure glaucoma associated with drug sensitivity to hydrochlorothiazide. Arch Ophthalmol. 1995;113:1231-1232.
  23. Denis P, Charpentier D, Berros P, et al. Bilateral acute angle-closure glaucoma after dexfenfluramine treatment. Ophthalmologica. 1995;209:223-224.
  24. Grinbaum A, Ashkenazi I, Gutman I, et al. Suggested mechanism for acute transient myopia after sulfonamide treatment. Ann Ophthalmol. 1993;25:224-226.
  25. Postel EA, Assalian A, Epstein DL. Drug-induced transient myopia and angle-closure glaucoma associated with supraciliary choroidal effusion. Am J Ophthalmol. 1996;122:110-112.
  26. Ates H, Kayikcioglu O, Andac K. Bilateral angle-closure glaucoma following general anesthesia. Int Ophthalmol. 1999;23:129-130.
  27. Ujino H, Morimoto O, Yukioka H, et al. Acute angle-closure glaucoma after total hip replacement surgery [in Japanese]. Masui. 1997;46:823-826.
  28. Lachkar Y, Bouassida W. Drug-induced acute angle-closure glaucoma. Curr Opin Ophthalmol. 2007;18:129-133.

Answers: 1. C; 2. B; 3. D; 4.C; 5. B.

Related Videos
© 2024 MJH Life Sciences

All rights reserved.