Acute Angle Closure Glaucoma

Acute angle closure glaucoma results from a sudden increase in intraocular pressure due to blockage of the flow of the aqueous humor within the eye.

  • Processes: endocrine
  • Incidence: 71 / 100.000

Overview

Acute angle closure glaucoma is caused by blockage of the drainage system of the aqueous humor in the compartments of the eye. Most commonly, it results from close contact between the lens and the iris, closing the pupil and preventing the passage of the aqueous humor from the posterior to the anterior chamber. Furthermore, the angle of the eye is blocked and the aqueous humor is unable to pass into the Schlemm's canal and the vascular system, resulting in increased intraocular pressure and subsequent damage to the optic nerve and visual acuity. Several factors can considerably increase this risk. They include dim light, certain drugs like anticholinergics, anticonvulsants, antidepressants and sympathomimetics, anatomical predisposition and old age. Patients present with redness in the eye, acute onset of orbital and periorbital pain, nausea, vomiting and a feeling of illness. Diagnosis is clinical and can be established with history and physical exam. Laboratory blood tests and imaging studies are usually not required. Treatment needs to be initiated immediately and consists of timolol, pilocarpine, apraclonidine, acetazolamide and osmotic agents. Pilocarpine is also used for chronic treatment to prevent recurrence and further damage, although it is thought to worsen outcomes in certain cases. Laser therapy is recommended to provide long-term treatment and can be used as a preventive method in very high-risk individuals. Outcomes vary but they are favorable in case treatment is initiated immediately without delay [1].

Etiology

Acute angle closure glaucoma results due to the blocking of the drainage of the aqueous chamber in the eye, raising the intraocular pressure which damages the optic nerve. Many causes may end up pushing or pulling the iris to the point of contact between the iris and cornea and physically block important ducts in the anterior chamber. Factors associated with an increased risk include the following: a shorter axis of the eye, a thick iris, a lens that is located anteriorly, a narrow angle, dim light, hyperglycemia that is corrected too rapidly and the intake of certain drugs like anticonvulsants, antidepressants, anticholinergics, cocaine, sulfonamides, botulinum toxin and sympathomimetics [2] [3]. It may also be associated with trauma, giant cell arteritis, carotid-cavernous sinus fistula, and prone position during surgery [4].

Pupil dilation in certain individuals at high risk can precipitate acute angle closure glaucoma. This is because, with pupil dilation, the lens comes in contact with the back of the iris, stopping the flow of the aqueous humor from the anterior chamber through the pupil or from the posterior chamber through the iris. This series of events is eventually exacerbated by the collection of aqueous fluid behind the iris, blocking the trabecular meshwork and the drainage of aqueous fluid in the eyes. The ultimate result is a progressive and rapid elevation of the pressure, leading to the clinical features of acute angle closure glaucoma.

Epidemiology

Prevalence of acute angle closure glaucoma in the United States is 1 to 40 cases for every 1000 Americans. This value varies considerably with ethnicity. Prevalence is 1 in 1000 among Caucasians, 1 to 100 amongst Asians and can reach 2-4 in 100 in Eskimos. It is also more likely to occur among women because of a shallow anterior chamber. Older individuals in their sixth or seventh decades are prone to the highest risk.

Outcomes of acute angle closure glaucoma vary according to the disease responsible for triggering the increased pressure, the ethnicity of the patient and the time lapse between the initial event and the onset of treatment. In particular, individuals with an Asian background do not respond as well to the initial treatment and are at a higher risk for subsequent complications, such as damage to visual acuity and progressive increase in intraocular pressure. In general, however, the level of intraocular pressure increase will not affect visual acuity and around 66% of individuals will not experience any visual field loss [5][6][7].

Pathophysiology

Acute angle closure glaucoma occurs due to blockage of aqueous humor drainage in the eye. Normally, aqueous humor is produced by the ciliary body and passes from the posterior chamber to the anterior chamber through the pupil. It subsequently diffuses from the anterior chamber to blood vessels through the Schlemm's canal and the trabecular network situated in the angle of the eye [8] [9].

Acute angle-closure glaucoma occurs when there is blockage of the pupil due to close contact of the lens with the iris. Nonetheless, several mechanisms that diverge from the historically accepted theory have been proposed. Cronemberger et al. suggest that an increase in sympathetic tone, as well as over developed iris dilator muscles, can eventually lead to the thickening of the middle peripheral iris, leading to the closure of the angle [10]. The anterior insertion of the iris has also been proposed to block the Schlemm's canal and the trabecular network, and induce increased intraocular pressure. Other much rarer mechanisms include ciliary block and lens swelling. Lens swelling is associated with cataracts and results in the crowding of the anterior chamber. Ciliary block takes place due to forces present posterior to the lens that push the lens and the iris closer to each other. It is thought to occur in uveitis, scleral buckles, and panretinal photocoagulation.

Prognosis

Prognosis is generally favorable, although it varies according to several factors. Prompt treatment and diagnosis is critical, and laser treatment or surgery can prevent further relapses. Nonetheless, with strong attacks and delays in treatment, damage to the optic nerve and the associated blood vessels may occur, manifesting in the future with permanent visual damage. 

Presentation

Acute angle closure glaucoma can manifest with a number of symptoms. These include eye erythema, a sudden onset of severe pain within and around the eye that can later become a headache accompanied by nausea, vomiting, a general ill feeling, a hazy looking cornea, blurred vision, appearance of halos around lights and a feeling of hard and tender eyes [11]. Extraocular symptoms are the most common and patients most frequently complain of headaches. This can eventually lead to migraine treatment or a suspicion of subarachnoid hemorrhage. Case reports also describe patients wrongly diagnosed as having gastroenteritis when they presented with vomiting and abdominal pain [12].

On the other hand, intermittent acute angle closure glaucoma is characterized by mild symptoms that are non-continuous and painless, along with halos and blurring of vision. These attacks end when the patient sleeps or moves to a room with good lighting. Nonetheless, they tend to recur and may significantly damage vision in the long term.

History is important in elucidating the risk factors that have triggered the attack. Most individuals are elderly, have been already diagnosed with hyperopia and report no prior history of glaucoma.

Physical examination will address the visual fields, the external eye, and visual acuity. It will also include an examination of the fundus, an assessment of the pupils and of ocular motility, as well as measurements of the intraocular pressure. Visual exam reveals severe decrease in visual acuity, and patients are frequently incapable of identifying letters and numbers viewed from a distance and may only detect hand movements. Fundoscopic examination is usually not possible due to the presence of edema with a blurred cornea. Findings on slit-lamp examination include synechiae, a pupil that is irregular both in shape and function, corneal edema and segmental iris atrophy. The physical exam will also reveal pain with eye movements, a firm globe and a non-reactive pupil that is mildly dilated. Finally, intraocular pressure is usually above 10 to 20 mm Hg.

Workup

Workup of angle closure glaucoma depends on whether the condition is acute or chronic. Acute angle closure glaucoma may only necessitate history taking, a physical exam and a measurement of the intraocular pressure whereas the chronic form can sometimes require a gonioscopy. The latter will usually show visual field and optic nerve abnormalities, along with peripheral anterior synechiae. In many cases, however, gonioscopy is difficult to perform because of the friability of the epithelium and the clouding of the cornea. In this case, the physician may opt to perform it in the other eye. It will usually show a narrow angle. Acute angle closure glaucoma can be ruled out if the other eye has features of a wide angle.

Laboratory or imaging studies are rarely useful in the diagnosis and management of acute or chronic angle closure glaucoma.

Treatment

It is critical to start immediate management. Treatment is initiated with timolol, pilocarpine, apraclonidine, acetazolamide and an osmotic agent, for example, oral glycerol diluted with water, isosorbide or mannitol. Treatment response can be monitored with measurements of the intraocular pressure. In case the intraocular pressure is greater than 40 to 50 mm Hg, miotic drugs are usually not beneficial, as the pupillary sphincter becomes anoxic.

Pilocarpine can also be used in the treatment of chronic angle closure glaucoma [13]. It works through the constriction of the ciliary muscle, which can result in an increase in the thickness of the lens and subsequent anterior movement of the chamber. Nonetheless, some concerns exist for its usage. It can paradoxically reduce the depth of the anterior chamber, thereby exacerbating the clinical symptoms.

Long term treatment is instituted with laser therapy, in a procedure called laser peripheral iridotomy (LPI). Laser peripheral iridotomy works by creating a new channel in the eye, connecting the anterior to the posterior chambers, and thus breaking the blockage caused by the pupil. The procedure is done when inflammation has resolved and the clouding of the cornea has subsided. Laser peripheral iridotomy is performed on both eyes because of a very high risk of acute angle closure glaucoma in the other eye (around an 80% chance). It is usually conducted from hours to a couple of days after the lowering of the intraocular pressure. This depends on the time the cornea takes to become clear again.

Laser peripheral iridotomy is associated with certain complications, although they pale in comparison with its benefits. The most common side effect is glare, which results from a false placing of the iridotomy, preventing its coverage by the upper eyelid.

Prevention

Individuals at high risk should be advised to avoid medication or eye drops that can trigger a reaction. Furthermore, those at a particularly high risk, have the option of undergoing laser iridotomy even before experiencing an attack.

Patient Information

Acute angle closure glaucoma is a medical condition that affects the eyes and that results from the blockage of the channels in which fluid passes within the chambers of the eyes and to the blood. This blockage can eventually lead to an increase in the pressure within the compartments of the eye, with subsequent damage to the optic nerve and visual acuity. The condition is usually triggered by dilation of the pupil in an environment with dim lights or after the intake of certain medications. Older individuals and those with anatomical predisposition are particularly at risk. Patients present with eye redness, sudden pain in the eye that later becomes a headache associated with nausea, vomiting, a general ill feeling along with blurred vision and seeing halos around lights. The physician may need to take an extensive history and perform a detailed physical exam to establish the diagnosis. Laboratory tests and imaging studies are usually not required. Acute angle closure glaucoma is an emergency and the patient needs to be immediately started on medications that include timolol, pilocarpine, apraclonidine, acetazolamide and an osmotic agent. Pilocarpine is also used for chronic treatment to prevent relapse and gradual increase of pressure. Laser therapy is used to create a channel in the eye to facilitate fluid movement, decrease pressure and ensure good resolution and treatment of the condition. Acute angle closure glaucoma has, in general, a good prognosis, if the illness is caught early and treated immediately.

References

  1. Berkoff DJ, Sanchez LD. An uncommon presentation of acute angle closure glaucoma. J Emerg Med. 2005 Jul.; 29(1):43-4.
  2. Croos R, Thirumalai S, Hassan S, Davis Jda R. Citalopram associated with acute angle-closure glaucoma: case report. BMC Ophthalmol. 2005 Oct 4.; 5:23.
  3. Natesh S, Rajashekhara SK, Rao AS, Shetty B. Topiramate-induced angle closure with acute myopia, macular striae. Oman J Ophthalmol. 2010 Jan.; 3(1):26-8.
  4. Tse DM, Titchener AG, Sarkies N, Robinson S. Acute angle closure glaucoma following head and orbital trauma. Emerg Med J. 2009 Dec.; 26(12):913.
  5. Ang LP, Ang LP. Current understanding of the treatment and outcome of acute primary angle-closure glaucoma: an Asian perspective. Ann Acad Med Singapore. 2008 Mar.; 37(3):210-5.
  6. He M, Foster PJ, Ge J, Huang W, Zheng Y, Friedman DS. Prevalence and clinical characteristics of glaucoma in adult Chinese: a population-based study in Liwan District, Guangzhou. Invest Ophthalmol Vis Sci. 2006 Jul.; 47(7):2782-8.
  7. Vijaya L, George R, Arvind H, Baskaran M, Paul PG, Ramesh SV. Prevalence of angle-closure disease in a rural southern Indian population. Arch Ophthalmol. 2006 Mar.; 124(3):403-9.
  8. Yip LW, Aquino MC, Chew PT. Measurement of anterior lens growth after acute primary angle-closure glaucoma. Can J Ophthalmol. 2007 Apr; 42(2):321-2.
  9. Wang BS, Narayanaswamy A, Amerasinghe N, et al. Increased iris thickness and association with primary angle closure glaucoma. Br J Ophthalmol. 2011 Jan;95(1):46-50.
  10. Cronemberger S, Calixto N, de Andrade AO, Mérula RV. New considerations on pupillary block mechanism.Arq Bras Oftalmol. 2010 Feb.; 73(1):9-15.
  11. Rahim SA, Sahlas DJ, Shadowitz S. Blinded by pressure and pain. Lancet. 2005 Jun 25-Jul 1.; 365(9478):2244.
  12. Cholongitas E, Pipili C, Dasenaki M. Acute angle closure glaucoma presented with nausea and epigastric pain. Dig Dis Sci. 2008 May.; 53(5):1430-1.
  13. Day AC, Nolan W, Malik A, Viswanathan AC, Foster PJ. Pilocarpine induced acute angle closure. BMJ Case Rep. 2012 May; 8;2012.

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