What are the main causes of acute angle-closure glaucoma. How does acute angle-closure glaucoma present clinically. What is the initial management approach for acute angle-closure glaucoma. Who is at highest risk for developing acute angle-closure glaucoma.

Understanding Acute Angle-Closure Glaucoma: A Sight-Threatening Emergency

Acute angle-closure glaucoma (AACG) is a serious ocular emergency characterized by a rapid increase in intraocular pressure (IOP) due to obstruction of aqueous humor outflow. This condition requires immediate medical attention to prevent permanent vision loss. To fully grasp the severity and implications of AACG, it’s crucial to understand its underlying mechanisms, risk factors, and clinical presentation.

The Pathophysiology Behind Acute Angle-Closure Glaucoma

The primary factor contributing to AACG is the anatomical structure of the anterior chamber. A shallower angle between the iris and cornea predisposes individuals to this condition. But how exactly does this lead to an acute attack?

• Pupillary block: The shallow anterior chamber causes increased contact between the iris and lens, impeding aqueous humor flow from the posterior to anterior chamber.
• Pressure differential: This blockage creates a pressure difference between the two chambers, known as pupillary block.
• Iris bowing: The pressure differential causes the iris to bow forward, further narrowing the anterior chamber angle.
• Outflow obstruction: As the angle narrows, it obstructs the trabecular meshwork and Schlemm’s canal, the primary outflow pathways for aqueous humor.
• IOP spike: With outflow obstructed but production continuing, intraocular pressure rises rapidly.

This cascade of events creates a vicious cycle, perpetuating the increase in IOP and leading to the acute presentation of angle-closure glaucoma.

Risk Factors and Epidemiology of Acute Angle-Closure Glaucoma

Certain demographic and anatomical factors increase the risk of developing AACG. Understanding these risk factors can help identify individuals who may benefit from preventive measures or closer monitoring.

Age-Related Risk

Why does age play a role in AACG risk? The average age at presentation is 60 years, with prevalence increasing thereafter. This age-related risk is primarily attributed to the natural enlargement of the lens over time, which can exacerbate a predisposition to a narrow angle.

Gender Disparity

Is AACG equally common in men and women? Interestingly, there is a significant gender disparity in AACG incidence. Women are four times more likely than men to experience an acute attack. This difference may be related to anatomical variations in anterior chamber depth and angle width between genders.

Racial Predisposition

Are certain ethnic groups more susceptible to AACG? Yes, there are notable racial differences in AACG prevalence:

• Higher risk: Southeast Asians, Chinese, and Inuit populations have a higher incidence of AACG.
• Lower risk: Black populations have a lower incidence of AACG.
• Intermediate risk: In white populations, AACG accounts for approximately 6% of all glaucoma diagnoses.

Genetic Factors

Can AACG run in families? Yes, there is a hereditary component to AACG risk. The ocular anatomic features that predispose individuals to narrow angles and AACG are inherited. This underscores the importance of family history in assessing an individual’s risk.

Clinical Presentation: Recognizing the Signs and Symptoms of AACG

The sudden onset of AACG often presents with a constellation of alarming symptoms. Recognizing these signs promptly is crucial for timely intervention and preservation of vision.

Characteristic Symptoms

What are the hallmark symptoms of an AACG attack? Patients typically experience:

• Severe unilateral eye pain or headache
• Sudden onset of blurred vision
• Perception of rainbow-colored halos around bright lights
• Nausea and vomiting (due to the shared innervation of the eye and gastrointestinal system)

Physical Examination Findings

What would an ophthalmologist observe during an examination of a patient with AACG? Key findings include:

• Fixed, mid-dilated pupil unresponsive to light
• Hazy or cloudy cornea due to edema
• Marked conjunctival injection (redness)
• Shallow anterior chamber upon slit-lamp examination
• Dramatically elevated intraocular pressure (often >50 mmHg)

Precipitating Factors: What Triggers an Acute Attack?

Understanding the factors that can precipitate an AACG attack is crucial for both prevention and management. These triggers often involve situations that cause pupillary dilation, exacerbating the underlying anatomical predisposition.

Common Precipitating Factors

• Dim lighting conditions
• Emotional stress
• Certain medications (e.g., anticholinergics, sympathomimetics)
• Mydriatic eye drops used for dilated eye examinations
• Prone positioning for extended periods

By identifying and avoiding these triggers, individuals at risk for AACG may be able to prevent an acute attack.

Emergency Management: The Critical First Steps

When a patient presents with suspected AACG, rapid intervention is essential to prevent irreversible optic nerve damage and vision loss. The primary goal of initial management is to lower the intraocular pressure as quickly as possible.

Immediate Medical Interventions

What are the first-line treatments for AACG? The initial management typically involves a combination of the following:

1. Topical beta-blockers (e.g., timolol) to decrease aqueous production
2. Alpha-2 agonists (e.g., brimonidine) to reduce aqueous production and increase uveoscleral outflow
3. Topical and oral carbonic anhydrase inhibitors (e.g., dorzolamide eye drops and acetazolamide tablets) to reduce aqueous production
4. Pilocarpine eye drops to constrict the pupil and pull the iris away from the angle
5. Hyperosmotic agents (e.g., intravenous mannitol) to reduce vitreous volume and posterior chamber pressure

Monitoring and Follow-up

How is the patient’s response to treatment assessed? Close monitoring of intraocular pressure is crucial. Pressure should be checked every 15-30 minutes initially. If pressure does not decrease within 1-2 hours of medical therapy, more aggressive interventions may be necessary.

Definitive Treatment: Beyond the Acute Phase

Once the acute attack is controlled, definitive treatment is necessary to prevent recurrence and manage the underlying anatomical predisposition.

Laser Iridotomy

What is the gold standard for preventing recurrent AACG attacks? Laser peripheral iridotomy (LPI) is the definitive treatment for AACG. This procedure creates a small hole in the peripheral iris, allowing aqueous to flow directly from the posterior to the anterior chamber, bypassing the pupillary block.

Surgical Options

Are there alternatives to laser iridotomy? In cases where LPI is not successful or not possible, other surgical interventions may be considered:

• Lens extraction (if the patient has a cataract)
• Trabeculectomy
• Drainage implant surgery

These procedures aim to either eliminate the anatomical predisposition or create alternative outflow pathways for aqueous humor.

Long-term Management and Prognosis

The management of AACG doesn’t end with the resolution of the acute attack. Long-term follow-up and care are essential to preserve vision and prevent complications.

Follow-up Care

What does long-term management involve? Patients who have experienced an AACG attack require:

• Regular intraocular pressure checks
• Gonioscopy to assess the anterior chamber angle
• Visual field testing to monitor for glaucomatous damage
• Optical coherence tomography (OCT) to evaluate the optic nerve and retinal nerve fiber layer

Prognosis and Visual Outcomes

What factors influence the long-term prognosis after an AACG attack? The visual outcome depends on several factors:

• Duration of the acute attack before treatment
• Peak intraocular pressure reached
• Presence of pre-existing glaucomatous damage
• Effectiveness of the definitive treatment (e.g., success of laser iridotomy)

Prompt recognition and treatment of AACG generally lead to good visual outcomes, highlighting the importance of public awareness and healthcare provider education about this ocular emergency.

Prevention Strategies: Identifying and Managing At-Risk Individuals

Given the potentially devastating consequences of AACG, prevention plays a crucial role in management. Identifying at-risk individuals and implementing preventive measures can significantly reduce the incidence of acute attacks.

Screening for Narrow Angles

How can potential AACG be identified before an acute attack? Regular comprehensive eye exams, especially for individuals over 40, can help identify those with narrow angles. Gonioscopy, anterior segment OCT, and ultrasound biomicroscopy are valuable tools for assessing angle anatomy.

Prophylactic Iridotomy

When should preventive laser iridotomy be considered? For individuals with very narrow or occludable angles, especially those with a history of angle-closure in the fellow eye, prophylactic laser iridotomy may be recommended. This procedure can prevent an acute attack by eliminating pupillary block.

Patient Education

What role does patient education play in AACG prevention? Educating at-risk individuals about the symptoms of AACG and potential triggering factors is crucial. Patients should be advised to:

• Seek immediate medical attention if they experience symptoms suggestive of an acute attack
• Avoid medications that can cause pupillary dilation without medical supervision
• Inform all healthcare providers about their predisposition to angle-closure

By implementing these preventive strategies, the incidence of AACG can be significantly reduced, potentially saving sight for many at-risk individuals.

The Role of Interprofessional Care in AACG Management

Effective management of AACG requires a collaborative approach involving various healthcare professionals. This interprofessional team approach ensures comprehensive care from the acute phase through long-term management.

Key Team Members

Who are the essential members of the AACG management team?

• Ophthalmologists: Provide specialized eye care, perform definitive treatments like laser iridotomy
• Emergency physicians: Often the first to encounter and diagnose AACG
• Optometrists: Play a crucial role in screening and identifying at-risk individuals
• Nurses: Assist in acute management, patient education, and monitoring
• Pharmacists: Ensure appropriate medication selection and dosing, educate about potential drug interactions

Collaborative Care Model

How does the interprofessional team work together in AACG management?

1. Rapid assessment and diagnosis: Emergency physicians and ophthalmologists collaborate for prompt recognition and treatment initiation.
2. Acute management: Nurses assist in medication administration and monitoring, while pharmacists ensure appropriate drug therapy.
3. Definitive treatment: Ophthalmologists perform laser or surgical interventions as needed.
4. Long-term follow-up: Optometrists and ophthalmologists share responsibility for ongoing monitoring and management.
5. Patient education: All team members contribute to patient and family education about the condition, its management, and prevention strategies.

This collaborative approach ensures that patients receive comprehensive, coordinated care throughout their AACG journey, from acute presentation to long-term management.

Future Directions in AACG Research and Management

As our understanding of AACG continues to evolve, new avenues for research and management are emerging. These advancements hold promise for improving prevention, diagnosis, and treatment of this sight-threatening condition.

Emerging Diagnostic Technologies

What new tools are being developed to improve AACG diagnosis and risk assessment?

• Advanced imaging techniques: High-resolution OCT and artificial intelligence-assisted image analysis for more accurate angle assessment
• Genetic testing: Identification of genetic markers associated with increased AACG risk
• Portable IOP monitoring devices: For more frequent and convenient pressure checks in at-risk individuals

Novel Treatment Approaches

What innovative therapies are on the horizon for AACG management?

• Targeted drug delivery systems: To improve efficacy and reduce side effects of IOP-lowering medications
• Minimally invasive glaucoma surgeries (MIGS): Less invasive alternatives to traditional glaucoma surgeries
• Neuroprotective agents: To preserve optic nerve function even in the face of elevated IOP

As research in these areas progresses, we can anticipate more personalized and effective approaches to AACG prevention and management, potentially reducing the global burden of this vision-threatening condition.

Acute Closed Angle Glaucoma – StatPearls

Babak Khazaeni; Leila Khazaeni.

Author Information and Affiliations

Last Update: January 2, 2023.

Continuing Education Activity

Acute angle-closure glaucoma is an ocular emergency that results from a rapid increase in intraocular pressure due to outflow obstruction of aqueous humor. Several factors lead to the obstruction in acute angle-closure glaucoma, but the major predisposing factor is the structural anatomy of the anterior chamber, leading to a shallower angle between the iris and the cornea. Acute angle-closure glaucoma presents as a sudden onset of severe unilateral eye pain or a headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with marked conjunctival injection. This activity reviews the evaluation and management of patients with acute angle-closure glaucoma and highlights the role of the interprofessional team in managing patients with this condition.

Objectives:

• Describe the pathophysiology of acute angle-closure glaucoma.

• Summarize how a patient with acute angle-closure glaucoma is likely to present.

• Identify the critical immediate steps to take when managing a patient with acute angle-closure glaucoma.

• Outline the role of a collaborative interprofessional team in providing well-coordinated care to patients presenting with acute angle-closure glaucoma.

Access free multiple choice questions on this topic.

Introduction

Glaucoma is a set of ocular disorders often defined by increased intraocular pressures leading to optic neuropathy and vision loss if untreated.[1] Glaucoma has traditionally been classified as open-angle or closed-angle and as primary or secondary. The angle refers to the angle between the iris and the cornea in the anterior chamber, which can become structurally obstructed. By definition, primary glaucomas are not associated with known ocular or systemic disorders and usually affect both eyes. Secondary glaucomas are associated with ocular or systemic disorders and are often unilateral. Acute angle-closure glaucoma is a subset of primary angle-closure glaucoma.

The commonly accepted range for intraocular pressure is 10 to 22 mmHg. Three factors that affect the intraocular pressure are the rate of production of aqueous humor by the ciliary body, the resistance to aqueous outflow through the trabecular meshwork and Schlemm’s canal, and the episcleral venous pressure. The normal flow of aqueous humor starts in the ciliary body, goes through the pupil, and out through the trabecular meshwork and Schlemm’s canal in the angle of the anterior chamber. In acute angle-closure glaucoma, intraocular pressure increases rapidly due to outflow obstruction of the aqueous humor. Several factors lead to the obstruction in acute angle-closure glaucoma, but the major predisposing factor is the structural anatomy of the anterior chamber leading to a shallower angle.[2][3]

Etiology

Blockage to the flow of aqueous humor occurs due to a number of predisposing anatomic variations. These variations include a shallower anterior chamber, lens size, anterior location of the iris-lens diaphragm, and a narrow entrance to the anterior chamber angle. The shallower anterior chamber angle leads to a large area of the iris and lens being in contact with each other, slowing the flow of aqueous humor from the posterior chamber to the anterior chamber. This, in turn, leads to a pressure difference between the chambers called a pupillary block.[4] 

The pupillary block causes bowing of the iris, which narrows the angle of the anterior chamber further. This cycle will perpetuate increasing intraocular pressures leading to the clinical presentation of acute angle-closure glaucoma.

Epidemiology

There are several risk factors for acute angle-closure glaucoma, including age, gender, race, and family history.[5]

• Age: The average age at presentation is 60, and prevalence increases thereafter. This is felt to be due to the increasing size of the lens with age.

• Gender: There is a 4 to 1 ratio of the incidence of angle-closure glaucoma in women versus men.

• Race: Angle-closure glaucoma is more common in Southeast Asians, Chinese, and Eskimos. It is uncommon in black populations. In whites, acute angle-closure glaucoma accounts for 6% of all glaucoma diagnoses.[6]

• Family history: Ocular anatomic features are inherited. 

Pathophysiology

An acute attack of angle-closure glaucoma is precipitated by pupillary dilatation, leading to increasing iris and lens contact increasing the pupillary block.[7] The increasing pupillary block leads to bulging of the iris, acutely closing the angle between the iris and cornea, thus obstructing the aqueous humor outflow tract. The intraocular pressure rises acutely, leading to symptomology.

History and Physical

Acute angle-closure glaucoma presents as a sudden onset of severe unilateral eye pain or a headache associated with blurred vision, rainbow-colored halos around bright lights, nausea, and vomiting. The physical exam will reveal a fixed midpoint pupil and a hazy or cloudy cornea with marked conjunctival injection (most prominent at the limbus). Intraocular pressure will be elevated and can be as high as 60 to 80 mm Hg in an acute attack. A mild amount of aqueous flare and cells may be seen. The optic nerve may also be swollen during an acute attack.[8][9]

Evaluation

Measuring elevated intraocular pressure is diagnostic. There is no need for any imaging studies. A basic metabolic panel should be checked if osmotic agents are used in the treatment regime. A gonioscopic examination by an ophthalmologist to verify angle-closure makes the definitive diagnosis. Gonioscopy of the unaffected eye will reveal a narrow occludable angle given the anatomic predisposing factors to acute angle-closure glaucoma (See other issues for further discussion). Glaucomflecken (grey-white opacities on the anterior lens capsule) may be visible if previous attacks of angle-closure glaucoma have occurred. [10]

Treatment / Management

The medical treatment for acute angle-closure glaucoma aims to decrease the intraocular pressure by blocking the production of aqueous humor, increasing the outflow of aqueous humor, and reducing the volume of the aqueous humor.[11][12]

Initial medical therapy includes a combination of the following medications:

• Intravenous acetazolamide 500 mg to block the production of aqueous humor.

• Intravenous mannitol 1 to 2 grams/kg can be given (if there is no contraindication) to rapidly reduce the volume of aqueous humor.

• Topical beta-blocker (timolol 0.5%) one drop to block the production of aqueous humor.

• Topical alpha 2-agonist (apraclonidine 1%) one drop to block the production of aqueous humor.

• Topical pilocarpine 1% to 2% one drop every 15 minutes for two doses once intraocular pressure is below 40 mm Hg to increase the outflow of aqueous humor. This is not effective at higher pressures due to pressure-induced ischemic paralysis of the iris.

Intraocular pressure needs to be checked every hour.

Definitive treatment is peripheral iridectomy after the acute episode subsides. Laser iridectomy is the treatment of choice. Surgical iridectomy is indicated when laser iridectomy can not be accomplished. Iridectomy relieves the pupillary block as the pressure between the posterior and anterior chamber approaches zero by allowing the flow of aqueous humor through a different route. Iridectomy should be as peripheral as possible and covered by the eyelid to avoid monocular diplopia through this second hole in the pupil.[13]

Differential Diagnosis

• Allergic conjunctivitis

• Bacterial conjunctivitis (pink eye)

• Viral conjunctivitis 

• Drug-induced glaucoma

• Malignant glaucoma

• Neovascular glaucoma

• Phacomorphic glaucoma

• Senile cataract (age-related cataract)

• Lens subluxation[14]

• Migraine headache[15]

• Cluster headache

• Suprachoroidal hemorrhage

Prognosis

The prognosis depends on early detection and prompt treatment of acute closed-angle glaucoma. A study conducted on 116 cases of acute angle-closure glaucoma concluded that the delay in presentation and the time taken to end the acute episode was the most important factor in determining the final outcome of these patients. High intraocular pressure was less effective in determining the long-term prognosis of this condition.[16]

Complications

If acute closed-angle glaucoma is not detected and treated in its initial stages, it can lead to temporary loss of vision or blindness. There is a loss of peripheral vision, followed by a loss of central vision. There can be a significant increase in IOP in patients with peripheral patent iridotomy and a flat anterior chamber. This condition is called malignant glaucoma. This condition is difficult to treat and progressively leads to blindness.[17]

Deterrence and Patient Education

Patients with a history of acute angle-closure glaucoma should avoid dim light. Pupils dilate in response to dim light, further narrowing the iridocorneal angle. Patients with hypermetropia are at an increased risk of developing angle-closure glaucoma.

Pearls and Other Issues

An untreated opposite eye has a 40% to 80% chance of developing an acute attack of angle-closure glaucoma over 5 to 10 years as it shares the same anatomic predisposing factors as the first eye.[18] Hence peripheral iridectomy should be performed in the other eye as well as the affected eye.

The gender and ethnicity predisposing factors to acute angle-closure glaucoma hint at a genetic predisposition to the disease in certain populations. Recent large-scale studies have shown a clear association to several genes and genetic loci with primary open-angle glaucoma, but evidence for acute angle-closure glaucoma is sparse. So far, only one study has shown a genetic locus on Chromosome 11 that can cause acute angle-closure glaucoma. Studies have been conducted on possible therapeutic targets in patients with early-onset glaucoma based on molecular and cellular events caused by MYOC, OPTN, and TBK1 mutations. [19]

Enhancing Healthcare Team Outcomes

Acute angle-closure glaucoma is best managed by an interprofessional team, including an ophthalmologist, family clinician, an ophthalmology nurse, and the pharmacist. After managing the emergency with eye drops, the patient should be scheduled for an iridectomy. Clinicians need to be aware that the other eye is also at risk for acute angle-closure glaucoma, and prophylactic surgery is recommended.

The outcomes for patients with acute angle-closure glaucoma are good following treatment. However, delay in treatment can lead to damage to the optic nerve and vision loss.

Review Questions

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• Comment on this article.

References

1.

Prum BE, Herndon LW, Moroi SE, Mansberger SL, Stein JD, Lim MC, Rosenberg LF, Gedde SJ, Williams RD. Primary Angle Closure Preferred Practice Pattern(®) Guidelines. Ophthalmology. 2016 Jan;123(1):P1-P40. [PubMed: 26581557]

2.

Pohl H, Tarnutzer AA. Acute Angle-Closure Glaucoma. N Engl J Med. 2018 Mar 08;378(10):e14. [PubMed: 29514027]

3.

Sun X, Dai Y, Chen Y, Yu DY, Cringle SJ, Chen J, Kong X, Wang X, Jiang C. Primary angle closure glaucoma: What we know and what we don’t know. Prog Retin Eye Res. 2017 Mar;57:26-45. [PubMed: 28039061]

4.

Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014 May 14;311(18):1901-11. [PMC free article: PMC4523637] [PubMed: 24825645]

5.

Anderson DR, Jin JC, Wright MM. The physiologic characteristics of relative pupillary block. Am J Ophthalmol. 1991 Mar 15;111(3):344-50. [PubMed: 2000905]

6.

Ahram DF, Alward WL, Kuehn MH. The genetic mechanisms of primary angle closure glaucoma. Eye (Lond). 2015 Oct;29(10):1251-9. [PMC free article: PMC4815686] [PubMed: 26206529]

7.

Bourne RR, Taylor HR, Flaxman SR, Keeffe J, Leasher J, Naidoo K, Pesudovs K, White RA, Wong TY, Resnikoff S, Jonas JB. , Vision Loss Expert Group of the Global Burden of Disease Study. Number of People Blind or Visually Impaired by Glaucoma Worldwide and in World Regions 1990 – 2010: A Meta-Analysis. PLoS One. 2016;11(10):e0162229. [PMC free article: PMC5072735] [PubMed: 27764086]

8.

Collignon NJ. Emergencies in glaucoma: a review. Bull Soc Belge Ophtalmol. 2005;(296):71-81. [PubMed: 16050422]

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Watkinson S. Assessment and management of patients with acute red eye. Nurs Older People. 2013 Jun;25(5):27-34; quiz 35. [PubMed: 23914708]

10.

Garala P, Bansal A. Acute Secondary Optic Neuropathy as a Complication of a Single Episode of Acutely Raised Intraocular Pressure: A Case Series. J Glaucoma. 2019 Jan;28(1):e10-e13. [PubMed: 30234746]

11.

Shaw AD, Burnett CA, Eke T. A simple technique for indirect gonioscopy for patients who cannot be examined at the slit lamp. Br J Ophthalmol. 2006 Sep;90(9):1209. [PMC free article: PMC1857408] [PubMed: 16929072]

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Anwar F, Turalba A. An Overview of Treatment Methods for Primary Angle Closure. Semin Ophthalmol. 2017;32(1):82-85. [PubMed: 27686782]

13.

He M, Jiang Y, Huang S, Chang DS, Munoz B, Aung T, Foster PJ, Friedman DS. Laser peripheral iridotomy for the prevention of angle closure: a single-centre, randomised controlled trial. Lancet. 2019 Apr 20;393(10181):1609-1618. [PubMed: 30878226]

14.

Xing X, Huang L, Tian F, Zhang Y, Lv Y, Liu W, Liu A. Biometric indicators of eyes with occult lens subluxation inducing secondary acute angle closure. BMC Ophthalmol. 2020 Mar 05;20(1):87. [PMC free article: PMC7059282] [PubMed: 32138781]

15.

Renton BJ, Bastawrous A. Acute Angle Closure Glaucoma (AACG): an important differential diagnosis for acute severe headache. Acute Med. 2011;10(2):77-8. [PubMed: 22041605]

16.

David R, Tessler Z, Yassur Y. Long-term outcome of primary acute angle-closure glaucoma. Br J Ophthalmol. 1985 Apr;69(4):261-2. [PMC free article: PMC1040578] [PubMed: 3994941]

17.

Shahid H, Salmon JF. Malignant glaucoma: a review of the modern literature. J Ophthalmol. 2012;2012:852659. [PMC free article: PMC3321564] [PubMed: 22545204]

18.

Atalay E, Nongpiur ME, Baskaran M, Sharma S, Perera SA, Aung T. Biometric Factors Associated With Acute Primary Angle Closure: Comparison of the Affected and Fellow Eye. Invest Ophthalmol Vis Sci. 2016 Oct 01;57(13):5320-5325. [PubMed: 27727395]

19.

Wiggs JL, Pasquale LR. Genetics of glaucoma. Hum Mol Genet. 2017 Aug 01;26(R1):R21-R27. [PMC free article: PMC6074793] [PubMed: 28505344]

20.

Nuessle S, Luebke J, Boehringer D, Reinhard T, Anton A. [Acute angle closure : An ophthalmological emergency in the emergency room]. Med Klin Intensivmed Notfmed. 2022 Mar;117(2):137-143. [PMC free article: PMC8897352] [PubMed: 33580819]

Disclosure: Babak Khazaeni declares no relevant financial relationships with ineligible companies.

Disclosure: Leila Khazaeni declares no relevant financial relationships with ineligible companies.

Acute Angle Closure Glaucoma: Causes, Symptoms, Treatment

Written by Rachel Reiff Ellis

• Causes
• Symptoms
• Diagnosis
• Treatment
• Prevention

This serious condition makes the pressure inside your eye (your doctor may call it intraocular pressure, or IOP) go up suddenly. It can rise within a matter of hours. It happens when fluid in your eye can’t drain the way it should. It isn’t as common as other types of glaucoma, which cause pressure buildup much more slowly over time.Acute angle-closure glaucoma is caused by a rapid or sudden increase in pressure inside the eye, called intraocular pressure (IOP).

Fluid drains out of your eye through a system of canals. These canals live in a mesh of tissue between your iris (the colored part of your eye) and your cornea (the clear outer layer).

When your iris and cornea move closer together, it “closes the angle” between them. When this happens suddenly, it’s called an acute attack and is very painful.

Acute angle closure glaucoma completely blocks your canals. It stops fluid from flowing through them, kind of like a piece of paper sliding over a sink drain. The pressure that builds up can damage your optic nerve. If you don’t treat the problem quickly enough, you could lose your sight completely.

You might have an attack of angle closure glaucoma if you have narrow drainage systems and your eyes dilate (your pupil gets bigger) too much or too quickly. This can normally happen when you:

• Go into a dark room
• Get drops that dilate your eyes
• Are excited or stressed
• Take certain drugs like antidepressants, cold medications, or antihistamines

Some health conditions can also cause angle closure glaucoma:

• Cataracts
• Ectopic lens (when your lens moves from where it should be)
• Diabetic retinopathy
• Ocular ischemia (narrowed blood vessels to the eye)
• Uveitis (eye inflammation)
• Tumors

Women are 2 to 4 times more likely to get it than men. You’re also more likely to have it if you’re:

• Asian or Inuit
• Farsighted
• Between 55 and 65

Or if you:

• Have a family history of it
• Use medications that dilate your pupils
• Use other medications that cause your iris and cornea to come together, like sulfonamides, topiramate, or phenothiazines

If you have acute angle closure glaucoma in one eye, you’re also more likely to get it in the other.

They come on quickly. You won’t be able to ignore them. They include:

• Eye pain
• Severe headache
• Nausea or vomiting
• Very blurry or hazy vision
• Seeing rainbows or halos around lights
• Redness in the white part of the affected eye
• Pupils of different sizes
• Sudden loss of sight

When your doctor examines you, they may also notice that your pupils no longer get smaller or bigger when they shine light on them.

If you think you have acute angle closure glaucoma, you’ll need to see an ophthalmologist right away — it’s an emergency. They’ll examine you and ask about your symptoms. They may do one or more tests to find out more about what’s going on inside your eye:

• Gonioscopy: The doctor uses a lens with a simple microscope called a slit lamp to look into your eye. A beam of light checks the angle between your iris and cornea and see how well fluid drains.
• Tonometry: This test uses a tool to measure the pressure inside your eye.
• Ophthalmoscopy: Your doctor checks for damage to your optic nerve with a small lighted device.

The first thing your doctor will do to treat your acute angle closure attack is try to get rid of some of the pressure in your eye. They might use:

• Drops that narrow your pupil
• Medication to lowers the amount of fluid your eye makes

Once your IOP has dropped a little, your doctor may use a laser to:

• Make a small hole in your iris. This is called a laser iridotomy, and it helps the fluid start flowing again inside your eye. It’s an outpatient treatment, and takes a few minutes.
• Pull the edges of your iris away from your drainage canals. This called laser iridoplasty or gonioplasty.

If you have cataracts, your doctor may consider surgery to replace the lens in your eye. This type of surgery can be harder to do when you’re having an acute attack.

Even if your acute angle closure glaucoma is in only one eye, your doctor will probably treat both eyes, just to be safe. You may need further surgery if this does not allow a passage for enough drainage of fluid.

The best way to prevent an acute angle closure glaucoma attack is to get your eyes checked regularly, especially if you’re at high risk. Your doctor can keep tabs on pressure levels and how well fluid drains. If they think your risk is unusually high, they may suggest laser treatment to hold off an attack.

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Angle-closure glaucoma

Angle-closure glaucoma: symptoms, treatment, recommendations

The term “glaucoma” unites a large group of diseases of the organs of vision, which are characterized by the following symptoms: high intraocular pressure, decreased function of peripheral vision and atrophy of the optic nerve. These changes lead to irreversible deterioration of vision up to the development of complete blindness. In Russia, the main cause of visual impairment (up to 28%) is glaucoma.

What is angle-closure glaucoma?

Ulcer-closure glaucoma is a pathology that occurs as a result of a disorder in the microcirculation of the intraocular fluid when the anterior corner of the eye is blocked. The eye constantly produces aqueous humor, which is necessary to nourish those internal structures where there are no blood vessels. The fluid through the drainage system located in the anterior corner of the eye flows into the superficial veins of the sclera. If the outflow is disturbed, fluid accumulates, intraocular pressure increases. Irritation of pain receptors causes a further reactive rise in pressure. Compression leads to impaired blood supply, dystrophy and atrophy of nerve fibers, which gradually causes atrophy and death of the optic nerve.

Scientists came to the conclusion that the development and progression of glaucoma is a combined action of various risk factors that lead to the triggering of the disease mechanism.

Risk factors:

• Age category over 40 years.
• Race. The most susceptible to pathology are people of the Negroid and Mongoloid races.
• Hereditary predisposition.
• Refractive error: high degrees of myopia or hyperopia.
• Condition after injury to the eye or the consequences of surgical operations.
• Frequently recurring stressful situations.
• Chronic cardiovascular diseases.
• Endocrine pathologies.

Stages of the pathological process in glaucoma:

• Violation of the circulation of the eye fluid.
• High intraocular pressure.
• Deterioration of the blood supply to the tissues and structures of the eye.
• The growth of destructive-dystrophic processes leading to atrophy of the optic fibers.
• Formation of glaucomatous optic neuropathy.

Forms of angle-closure glaucoma

The most common form (up to 80%) is pupillary block glaucoma. Attack periods are replaced by asymptomatic remissions. Each attack leaves adhesions in the drainage system, which further disrupts the normal outflow of eye fluid. Due to this, a constantly high pressure in the anterior chamber of the eye is maintained, which is accompanied by disorders of visual functions typical of glaucoma.

Angle-closure glaucoma with flat iris occurs in 10% of all cases. An exacerbation can develop when the pupil expands under the influence of various reasons: during stress, in the dark, when mydriatic drops are instilled into the eye.

In 7%, a “creeping” form is observed, in which, for unknown reasons, the iris root is fused with the angle of the anterior chamber. The disease begins imperceptibly and is often detected by chance during preventive examinations of the organ of vision. Later, ophthalmohyperthesia and a typical clinical picture of angle-closure glaucoma join.

The rarest (about 1%) malignant form is glaucoma with vitreous lens block. Its appearance is associated with the anatomical and physiological features of the eye: an enlarged lens, a small size of the eyeball, and a dense ciliary body. The iris-lenticular septum tilts anteriorly and obstructs the angle of the anterior chamber, while fluid collects behind the vitreous in the posterior chamber of the eye.

Symptoms of angle-closure glaucoma

The initial stages of the pathological process develop imperceptibly for the patient.

Signs of the disease appear during attacks, without exacerbation there are no symptoms.

In the clinic of angle-closure glaucoma, acute and subacute attacks are distinguished.

An acute attack begins suddenly with the appearance of a sharp pain in the eye with irradiation on the side of the lesion along the projection of the trigeminal nerve to the forehead and temples, vision is blurred, circles of all colors of the rainbow appear when looking at bright light. The general condition also worsens: malaise, weakness, pain in the heart, nausea, vomiting.

The sclera is hyperemic, the cornea is edematous, the pupil is sharply dilated, deformed; foci of cloudiness are noted on the lens.

An acute attack is characterized by a maximum rise in intraocular pressure. Rough adhesions formed in the anterior corner of the eye between the root of the iris and the cornea completely block the drainage system. With a strong compression of the vessels of the iris, a local circulatory disorder develops, from which the optic nerve also suffers.

In a subacute attack, the angle of the anterior chamber of the eye is partially closed, which determines the clinic of the disease. With a mild course (intraocular pressure of 40 mm Hg), when at least the minimum circulatory movement of the eye fluid is preserved, the patient has only hazy blurred vision and multi-colored circles before the eyes in bright light.

At pressures above 60 mmHg. Art. symptoms of glaucoma become more pronounced: there are painful sensations in the eye, forehead, superciliary arches. The subacute form does not cause deformation of the pupil, does not provoke the development of segmental atrophy and adhesions in the corner of the anterior chamber of the eye.

The most common motive in the development of an acute attack of glaucoma is:

• Emotional overexcitation.
• Physical work associated with frequent torso bending.
• Drinking too much liquid.
• Prolonged exposure to a darkened room.
• Hypothermia.
• Taking alcohol and drugs that stimulate the nervous system.

Diagnosis

Modern ophthalmology uses several methods for diagnosing glaucoma:

• Visometry – determination of visual acuity.
• Biomicroscopy.
• Gonioscopy – assessment of the condition of the anterior chamber of the eye.
• Ocular tonometry – measurement of intraocular pressure.

Treatment of angle-closure glaucoma

Tactics treatment of angle-closure glaucoma is different and depends on the clinical picture of the disease.

In case of an acute attack of glaucoma, medical attention should be provided immediately, since prolonged exposure to high pressure structures of the eye can lead to a complete loss of visual functions.

Acute glaucoma drugs:

Eye drops with β-blockers that reduce the production of intraocular fluid: Glaumol, Okukap.

Medicated pupil constriction drops. The pupil, contracting, pulls the iris behind it, which allows you to move it away from the angle of the anterior chamber and unblock the outflow of fluid: “Pilocarpine”, “Oftan”.

Diuretics, analgesics and antiemetics are used as systemic pharmaceuticals.

If an attack of glaucoma persists for more than 24 hours and medical treatment fails, surgical treatment is indicated. If the attack stops, then the operation is performed at a later date.

Methods of surgical treatment of angle-closure glaucoma are determined by the form, stage and presence of concomitant pathologies.

Surgical treatment of angle-closure glaucoma consists in creating artificial micro-holes at the root of the iris, blocking the entrance to the drainage system. The operation is called iridectomy, which opens the anterior corner of the eye, and the pressure between the anterior and posterior chambers equalizes.

Laser iridotomy is also used in ophthalmology for the treatment of glaucoma. The purpose of the operation is to form a channel between the anterior and posterior chambers of the eye, as a result of which the hydrostatic pressure is normalized.

Professor Trubilin’s clinic uses non-penetrating deep sclerectomy as a surgical treatment for glaucoma. The operation is performed without opening the eyeball, only within the drainage system, which allows creating a good hypotensive effect. In advanced clinical cases, it is proposed to implant a mini-shunt under the sclera, which will take on the function of drainage, through which the outflow of intraocular fluid will pass.