What are the risk factors for acute angle-closure glaucoma. How does acute angle-closure glaucoma present clinically. What is the pathophysiology behind acute angle-closure glaucoma. What are the immediate steps in managing acute angle-closure glaucoma. How can acute angle-closure glaucoma be prevented.

Understanding Acute Angle-Closure Glaucoma: A Comprehensive Overview

Acute angle-closure glaucoma (AACG) is a sight-threatening ocular emergency characterized by a rapid increase in intraocular pressure due to obstruction of aqueous humor outflow. This condition requires immediate medical attention to prevent permanent vision loss. Let’s delve into the intricacies of AACG, exploring its causes, symptoms, and management strategies.

The Anatomy and Pathophysiology of Acute Angle-Closure Glaucoma

To understand AACG, it’s crucial to grasp the underlying anatomy and pathophysiology. The anterior chamber angle, formed between the iris and cornea, plays a pivotal role in the development of this condition.

Anatomical Predisposition

Several anatomical factors contribute to the risk of AACG:

• Shallow anterior chamber
• Enlarged lens
• Anterior positioning of the iris-lens diaphragm
• Narrow entrance to the anterior chamber angle

These variations create an environment conducive to angle closure. How does this anatomical predisposition lead to AACG? The shallow anterior chamber angle results in a larger area of contact between the iris and lens, impeding the flow of aqueous humor from the posterior to the anterior chamber.

Pupillary Block and Angle Closure

The restricted flow of aqueous humor creates a pressure differential between the posterior and anterior chambers, known as pupillary block. This pressure difference causes the iris to bow forward, further narrowing the already compromised angle. As this cycle continues, intraocular pressure rises precipitously, leading to the clinical manifestation of AACG.

What triggers an acute attack of angle-closure glaucoma? Pupillary dilation often precipitates an attack by increasing contact between the iris and lens, exacerbating the pupillary block. This can occur in various situations, such as dim lighting conditions or the use of certain medications.

Risk Factors and Epidemiology of Acute Angle-Closure Glaucoma

Understanding the risk factors and epidemiology of AACG is essential for identifying individuals at higher risk and implementing preventive measures.

Age-Related Risk

AACG predominantly affects older individuals, with the average age of onset being around 60 years. Why does age play a role in AACG risk? The lens continues to grow throughout life, gradually increasing in size. This growth can contribute to a narrowing of the anterior chamber angle, elevating the risk of angle closure.

Gender Disparity

Interestingly, AACG exhibits a significant gender bias. Women are four times more likely to develop AACG compared to men. While the exact reasons for this disparity are not fully understood, it’s thought that anatomical differences in ocular structures between genders may contribute to this increased risk.

Racial and Ethnic Variations

The prevalence of AACG varies considerably among different racial and ethnic groups:

• Higher incidence in Southeast Asians, Chinese, and Eskimo populations
• Lower incidence in black populations
• In white populations, AACG accounts for approximately 6% of all glaucoma diagnoses

These variations highlight the importance of considering racial and ethnic background when assessing an individual’s risk for AACG.

Genetic Factors

Family history plays a significant role in AACG risk. The anatomical features predisposing an individual to AACG are often inherited. This genetic component underscores the importance of screening family members of AACG patients for early detection and prevention.

Clinical Presentation and Symptoms of Acute Angle-Closure Glaucoma

Recognizing the signs and symptoms of AACG is crucial for prompt diagnosis and treatment. The onset of AACG is typically sudden and severe, often catching patients off guard.

Ocular Symptoms

The hallmark symptoms of AACG include:

• Severe unilateral eye pain
• Blurred vision
• Perception of rainbow-colored halos around bright lights
• Redness of the affected eye

Why do patients with AACG see rainbow-colored halos? This phenomenon, known as rainbow vision, occurs due to corneal edema resulting from the elevated intraocular pressure. The edema causes light to scatter as it enters the eye, creating the perception of colored halos around light sources.

Associated Systemic Symptoms

AACG can also manifest with systemic symptoms, including:

• Headache (often mistaken for a migraine)
• Nausea
• Vomiting

These systemic symptoms can sometimes lead to misdiagnosis, emphasizing the importance of considering AACG in patients presenting with these complaints, especially when accompanied by ocular symptoms.

Physical Examination Findings

On examination, several key findings may be observed:

• Fixed, mid-dilated pupil
• Hazy or cloudy cornea
• Marked conjunctival injection (redness)
• Shallow anterior chamber
• Severely elevated intraocular pressure (often >50 mmHg)

How does the pupil appear in AACG? The pupil typically becomes fixed in a mid-dilated position due to iris ischemia resulting from the markedly elevated intraocular pressure.

Diagnosis and Immediate Management of Acute Angle-Closure Glaucoma

Prompt diagnosis and immediate management are crucial in preventing irreversible vision loss in AACG. The diagnosis is primarily clinical, based on the presenting symptoms and examination findings.

Diagnostic Procedures

While the diagnosis is often made clinically, several diagnostic procedures can confirm AACG:

• Tonometry to measure intraocular pressure
• Gonioscopy to visualize the anterior chamber angle
• Slit-lamp examination to assess corneal edema and anterior chamber depth

What is the role of gonioscopy in diagnosing AACG? Gonioscopy allows direct visualization of the anterior chamber angle, confirming its closure. However, it’s often deferred in the acute setting due to patient discomfort and the risk of further increasing intraocular pressure.

Immediate Management Steps

The primary goal of immediate management is to rapidly lower the intraocular pressure. This typically involves a combination of medical and laser treatments:

1. Topical pressure-lowering medications (e.g., beta-blockers, alpha-agonists)
2. Oral or intravenous carbonic anhydrase inhibitors
3. Oral or intravenous hyperosmotic agents (e.g., mannitol)
4. Laser peripheral iridotomy to create a bypass channel for aqueous flow

Why is laser peripheral iridotomy performed? This procedure creates a small opening in the peripheral iris, allowing aqueous humor to bypass the pupillary block and flow directly from the posterior to the anterior chamber, equalizing pressure and opening the angle.

Long-Term Management and Prevention of Acute Angle-Closure Glaucoma

After the acute attack is resolved, long-term management focuses on preventing recurrence and managing any residual glaucomatous damage.

Surgical Interventions

In some cases, surgical intervention may be necessary:

• Lens extraction (if the lens is contributing significantly to angle closure)
• Trabeculectomy (in cases of persistent elevated intraocular pressure)

How does lens extraction help in managing AACG? Removing the lens, especially if it’s enlarged or cataractous, can deepen the anterior chamber and widen the angle, reducing the risk of future attacks.

Preventive Measures

Preventing AACG involves identifying at-risk individuals and taking proactive steps:

• Regular eye examinations, especially for those with risk factors
• Prophylactic laser peripheral iridotomy in high-risk patients
• Education about symptoms and the importance of seeking immediate care
• Caution with medications that can precipitate angle closure (e.g., certain antidepressants, antihistamines)

What is the role of prophylactic laser peripheral iridotomy? This procedure can prevent AACG in high-risk individuals by creating a bypass channel for aqueous flow before an acute attack occurs.

The Role of the Interprofessional Team in Managing Acute Angle-Closure Glaucoma

Effective management of AACG requires a collaborative effort from an interprofessional team. This team typically includes:

• Emergency physicians for initial assessment and management
• Ophthalmologists for definitive diagnosis and treatment
• Nurses for patient monitoring and education
• Pharmacists for medication management
• Primary care physicians for long-term follow-up and management of associated conditions

How does interprofessional collaboration improve outcomes in AACG? A well-coordinated team approach ensures rapid diagnosis, prompt initiation of treatment, and comprehensive follow-up care, ultimately leading to better visual outcomes and reduced risk of recurrence.

Future Directions in Acute Angle-Closure Glaucoma Research and Management

As our understanding of AACG continues to evolve, several areas of research hold promise for improving diagnosis, treatment, and prevention:

Advanced Imaging Techniques

Emerging imaging technologies, such as anterior segment optical coherence tomography (AS-OCT), offer new possibilities for early detection and risk assessment. These techniques provide detailed visualization of anterior segment structures, potentially allowing for more precise identification of at-risk individuals.

Genetic Studies

Ongoing genetic research aims to identify specific genes associated with AACG risk. This could lead to more targeted screening programs and personalized prevention strategies. What potential impact could genetic screening have on AACG management? Identifying genetic markers for AACG risk could allow for earlier intervention in high-risk individuals, potentially preventing acute attacks before they occur.

Novel Therapeutic Approaches

Research into new therapeutic modalities continues, with a focus on developing treatments that can rapidly and safely lower intraocular pressure during acute attacks. Additionally, investigations into therapies that can modify the anatomical risk factors for AACG are ongoing.

Telemedicine and Remote Monitoring

The integration of telemedicine and remote monitoring technologies in ophthalmology presents new opportunities for AACG management. These tools could enable earlier detection of at-risk patients and facilitate rapid triage of acute cases, particularly in underserved areas.

How might telemedicine impact AACG outcomes? By enabling remote screening and rapid consultation with specialists, telemedicine could reduce delays in diagnosis and treatment, potentially improving visual outcomes in AACG patients.

In conclusion, acute angle-closure glaucoma remains a challenging and potentially devastating ocular emergency. However, with ongoing advances in our understanding of its pathophysiology, risk factors, and management strategies, we are better equipped than ever to diagnose, treat, and prevent this condition. By staying informed about the latest developments and maintaining a collaborative approach to care, healthcare professionals can continue to improve outcomes for patients at risk of or experiencing acute angle-closure glaucoma.

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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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]

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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]

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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]

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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]

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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]

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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]

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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]

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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]

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

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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.

Angle-Closure Glaucoma – Eye Disorders

By

Douglas J. Rhee

, MD, University Hospitals/Case Western Reserve University

Reviewed/Revised Apr 2023

View Patient Education

Topic Resources

Angle-closure glaucoma is glaucoma associated with a physically obstructed anterior chamber angle, which may be chronic or, rarely, acute. Symptoms of acute angle closure are severe ocular pain and redness, decreased vision, colored halos around lights, headache, nausea, and vomiting. Intraocular pressure (IOP) is elevated. Immediate treatment of the acute condition with multiple topical and systemic medications is required to prevent permanent vision loss, followed by the definitive treatment, iridotomy.

(See also Overview of Glaucoma Overview of Glaucoma Glaucomas are a group of eye disorders characterized by progressive optic nerve damage in which an important part is a relative increase in intraocular pressure (IOP) that can lead to irreversible… read more .)

Angle-closure glaucoma accounts for about 10% of all glaucomas in the United States.

Angle-closure glaucoma is caused by factors that either pull or push the iris up into the angle (ie, junction of the iris and cornea at the periphery of the ), physically blocking drainage of aqueous and raising intraocular pressure (IOP) (see table ). Elevated IOP damages the optic nerve.

Angle closure may be primary (cause is unknown) or secondary to another condition and can be acute, subacute (intermittent), or chronic.

Narrow angles are not present in young people. As people age, the lens of the eye continues to grow. In some but not all people, this growth pushes the iris forward, narrowing the angle. Risk factors for developing narrow angles include family history, advanced age, and race; risk is higher in Asian and Inuit populations and lower in European and African populations.

In people with narrow angles, the distance between the iris at the pupil and the lens is also very narrow. When the iris dilates, forces pull the iris centripetally and posteriorly causing increasing iris–lens contact, which prevents aqueous from passing between the lens and iris, through the pupil, and into the anterior chamber (this mechanism is termed pupillary block). Pressure from the continued secretion of aqueous into the posterior chamber by the ciliary body pushes the peripheral iris anteriorly (causing a forward-bowing iris called iris bombe), closing the angle. This closure blocks aqueous outflow, resulting in rapid (within hours) and severe (> 40 mm Hg) elevation of intraocular pressure (IOP). Nonpupillary block mechanisms include plateau iris syndrome, in which the central anterior chamber is deep but the peripheral anterior chamber is made shallow by a ciliary body that is displaced forward.

Acute angle-closure glaucoma requires immediate recognition and treatment because vision can be lost quickly and permanently.

Intermittent angle-closure glaucoma occurs if the episode of pupillary block resolves spontaneously after several hours, usually after sleeping supine.

Chronic angle-closure glaucoma occurs if the angle narrows slowly, allowing scarring between the peripheral iris and trabecular meshwork; IOP elevation is slow.

Pupillary dilation (mydriasis) can push the iris into the angle and precipitate acute angle-closure glaucoma in any person with narrow angles.

The mechanical obstruction of the angle is due to a coexisting condition, such as proliferative diabetic retinopathy Diabetic Retinopathy In patients with diabetes mellitus, years of poorly controlled hyperglycemia lead to multiple, primarily vascular, complications that affect small vessels (microvascular), large vessels (macrovascular)… read more (PDR), ischemic central vein occlusion Central Retinal Vein Occlusion and Branch Retinal Vein Occlusion Central retinal vein occlusion is a blockage of the central retinal vein by a thrombus. It causes painless vision loss, ranging from mild to severe, and usually occurs suddenly. Diagnosis is… read more , uveitis Overview of Uveitis Uveitis is defined as inflammation of the uveal tract—the iris, ciliary body, and choroid. However, the retina and fluid within the anterior chamber and vitreous are often involved as well…. read more , or epithelial down-growth. Contraction of a neovascular membrane (eg, in PDR) or inflammatory scarring can pull the iris into the angle.

Patients have severe ocular pain and redness, decreased vision, colored halos around lights, headache, nausea, and vomiting. The systemic complaints may be so severe that patients are misdiagnosed as having a neurologic or gastrointestinal problem. Examination typically reveals conjunctival hyperemia, a hazy cornea, a fixed mid-dilated pupil, and anterior chamber inflammation. Vision is decreased. Intraocular pressure (IOP) measurement is usually 40 to 80 mm Hg. The optic nerve is difficult to visualize because of corneal edema, and visual field testing is not done because of discomfort. For primary mechanisms of angle-closure (eg, pupillary block and plateau iris), examination of the uninvolved contralateral eye can indicate the diagnosis.

Pearls & Pitfalls

This type of glaucoma manifests similarly to open-angle glaucoma Primary Open-Angle Glaucoma Primary open-angle glaucoma is a syndrome of optic nerve damage associated with an open anterior chamber angle and an elevated or sometimes average intraocular pressure (IOP). Symptoms are a… read more . Some patients have ocular redness, discomfort, blurred vision, or headache that lessens with sleep (perhaps because of sleep-induced miosis and posterior displacement of the lens by gravity). On gonioscopy, the angle is narrow, and peripheral anterior synechiae (PAS), which are adhesions between the peripheral iris and angle structure causing blockage of trabecular meshwork and/or ciliary body face, may be seen. IOP may be normal but is usually higher in the affected eye.

Diagnosis of acute angle-closure glaucoma is clinical and by measurement of IOP. Gonioscopy may be difficult to do in the involved eye because of a clouded cornea with friable corneal epithelium. However, examination of the other eye reveals a narrow or occludable angle. If the other eye has a wide angle, a diagnosis other than primary angle-closure glaucoma should be considered. Pupillary block mechanism can be recognized as iris bombe, an anterior bowing or arc of the iris between the angle and the pupil.

Diagnosis of chronic angle-closure glaucoma is based on the presence of peripheral anterior synechiae on gonioscopy and characteristic optic nerve and visual field changes (see symptoms and signs of primary open-angle glaucoma Symptoms and Signs Primary open-angle glaucoma is a syndrome of optic nerve damage associated with an open anterior chamber angle and an elevated or sometimes average intraocular pressure (IOP). Symptoms are a… read more ).

Before giving or prescribing mydriatic eye drops (which can trigger acute narrow-angle glaucoma in patients at risk), anterior chamber depth should be assessed. If gonioscopy is unavailable, the chamber depth can be more crudely assessed using a slit lamp or even a penlight; the penlight is held next to the temporal side of the eye, with the light beam parallel to the iris. If a shadow is cast on the nasal iris, the angle is probably narrow, because the temporal iris bows forward and blocks the light.

• Acute: Timolol, pilocarpine, and brimonidine drops, oral acetazolamide, and a systemic osmotic agent, followed by laser peripheral iridotomy

• Chronic: Similar to primary open-angle glaucoma except that laser peripheral iridotomy should be done if the ophthalmologist feels that the procedure may slow mechanical closing of the angle. Cataract Cataract A cataract is a congenital or degenerative opacity of the lens. The main symptom is gradual, painless vision blurring. Diagnosis is by ophthalmoscopy and slit-lamp examination. Treatment is… read more removal helps delay the progression of chronic angle-closure glaucoma.

Pupillary dilation should be avoided in people at risk, something important when considering applying topical agents to dilate the eye for examination (eg, cyclopentolate, phenylephrine) or for treatment (eg, homatropine) or when giving systemic medications that have the potential to dilate the pupils (eg, scopolamine, alpha-adrenergic agonists commonly used to treat urinary incontinence, medications with anticholinergic effects).

Treatment must be initiated immediately because vision can be lost quickly and permanently. The patient should receive several medications at once. A suggested regimen is timolol 0.5% one drop every 30 minutes for 2 doses, pilocarpine 2 to 4% one drop every 15 minutes for 2 doses, brimonidine (0.15 or 0.2%) one drop every 15 minutes for 2 doses, acetazolamide 500 mg orally initially (IV if patients are nauseated) followed by 250 mg every 6 hours, and an osmotic agent, such as oral glycerol 1 mL/kg diluted with an equal amount of cold water, mannitol 1. 0 to 1.5 mg/kg IV, or isosorbide 100 g orally (220 mL of a 45% solution). (NOTE: This form of isosorbide is not isosorbide dinitrate.) Response is evaluated by measuring intraocular pressure (IOP). Miotics (eg, pilocarpine) are generally not effective when IOP is > 40 or 50 mm Hg because of an anoxic pupillary sphincter.

Definitive treatment is with laser peripheral iridotomy (LPI), which opens another pathway for fluid to pass from the posterior to the anterior chamber, breaking the pupillary block. It is done as soon as the cornea is clear and inflammation has subsided. In some cases the cornea clears within hours of lowering the IOP; in other cases, it can take 1 to 2 days. Because the chance of having an acute attack in the other eye is 80%, LPI is done on both eyes.

The risk of complications with LPI is extremely low compared with its benefits. Glare, which can be bothersome, may occur.

Patients with chronic, subacute, or intermittent angle-closure glaucoma should also have LPI. Additionally, patients with a narrow angle, even in the absence of symptoms, should undergo prompt LPI to prevent angle-closure glaucoma. If a cataract is present, cataract removal Cataract extraction and lens implant procedures A cataract is a congenital or degenerative opacity of the lens. The main symptom is gradual, painless vision blurring. Diagnosis is by ophthalmoscopy and slit-lamp examination. Treatment is… read more can dramatically delay the progression of chronic angle-closure glaucoma.

The medications and full-thickness incisional surgical treatments used for angle-closure glaucoma are the same as those used for open-angle glaucoma. However, laser trabeculoplasty is relatively contraindicated if the angle is so narrow that additional peripheral anterior synechiae may form after the laser procedure. Typically, partial-thickness procedures are not indicated.

• Angle-closure glaucoma can develop acutely, intermittently, or chronically.

• Suspect acute angle-closure glaucoma based on clinical findings and confirm it by measuring intraocular pressure.

• Confirm chronic angle-closure glaucoma by peripheral anterior synechiae and optic nerve and visual field changes.

• Treat acute angle-closure glaucoma as an emergency.

• Consult an ophthalmologist to arrange laser peripheral iridotomy for all patients with angle-closure glaucoma.

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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.