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Acute Angle-Closure Glaucoma
Introduction
Glaucoma, characterized by increased intraocular pressure (IOP), can result in optic neuropathy and vision loss if left untreated.[1] Glaucoma is classified as open-angle or closed-angle and as primary or secondary, depending on the obstruction in the anterior chamber. The angle refers to the space between the iris and the cornea in the anterior chamber, which can become structurally obstructed.
Primary glaucomas are not associated with known ocular or systemic disorders and usually affect both eyes. In contrast, secondary glaucomas are often unilateral and linked to ocular or systemic diseases. Acute closed-angle glaucoma (ACAG) is a subset of primary angle-closure glaucoma. Acute angle-closure (AAC) is an ophthalmologic emergency with elevated IOP, posing a risk of irreversible damage and potential blindness if not treated promptly.[2]
AAC usually presents with significant and distressing symptoms such as unilateral intense periocular pain, redness in the eye, rapid vision loss, systemic symptoms, nausea, headache, multicolored halos around light sources, and vomiting.[3] Nonophthalmologic practitioners may misinterpret these symptoms as neurological conditions, leading to unnecessary cranial imaging and neurologic consultations before ophthalmologic examinations are conducted.[4]
The diagnosis of AAC is confirmed by an elevated IOP measured by tonometry, typically 50 to 80 mm Hg.[5] Examination with a slit-lamp microscope usually reveals a shallow anterior chamber, corneal edema, fixed dilated pupil, conjunctival injection around the limbus (ciliary flush), and a closed angle on gonioscopy.[6] Treatment options include medical, laser, and surgical interventions to reduce IOP, relieve acute symptoms, and prevent future angle closures.[7]
The normal range for IOP measured by tonometry is 10 to 21 mm Hg.[8] IOP is influenced by the ciliary body's production rate of aqueous humor, the resistance to aqueous outflow through the trabecular meshwork and Schlemm's canal, and the episcleral venous pressure. Aqueous humor is produced in the ciliary body, passes through the pupil, and drains through the trabecular meshwork (TM) and Schlemm's canal at the anterior chamber angle. In ACAG, IOP increases rapidly due to outflow obstruction of the aqueous humor. The main predisposing factor for ACAG is the anterior chamber's structural anatomy, which can lead to a shallower angle.[9][10]
Etiology
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Etiology
Primary angle closure is characterized by a reversible (appositional) closure of the anterior chamber angle or an adhesional (synechial) closure. It can present in acute or chronic forms. Acute angle closure occurs when there is a sudden increase in IOP due to blockage of aqueous outflow from the trabecular meshwork (TM), resulting from a pupillary block of the iris that leads to complete closure of the angle.[11]
Recurrent, self-limiting symptomatic episodes characterize the subacute or intermittent form of primary angle closure.[12] In contrast, the chronic condition involves recurrent episodes of angle closure, resulting in elevated IOP without symptoms and causing structural damage to the angle due to prolonged contact between the trabecular meshwork and the peripheral iris.[13] This can lead to synechial closure and both structural and functional impairment in the angle over time.[14]
Aqueous humor flow obstruction in primary angle closure is attributed to various anatomic factors, including a shallow anterior chamber, lens size, anterior positioning of the iris-lens diaphragm, and a narrow entrance to the anterior chamber angle.[15] A shallow anterior chamber angle results in extensive contact between the iris and the lens, thereby impeding aqueous humor flow from the posterior to the anterior chamber. This results in a pressure difference between the chambers, known as a pupillary block.[16]
The pupillary block mechanism induces iris bowing, thereby further narrowing the anterior chamber angle. This ongoing cycle perpetuates increasing IOP, leading to the clinical manifestation of ACAG.[17]
The American Academy of Ophthalmology guidelines classify primary angle closure based on specific criteria, including a narrow angle, more than 180° of iridotrabecular contact (ITC), peripheral anterior synechiae (PAS), elevated IOP, and signs of optic nerve damage.[18] Primary angle closure suspect (PACS) refers to an eye with ITC but no elevated IOP or PAS. "Primary angle closure" (PAC) is diagnosed when ITC is present with PAS, IOP, or both. The term "primary angle-closure glaucoma" (PACG) is used when there is evidence of a glaucomatous retinal nerve fiber layer with or without optic nerve damage.
Epidemiology
The number of people worldwide affected by glaucoma was reported to be approximately 65 million in 2013. However, incidence was estimated to have increased to as high as 76 million in 2020 and is projected to reach over 110 million by 2040.[19] Among these cases, one-third are due to PACG. Meta-analyses have consistently demonstrated that PACG is more likely to lead to blindness than primary open-angle glaucoma.[20]
Acute angle-closure (AAC) glaucoma is considered rare. The incidence of AAC in white individuals has been reported to be approximately 2 to 4 cases per 100,000 people.[6] However, incidence has been higher in certain populations, including Singapore and other Asian countries, with rates ranging from 6 to 12 cases per 100,000 inhabitants.[21][22]
Identified risk factors associated with AAC include the following:[23]
- Age: AAC typically manifests between ages 55 and 65, and its prevalence increases with age. This is likely due to age-related increases in lens thickness and decreases in anterior chamber depth.[24]
- Gender: Studies indicate that females have a 2-4 times higher incidence of AAC than males.[22]
- Race: AAC is commonly observed in Southeast Asian, Chinese, and Inuit peoples, while remaining relatively uncommon in black populations. Variability among ethnicities could be due to anatomical differences in the ciliary body and iris.[2] In white people, AAC accounts for 6% of all glaucoma diagnoses.[25]
- Family history: Predisposed ocular anatomic features at risk can be inherited.[26][27]
- Hyperopia: Certain ocular anatomical features associated with an increased risk of AAC can be inherited. The predisposition to develop AAC can be inherited.[28]
- Medications: Over 60 drugs have been reported to be associated with AAC and are considered risk factors, particularly for individuals with ocular predispositions. These drugs include topical anticholinergic pupil dilators, such as atropine and cyclopentolate, and systemic medication, including topiramate, sulfonamides, duloxetine, and phenothiazines.[29] Patients taking these medications should undergo regular ophthalmic examinations, particularly if they have AAC risk factors.[30]
Pathophysiology
AAC is precipitated by the blockage of aqueous outflow from the TM, resulting in a sudden and non—self-resolving increase in IOP. This elevated pressure leads to significant systemic and ophthalmologic signs and symptoms.
Primary angle closure refers to cases in which angle closure occurs in isolation, without underlying causes or associated diseases.[31] It occurs due to anatomical factors, such as a shallow anterior chamber or a narrow angle, which predispose the individual to sudden angle-closure. On the other hand, secondary AAC refers to cases in which angle closure results from underlying causes or diseases other than primary angle-closure glaucoma.[32] These underlying factors may include trauma, inflammation, tumors, or systemic conditions that affect ocular structures or the flow of aqueous humor.
The most common cause of primary AAC is pupillary block.[33] In certain conditions, like mydriasis and posterior synechiae in eyes at risk of AAC, increased apposition between the lens and iris can disrupt the normal movement of aqueous humor from the posterior chamber.
As a result of this disruption, fluid forces are built behind the iris, pushing and bulging the peripheral iris. This bulging causes the iris to contact the TM, leading to acute closure of the angle between the iris and the cornea.[34] This mechanism obstructs aqueous humor outflow, resulting in an acute and abrupt rise in IOP.[35]
Nonpupillary block mechanisms can also cause angle closure and obstruct aqueous outflow from the TM. These conditions include plateau iris syndrome, ciliary body edema, an anteriorly displaced or enlarged lens, and malignant glaucoma.[36]
History and Physical
AAC typically presents with sudden and severe symptoms, which may include:
- Eye pain or headache
- Blurred vision and reduced visual acuity
- Rainbow-colored halos
- Nausea and vomiting
During a physical examination, the following findings may be observed:
- Fixed midpoint dilated pupil
- Engorged conjunctival vessels
- Hazy or cloudy cornea
- Marked conjunctival injection
- Elevated intraocular pressure: Intraocular pressure is significantly elevated during an acute attack and can reach levels of 60-80 mm Hg.
- Mild aqueous flare and cells: Examination of the anterior chamber may reveal a slight amount of aqueous flare (haziness) and cells, indicating inflammation.
- Angle-closure on gonioscopy: Gonioscopy will reveal angle closure for 360 degrees, confirming the diagnosis of AAC.
- Swollen optic nerve: The optic nerve may appear swollen during an acute attack, indicating optic nerve head edema.[37][38]
Evaluation
Several diagnostic procedures are commonly performed in evaluating a patient with suspected AAC and include the following:
Slit-lamp examination: Slit-lamp examination is essential for a detailed assessment of the anterior segment of the eye. It allows close examination of the cornea, iris, and anterior chamber to detect abnormalities, such as corneal edema, conjunctival injection, or an anatomically narrow angle.
Measurement of intraocular pressure (IOP): Elevated intraocular pressure is a hallmark of AAC. Measuring the IOP using tonometry is a critical diagnostic step. Elevated IOP levels are typically observed in AAC, and values can be markedly high during an acute attack.
Imaging studies: In the acute phase of AAC, imaging studies are generally unnecessary for diagnosis. The clinical signs and symptoms, along with findings from slit-lamp examination and IOP measurement, are usually sufficient to establish a diagnosis.
Basic metabolic panel: If osmotic agents, such as mannitol or glycerin, are used as part of the treatment regimen, a basic metabolic panel can help monitor electrolyte levels and renal function due to their potential systemic effects.
Gonioscopic examination: A gonioscopic examination, performed by an ophthalmologist, is crucial for verifying angle closure and making a definitive diagnosis of AAC. It involves evaluating the angle between the iris and cornea to determine the extent of closure. Gonioscopy of the unaffected eye may reveal a narrow, almost occluded angle, considering the anatomic predisposing factors for angle-closure glaucoma.
Glaucomflecken: Glaucomflecken refers to grey-white opacities that may be visible on the anterior lens capsule, typically following previous episodes of angle-closure glaucoma. These opacities can be observed during a slit-lamp examination, providing evidence of past attacks.[39]
Visual field testing with automated static perimetry and optical coherence tomography (OCT) is crucial in the care of patients with AAC to assess multiple aspects of the condition and to guide treatment decisions.
Visual field testing: Automated static perimetry helps assess the extent and severity of glaucomatous visual field loss attributable to AAC. It measures the patient's ability to perceive visual stimuli at different locations within their visual field. Serial visual field testing over time can provide valuable information about the condition's progression and the treatment's effectiveness.
Optical Coherence Tomography (OCT): OCT is a noninvasive imaging technique that provides detailed cross-sectional images of the retina and optic nerve head. It helps when assessing retinal nerve fiber layer (RNFL) thickness and indicates AAC-related damage. OCT can also help detect structural abnormalities and optic nerve head changes characteristic of glaucoma. Serial OCT scans enable monitoring of changes over time and the assessment of treatment response.
Anterior segment OCT and ultrasound biomicroscopy: In patients with risk factors for AAC, such as hyperopia, a shallow anterior chamber, or a history of AAC in the fellow eye, these imaging modalities can be helpful. These imaging modalities provide detailed visualization of the anterior segment structures, including the angle, iris, and ciliary body. They can help assess anatomical features associated with angle closure and inform decision-making regarding preventive measures or further interventions.
Treatment / Management
The medical treatment of acute angle-closure glaucoma focuses on rapidly lowering IOP by blocking the production of aqueous humor, increasing the outflow of aqueous humor, and reducing the volume of aqueous humor.[18][40](B3)
Initial medical therapy typically involves a combination of medications to reduce IOP and relieve symptoms rapidly. The following medications are commonly used:
- Oral or intravenous acetazolamide: Acetazolamide, a carbonic anhydrase inhibitor, is administered orally or intravenously to reduce aqueous humor production. It lowers IOP by inhibiting the enzyme that generates bicarbonate ions, thereby decreasing aqueous humor secretion.[41] The dose is 500 mg orally or IV.
- Intravenous mannitol: Mannitol, an osmotic diuretic, is given intravenously to decrease the volume of aqueous humor and lower IOP rapidly. It draws fluid out of the eye, thereby reducing intraocular pressure.[42] The dosage is typically 1 to 2 g/kg body weight.
- Topical beta-blocker: A topical beta-blocker, such as timolol 0.5%, is applied as eye drops to block aqueous humor production. Beta-blockers reduce IOP by inhibiting the beta-adrenergic receptors in the ciliary body, thereby decreasing aqueous humor production.[43] Apply 1 drop of timolol 0.5% to the affected eye.
- Topical alpha 2-agonist: An alpha 2-agonist, like apraclonidine 1%, is used as eye drops to block aqueous humor production. These medications reduce aqueous humor production and enhance outflow through the trabecular meshwork.[44] The dose is apraclonidine 1%; apply 1 drop to the affected eye.
- Topical pilocarpine: Pilocarpine, a miotic agent, is instilled as eye drops to increase the outflow of aqueous humor. It works by constricting the pupil and increasing iris tension, thereby widening the angle between the iris and the cornea and facilitating drainage of aqueous humor. Pilocarpine is usually administered once the intraocular pressure is below 40 mm Hg. The dose is pilocarpine 1% to 2%; apply 1 drop every 15 minutes for 2 doses once IOP is below 40 mm Hg.[45] (B3)
During the acute phase of AAC, it is crucial to closely monitor IOP to assess treatment effectiveness and ensure it returns to normal values. Frequent IOP measurements are necessary to evaluate the response to therapy and make any necessary adjustments. The recommended frequency of IOP checks may vary depending on the specific situation and treatment response. In general, it is advisable to measure IOP at least hourly after the initial onset of symptoms until it stabilizes.
After the acute episode of AAC subsides, definitive treatment focuses on preventing future angle-closure attacks and managing the underlying anatomical risk factors. The following treatment options are commonly employed:
Laser peripheral iridotomy (LPI) is the treatment of choice.[46] LPI involves using a laser to create a small hole in the peripheral iris, allowing aqueous humor to flow from the posterior chamber to the anterior chamber, bypassing the blocked angle. LPI helps to relieve pupillary block and prevent future angle-closure episodes. LPI is a minimally invasive procedure performed on an outpatient basis.
Surgical iridectomy is indicated when laser iridectomy cannot be performed or is insufficient.[47] This involves surgically removing a portion of the iris to create a permanent opening and relieve the pupillary block. Surgical iridectomy is typically reserved for situations where laser treatment is not feasible or unsuccessful.(A1)
Iridectomy or iridotomy relieves the pupillary block as the pressure between the posterior and anterior chambers approaches zero by allowing the flow of aqueous humor through a different route. Iridectomy/iridotomy should be as peripheral as possible and covered by the eyelid to avoid monocular diplopia through this second hole in the pupil.[48](A1)
Lens extraction can be considered when significant anatomical risk factors are present. In these cases, lens extraction may be considered as a first-line treatment.[49] Lens extraction involves removing the crystalline lens, thereby relieving the anatomical factors contributing to angle closure. This approach is often beneficial in eyes with advanced AAC.
If elevated IOP persists after the acute phase of AAC, treatment strategies similar to those used in open-angle glaucoma can be employed. These include topical medical therapy, laser treatment, and surgical interventions.
Routine ophthalmologic examinations, visual field testing, and OCT should be considered for patients at risk of developing elevated IOP and future glaucomatous damage.
Differential Diagnosis
Numerous conditions can lead to elevated IOP, corneal haze, inflammation of the conjunctiva and the anterior segment, and similar signs and symptoms seen in patients with AAC. When evaluating a patient presenting with these manifestations, the following differential diagnosis should be considered:
- Allergic conjunctivitis
- Bacterial conjunctivitis (pink eye)
- Viral conjunctivitis
- Keratitis
- Episcleritis or scleritis
- Eye trauma
- Chemical injury
- Corneal ulcer
- Open-angle glaucoma
- Drug-induced glaucoma
- Malignant glaucoma
- Neovascular glaucoma
- Phacomorphic glaucoma
- Senile cataract (age-related cataract)
- Lens subluxation [50]
- Migraine headache [51]
- Cluster headache
- Suprachoroidal hemorrhage
Prognosis
The prognosis of AAC is significantly influenced by early detection and prompt treatment. A study of 116 AAC cases found that the timing of presentation and the duration of the acute episode were crucial determinants of patient outcomes. High IOP was found to have less impact on the long-term prognosis of this condition.[52]
Complications
If AAC goes undetected and untreated in its early stages, it can result in temporary vision loss or blindness. The condition's progression typically involves a sequential loss of peripheral vision followed by a loss of central vision. However, in some cases, AAC can develop into a more severe and challenging-to-treat form known as malignant glaucoma.
A significant increase in IOP characterizes malignant glaucoma despite a patent iridotomy. In this condition, the eye's anterior chamber becomes flat due to a fluid imbalance, leading to further elevation of IOP. Malignant glaucoma is also called aqueous misdirection syndrome or ciliary block glaucoma. This condition is challenging to treat and progressively leads to blindness.[53]
Deterrence and Patient Education
Patients with a history of acute angle-closure glaucoma should be advised to avoid dim lighting conditions. Dim light can cause pupil dilation, thereby further narrowing the iridocorneal angle.
Patients with hypermetropia are at an increased risk of developing angle-closure glaucoma. This is because hypermetropia is often associated with specific anatomical predispositions that can contribute to angle closure, such as a shallow anterior chamber depth or a more anterior lens position. LPI is a recommended preventative measure in individuals with AAC risk factors.[48]
Pearls and Other Issues
In patients with an AAC, the untreated opposite eye shares the same anatomic predisposing factors as the first eye. The untreated eye has a 40% to 80% chance of developing an AAC glaucoma within 5 to 10 years.[54] Therefore, it is recommended to perform LPI in both eyes to reduce the risk of such an attack.
The presence of gender and ethnicity as predisposing factors for AAC glaucoma suggests a genetic predisposition to the disease in specific populations. Recent large-scale studies have provided strong evidence that several genes and genetic loci are associated with primary open-angle glaucoma. However, evidence for acute angle-closure glaucoma is sparse. Only 1 study has identified a genetic locus on chromosome 11 that can contribute to the development of AAC glaucoma.
Research has explored potential therapeutic targets for patients with early-onset glaucoma, focusing on molecular and cellular events triggered by mutations in the myocilin (MYOC), optineurin (OPTN), and TANK-binding kinase 1 (TBK1) genes.[55]
Enhancing Healthcare Team Outcomes
The optimal management of AAC glaucoma requires a collaborative approach involving an interprofessional team comprising an ophthalmologist, an emergency physician, a nurse, and a pharmacist. In initial emergency management, administering appropriate eye drops is crucial. However, it is essential to note that this is typically a temporary measure.
Following the emergency intervention, it is essential to schedule the patient for an iridectomy. Healthcare practitioners should be mindful that the contralateral eye is susceptible to AAC glaucoma. Thus, prophylactic surgery, such as laser peripheral iridotomy, is also recommended to reduce the risk in that eye.
Patients with AAC glaucoma generally have favorable outcomes if timely treatment is provided. However, it is crucial to emphasize that any delay in treatment can have serious consequences, including optic nerve damage and vision loss. Swift intervention is essential to alleviate intraocular pressure and preserve visual function. Therefore, prompt recognition and appropriate management are paramount for optimizing prognosis in individuals with AAC glaucoma.
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