Introduction
Glaucoma, a condition marked by elevated intraocular pressure (IOP), can lead to optic nerve damage and irreversible vision loss if left unaddressed.[1] It is broadly categorized into open-angle and closed-angle types, and further classified as primary or secondary based on the obstruction site within the eye’s anterior chamber. The “angle” refers to the space between the iris and cornea, a critical area for fluid drainage that can become structurally blocked. Accurate and timely Acute Glaucoma Diagnosis is crucial for effective management and preventing severe outcomes.
Primary glaucomas arise without known ocular or systemic causes and typically affect both eyes. Secondary glaucomas, conversely, are often unilateral and linked to other eye or systemic diseases. Acute angle-closure glaucoma (ACAG) is a critical subtype of primary angle-closure glaucoma. Acute angle-closure (AAC) represents a serious ophthalmologic emergency characterized by a rapid spike in IOP, carrying a significant risk of permanent damage and potential blindness if immediate treatment is not initiated.[2]
AAC often manifests with alarming and painful symptoms, including intense, one-sided eye pain, redness, rapid vision impairment, systemic symptoms like nausea and headache, seeing rainbow-colored halos around lights, and vomiting.[3] It’s important to note that non-eye care practitioners might mistake these symptoms for neurological issues, potentially leading to unnecessary brain scans and neurology consultations before an eye exam is performed.[4] Therefore, understanding acute glaucoma diagnosis is vital for all medical professionals.
Confirmation of AAC diagnosis relies on measuring elevated IOP using tonometry, often reaching levels between 50 to 80 mm Hg.[5] A slit-lamp microscope examination typically reveals a shallow anterior chamber, corneal swelling (edema), a fixed and dilated pupil, redness around the cornea (ciliary flush), and a closed angle upon gonioscopy.[6] Treatment strategies encompass medications, laser procedures, and surgery, all aimed at lowering IOP, alleviating acute symptoms, and preventing future angle closures.[7] Prompt and accurate acute glaucoma diagnosis is the first step towards effective intervention.
Normal IOP ranges from 10 to 21 mm Hg.[8] IOP is determined by the rate of aqueous humor production by the ciliary body, the resistance to its outflow through the trabecular meshwork and Schlemm’s canal, and episcleral venous pressure. Aqueous humor, produced in the ciliary body, flows through the pupil and drains via the trabecular meshwork (TM) and Schlemm’s canal at the anterior chamber angle. In ACAG, IOP surges because of blocked aqueous humor outflow. The primary risk factor for ACAG is the anterior chamber’s anatomy, which can predispose to a shallow angle.[9][10] Early acute glaucoma diagnosis can significantly improve patient outcomes.
Etiology of Acute Angle-Closure Glaucoma
Primary angle closure is characterized by either a reversible (appositional) or irreversible (synechial) closure of the anterior chamber angle. It can manifest acutely or chronically. Acute angle closure occurs when a sudden IOP increase is triggered by blocked aqueous outflow from the trabecular meshwork (TM). This blockage is often due to a pupillary block of the iris, resulting in complete angle closure.[11] A swift and accurate acute glaucoma diagnosis is essential in these cases.
Subacute or intermittent primary angle closure involves recurring, symptomatic episodes that resolve on their own.[12] Chronic angle closure, on the other hand, involves repeated episodes leading to sustained elevated IOP without noticeable symptoms initially, causing structural damage to the angle due to prolonged contact between the trabecular meshwork and the peripheral iris.[13] This can progress to synechial closure and both structural and functional angle impairment over time.[14] Even in chronic cases, understanding the underlying mechanisms is crucial for effective acute glaucoma diagnosis and management during exacerbations.
Aqueous humor flow obstruction in primary angle closure is linked to anatomical factors such as a shallow anterior chamber, lens size, the forward positioning of the iris-lens diaphragm, and a narrow angle entrance.[15] A shallow anterior chamber angle leads to increased contact between the iris and lens, hindering aqueous humor flow from the posterior to the anterior chamber. This creates a pressure difference between the chambers, known as a pupillary block.[16] Recognizing these anatomical risk factors is important for acute glaucoma diagnosis and preventative measures.
The pupillary block mechanism causes the iris to bow forward, further narrowing the anterior chamber angle. This cycle perpetuates rising IOP, culminating in the clinical presentation of ACAG.[17] Therefore, acute glaucoma diagnosis involves identifying and addressing this pupillary block mechanism.
The American Academy of Ophthalmology classifies primary angle closure based on criteria including a narrow angle, more than 180° of iridotrabecular contact (ITC), peripheral anterior synechiae (PAS), elevated IOP, and optic nerve damage signs.[18] Primary angle closure suspect (PACS) refers to eyes with ITC but no elevated IOP or PAS. “Primary angle closure” (PAC) is diagnosed with ITC and either PAS, elevated IOP, or both. “Primary angle-closure glaucoma” (PACG) is diagnosed when there is glaucomatous retinal nerve fiber layer damage, with or without optic nerve damage. These classifications are essential for accurate acute glaucoma diagnosis and staging the condition.
Epidemiology of Acute Angle-Closure Glaucoma
In 2013, approximately 65 million people globally were affected by glaucoma. Estimates suggest this number rose to 76 million by 2020 and is projected to exceed 110 million by 2040.[19] About one-third of these cases are attributed to PACG. Meta-analyses indicate that PACG is more likely to cause blindness compared to primary open-angle glaucoma.[20] This highlights the importance of early acute glaucoma diagnosis and intervention to prevent vision loss.
Acute angle-closure (AAC) glaucoma is considered relatively rare. The incidence in white populations is reported to be about 2 to 4 cases per 100,000 people.[6] However, incidence is higher in specific populations, particularly in Singapore and Asia, ranging from 6 to 12 cases per 100,000 inhabitants.[21][22] Geographic and ethnic variations in incidence underscore the need for targeted acute glaucoma diagnosis strategies in high-risk populations.
Identified risk factors for ACAG include:[[23]](#article-22261.r23]
- Older age: The risk increases with age due to lens thickening and anterior chamber shallowing.[24]
- Female gender: Women are more predisposed, possibly due to shallower anterior chambers.[25]
- Asian ethnicity: Individuals of Asian descent have a higher prevalence of angle closure.[26][27]
- Hyperopia (farsightedness): Smaller eyes with shallower anterior chambers are more susceptible.[28]
- Family history: Genetic predisposition plays a role in angle closure glaucoma.[[23]](#article-22261.r23]
- Shallow anterior chamber depth: Anatomical predisposition is a primary risk factor.
- Small corneal diameter: Correlated with smaller anterior segment dimensions.
- Increased lens thickness: Thicker lenses can narrow the anterior angle.
- Certain medications: Drugs causing pupillary dilation can trigger angle closure in susceptible individuals.[29][30] Awareness of these risk factors is critical for proactive acute glaucoma diagnosis and preventative care.
Pathophysiology of Acute Angle-Closure Glaucoma
AAC is triggered by the blockage of aqueous outflow from the TM, leading to a sudden and persistent increase in IOP. This elevation causes significant systemic and ocular symptoms. Understanding this pathophysiology is key to effective acute glaucoma diagnosis and treatment.
Primary AAC occurs when angle closure develops in isolation without underlying causes or associated diseases.[31] It is primarily due to anatomical factors like a shallow anterior chamber or narrow angle. Secondary AAC, in contrast, is angle closure resulting from other conditions or diseases.[32] These can include trauma, inflammation, tumors, or systemic conditions affecting eye structures or aqueous humor flow. Distinguishing between primary and secondary AAC is important for accurate acute glaucoma diagnosis and management.
Pupillary block is the most common mechanism in primary AAC.[33] In conditions like mydriasis and posterior synechiae in eyes at risk, increased contact between the lens and iris can disrupt normal aqueous humor movement from the posterior chamber. This mechanism is central to acute glaucoma diagnosis and treatment strategies.
This disruption leads to fluid pressure buildup behind the iris, pushing the peripheral iris forward. This bulging iris then contacts the TM, acutely closing the angle between the iris and cornea.[34] This obstruction blocks aqueous humor outflow, causing a rapid and significant IOP rise.[35] Rapid IOP elevation is the hallmark of AAC and a critical diagnostic indicator for acute glaucoma diagnosis.
Nonpupillary block mechanisms can also cause angle closure, including plateau iris syndrome, ciliary body swelling (edema), anteriorly displaced or enlarged lens, and malignant glaucoma.[36] These less common mechanisms must also be considered in the differential acute glaucoma diagnosis.
History and Physical Examination for Acute Glaucoma Diagnosis
AAC typically presents with sudden and severe symptoms, including:
- Eye pain or headache: Often intense and localized around the eye or brow.
- Blurred vision and reduced visual acuity: Vision can become significantly impaired rapidly.
- Rainbow-colored halos: Caused by corneal edema scattering light.
- Nausea and vomiting: Systemic symptoms due to severe pain and vagal nerve stimulation.
During a physical examination, key findings may include:
- Fixed midpoint dilated pupil: Pupil is unresponsive to light and moderately dilated.
- Engorged conjunctival vessels: Eye appears red due to dilated blood vessels.
- Hazy or cloudy cornea: Corneal edema reduces corneal transparency.
- Marked conjunctival injection: Significant redness of the conjunctiva.
- Elevated intraocular pressure: IOP is markedly elevated, typically 60 to 80 mm Hg.
- Mild aqueous flare and cells: Slight inflammation in the anterior chamber.
- Angle-closure on gonioscopy: Gonioscopy confirms 360-degree angle closure.
- Swollen optic nerve: Optic nerve head edema may be present. [37][38] These clinical signs and symptoms are crucial for prompt acute glaucoma diagnosis during physical examination.
Evaluation and Diagnostic Procedures for Acute Glaucoma Diagnosis
Several diagnostic procedures are essential in evaluating suspected AAC, ensuring accurate acute glaucoma diagnosis:
Slit-lamp examination: This is vital for detailed anterior segment assessment. It allows close examination of the cornea, iris, and anterior chamber to identify corneal edema, conjunctival injection, and a narrow angle. Slit-lamp findings are a cornerstone of acute glaucoma diagnosis.
Measurement of intraocular pressure (IOP): Elevated IOP is a hallmark of AAC. Tonometry is crucial for measuring IOP, which is typically markedly high during an acute attack. Elevated IOP is a primary diagnostic criterion for acute glaucoma diagnosis.
Imaging studies: In the acute phase, imaging is generally not needed for acute glaucoma diagnosis. Clinical signs, symptoms, slit-lamp findings, and IOP measurement usually suffice.
Basic metabolic panel: If osmotic agents like mannitol or glycerin are used for treatment, a basic metabolic panel monitors electrolyte levels and kidney function due to potential systemic effects. While not directly for acute glaucoma diagnosis, it’s important for managing treatment side effects.
Gonioscopic examination: Performed by an ophthalmologist, gonioscopy is crucial for confirming angle closure and definitive acute glaucoma diagnosis. It evaluates the angle between the iris and cornea to determine closure extent. Gonioscopy of the unaffected eye may reveal a narrow angle, indicating predisposition.
Glaucomflecken: These grey-white lens capsule opacities, visible on slit-lamp examination, indicate past angle-closure glaucoma episodes. They are supportive evidence for acute glaucoma diagnosis in recurrent cases.
Visual field testing (automated static perimetry) and Optical Coherence Tomography (OCT): These are crucial in managing AAC patients to assess glaucomatous damage and guide treatment.
- Visual field testing: Automated static perimetry assesses glaucomatous visual field loss, measuring the patient’s ability to perceive stimuli in their visual field. Serial testing monitors progression and treatment effectiveness.
- Optical Coherence Tomography (OCT): OCT provides detailed retinal and optic nerve head images, assessing retinal nerve fiber layer (RNFL) thickness, indicating AAC-related damage. Serial OCT monitors changes and treatment response.
- Anterior segment OCT and ultrasound biomicroscopy: In patients at risk (hyperopia, shallow anterior chamber, contralateral AAC history), these modalities visualize anterior segment structures (angle, iris, ciliary body). They assess anatomical features related to angle closure, aiding preventative decisions. These advanced imaging techniques enhance the precision of acute glaucoma diagnosis and risk assessment.
Treatment and Management of Acute Angle-Closure Glaucoma
Medical treatment for acute angle-closure glaucoma aims to rapidly lower IOP by reducing aqueous humor production, increasing outflow, and decreasing aqueous humor volume.[18][40] Effective management follows accurate acute glaucoma diagnosis.
Initial medical therapy typically combines medications to quickly reduce IOP and relieve symptoms. Common medications include:
- Topical beta-blockers (e.g., timolol): Reduce aqueous humor production.
- Alpha-adrenergic agonists (e.g., apraclonidine, brimonidine): Decrease aqueous production and increase outflow.
- Carbonic anhydrase inhibitors (CAIs) (e.g., oral acetazolamide, topical dorzolamide): Significantly reduce aqueous humor production.
- Miotics (e.g., pilocarpine): Constrict the pupil, potentially pulling the iris away from the angle (used cautiously after IOP reduction).
- Osmotic agents (e.g., intravenous mannitol, oral glycerin): Reduce aqueous humor volume systemically (used in severe cases). These medications are used in conjunction following acute glaucoma diagnosis to rapidly reduce IOP.
During the acute phase, close IOP monitoring is critical to assess treatment effectiveness. Frequent IOP measurements, generally hourly initially until stabilization, are necessary. Continuous monitoring is essential post acute glaucoma diagnosis to ensure treatment efficacy.
After the acute episode subsides, definitive treatment focuses on preventing future angle-closure attacks and managing anatomical risk factors. Common options include:
-
Laser peripheral iridotomy (LPI): The preferred treatment.[46] LPI creates a small iris hole, allowing aqueous humor flow from the posterior to anterior chamber, bypassing the blocked angle. It relieves pupillary block and prevents future episodes. LPI is minimally invasive and outpatient-based. LPI is a definitive treatment following acute glaucoma diagnosis to prevent recurrence.
-
Surgical iridectomy: Indicated when LPI is not feasible or insufficient.[47] This surgically removes a portion of the iris to create a permanent opening and relieve pupillary block. Reserved for cases where laser treatment fails or is not possible.
-
Iridectomy or iridotomy: These relieve pupillary block by equalizing pressure between the posterior and anterior chambers. The opening should be peripheral and covered by the eyelid to avoid double vision. [48]
-
Lens extraction: May be considered as a first-line treatment in cases with significant anatomical risk factors, especially with advanced AAC.[49] Removing the crystalline lens can alleviate anatomical factors causing angle closure.
If elevated IOP persists post-acute phase, management strategies similar to open-angle glaucoma are used, including topical medications, laser treatment, and surgery. Long-term management strategies are implemented after successful acute glaucoma diagnosis and initial treatment.
Routine ophthalmologic exams, visual field testing, and OCT are recommended for patients at risk of developing elevated IOP and future glaucomatous damage. Ongoing monitoring is crucial even after successful acute glaucoma diagnosis and treatment.
Differential Diagnosis for Acute Glaucoma Diagnosis
Several conditions can mimic AAC with elevated IOP, corneal haze, conjunctival and anterior segment inflammation. Differential acute glaucoma diagnosis must consider:
- 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
A thorough examination and appropriate diagnostic tests are essential to differentiate AAC from these conditions and ensure accurate acute glaucoma diagnosis.
Prognosis of Acute Angle-Closure Glaucoma
Prognosis for AAC is significantly improved by early detection and prompt treatment. A study of 116 ACAG cases found that presentation timing and acute episode duration were critical outcome factors. High IOP had less impact on long-term prognosis than timely intervention.[52] Early acute glaucoma diagnosis is paramount for a favorable prognosis.
Complications of Untreated Acute Angle-Closure Glaucoma
Untreated ACAG can lead to temporary or permanent vision loss and blindness. Progression typically involves peripheral vision loss followed by central vision loss. In severe cases, malignant glaucoma, a challenging and vision-threatening condition, can develop. Avoiding these complications relies on timely acute glaucoma diagnosis and treatment.
Malignant glaucoma is characterized by persistently elevated IOP despite patent iridotomy. The anterior chamber flattens due to fluid imbalance, further elevating IOP. Also known as aqueous misdirection syndrome or ciliary block glaucoma, it is difficult to treat and can lead to blindness.[53] Prompt acute glaucoma diagnosis and management can prevent progression to malignant glaucoma.
Deterrence and Patient Education for Acute Angle-Closure Glaucoma
Patients with a history of AAC should avoid dim lighting, which can dilate pupils and further narrow the iridocorneal angle. Patient education is crucial following acute glaucoma diagnosis and treatment to prevent future episodes.
Patients with hyperopia are at increased risk due to anatomical predispositions like shallow anterior chambers or anterior lens position. LPI is recommended as a preventative measure for individuals with AAC risk factors.[48] Risk factor awareness and preventative LPI are important aspects of post acute glaucoma diagnosis care.
Pearls and Other Issues in Acute Angle-Closure Glaucoma
In AAC, the untreated opposite eye shares the same anatomical risk factors and has a 40% to 80% chance of developing AAC glaucoma within 5 to 10 years.[54] Prophylactic LPI is recommended for the fellow eye to reduce this risk. Bilateral preventative measures are crucial after acute glaucoma diagnosis in one eye.
Gender and ethnicity as risk factors suggest a genetic predisposition. While genetic links are strong for open-angle glaucoma, evidence for AAC glaucoma is sparser. One study identified a genetic locus on chromosome 11 potentially contributing to AAC glaucoma. Further research is needed to understand the genetic basis of acute glaucoma diagnosis and risk.
Research is exploring therapeutic targets for early-onset glaucoma, focusing on molecular and cellular events triggered by mutations in MYOC, OPTN, and TBK1 genes.[55] Ongoing research aims to improve understanding and treatment strategies related to acute glaucoma diagnosis and management.
Enhancing Healthcare Team Outcomes in Acute Angle-Closure Glaucoma
Optimal AAC management requires an interprofessional team: ophthalmologist, family practitioner, ophthalmology nurse, and pharmacist. Initial emergency management includes appropriate eye drop administration, typically a temporary measure. Collaborative care is essential for effective acute glaucoma diagnosis and management.
Following emergency intervention, scheduling an iridectomy is essential. Healthcare practitioners should be aware of the contralateral eye’s susceptibility and recommend prophylactic LPI for it. Team communication and coordinated care are vital after acute glaucoma diagnosis.
Patients with AAC generally have favorable outcomes with timely treatment. However, treatment delays can have serious consequences, including optic nerve damage and vision loss. Prompt recognition and management are paramount for optimizing prognosis. Rapid and accurate acute glaucoma diagnosis and swift intervention are key to preserving vision in AAC.
Review Questions
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References
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Disclosure: Babak Khazaeni declares no relevant financial relationships with ineligible companies.
Disclosure: Marco Zeppieri declares no relevant financial relationships with ineligible companies.
Disclosure: Leila Khazaeni declares no relevant financial relationships with ineligible companies.
