Angle-closure glaucoma

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Major Review

Angle-closure glaucoma ABSTRACT In India primary angle closure disease comprises approximately fifty percent of primary glaucoma. It is the leading cause of blindness from glaucoma. Appropriate identification and institution of therapy can prevent long term morbidity from this disease. The use of Pilocarpine and the application of laser iridotomy early in the treatment of angle closure glaucoma has to be underscored. Long term prognosis depends upon identification of the variety of presentations and appropriate use of medical and laser and surgical therapy to maintain a good quality of life for the patients. Family screening plays an important role in detecting new patients at an early stage of the disease. Keywords: Angle‑closure glaucoma, iridotomy, pilocarpine

EPIDEMIOLOGY

DEFINITION AND CLASSIFICATION

Angle‑closure glaucoma is considered as the leading cause of irreversible blindness worldwide and the incidence of primary angle‑closure glaucoma (PACG) is higher in Asians. [1] It is estimated that about 15 million people worldwide have been affected by angle‑closure disease in 2010 and the number is expected to increase to 21 million by 2020.[2]

Angle‑closure disease has two forms: Primary and secondary.

Tham et al. estimated that the number of people that will be affected with PACG worldwide would be 23.36 million and 32.04 million in 2020 and 2040, respectively. Similarly, in Asians, it would be 17.96 million and 24.5 million, respectively.[3] RISK FACTORS • • • • •

Age: Increased frequency with advancing age[4] Gender: 2–3 times more common in women[5] Ethnicity: Asians, more common in Chinese[2] Family history of angle closure[6] Refractive error: Prevalence is higher in individuals with hyperopic eyes[7] • Shallow anterior chamber depth[8] • Shorter axial length • Thicker lens.[9]

The primary angle closure disease (PACD) according to the natural history is classified based on the definition proposed by the International Society for Geographical and Epidemiological Ophthalmology as.[10] Primary angle‑closure suspect The presence of iridotrabecular contact for at least 270° on gonioscopy (with the eye in the primary position, without indentation), with normal intraocular pressure (IOP), optic disc, and visual fields. Primary angle closure The presence of iridotrabecular contact for at least 270°, with either raised IOP and/or peripheral anterior synechiae (PAS), but with normal optic disc and visual fields. Other signs which suggest PAC include loss of pupillary riff, iris whorling, glaukomflecken, and endothelial cell damage. Lakshmi Sravani Mandava, Ganesh V. Raman Department of Glaucoma, Aravind Eye Hospital, Coimbatore, Tamil Nadu, India Address for correspondence: Dr. Ganesh V. Raman, Glaucoma Clinic, Aravind Eye Hospital, Avinashi Road, Coimbatore ‑ 641 014, Tamil Nadu, India. E‑mail: [email protected]

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DOI: 10.4103/kjo.kjo_23_18

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How to cite this article: Mandava LS, Raman GV. Angle-closure glaucoma. Kerala J Ophthalmol 2018;30:12-6.

© 2018 Kerala Journal of Ophthalmology | Published by Wolters Kluwer - Medknow


Mandava and Raman: Major review angle‑closure disease

Primary angle‑closure glaucoma The presence of iridotrabecular contact for >270°, with raised IOP and optic nerve and visual field damage. Some authors modify and even take >180° of iridotrabecular contact as an indication for intervention. Primary angle‑closure disease is classified based on the mechanism of closure into: 1. Iris–pupil obstruction (e.g., pupillary block) 2. Ciliary body anomalies (e.g., plateau iris syndrome) 3. Phacomorphic mechanism 4. Thick iris/thick last peripheral roll of iris induced angle closure. Pathophysiology In majority of cases, primary angle closure is caused by relative pupillary block, in which aqueous encounters increased resistance as it flows from the posterior to anterior chamber. The risk of pupillary block is high in a mid‑dilated pupil as there is maximum contact between the iris and the lens. The increased pressure gradient across the pupil causes the peripheral iris to bow forward and cover the filtering portion of the trabecular meshwork, leading to appositional angle closure. Prolonged and repeated contact between the peripheral iris and trabecular meshwork leads to PAS formation. A less common cause of primary angle closure is plateau iris configuration. It is characterized by a normal central anterior chamber depth, flat iris plane, and crowding of the angle by the iris base as it is displaced forward by anteriorly located ciliary processes. This can lead to subsequent angle closure. Secondary angle closure It is caused by an underlying identifiable pathologic event. When associated with elevated IOP and glaucomatous disc damage, it is referred to as secondary angle‑closure glaucoma. The underlying causes are listed below according to the pathophysiology of obstruction. Anterior “pulling mechanism” The iris is pulled forward by some process in the angle, often by the contraction of a membrane or PAS. a. Neovascular glaucoma b. Iridocorneal endothelial syndromes (e.g., Chandler’s syndrome) c. Epithelial downgrowth d. Fibrous ingrowth e. Flat anterior chamber f. Inflammation g. Penetrating keratoplasty.

Posterior “pushing mechanism” The iris is pushed forward by some condition in the posterior segment. Often, the ciliary body is rotated anteriorly, allowing the lens to come forward also. a. Malignant glaucoma b. Cysts of the iris and ciliary body c. Intraocular tumors, silicone oil, or gas d. Nanophthalmos e. Drug induced (e.g., systemic topiramate) f. Suprachoroidal hemorrhage, choroidal effusion g. Scleral buckle h. Anteriorly displaced lens i. Contracting retrolental tissue as seen in retinopathy of prematurity. CLINICAL PRESENTATION Acute attack of primary angle‑closure glaucoma Signs and symptoms The typical patient with an acute attack of PACG from the papillary block will have a sudden onset of pain or aching on the side of the affected eye. The eye pain appears to be related more to the rapid rate of the rise in IOP than to the absolute level of the pressure itself. This pain is accompanied by blurred vision or colored haloes around lights and ocular congestion. Autonomic stimulation during an acute attack can result in nausea, vomiting, sweating, and bradycardia. Clinical examination 1. Diminished visual acuity 2. Circumcorneal conjunctival congestion 3. Corneal edema, usually involving only the epithelium, but occasionally thickening the stroma also 4. A shallow anterior chamber both centrally and peripherally 5. Minimal anterior chamber reaction caused by increased aqueous humor protein concentration 6. A moderately dilated, vertically oval, sluggish, or nonreactive pupil as the high IOP causes ischemia and paresis of the pupillary sphincter 7. Markedly elevated IOP, usually in the range of 35–75 mmHg 8. A closed angle on gonioscopy, which is the critical test for diagnosing angle‑closure glaucoma. It is sometimes difficult to evaluate the angle during an acute attack because of corneal edema and hazy media. In this situation, gonioscopy should be repeated after the IOP is reduced by medical treatment 9. Sometimes a hyperemic, swollen optic disc is seen probably from impaired axoplasmic flow.

Kerala Journal of Ophthalmology / Volume 30 / Issue 1 / January‑April 2018

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MANAGEMENT The rationale of treatment, once angle closure has been diagnosed, is to: 1. Eliminate pupillary block 2. Assess the extent of angle closure 3. Document baseline features following iridotomy in terms of goniosopy, optic disc, and visual field assessment 4. Follow‑up in terms of IOP monitoring, progression of angle closure, disc, and field changes 5. Protection of the fellow eye. Diagnostic modalities Provocative tests Various provocative tests have been developed to find out patients who may be at higher risk of angle closure. The test is considered positive if the IOP increases by 8 mmHg or more. Commonly used tests are as follows: 1. Dark‑room test – the patients are placed in a dark room for 1–2 h to dilate the pupil and increase resistance at iris–lens diaphragm 2. Prone test – the patient is placed in prone position for 1–2 h to displace the lens anteriorly and increase pupillary block 3. Mydriatic provocative test – causes pupillary dilatation and increase pupillary block. However, these tests are not found to be very predictive of angle closure.[11] Imaging techniques These provide detailed images of various structures and also help in quantitative measurements. They are useful in detecting both primary and secondary cases of angle closure. 1. Ultrasound biomicroscopy: It is a high‑frequency B scan ultrasound which provides high‑resolution cross‑sectional images of the anterior segment of the eye up to the anterior vitreous. It is particularly useful in evaluating plateau iris and any pathology related to the ciliary body[12] 2. Anterior segment optical coherence tomography: It utilizes diode light source to produce detailed images of cornea, angle, and anterior ciliary body. However, it is unable to image structures posterior to the iris. Medical management of acute primary angle‑closure glaucoma Patient comfort and lowering of the IOP are the first priorities in managing an acute crisis of PACG. When these are achieved, one can proceed to more definitive interventions with the laser, such as iridotomy, pupilloplasty, or iridoplasty. 14

Topical anti‑glaucoma medications which can be used are topical beta‑blocker (timolol maleate 0.5% bid), topical carbonic anhydrase inhibitors (dorzolamide 2% bid/brinzolamide 1%). Pilocarpine 2% tid can also be used and should be used once treatment for the acute phase of IOP is initiated. Alpha‑adrenergic agonist (brimonidine 0.15%–0.2%) may also be used, but personally, I avoid it because of its mydriatic property. Oral carbonic anhydrase inhibitors such as acetazolamide 500 mg is given in tid dosage. If the patient is nauseous, intravenous acetazolamide 250–500 mg can be given. Systemic hyperosmotic agents dehydrate the vitreous and allow the lens–iris diaphragm to move posteriorly. They are often the most effective means of lowering IOP during acute episodes of angle‑closure glaucoma. Oral glycerin is administered as a 50% solution in a dose of 1.5–4 ml/kg. In diabetes patients, oral 45% isosorbide solution can be given in a similar dose. If the patient is nauseous or vomiting, 20% mannitol is administered in a dose of 2.0–7 ml/kg over 30–45 min. It is to be used with caution as it may induce cardiac overload, especially in elderly patients with cardiovascular disease. In most acute attacks of angle‑closure glaucoma with pupillary block, the high IOP leads to ischemia of the pupillary sphincter muscle making it unresponsive to topical miotics. Therefore, pilocarpine is by itself less likely to bring down the high pressure of an acute attack. Pilocarpine still remains the drug of choice in angle‑closure glaucoma and is to be used with simultaneous efforts to bring down the raised IOP or after bringing down the raised IOP. To reduce anterior chamber inflammation and the chance of both anterior and posterior synechiae formation, topical steroids are to be used. Once adequate lowering of IOP has been achieved and intraocular inflammation has subsided, laser peripheral iridotomy (LPI) or surgical iridectomy is be performed. It is imperative to perform laser iridotomy in the fellow eye as the prognosis of the eye with acute attack is guarded, and the fellow eye has been known to progress to chronic glaucoma and resultant blindness if left untreated. Laser peripheral iridotomy Peripheral laser iridotomy with Nd:YAG or Argon laser is the definitive treatment for acute angle‑closure glaucoma with the pupillary block. It establishes free communication between the posterior and anterior chambers, and there is an insufficient




pressure differential to push the peripheral iris forward against the trabecular meshwork. The peripheral anterior chamber depth usually increases after iridotomy, in the absence of extensive PAS, whereas the central depth is unchanged. Although surgical iridectomy is a relatively safe and simple procedure, it is invasive and presents a small risk of intraocular complications such as bleeding, cataract, and endophthalmitis. Surgical iridectomy is now reserved for such infrequent situations such as the laser fails to produce a patent iridotomy, laser iridotomy repeatedly closes, a laser is neither available nor functioning properly, opacities of the cornea interfere with laser treatment, or the patient is uncooperative or unable to sit at the slit lamp. Laser iridoplasty and pupilloplasty The peripheral iridoplasty is a usually done in the following settings: 1. Acute PACG from pupillary block, unresponsive to medical treatment, and where a laser iridotomy is precluded by excessive shallowing of the anterior chamber, inflammation or corneal edema[13,14] 2. Plateau iris syndrome and 3. Acute phacomorphic angle closure. In laser iridoplasty, burns of long duration and low power are placed on the peripheral iris which contracts the iris and physically pulls the iris away from the angle in an attempt to open the angle. It is only useful in short‑term lowering of IOP and does not relieve pupillary block.[15] It is the treatment of choice in plateau iris syndrome where peripheral iridotomy is not helpful. Pupilloplasty refers to a laser technique which can interrupt pupillary block by distorting the pupil into a tear‑shaped configuration by applications of intense, small bursts of argon laser 2–3 mm eccentric to the pupillary margin superiorly, thus facilitating aqueous flow into the anterior chamber. Surgical management of primary angle‑closure glaucoma 1. Lens extraction: It is believed that increasing lens thickness and relative anterior lens position may be responsible for the crowding of the angle, and this may be ameliorated by removing the crystalline lens and implanting an intraocular lens. However, the surgeon may face with intra‑operative challenges such as a shallow anterior chamber, a convex lens prone to anterior capsular tears, and a flaccid iris from ischemic damage. Although according to EAGLE study, clear lens extraction showed greater efficacy and was more cost‑effective than LPI, the IOP reduction was found insufficient in the long term and the general consensus was that lens extraction may be useful in population where

access to glaucoma services is sporadic[15] 2. Trabeculectomy: In patients unresponsive to medical treatment, especially if residual PAS extending to >180° is present, laser therapy in the setting of an acute attack may not be possible. In such situation, trabeculectomy may provide an alternative solution. It is also useful when signs of disc damage are already present. However, this is associated with a high risk of surgical failure and complications.[16,17] Combined cataract with filtration surgery and cataract with glaucoma drainage device can also be attempted. In a study by Tsai et al., in patients with PACG, the long‑term IOP‑lowering effect and surgical complications of combined trabeculectomy and cataract extraction are comparable with those of trabeculectomy alone. However, the combined surgery incurred fewer subsequent surgical interventions[18] 3. Goniosynechialysis: It refers to the deliberate intra‑operative shearing or peeling of synechial adhesions in the angle, either mechanically using forceps or cyclodialysis spatula or with a viscoelastic dissection, for at least 180°.[19] Management of the fellow eye Fellow eye of an eye presenting with acute PACG requires a laser iridotomy as most of these eyes steadily progress through the natural history of the condition, unless that course is interrupted.[20] In Asian population with acute PAC, prophylactic laser iridotomy is safe and effective in preventing acute angle closure in fellow eyes.[21] The rate of progression in primary angle closure suspect (PACS) is slower compared to PAC. According to the Chennai eye disease incidence study, there was significant cataract progression in 6 years following LPI in PACS.[22] Hence, the decision to treat PACS should be taken after carefully evaluating the risk and benefit in that particular patient. Screening Due to the high prevalence and morbidity associated with angle‑closure glaucoma, there is a need for screening methods. At the community level, evaluation of the anterior chamber depth can be done using flashlight, where light is held from the temporal side and the shadow projected onto the nasal iris is observed. The presence of this shadow indicates a shallow anterior chamber as the iris is bowing forward and blocking the light pathway. The absence of this shadow indicates an open angle. Pupillary reaction can be assessed and a relative afferent pupillary defect can be noticed in advanced glaucoma. On slit‑lamp examination by a general ophthalmologist, the anterior chamber depth can be assessed using Van Herick method, where a narrow slit is projected just adjacent to the limbus and the distance between the anterior surface of the


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iris and the posterior surface of cornea is compared to that of the corneal thickness. Screening of the family members of patients with glaucoma is also necessary. In the South Indian population screened, siblings of angle closure patients had a >1 in 3 risk of prevalent angle closure, whereas siblings of PAC/PACG patients had a >10% risk of prevalent PAC/PACG.[23] Secondary angle closure Diagnosis of primary or secondary angle closure is based on the history and clinical examination. In secondary cases, a clue to the diagnosis can be obtained by taking detailed ocular and systemic history regarding trauma, previous intraocular surgery, laser, history of diabetes, hypertension, carotid stenosis, and use of systemic medications like topiramate. On examination, one should look for signs of trauma, anterior chamber reaction, iris lesions, neovascularization, lens status and position, posterior segment vascular changes, intraocular tamponade agents, scleral buckle, etc. Treatment of secondary angle closure is aimed at primarily treating the causative factor as well as controlling IOP.

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CONCLUSION Angle‑closure glaucoma is the most common cause of hospital‑based blindness due to glaucoma. Comprehensive examination by the ophthalmologist and serial gonioscopic examination in cases of suspects will go a long way in controlling blindness due to this disease. Appropriate management of acute glaucoma with immediate laser iridotomy (or surgical iridectomy) helps relieve symptoms of acute attack, preserves vision, and establishes better doctor–patient relationship. Opportunistic screening of family members is now the only cost‑effective method to detect new patients of PACD.

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Acknowledgments 1. Dr. Shabana Bharathi, Ex Glaucoma Fellow, Aravind Eye Hospital, Coimbatore. 2. Dr. Mrunali Dhavaliker, Medical Officer, Department of Glaucoma, Aravind Eye Hospital, Coimbatore. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. 16

20. 21. 22.

23.

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