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1. General examination  External Adnexae • Tuberous Sclerosis (Bourneville Syndrome) • the “ash-leaf sign” & adenoma sebaceum • Neurofibromatosis – Subcutaneous plexiform neuromas • Juvenile Xanthogranuloma, • yellow and/or orange papules • Oculodermal melanocytosis (nevus of Ota). • skin pigmentation 3
2. Cont… • In the Baltimore Eye Survey, the prevalence of POAG among White individuals ranged from 0.9% in those aged 40–49 years • 2.2% in those aged ≥80 years, • whereas the prevalence among Black individuals ranged from 1.2% to 11.3%, respectively. 5
3. Cont… • The prevalence of PACG varies among racial and ethnic groups. • A meta- analysis estimated the prevalence – Asia to be 1.1% among individuals aged 40–80 years; however, it is even higher in east Asia. – Among people of European ancestry >40 yrs,estimated to be 0.1% to 0.4%. – The estimated prevalence in African populations ranges from 0.1% to 0.6%. – The highest- known prevalence, estimated to be between 2.5% and 4.8%, is found in Inuit populations >40 years in Alaska and Greenland. 6
4. Cont… • Ocular hypertension (OHT) is defined as the presence of statistically elevated IOP in the absence of glaucomatous visual field or optic disc damage. • A large proportion of patients with OHT do not go on to develop glaucoma. 7
5. Pathogenesis of Glaucoma • Glaucoma is a progressive disease characterized by slow degeneration of retinal ganglion cells (RGCs) and optic nerve axons. • The pathogenesis is not fully understood but several theories are in vogue to explain the varied clinical manifestations. • There is evidence that RGC death in glaucoma may occur through a type of degeneration defined as apoptosis. 8
6. Cont.….. • Apoptosis can be initiated by various mechanisms: • Inflammation • Ischemia • Neurotoxicity  Glutamate excitotoxicity  Nitrous oxide toxicity • Neurotrophin deprivation • Oxidative stress • Mitochondrial dysfunction 9
7. • 10
8. Cont.… • corectopia (displacement of the pupil), • nevi, nodules, • exfoliative material • Transillumination defects, the presence and patency of an iridotomy or iridectomy, and any surgically induced iris abnormalities. • Iris color should be noted, especially in patients being considered for treatment with a prostaglandin analogue 11
9. Cont… • Early stages of neovascularization of the anterior segment may appear as – Either fine tufts at the pupillary margin or – A fine network of vessels on the surface of the iris adjacent to the iris root. • ocular trauma, such as – Iris sphincter tears, – Iridodialysis (tear in the iris root), or – Iridodonesis 12
10. Cont.… • contour of the iris – clues about the under lying mechanism of angle closure. – choroidal effusion or hemorrhage – iris or ciliary body cyst or, rarely, uveal melanoma; 13
11. Central Anterior Chamber (Ghorbani-Smith Method) • 17
12. 19
13. 20
14. •
15. 28
16. Laser Trabeculoplasty • (LTP), laser energy is applied to the trabecular meshwork in discrete spots, usually covering 180°–360° per treatment. • The goal of LTP is to reduce IOP by increasing outflow facility. • Different laser wavelengths and delivery systems can be used 29
17. Cont… • In all forms of LTP, possible mechanisms of action include the following: • stimulation of cell division • release of cytokines from treated trabecular meshwork cells resulting in alterations of the extracellular matrix of the TM or biomechanical changes in the Schlemm canal endothelial cells • recruitment of monocytes and macrophages in the TM • increased phagocytic activity of cells in the TM 30
18. Cont…. 31
19. Cont… • Complications – transient rise in IOP – Low-grade anterior uveitis – PAS – hyphema, corneal inflammation and edema – reactivation of herpes simplex virus, and persistently elevated IOP • Results and long-term follow-up – 4–6 weeks before evaluating the full effect of treatment – 80% of patients medically uncontrolled IOP results drop upto 6-12moths – 50% of patients with an initial response maintain a significantly lower IOP level for 3–5 years after treatmet – The success rate at 10 years is approximately 30%. 32
20. • Laser Iridotomy – pupillary block resulting in primary angle closure (PAC) or acute PAC – PAC suspect (PACS) 33
21. Cont…. • Contraindications – completely flat anterior chamber – opacified or edematous cornea – 360° of synechial angle closure – Other Angle closure 34
22. cont… • Laser Gonioplasty, or Peripheral Iridoplasty – is a technique to deepen the angle. – plateau iris syndrome, nanophthalmos, and lens-related angle-closure. • Contraindications – tumors of the iris or ciliary body and uveitis 35
23. Cyclodestruction • Internal cyclodestruction (endocyclophotocoagulation) • External cyclodestruction (trans scleral cyclophotocoagulation) • destroying a portion of the ciliary body. • Cyclocryotherapy • Nd: YAG cyclodestruction • Endoscopic cyclophotocoagulation • Trans scleral cyclophotocoagulation 36
24. Incisional Surgery • trabeculectomy • implantation of tube shunts. • MIGS 37
25. 38
26. 39
27. 40
28. Cont… 41

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In tuberous sclerosis, glaucoma may occur secondary to vitreous hemorrhage, anterior segment neovascularization, or retinal detachment. A typical external sign of tuberous sclerosis is pink to red- brown angiofibromas,which are often found on the face and chin.
In juvenile xanthogranuloma, yellow or orangepapules or nodules can be pre sent on the eyelids or face. In oculodermal melanocytosis,blue to brown discoloration or darkening occurs on the periocular skin. It can be unilateralor bilateral, and it may be subtle, particularly in persons of African, Asian, or Hispanicancestry.The presence of subcutaneous eyelid plexiform neurofibromas is a hallmark of the type1 variant of neurofibromatosis (NF1, or von Recklinghausen disease). Although glaucoma isgenerally uncommon in patients with NF1, it occurs in 25%–50% of those who have an eyelid plexiform neurofibroma. In these patients, glaucoma is usually unilateral and ipsilateralto the eyelid neurofibroma.Several disease pro cesses with ocular adnexal abnormalities are associated with elevated episcleral venous pressure (see Chapter 8). The presence of a facial cutaneousangioma (nevus flammeus, or port- wine stain) can indicate encephalotrigeminal angiomatosis (Sturge- Weber syndrome). The cutaneous hemangiomas of a closely related condition, Klippel- Trénaunay- Weber syndrome, extend over an affected limb and may alsoinvolve the face and eyes. Orbital varices, arteriovenous fistulas, and superior vena cavasyndrome may also be associated with elevated episcleral venous pressure and secondaryglaucoma. Intermittent unilateral proptosis and dilated eyelid veins are key external signsof orbital varices. Carotid- cavernous, dural- cavernous, and other arteriovenous fistulascan produce orbital bruits, restricted ocular motility, proptosis, and pulsating exophthalmos. Superior vena cava syndrome can cause proptosis and facial and eyelid edema, aswell as conjunctival chemosis. Thyroid eye disease may also be associated with glaucoma;ocular adnexal features of this disease include exophthalmos, eyelid retraction, and motility disorders.Long- term use of prostaglandin analogues may result in ocular adnexal abnormalities, including increased periocular pigmentation and hypertrichosis of the eyelashes.Other reported external abnormalities include orbital fat atrophy, enophthalmos, deepening of the upper eyelid sulcus, upper eyelid ptosis, inferior scleral show, and tightening ofthe eyelids
Examination and assessment of the external ocular adnexae is useful for determining the presence of a variety of conditions associated with secondary glaucomas as well as external ocular manifestations of glaucoma therapy. The entities described in this section are discussed in greater depth andillustrated in other volumes of the BCSC series; consult the Master Index.An example of an association between adnexal changes and systemic disease is tuberous sclerosis (Bourneville syndrome), in which glaucoma may occur secondary to vitreous hemorrhage, anterior segment neovascularization, or retinal detachment. Typical external and cutaneous signs of tuberoussclerosis include a hypopigmented lesion termed the “ash-leaf sign” and a red-brown papular rash (adenoma sebaceum) that is often found on the face and chin. Other changes in the ocular adnexa associated with secondary glaucoma include the subcutaneous plexiform neuromas that are a hallmark of the type 1 variant of neurofibromatosis, the yellow and/or orange papules in juvenile xanthogranuloma, and the skin pigmentation seen in oculodermalmelanocytosis (nevus of Ota).
The overall populationbased prevalence was 4–5 times higher among Black individuals than White individuals.In the Rotterdam Study, a longitudinal population- based study of northern Eu ro peans,the observed prevalence was 1.1% among subjects ≥55 years of age. In the same study cohort, the incident risk of developing glaucoma at 10 years was 2.8%. In both the BaltimoreEye Survey and the Rotterdam Study, half of the subjects with glaucoma were unaware oftheir diagnosis.
Blindness and low vision in Jimma Zone, Ethopia: results of a population-based survey

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Original Article
Blindness and low vision in Jimma Zone, Ethopia: results of a population-based survey
Negussie Zerihun & Denise Mabey
Pages 19-26 | Accepted 25 Jun 1996, Published online: 08 Jul 2009
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https://doi.org/10.3109/09286589709058057
A population-based study on the prevalence of blindness and low vision was carried out in Jimma Zone, south-western Ethiopia between November 1994 and January 1995. A total of 7423 people from a sample of 8215 (90.4%) was examined. Sixty-three (0.85%) were blind (visual acuity less than 3/60 in the better eye) and 125 people (1.7%) had low vision (less than 6/18–3/60).
Cataract and aphakia (52.4%), corneal opacity and phthisis bulbi (25.4%), and glaucoma (9.5%) were the major causes of blindness. Cataract (56.8%), refractive errors (28.8%), and corneal opacity (12.8%) were the major causes of low vision. Corneal opacity from trachoma was responsible for 20.6% of all blindness and 10.4% of low vision. The prevalence of visual impairment due to refractive errors was 5.1/1000 population. Almost 25% of the study population had active trachoma, and 0.9% of pre-school children had signs of vitamin A deficiency.
Out of a total population of 2 million an estimated 17,000 people are blind and 34,000 have low vision (i.e., a total of 51,000 people with visual impairment). Approximately 20,000 people require cataract surgery, 52,000 require lid surgery for trichiasis, 24,000 require spectacles (excluding presbyopia), including 10,000 for significant refractive errors, half a million require treatment for active trachoma and 4,000 require glaucoma treatment.

Aim: To evaluate the prevalence of glaucoma, treatment patterns and patient attitudes in Ethiopia. • Methods: A survey was administered to glaucoma patients in hospitals in Addis Ababa, Ethiopia. • Results: Of the 415 qualified patients, exfoliative glaucoma (17%) was most commonly found in the Gurage population (33%), whereas chronic angle-closure glaucoma (5%) was found in the Amhara/Tigre (6%) population (P = 0.006). Patients were treated with an average of 1.4 ± 0.8 medications: 52% admitted recent noncompliance and 36% had undergone filtering surgery. Patients believed their physician was trying to help them (93%). God wanted them to receive treatment (89%) and their spouse was sympathetic to their disease (82%). Patients noted their community was unaware of their condition (87%) with Muslims [most common in the Gurage population (31%, P < 0.0001)] reporting this the most (25%, P = 0.01). Amhara/Tigre patients strongly believed their doctors were concerned about them (94%, P = 0.04). • Conclusion: The prevalence of glaucoma type varies among ethnic groups in Ethiopia with exfoliation more common in the Gurage population and chronic angle-closure glaucoma more frequent in the Amhara/Tigre population.
A glaucoma suspect is defined as an individual who has 1 or more of the following characteristics:• a suspicious optic nerve or nerve fiber layer appearance in the absence of a visualfield defect• a visual field defect suggestive of glaucoma in the absence of a corresponding glaucomatous optic nerve abnormality• a family history of glaucoma in a first- degree relative• elevated IOP without evidence of optic nerve damage (see the following section OcularHypertension)
Histopathological evaluation shows that the primary site of damage is:• Retinal ganglion cells• Glial cells including the astrocytes and the Müller cells
Apoptosis has been accepted as an important component of glaucomatous neuro degeneration.
Retinal ganglion cells respond to a variety of neurotrophins, such as brain-derived neurotrophic factor, ciliary nerve trophic factor,glial cell-derived neurotrophic factor, and nerve growth factor. These trophic factors are neuroprotective.Impaired neurotrophin transport from the visual thalamus to the soma of RGCs results in their destruction by apoptosis. The retrograde and anterogradeneuronal transport in glaucomatous eyes is disturbed or interrupted at LC.An increased IOP leads to a contusion of nerve fibers squeezing throughcollagenous plates of LC. Additionally, the cerebrospinal fluid pressureinfluences the degree of mechanical stress, due to a pressure gradient acrossthe tissue of the ONH.
Genetic mutations of myocilin (MYOC) are speculated to cause 2–4% of the POAG in the world.
MYOC is exhibited in human trabecular meshwork and several other tissues but not enough is known about its cellular function.• The gene family bcl-2 is capable of producing several proteins that play important anti apoptotic functions, whereas the bax genes produce pro apoptotic proteins. Whether a cell undergoes apoptosis appears to depend on the relative concentrations of proteins each of these gene families is responsible for producing.• After the increased production of bax, a group of cysteine proteases calledcaspases appears to be the key molecules that determine the point of commitment to apoptosis.
Glutamate excitotoxicity: Excess glutamate induces neuronal changes leadingto RGC death, and this paradoxical phenomenon is termed excitotoxicity.Glutamate transporters like glutamate–aspartate transporter and excitatoryamino acid carrier 1 and glutamate receptors are downregulated inglaucomatous eyes following astrocyte activation. This results in deficientglutamate removal from the extracellular space. An elevated extracellularconcentration of glutamate will lead to an increased inflow of calcium into theRGCs through an activation of voltage-gated calcium channels. An excessiveintracellular concentration of calcium leads to neuron damage. After theincrease in neuronal intracellular calcium, there is an increased productionof free radicals including nitric oxide (NO). Nitric oxide neurotoxicity: As a free radical, NO can start a chain of reactions including activation of the p53 protein, disruption of mitochondria function,and the degradation of deoxyribonucleic acid (DNA) that ultimately results in apoptosis. Nitric oxide rapidly reacts with superoxide to form peroxynitrate,which is a toxic free radical capable of extensive neuro degeneration. Ionotrophic receptors neurotoxicity: Activation of N-methyl-D-aspartate(NMDA) and non-NMDA receptors increases the intracellular calcium thatstimulates various enzymes that lead to RGC death. Neuroinflammation: Patients with primary open-angle glaucoma and NTGhave a significant increase in cytokine receptors suggestive of T cell overactivation, which is a result of long-term presence of lymphocytes andantigens from sustained neurodegeneration.Normal-tension glaucoma has been suggested to be an autoimmune neuropathy with presence of autoantigens in these patients and there is epidemiological association of immune-related diseases with 30% of patients with NTG. Heat shock proteins (HSP) and caspase: These assist in protein folding andassembly and help by responding to stress induced by increased IOP. Butwhen they persist, they can induce neuronal apoptosis. Ischemia andexcessive production of HSP antibodies activate caspase. Caspase depletesthe energy sources of the cell, Nicotinamide adenine dinucleotide (NAD),and adenosine triphosphate and thus eventually cleaves and unravels thecellular DNA. It is this rapid cascade of caspase activation that is responsiblefor the speed of cell death that occurs in apoptosis.It has been suggested that excitotoxicity could play a bigger role in damage due to ischemia because there is extensive research linking excitotoxicityto hypoxic conditions. The neurotrophin deprival hypothesis meshes wellwith the traditional mechanical theory.Glial cell activation is noted in glaucoma and the affected cells are theastrocytes in ONH and retina and the retinal Müller cells. The characteristicclinical finding in glaucoma is the ONH excavation that implies tissueremodeling.Ocular blood flow is affected in glaucoma, but it is not well understood ifit is secondary or causal to tissue atrophy. Role of ROSExperimental data suggests:• Hydrogen peroxide can cause trabecular meshwork degeneration thatleads to increased resistance to aqueous outflow.• Trabecular meshwork has antioxidant activities, mainly related to superoxide dismutase–catalase and glutathione pathways, but these are alteredin patients with glaucoma.• Increase in IOP and severity of visual-field defects in patients withglaucoma parallel the amount of oxidative DNA damage affectingtrabecular meshwork.• Vascular alterations associated with glaucoma contribute to the generation of oxidative damage.• Oxidative stress in retinal cells appears to be involved in the neuronal celldeath affecting the optic nerve in POAG.Glaucomatous subjects might have a genetic predisposition renderingthem more susceptible to ROS-induced damage. Clinical trials testing theefficacy of antioxidant drugs for POAG management is an arena of furtherresearch.Role of MetalloproteinasesMetalloproteinases are zinc-containing enzymes that digest extracellularmatrix. The turnover of the matrix is increased in glaucoma that is speculatedto be result of oxidative stress in response to reperfusion injury.Metalloproteinase 9 is secreted by lymphocytes in glaucoma and it:• Is a prerequisite for apoptosis of RGCs.• Is involved in tissue remodeling and is thus responsible for changes inONH and LC.• Is important in the breakdown of the blood–brain barrier and may contribute to development of splinter hemorrhages.• Regulates the corneal thickness.
Posterior bowing of the peripheral parts of the iris result in aconcave peripheral iris, a reverse pupillary blockwith higher pressure in the anterior chamberthan in the posterior chamber. The peripheralpigmented layer of the iris will be rubbed off bythe zonular fi bers during movements of the pupil.This leads to radial transillumination defects orthe so-called “church-window” phenomenon,seen as a crown-like red re fl ex of the fundusthat resembles a rosetta window of a gothicchurch (Fig. 6.4). Pigmented cells are releasedinto the aqueous humor and may be found onthe anterior surface of the iris (Fig. 6.5). Theyare phagocytosed by the endothelial cells of theFig. 6.1 Pseudoexfoliation material on the anterior surface of the lens, some of which has been rubbed off in themid-periphery by the pupilFig. 6.2 Chamber angle of an eye with pseudoexfoliation(arrow white Schwalbe’s ring). In the direction towardsthe cornea there is a very thin dark line (Sampaolesi’sline). Asterisk indicates the bright white scleral spur.Between the scleral spur and Schwalbe’s line is the pigmented trabecular meshwork (grade +3)Fig. 6.3 Chamber angle of an eye with pseudoexfoliation(asterisks bright white scleral spur). Black pigment granules are present in the inferior part of the angle at6 o’clock6.2 The Chamber Angle in Secondary Open-Angle Glaucoma 41trabecular meshwork. This induces an intense orvery intense brown pigmentation of the trabecular meshwork (Scheie grade +3 or +4), especially in the inferior part (Fig. 6.6). AdditionallySampaolesi’s line is very often present. Verticaldeposits of pigment on the corneal endotheliumare called Krukenberg spindle (Fig. 6.7). Eventhe zonular fi bers and the peripheral posteriorsurface of the lens (Scheie’s stripe) are full ofpigment cells (Fig. 6.8).Course: The IOP shows high fl uctuations.Over time – when accommodation is lost due to aging – most of the pigment has been released and the pigment dispersion or glaucoma has“burned out”. Then the pigmentation of the trabecular meshwork becomes less in the inferior part and more prominent in the superior half (“pigment reversal”)
Use the slit lamp and at fi rst adjust the slit in ahorizontal position. Fix the arm of the slit lamp temporally at 60°. The microscope is pointedstraight ahead and the patient is asked to look straight ahead. Shorten the slit to 1–2 mm andmove the slit lamp until it is focused at the cornea. You will fi nd a second slit on the surface ofthe iris and/or the lens (depending on the width of the pupil), that is slightly unfocused (Fig. 5.4).Increase the length of the slit until the two slits meet (Figs. 5.5 and 5.6). Read the length at the scale of the slit lamp (Fig. 5.7) and multiply thisvalue by 1.4 (for values between 1 and 2.5 mm)or add 10% of the value and 0.5 mm. This willgive you the central anterior chamber depth (corneal endothelium to the anterior surface of thelens) in millimeters. An eye with a central chamber depth of 2 mm or less is at risk of developing angle closure. If you measure the right eye youmust only use the right ocular and vice versa forthe left eye.
Fig. 2.1 (a) Cirrus HD-OCT RNFL thickness map of theright eye demonstrating robust RNFL arcuate bundles. No defects are detected on the RNFL deviation map. AverageRNFL thickness, rim area, average C/D ratio, vertical C/Dratio, and cup volume are within normal distribution as compared with age-matched controls within the referencepopulation. Sectoral analysis is also within normal distribution.
(b) The same patient’s left eye, which demonstrates RNFL thinning and attenuation on the thicknessmap, noted by the paucity of orange and red along thenormal RNFL arcuate distribution. On the RNFL deviation map, clear inferotemporal and superotemporal RNFLdefects are noted in wedge-shaped distributions. AverageRNFL thickness, RNFL symmetry between the eyes, rimarea, average C/D ratio, vertical C/D, and cup volume areall below 1% of age-matched controls within the reference population. Sectoral analysis also confirms relativethinning of the superior and inferior quadrants below 1%of the average reference population
Maximal tolerable medical therapy may be defined as the therapeuticregimen that maximizes the benefits of medical therapy while maintaining the quality of life of the patient with glaucoma.• It focuses on both the tolerability of side effects and the therapeuticefficacy of medication. Patients are generally unable to support more thanfour glaucoma medications, and in case of intolerable side effects with<4 medications also, they may be considered to be appropriate candidates for glaucoma surgery.• Since the IOP drop with each additional medication diminishes, patientsdo not significantly benefit from two or more glaucoma drugs at the sametime. An additional 2 mm Hg IOP lowering when adding a second agent toa prostaglandin is difficult to achieve, and the third agent results in almostinsignificant IOP drop.• It is therefore more judicious to think in terms of optimal medical therapy,which generally includes two or three medications, rather than maximalmedical therapy.• Systemic medications including systemic CAIs and hyperosmotic agentsare beyond the scope of maximal tolerable medical therapy. These are,therefore, primarily used as temporising measures, or to overcome a glaucomatous crisis.
EfficacySLT and ALT seem to have similar efficacy in lowering IOP. Approximately 80% of patientswith medically uncontrolled OAG experience a drop in IOP for at least 6 months following LTP. Among patients who had an initial response, 50% maintain a significantly lowerIOP level for 3–5 years after treatment. The success rate at 10 years is about 30%. Highersuccess rates are seen in older patients with primary open- angle glaucoma (POAG) andpseudoexfoliative glaucoma.Treatment can be repeated with SLT and MLT, although success rates seem to declinewith each subsequent treatment. Because the initial ALT treatment is usually applied toonly 180° of the trabecular meshwork, the laser can be applied to the untreated half of themeshwork later, if needed. However, in previously treated areas, repeat ALT may be lesseffective and associated with an increased risk of IOP elevation. SLT can be used in areasof prior ALT treatment, with results similar to those in eyes undergoing repeat SLT. LTP isless effective in patients with angle- recession glaucoma, inflammatory glaucoma, or abnormalangle structure.The Glaucoma Laser Trial (GLT) was a multicenter randomized clinical trial that assessed the efficacy and safety of ALT as an alternative to topical medical therapy in patientswith newly diagnosed, previously untreated POAG. As initial therapy, ALT appeared to beat least as effective as medi cation in reducing IOP, preventing visual field loss, and slowing an increase in cup–disc ratio. The study was flawed in that 1 eye was assigned to ALTwhile the fellow eye was assigned to timolol treatment, which can have an IOP- loweringeffect on the contralateral eye, potentially confounding the results. More than half of theeyes treated initially with laser required the addition of 1 or more medi cations to controlIOP over the course of the study.The Laser in Glaucoma and Ocular Hypertension (LiGHT) Trial was a prospectiverandomized study that compared SLT to medical treatment in the initial management ofocular hypertension and glaucoma. At 36 months, IOP control was similar between the2 groups, while SLT was more cost- effective. Patients who had SLT scored similarly or better on quality- of- life mea sures compared with patients using
ang W, He M, Zhou M, Zhang X. Selective laser trabeculoplasty versus argon laser trabeculoplasty in patients with open-angle glaucoma: a systematic review and meta-analysis. PLoS One. 2013;8(12):e84270.
he risk of hyphema canbe reduced by pretreating dark irides with an argon or diode laser prior to penetration withNd:YAG laser and/or by coagulating an actively bleeding blood vessel with argon or diode laser.Identify a suitable iridotomy site:▪ Superior site covered by normal lid position (to avoid glare andmonocular diplopia)▪ Nasal quadrant if possible to prevent macular damage (which is notusual)▪ Peripheral site, approximately one-third distance from limbus to pupil(to minimize damage to the lens)▪ Avoid the 12 o’clock position (bubbles produced during the proceduremay obscure the view, hyphema from 12 o’clock is more disturbing)▪ Iris crypt (thinner iris requires less laser energy, thus less damage tothe surrounding tissue and less postlaser inflammation)
The contra-indications of laser peripheral iridotomy are as follows:• Moderate-to-severe corneal edema or opacification• Flat anterior chamber• No or poor anterior chamber view• Corneal decompensation• Failed multiple attempts of laser peripheral iridotomy (LPI)• Poor patient cooperation (relative).In these cases if an iridotomy is required, a surgical iridectomy may beperformed
Peripheral iridoplasty (or gonioplasty) is performed by using a thermal laser (green ordiode) to treat the peripheral iris stroma. This causes contraction of collagen fibers andthinning of the peripheral iris, pulling it away from the angle recess.
Limited eye care service
Become symptomatic after advanced
Ongoing follow up
Economic problem

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