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Secondary angle closure glaucoma dr. rahul.pptx

The document discusses secondary angle closure glaucoma, which is caused by impaired aqueous outflow due to apposition between the peripheral iris and the trabeculum. It presents two fundamental mechanisms—anterior pulling and posterior pushing—and highlights the importance of diagnosis and treatment options, including panretinal photocoagulation and anti-VEGF therapies. The document also covers related conditions such as neovascular glaucoma, iridocorneal endothelial syndrome, and other factors contributing to this type of glaucoma.

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SECONDARY ANGLE CLOSURE GLAUCOMA PRESENTED BY, DR. RAHUL GUPTA 1ST YR. RESIDENT DEPT. OF oPHTHALMOLOGY 7TH JAN, 2024
CONTENTS 2  Definition  Mechanism ⚫ Anterior pulling mechanism ⚫ Posterior pulling mechanism  Diagnosis  Treatment
SECONDARY ANGLE CLOSURE GLAUCOMA  Caused by impairment of aqueous outflow secondary to apposition between the peripheral iris and the trabeculum.  Related or identifiable ophthalmic condition is known to be present with the onset of angle closure : “secondary” ACG 3
Two fundamental mechanisms:  Anterior pulling mechanism: peripheral iris pulled forward onto TM by contraction of a membrane, inflammatory exudate, or fibrous band  Posterior pushing mechanism: peripheral iris is displaced forward by lens, vitreous, or ciliary body
CLASSIFICATION 1. Anterior pulling mechanism: Contraction of an inflammatory, hemorrhagic, or vascular membrane, band, or exudate in the angle PAS Forward displacement of lens-iris interface Often accompanied by swelling and anterior rotation of ciliary body 5
ANTERIOR ‘PULLING MECHANISM a. Neovascular glaucoma b.Iridocorneal endothelial syndromes (e.g. Chandler’s syndrome) c. Posterior polymorphous dystrophy d. Epithelial down growth e. Fibrous ingrowth f. Flat anterior chamber g. Inflammation 6
NEOVASCULAR GLAUCOMA Secondary glaucoma resulting from neovascularization of anterior segment, including iris and angle often associated with retinal hypoxia. SYNONYMS 1. Hemorrhagic glaucoma 2. Thrombotic glaucoma 3. Rubeotic glaucoma 4. Congestive glaucoma 5. Diabetic hemorrhagic glaucoma 9
NEOVASCULAR GLAUCOMA (NVG)  Primary initiating events : hypoxia and poor retinal capillary circulation  Begins as formation of new vessels  Ends with fibrovascular membranes migrating over drainage angle, potentially leading to end-stage glaucoma 10
HISTORY 1906  Coates , NVI in CRVO termed as RUBEOSIS IRIDIS 1937  Kurtz , NVA leading to PAS formation 1963  Weiss et al, coined the term NEOVASCULAR GLAUCOMA
ETIOLOGY Diabetic retinopathy (M.C.C) CRVO/CRAO Ocular ischemic disease Carotid artery occlusive disease • 36% cases : arise from CRVO • 32% : proliferative diabetic retinopathy • 13% : carotid artery occlusive disease 13
PATHOGENESIS  Theory of angiogenesis factor: ⚫ Michaelson 1948 Postulated existence of “X factor”, a vasoformative factor which controlled development of new vessels ⚫ Folkman et al Isolated a soluble substance from a solid neoplasm capable of producing neovascularisaton and popularised the term “tumor angiogenesis factor”
 VEGF (Vascular endothelial growth factor) ⚫ Potent angiogenic stimulator ⚫ Has role in both normal and pathologic angiogenesis ⚫ Also known as “vascular permeability factor” as induces vascular hyperpermeability and endothelial cell proliferation ⚫ Four isoforms: 1. VEGF121 2. VEGF165 - 3. VEGF189 4. VEGF206 most abundant form in most tissues
 Lens and vitreous acts as mechanical barriers and also releases vaso inhibitory factors  So any complicated cataract surgery like PCR, APHAKIA can lead to more predisposition  VEGF is synthesised by all tissues in retina, mainly by MULLERS CELL. VEGF conc 50-100 times more in aqueous humour in NVG
Muller cells –primary source in conditions of retinal ischemia Retinal capillary or venous obstruction Hypoxia of retinal cells Production of vasoformative factor Diffuses anteriorly Stimulates iris angiogenesis
 Theory of vasoinhibitory factors (VIF): ⚫ Source of VIF : Vitreous, lens and retinal pigment epithelial cells ⚫ Risk increased by vitrectomy and lensectomy
CLINICAL PRESENTATION  Pain; Reduced vision  Congested eye  A/C reaction  Elevated IOP < 40 mmHg  Mid-dilated, non reactive pupil  Rubeosis irides (NVI)  Neovascularization of the angle (NVA)  Ectropion uveae
Features Normal vessels New vessels Location Iris stroma Pupillary margins Angles Arrangemen t Regular Irregular Appearance Tortuou s Thin Course Radial Arbourising Character Not fenestrated Fenestrate d Scleral spur Not cross Crosses Flouroscein No leakage leakag e
(A)Pre-glaucoma stage with new vessels appearing at pupillary margin and in angle. (B)Open-angle glaucoma stage with new vessels spreading and fibrovascular tissue covering angle. (C)Heavy neovascularization and extensive peripheral anterior synechiae. 25 Stages of neovascular glaucoma.
DIAGNOSIS:  Gonioscopy: vitally important to detect in early stage as NVA can occur without NVI  Strong association with CRVO Treatment of choice  Clear media : Panretinal photocoagulation  Cloudy media ⚫ Prevent laser therapy ⚫ Panretinal cryotherapy - alternative to Vitrectomy to clear the media with endophotocoagulation ⚫ Or subsequent panretinal photocoagulation  Anti -VEGF 33
IRIDOCORNEAL ENDOTHELIAL (ICE) SYNDROME  Group of disorders characterized by abnormal corneal endothelium  Usually includes- ⚫ iris atrophy ⚫ corneal edema ⚫ secondary angle-closure glaucoma without pupillary block
Cause: Abnormal corneal endothelium forming a membrane over anterior surface of iris and angle structures Contraction of this membrane Distorts iris and closes angle
In Variants:  In early to mid adult life  whites > blacks  women > men  U/L > B/L (fellow eye may have subclinical abnormalities)
PATHOGENESIS corneal contracts  Defect site: corneal endothelium – dysfunction edema  Corneal endothelium elaborates a membrane forms PAS glaucoma  Ischemia may be a secondary phenomenon ‘melt holes.’  Few postulations: ⚫ Abnormal proliferation of neural crest cells or a fetal crest of epithelial cells ⚫ Inflammatory endothelial proliferation ⚫ Electron micrographic, immunohistochemical, and serologic studies - herpes simplex virus and EBV as cause 38
CLINICAL PRESENTATION  PAS: extensive in quadrant toward which pupil is displaced  Thinner iris stroma in opposite quadrant to PAS  Full-thickness iris holes  Anteriorly projected pigmented lesions from iris surface with multilayered membrane
ENTITIES ⚫ Progressive iris atrophy ⚫ Chandler’s syndrome ⚫ Cogan-reese syndrome
 Slit-lamp: ‘beaten silver’ endothelium  Specular reflection: loss of the normal, regular endothelial mosaic  Specular microscopy: alterations in size and shape of endothelial 42
PROGRESSIVE (ESSENTIAL) IRIS ATROPHY  Corectopia and ectopion uvea (synechiae lift the iris off the surface of the lens)  Iris dissolution - patchy disappearance of the stroma progresses to full-thickness holes  ‘stretch holes’  ‘ melt holes’ Broad patchy PAS – extend ant to schwalbe line 43
Most common variant - Marked corneal changes - Corectopia is minimal or absent -Endothelium - hammered silver appearance.
 Iris involvement - mild and limited to superficial stromal dissolution.  Peripheral anterior synechiae - not diffuse - do not extend as far anteriorly as in progressive iris atrophy
THE IRIS NAEVUS (COGAN–REESE) SYNDROME  diffuse naevus which covers the anterior iris or iris nodules .  Iris atrophy - absent - 50% of case  mild to moderate although corectopia may be severe.
TREATMENT • Hypertonic solutions or soft contact lenses • If corneal edema produces pain or reduced vision if IOP is reduced - penetrating keratoplasty   Filtering surgery or glaucoma drainage devices used. Goniotomy- short term sucess
POSTERIOR POLYMORPHOUS DYSTROPHY  Disease of corneal endothelium sometimes associated with glaucoma  B/L  Inheritence: autosomal dominant trait (AR also reported)  Defect on: long arm of chromosome 20, three different forms PPCD 1-3
HISTOPATHOLOGY  Thin descemet’s membrane covered by multiple layers of collagen  Cell layers resembles endothelium, epithelium or fibroblasts  Some cases: membrane in angle and on anterior surface of iris
PATHOGENESIS  Cause - It is still controversial  Analogous to ICE syndrome  Some postulates: Dysplastic corneal endothelium produces BM-like material Onto iris Contraction of Iris atrophy, corectopia, and iridocorneal Extends into angle membrane adhesions  developmental disorder  Viral infection (herpes simplex)metaplasia of the corneal endothelium
CLINICAL PRESENTATION  Variable  Most typical physical finding: cluster or linear arrangement of vesicles in posterior cornea surrounded by a gray haze  Deep corneal stroma and DM : ⚫ Band-like thickenings ⚫ White patches ⚫ Peau d’orange appearance ⚫ excrescences projecting on AC
 Associated ⚫corneal edema ⚫iris atrophy ⚫mild corectopia ⚫iridocorneal adhesions
 Mostly non-progressive, asymptomatic  Good vision throughout life  Few cases: progressive corneal changes: corneal edema  Glaucoma seen in 10–15%  Differential diagnosis: ⚫ Fuchs’ corneal dystrophy ⚫ Congenital hereditary corneal dystrophy ⚫ Axenfeld’s syndrome ⚫ Congenital glaucoma: 55
TREATMENT  Most : need no treatment  For edematous cornea ⚫ Hypertonic solutions ⚫ Soft contact lenses ⚫ Penetrating keratoplasty (as needed)  glaucoma - medication - filtering surgery
EPITHELIAL DOWNGROWTH Pathophysiology  Due to entry of epithelial membrane via wound  Proliferation over corneal endothelium, TM, anterior iris surface, and vitreous face  Membrane in angle contracts  PAS  Severe angle-closure glaucoma without pupillary block
 Most common cause - Cataract surgery (ICCE) - penetrating keratoplasty - glaucoma surgery - penetrating trauma, - unsuccessful removal of epithelial cysts of anterior segment
CLINICAL PRESENTATION  low-grade persistent postoperative inflammation: ⚫ conjunctival injection ⚫ photophobia ⚫ Cells in AC ⚫ discomfort  Evidence of current or past wound leak 61
 Diagnostic finding: ⚫ Grayish white membrane with a scalloped, thickened leading edge on the posterosuperior corneal surface. ⚫ Cornea : edematous ⚫ Iris: drawn up to old wound or incision.  Advanced cases: ⚫ Painful eye with bullous keratopathy and intractable glaucoma 62
TREATMENT  Difficult and unrewarding  Techniques used are to close fistula and then to excise or destroy epithelium  For corneal portion of membrane: destroyed with cryotherapy or chemical cauterization.  Iris membrane: excised  Cryotherapy applied to any remaining membrane on ciliary body and retina  En-bloc excision of all involved tissues 63
FIBROVASCULAR INGROWTH  Occurs in an eye with open wound after penetrating trauma or surgery  Specially if associated with ⚫ Hemorrhage ⚫ Inflammation ⚫ Incarcerated tissue  Membrane is seen as interlacing pattern of gray fibers(woven cloth)
Attributing factor:  Invading fibroblasts to subconjunctival connective tissue, corneal stroma, limbal tissue, metaplastic endothelium Invading tissue grows over corneal endothelium, anterior iris surface, vitreous face, and angle Contraction of membrane Formation of PAS
 Other factors contributing to glaucoma: ⚫ Uveitis ⚫ Pupillary block ⚫ Underlying trauma ⚫ Less virulent in course than epithelial ingrowth
FLAT ANTERIOR CHAMBER After penetrating trauma or surgery Formation of PAS SACG without pupillary block  Development of synechiae ⚫ Duration of flat AC ⚫ Degree of inflammation  SACG common - AC remain flat for 5 days or more after cataract extraction 67
IRIDOSCHISIS  Patchy dissolution of iris in which the ant stroma separates from post stroma and muscle layer  rare condition  elderly  bilateral.
 Slit lamp biomicroscopy ⚫ Shallow anterior chamber ⚫ usually involves the inferior iris ⚫ severity ranges from intrastromal atrophy to disintegrated iris fibrils  Anterior stroma splits into strands  Project into AC  Touch cornea
 Gonioscopy - narrow occludable angle – may be associated with PAS.  Treatment ⚫ Peripheral laser iridotomy. ⚫ Subsequent treatment is aimed at limiting glaucomatous damage.
2. POSTERIOR ‘PUSHING MECHANISM a. Ciliary block glaucoma (malignant glaucoma) b. Intraocular tumors c. Nanophthalmos d. Suprachoroidal hemorrhage e. Intravitreal air injection (e.g., retinal pneumopexy) f. Ciliochoroidal effusions (e.g., panretinal photocoagulation) a. Inflammation (e.g., posterior scleritis) b. Central retinal vein occlusion g. Scleral buckling procedure h. Retrolental fibroplasias 72
POSTERIOR PUSHING (OR ROTATIONAL) MECHANISM  Peripheral iris is displaced by lens, vitreous, or ciliary body often accompanied by swelling and anterior rotation of the ciliary body 1. Swelling of ciliary body Rotates forward about its attachment at scleral spur Loosens the zonules Diminishes diameter of ciliary ring Displaces the root of iris Which further acts to close angle. 73
MECHANISMS 2. swelling of anterior uveal tract (inflammation or vascular congestion) Narrowing of ciliary ring Reduced tension on lens zonules Allows lens to come forward Displaces peripheral iris
3. Swelling of ciliary body is often accompanied by accumulation of suprachoroidal and supraciliary fluid further rotates ciliary body and iris root into angle
CILIARY BLOCK GLAUCOMA  Syn: ⚫ Aqueous misdirection ⚫ Malignant glaucoma ⚫ Hyaloid block glaucoma ⚫ Posterior aqueous entrapment  Described by von graefe 1869  Definition: A shallow or flat AC with an inappropriately high IOP despite a patent iridectomy  Affects primarily patients who have narrow anterior chamber angles 76
 Precipitating factors: ⚫ As a complication of a filtering procedure in eyes with pre-existing ACG or shallow AC ⚫ Laser iridotomy ⚫ Miotic usage ⚫ Infectious endophthalmitis 77
PATHOGENESIS…  Posterior misdirection of aqueous flow by a relatively impermeable hyaloid membrane into or behind vitreous body AC Increase in vitreous volume Shallower Increase in IOP Provocating factors:  Small, crowded anterior segment  Angle closure  Swelling and inflammation of ciliary processes  Anterior rotation of ciliary body  Movement of lens-iris diaphragm forward 79
OCULAR MANIFESTATIONS  red, painful eye: commonly after surgery for AACG  Timing: ⚫ Immediate- during surgery ⚫ Months to years later ⚫ Often corresponds to cessation by cycloplegic therapy or initiation due to miotic drops Slit-lamp examination  Shallow or flat anterior chamber(central and peripheral)  Asymmetry of AC with respect to fellow eye  No iris bombé 80
Aqueous misdirection: flat anterior chamber despite a patent iridectomy. 81
DIAGNOSIS  Clinical suspicion after ruling out ⚫ Pupillary block ⚫ Suprachoroidal hemorrhage ⚫ Serous choroidal effusions ⚫ Or other causes of a flat anterior chamber  High-resolution ultrasound biomicroscopy: ⚫ Anterior rotation of ciliary body against peripheral iris ⚫ Forward displacement of posterior chamber intraocular lens ⚫ Shallow central AC 83
TREATMENT  1st line: medical (cycloplegics and mydriatics)  Atropine 1% and phenylephrine 2.5% QID : move lens- iris diaphragm back and relax ciliary muscle  Decrease aqueous production by: ⚫ Topical β-blockers ⚫ Oral or topical CAI ⚫ α-agonists  Shrink the vitreous volume. : ⚫ Isosorbide 1.5 mg/kg orally ⚫ Mannitol 2 g/kg intravenously over a 45-minute 85
2nd line of treatment: laser therapy:  Neodymium:yttrium-aluminum-garnet (Nd:YAG) ⚫ To create a large PI and anterior hyaloid rupture ⚫ To release trapped aqueous from vitreous ⚫ Re-establish normal aqueous flow  Peripheral placement : ⚫ Enable anterior migration aqueous ⚫ Maximize likelihood of resolution of malignant glaucoma.
 Pars plana vitrectomy ⚫ Failed medical or laser therapy ⚫ Phakic eyes for which laser treatment is not a good option:  Narrow angle in fellow eye - laser peripheral iridectomy performed before any other surgical procedures.
INTRAOCULAR TUMORS  Ocular malignant melanoma Mechanisms:  Direct extension of tumor into TM  Seeding of tumor cells into outflow channels  Obstruction of meshwork by pigment or pigment- laden macrophages  Neovascularization  PAS  Iridocyclitis  Hyphema
 Iris melanoma. Invading angle Melanomas of choroid and ciliary body: •Displace lens–iris diaphragm •Angle-closure glaucoma without pupillary block
Leiomyoma pushing the peripheral iri9s1 forward and closing off chamber angle. Adenomas and leiomyomas: Pushes iris forward and cause angle-closure glaucoma.
 Retinoblastoma: frequently associated with glaucoma  Mechanisms  Neovascularization  Angle seeding  Iridocyclitis  Hyphema  By rapidly developing as posterior mass thus displacing lens–iris diaphragm  the mechanism in 27% of cases with elevated IOP.
NANOPHTHALMOS  Normal shaped but small sized eye  sporadic or inherited in an AD/AR pattern  B/L  M =F  Prevalence: 0.06% and 0.1%
Features:  Short AP length (20 mm)  Small corneal diameter  Lens: normal (even somewhat large, in size)  Volume of lens: volume of eye =10–25% (normal=3– 4%)  AC (central / peripheral): shallow  Iris: anteriorly displaced  Sclera: thick  High hyperopia
OCULAR DIMENSIONS OF NANOPHTHALMIC EYES
 Develop ACG :4th – 6th decades of life  Can progress to total synechial closure Angle closure precipitated by:  Development of a choroidal effusion  Rotates ciliary body anteriorly  Displaces peripheral iris  Loosens zonules  Allows lens to move forward
SUPRACHOROIDAL HEMORRHAGE  non-expulsive suprachoroidal hemorrhage  rapidly developing posterior mass  produce angle-closure glaucoma without pupillary block.  most often seen after filtering operations in aphakic eyes
POSTERIOR SEGMENT INFLAMMATORY DISEASE  Posterior scleritis - increased IOP in 12–46%  Mechanisms ⚫ increased viscosity of the aqueous humor ⚫ inflammation of the outflow channels ⚫ obstruction of the trabecular meshwork by inflammatory cells and debris ⚫ PAS ⚫ Neovascularization ⚫ Elevated episcleral venous pressure ⚫ also be associated with choroidal effusion ⚫ secondary angle-closure glaucoma without pupillary block ⚫ swelling and anterior rotation of the ciliary body
CLINICAL FEATURES ⚫ Shallow anterior chamber both centrally and peripherally, ⚫ partial to total angle closure ⚫ sectorial or circumferential choroidal effusion ⚫ IOP - normal, high, or even low depending on the rate of aqueous hum Treatment ⚫ Medical management - systemic non-steroidal anti-inflammatory agents - topical cycloplegic agents - topical and systemic corticosteroids - control IOP 99
CENTRAL RETINAL VEIN OCCLUSION  Vein occlusion interferes with the venous drainage of the uveal tract  swelling and anterior rotation of the ciliary body.  transudation of fluid into the choroid, retina, and vitreous.  Medical treatment  Laser gonioplasty  Pupillary block - laser iridectomy  If ischemia - retinal ablation after the anterior chamber deepens 100
SCLERAL BUCKLING PROCEDURE  Ocular pain, nausea, vomiting, and chemosis.  Examination ⚫ shallow anterior chamber both centrally and peripherally ⚫ corneal edema ⚫ total angle closure ⚫ Intraocular pressure - 25–50 mmHg ⚫ serous or bloody choroidal detachment 101
MECHANISM  displaces the lens, iris and ciliary body  encircling band - temporary interference with the venous drainage of the uveal tract  swelling and anterior rotation of the ciliary body and accumulation of supraciliary and suprachoroidal fluid.  buckle may directly compress one or more vortex veins, leading to vascular congestion and angle-closure glaucoma.. 102
PANRETINAL PHOTOCOAGULATION  Often followed by a shallow anterior chamber and angle  Asymptomatic  Examination ⚫ corneal epithelial edema ⚫ shallow anterior chamber both centrally and peripherally ⚫ myopic shift in refraction ⚫ choroidal detachment ⚫ IOP in the range of 20–50 mmHg ⚫ partial to total angle closure. 103
 Anterior chamber- deepens spontaneously over a few days to a few weeks  Mechanism ⚫ interference with the venous drainage of the uveal tract ⚫ leading to choroidal detachment ⚫ swelling and anterior rotation of the ciliary body.  Medical therapy 104
SECONDARY ANGLE CLOSURE WITH PUPILLARY BLOCK Lens-induced angle closure
PHACOMORPHIC GLAUCOMA  Abnormal lens either compromises the lens–iris channel (pupillary block) or mechanically pushes the peripheral iris forward into the angle structures.  intumescent cataracts - crowd the anterior chamber  swelling, dislocation or subluxation –laser iridotomy 106
Intumescent and swollen lens  Increased pupillary block - develop slowly with an age- related cataract or rapidly with a traumatic, swollen cataract.  Unilateral and resembles PACG  Definitive treatment - cataract extraction.  Iridotomy 107
ECTOPIA LENTIS : Displacement of lens from its normal anatomical position Forward displacement Iris bombe Shallowing of the anterior chamber angle Pupillary block Secondary angle closure. 109
CLINICAL PRESENTATION: ute: ⚫ Pain Conju nctiva l hypere mia ⚫ Los s of visi on 110
TREATMENT  Long term treatment with miotic agents to prevent forward movement of lens.  Treatment of choice to relieve pupillary block : ⚫ Two laser iridotomies (180° apart) pupillary block  Definitive t/m: lensectomy  Lens extraction- Indication: ⚫ to restore vision ⚫ to reduce risk of recurrence of pupillary block 111
APHAKIC OR PSEUDOPHAKIC ANGLE- CLOSURE GLAUCOMA  Extensive adhesions of the iris to the vitreous face - produce pupillary block and secondary angle- closure glaucoma  Iridectomy is not patent, occluded, or omitted  Adherence of the iris to an intraocular lens (IOL) 112
 With anterior chamber lenses the optic may form a ball valve type seal over the pupil while the haptic covers the iridectomy.  Iridectomies spaced far enough apart to prevent the haptics from occluding the openings 113
MICROSPHEROPHAKIA  Congenital  Spherical or globular lens  Often familial  May occur as an isolated condition  Or as part of either Weill-Marchesani or Marfan syndrome.  Can cause ectopia lentis and subsequent pupillary block and 114 ACG lens (arrow) is trapped anteriorly by pupil, resulting in iris bombe and dramatic shallowing of AC
TREATMENT 115  Cycloplegia ⚫ tighten zonule, flatten lens, and pull it posteriorly, breaking pupillary block  Miotics may worses the condition by ⚫ Rotating ciliary body forward ⚫ loosening the zonule ⚫ Allowing lens to become more globular
References 116 # Becker-Shaffer's Diagnosis and Therapy of the Glaucomas; 8th Ed. # American Academy of Ophthalmology BCSC. Section 10; 2015-2016 # Shields Textbook of Glaucoma; 6th Ed. # Yanoff and Duker Ophthalmology 5th Ed
Secondary angle closure glaucoma dr. rahul.pptx

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Secondary angle closure glaucoma dr. rahul.pptx

  • 1.
    SECONDARY ANGLE CLOSURE GLAUCOMA PRESENTEDBY, DR. RAHUL GUPTA 1ST YR. RESIDENT DEPT. OF oPHTHALMOLOGY 7TH JAN, 2024
  • 2.
    CONTENTS 2  Definition  Mechanism ⚫Anterior pulling mechanism ⚫ Posterior pulling mechanism  Diagnosis  Treatment
  • 3.
    SECONDARY ANGLE CLOSUREGLAUCOMA  Caused by impairment of aqueous outflow secondary to apposition between the peripheral iris and the trabeculum.  Related or identifiable ophthalmic condition is known to be present with the onset of angle closure : “secondary” ACG 3
  • 4.
    Two fundamental mechanisms: Anterior pulling mechanism: peripheral iris pulled forward onto TM by contraction of a membrane, inflammatory exudate, or fibrous band  Posterior pushing mechanism: peripheral iris is displaced forward by lens, vitreous, or ciliary body
  • 5.
    CLASSIFICATION 1. Anterior pullingmechanism: Contraction of an inflammatory, hemorrhagic, or vascular membrane, band, or exudate in the angle PAS Forward displacement of lens-iris interface Often accompanied by swelling and anterior rotation of ciliary body 5
  • 6.
    ANTERIOR ‘PULLING MECHANISM a.Neovascular glaucoma b.Iridocorneal endothelial syndromes (e.g. Chandler’s syndrome) c. Posterior polymorphous dystrophy d. Epithelial down growth e. Fibrous ingrowth f. Flat anterior chamber g. Inflammation 6
  • 7.
    NEOVASCULAR GLAUCOMA Secondary glaucomaresulting from neovascularization of anterior segment, including iris and angle often associated with retinal hypoxia. SYNONYMS 1. Hemorrhagic glaucoma 2. Thrombotic glaucoma 3. Rubeotic glaucoma 4. Congestive glaucoma 5. Diabetic hemorrhagic glaucoma 9
  • 8.
    NEOVASCULAR GLAUCOMA (NVG) Primary initiating events : hypoxia and poor retinal capillary circulation  Begins as formation of new vessels  Ends with fibrovascular membranes migrating over drainage angle, potentially leading to end-stage glaucoma 10
  • 9.
    HISTORY 1906  Coates, NVI in CRVO termed as RUBEOSIS IRIDIS 1937  Kurtz , NVA leading to PAS formation 1963  Weiss et al, coined the term NEOVASCULAR GLAUCOMA
  • 11.
    ETIOLOGY Diabetic retinopathy (M.C.C) CRVO/CRAO Ocularischemic disease Carotid artery occlusive disease • 36% cases : arise from CRVO • 32% : proliferative diabetic retinopathy • 13% : carotid artery occlusive disease 13
  • 12.
    PATHOGENESIS  Theory ofangiogenesis factor: ⚫ Michaelson 1948 Postulated existence of “X factor”, a vasoformative factor which controlled development of new vessels ⚫ Folkman et al Isolated a soluble substance from a solid neoplasm capable of producing neovascularisaton and popularised the term “tumor angiogenesis factor”
  • 13.
     VEGF (Vascularendothelial growth factor) ⚫ Potent angiogenic stimulator ⚫ Has role in both normal and pathologic angiogenesis ⚫ Also known as “vascular permeability factor” as induces vascular hyperpermeability and endothelial cell proliferation ⚫ Four isoforms: 1. VEGF121 2. VEGF165 - 3. VEGF189 4. VEGF206 most abundant form in most tissues
  • 14.
     Lens andvitreous acts as mechanical barriers and also releases vaso inhibitory factors  So any complicated cataract surgery like PCR, APHAKIA can lead to more predisposition  VEGF is synthesised by all tissues in retina, mainly by MULLERS CELL. VEGF conc 50-100 times more in aqueous humour in NVG
  • 16.
    Muller cells –primarysource in conditions of retinal ischemia Retinal capillary or venous obstruction Hypoxia of retinal cells Production of vasoformative factor Diffuses anteriorly Stimulates iris angiogenesis
  • 17.
     Theory ofvasoinhibitory factors (VIF): ⚫ Source of VIF : Vitreous, lens and retinal pigment epithelial cells ⚫ Risk increased by vitrectomy and lensectomy
  • 18.
    CLINICAL PRESENTATION  Pain; Reducedvision  Congested eye  A/C reaction  Elevated IOP < 40 mmHg  Mid-dilated, non reactive pupil  Rubeosis irides (NVI)  Neovascularization of the angle (NVA)  Ectropion uveae
  • 19.
    Features Normal vessels Newvessels Location Iris stroma Pupillary margins Angles Arrangemen t Regular Irregular Appearance Tortuou s Thin Course Radial Arbourising Character Not fenestrated Fenestrate d Scleral spur Not cross Crosses Flouroscein No leakage leakag e
  • 20.
    (A)Pre-glaucoma stage withnew vessels appearing at pupillary margin and in angle. (B)Open-angle glaucoma stage with new vessels spreading and fibrovascular tissue covering angle. (C)Heavy neovascularization and extensive peripheral anterior synechiae. 25 Stages of neovascular glaucoma.
  • 21.
    DIAGNOSIS:  Gonioscopy: vitallyimportant to detect in early stage as NVA can occur without NVI  Strong association with CRVO Treatment of choice  Clear media : Panretinal photocoagulation  Cloudy media ⚫ Prevent laser therapy ⚫ Panretinal cryotherapy - alternative to Vitrectomy to clear the media with endophotocoagulation ⚫ Or subsequent panretinal photocoagulation  Anti -VEGF 33
  • 22.
    IRIDOCORNEAL ENDOTHELIAL (ICE) SYNDROME Group of disorders characterized by abnormal corneal endothelium  Usually includes- ⚫ iris atrophy ⚫ corneal edema ⚫ secondary angle-closure glaucoma without pupillary block
  • 23.
    Cause: Abnormal corneal endotheliumforming a membrane over anterior surface of iris and angle structures Contraction of this membrane Distorts iris and closes angle
  • 24.
    In Variants:  Inearly to mid adult life  whites > blacks  women > men  U/L > B/L (fellow eye may have subclinical abnormalities)
  • 25.
    PATHOGENESIS corneal contracts  Defect site:corneal endothelium – dysfunction edema  Corneal endothelium elaborates a membrane forms PAS glaucoma  Ischemia may be a secondary phenomenon ‘melt holes.’  Few postulations: ⚫ Abnormal proliferation of neural crest cells or a fetal crest of epithelial cells ⚫ Inflammatory endothelial proliferation ⚫ Electron micrographic, immunohistochemical, and serologic studies - herpes simplex virus and EBV as cause 38
  • 27.
    CLINICAL PRESENTATION  PAS:extensive in quadrant toward which pupil is displaced  Thinner iris stroma in opposite quadrant to PAS  Full-thickness iris holes  Anteriorly projected pigmented lesions from iris surface with multilayered membrane
  • 28.
    ENTITIES ⚫ Progressive irisatrophy ⚫ Chandler’s syndrome ⚫ Cogan-reese syndrome
  • 29.
     Slit-lamp: ‘beatensilver’ endothelium  Specular reflection: loss of the normal, regular endothelial mosaic  Specular microscopy: alterations in size and shape of endothelial 42
  • 30.
    PROGRESSIVE (ESSENTIAL) IRISATROPHY  Corectopia and ectopion uvea (synechiae lift the iris off the surface of the lens)  Iris dissolution - patchy disappearance of the stroma progresses to full-thickness holes  ‘stretch holes’  ‘ melt holes’ Broad patchy PAS – extend ant to schwalbe line 43
  • 31.
    Most common variant -Marked corneal changes - Corectopia is minimal or absent -Endothelium - hammered silver appearance.
  • 32.
     Iris involvement- mild and limited to superficial stromal dissolution.  Peripheral anterior synechiae - not diffuse - do not extend as far anteriorly as in progressive iris atrophy
  • 33.
    THE IRIS NAEVUS(COGAN–REESE) SYNDROME  diffuse naevus which covers the anterior iris or iris nodules .  Iris atrophy - absent - 50% of case  mild to moderate although corectopia may be severe.
  • 34.
    TREATMENT • Hypertonic solutionsor soft contact lenses • If corneal edema produces pain or reduced vision if IOP is reduced - penetrating keratoplasty   Filtering surgery or glaucoma drainage devices used. Goniotomy- short term sucess
  • 35.
    POSTERIOR POLYMORPHOUS DYSTROPHY  Diseaseof corneal endothelium sometimes associated with glaucoma  B/L  Inheritence: autosomal dominant trait (AR also reported)  Defect on: long arm of chromosome 20, three different forms PPCD 1-3
  • 36.
    HISTOPATHOLOGY  Thin descemet’smembrane covered by multiple layers of collagen  Cell layers resembles endothelium, epithelium or fibroblasts  Some cases: membrane in angle and on anterior surface of iris
  • 37.
    PATHOGENESIS  Cause -It is still controversial  Analogous to ICE syndrome  Some postulates: Dysplastic corneal endothelium produces BM-like material Onto iris Contraction of Iris atrophy, corectopia, and iridocorneal Extends into angle membrane adhesions  developmental disorder  Viral infection (herpes simplex)metaplasia of the corneal endothelium
  • 38.
    CLINICAL PRESENTATION  Variable  Mosttypical physical finding: cluster or linear arrangement of vesicles in posterior cornea surrounded by a gray haze  Deep corneal stroma and DM : ⚫ Band-like thickenings ⚫ White patches ⚫ Peau d’orange appearance ⚫ excrescences projecting on AC
  • 39.
     Associated ⚫corneal edema ⚫irisatrophy ⚫mild corectopia ⚫iridocorneal adhesions
  • 40.
     Mostly non-progressive,asymptomatic  Good vision throughout life  Few cases: progressive corneal changes: corneal edema  Glaucoma seen in 10–15%  Differential diagnosis: ⚫ Fuchs’ corneal dystrophy ⚫ Congenital hereditary corneal dystrophy ⚫ Axenfeld’s syndrome ⚫ Congenital glaucoma: 55
  • 41.
    TREATMENT  Most :need no treatment  For edematous cornea ⚫ Hypertonic solutions ⚫ Soft contact lenses ⚫ Penetrating keratoplasty (as needed)  glaucoma - medication - filtering surgery
  • 42.
    EPITHELIAL DOWNGROWTH Pathophysiology  Dueto entry of epithelial membrane via wound  Proliferation over corneal endothelium, TM, anterior iris surface, and vitreous face  Membrane in angle contracts  PAS  Severe angle-closure glaucoma without pupillary block
  • 44.
     Most commoncause - Cataract surgery (ICCE) - penetrating keratoplasty - glaucoma surgery - penetrating trauma, - unsuccessful removal of epithelial cysts of anterior segment
  • 45.
    CLINICAL PRESENTATION  low-grade persistent postoperativeinflammation: ⚫ conjunctival injection ⚫ photophobia ⚫ Cells in AC ⚫ discomfort  Evidence of current or past wound leak 61
  • 46.
     Diagnostic finding: ⚫Grayish white membrane with a scalloped, thickened leading edge on the posterosuperior corneal surface. ⚫ Cornea : edematous ⚫ Iris: drawn up to old wound or incision.  Advanced cases: ⚫ Painful eye with bullous keratopathy and intractable glaucoma 62
  • 47.
    TREATMENT  Difficult andunrewarding  Techniques used are to close fistula and then to excise or destroy epithelium  For corneal portion of membrane: destroyed with cryotherapy or chemical cauterization.  Iris membrane: excised  Cryotherapy applied to any remaining membrane on ciliary body and retina  En-bloc excision of all involved tissues 63
  • 48.
    FIBROVASCULAR INGROWTH  Occursin an eye with open wound after penetrating trauma or surgery  Specially if associated with ⚫ Hemorrhage ⚫ Inflammation ⚫ Incarcerated tissue  Membrane is seen as interlacing pattern of gray fibers(woven cloth)
  • 49.
    Attributing factor:  Invadingfibroblasts to subconjunctival connective tissue, corneal stroma, limbal tissue, metaplastic endothelium Invading tissue grows over corneal endothelium, anterior iris surface, vitreous face, and angle Contraction of membrane Formation of PAS
  • 50.
     Other factorscontributing to glaucoma: ⚫ Uveitis ⚫ Pupillary block ⚫ Underlying trauma ⚫ Less virulent in course than epithelial ingrowth
  • 51.
    FLAT ANTERIOR CHAMBER Afterpenetrating trauma or surgery Formation of PAS SACG without pupillary block  Development of synechiae ⚫ Duration of flat AC ⚫ Degree of inflammation  SACG common - AC remain flat for 5 days or more after cataract extraction 67
  • 52.
    IRIDOSCHISIS  Patchy dissolutionof iris in which the ant stroma separates from post stroma and muscle layer  rare condition  elderly  bilateral.
  • 53.
     Slit lampbiomicroscopy ⚫ Shallow anterior chamber ⚫ usually involves the inferior iris ⚫ severity ranges from intrastromal atrophy to disintegrated iris fibrils  Anterior stroma splits into strands  Project into AC  Touch cornea
  • 54.
     Gonioscopy -narrow occludable angle – may be associated with PAS.  Treatment ⚫ Peripheral laser iridotomy. ⚫ Subsequent treatment is aimed at limiting glaucomatous damage.
  • 55.
    2. POSTERIOR ‘PUSHINGMECHANISM a. Ciliary block glaucoma (malignant glaucoma) b. Intraocular tumors c. Nanophthalmos d. Suprachoroidal hemorrhage e. Intravitreal air injection (e.g., retinal pneumopexy) f. Ciliochoroidal effusions (e.g., panretinal photocoagulation) a. Inflammation (e.g., posterior scleritis) b. Central retinal vein occlusion g. Scleral buckling procedure h. Retrolental fibroplasias 72
  • 56.
    POSTERIOR PUSHING (ORROTATIONAL) MECHANISM  Peripheral iris is displaced by lens, vitreous, or ciliary body often accompanied by swelling and anterior rotation of the ciliary body 1. Swelling of ciliary body Rotates forward about its attachment at scleral spur Loosens the zonules Diminishes diameter of ciliary ring Displaces the root of iris Which further acts to close angle. 73
  • 57.
    MECHANISMS 2. swelling ofanterior uveal tract (inflammation or vascular congestion) Narrowing of ciliary ring Reduced tension on lens zonules Allows lens to come forward Displaces peripheral iris
  • 58.
    3. Swelling ofciliary body is often accompanied by accumulation of suprachoroidal and supraciliary fluid further rotates ciliary body and iris root into angle
  • 59.
    CILIARY BLOCK GLAUCOMA Syn: ⚫ Aqueous misdirection ⚫ Malignant glaucoma ⚫ Hyaloid block glaucoma ⚫ Posterior aqueous entrapment  Described by von graefe 1869  Definition: A shallow or flat AC with an inappropriately high IOP despite a patent iridectomy  Affects primarily patients who have narrow anterior chamber angles 76
  • 60.
     Precipitating factors: ⚫As a complication of a filtering procedure in eyes with pre-existing ACG or shallow AC ⚫ Laser iridotomy ⚫ Miotic usage ⚫ Infectious endophthalmitis 77
  • 61.
    PATHOGENESIS…  Posterior misdirectionof aqueous flow by a relatively impermeable hyaloid membrane into or behind vitreous body AC Increase in vitreous volume Shallower Increase in IOP Provocating factors:  Small, crowded anterior segment  Angle closure  Swelling and inflammation of ciliary processes  Anterior rotation of ciliary body  Movement of lens-iris diaphragm forward 79
  • 62.
    OCULAR MANIFESTATIONS  red,painful eye: commonly after surgery for AACG  Timing: ⚫ Immediate- during surgery ⚫ Months to years later ⚫ Often corresponds to cessation by cycloplegic therapy or initiation due to miotic drops Slit-lamp examination  Shallow or flat anterior chamber(central and peripheral)  Asymmetry of AC with respect to fellow eye  No iris bombé 80
  • 63.
    Aqueous misdirection: flatanterior chamber despite a patent iridectomy. 81
  • 64.
    DIAGNOSIS  Clinical suspicionafter ruling out ⚫ Pupillary block ⚫ Suprachoroidal hemorrhage ⚫ Serous choroidal effusions ⚫ Or other causes of a flat anterior chamber  High-resolution ultrasound biomicroscopy: ⚫ Anterior rotation of ciliary body against peripheral iris ⚫ Forward displacement of posterior chamber intraocular lens ⚫ Shallow central AC 83
  • 65.
    TREATMENT  1st line:medical (cycloplegics and mydriatics)  Atropine 1% and phenylephrine 2.5% QID : move lens- iris diaphragm back and relax ciliary muscle  Decrease aqueous production by: ⚫ Topical β-blockers ⚫ Oral or topical CAI ⚫ α-agonists  Shrink the vitreous volume. : ⚫ Isosorbide 1.5 mg/kg orally ⚫ Mannitol 2 g/kg intravenously over a 45-minute 85
  • 66.
    2nd line oftreatment: laser therapy:  Neodymium:yttrium-aluminum-garnet (Nd:YAG) ⚫ To create a large PI and anterior hyaloid rupture ⚫ To release trapped aqueous from vitreous ⚫ Re-establish normal aqueous flow  Peripheral placement : ⚫ Enable anterior migration aqueous ⚫ Maximize likelihood of resolution of malignant glaucoma.
  • 67.
     Pars planavitrectomy ⚫ Failed medical or laser therapy ⚫ Phakic eyes for which laser treatment is not a good option:  Narrow angle in fellow eye - laser peripheral iridectomy performed before any other surgical procedures.
  • 68.
    INTRAOCULAR TUMORS  Ocularmalignant melanoma Mechanisms:  Direct extension of tumor into TM  Seeding of tumor cells into outflow channels  Obstruction of meshwork by pigment or pigment- laden macrophages  Neovascularization  PAS  Iridocyclitis  Hyphema
  • 69.
     Iris melanoma. Invading angle Melanomasof choroid and ciliary body: •Displace lens–iris diaphragm •Angle-closure glaucoma without pupillary block
  • 70.
    Leiomyoma pushing theperipheral iri9s1 forward and closing off chamber angle. Adenomas and leiomyomas: Pushes iris forward and cause angle-closure glaucoma.
  • 71.
     Retinoblastoma: frequentlyassociated with glaucoma  Mechanisms  Neovascularization  Angle seeding  Iridocyclitis  Hyphema  By rapidly developing as posterior mass thus displacing lens–iris diaphragm  the mechanism in 27% of cases with elevated IOP.
  • 72.
    NANOPHTHALMOS  Normal shapedbut small sized eye  sporadic or inherited in an AD/AR pattern  B/L  M =F  Prevalence: 0.06% and 0.1%
  • 73.
    Features:  Short APlength (20 mm)  Small corneal diameter  Lens: normal (even somewhat large, in size)  Volume of lens: volume of eye =10–25% (normal=3– 4%)  AC (central / peripheral): shallow  Iris: anteriorly displaced  Sclera: thick  High hyperopia
  • 74.
    OCULAR DIMENSIONS OFNANOPHTHALMIC EYES
  • 75.
     Develop ACG:4th – 6th decades of life  Can progress to total synechial closure Angle closure precipitated by:  Development of a choroidal effusion  Rotates ciliary body anteriorly  Displaces peripheral iris  Loosens zonules  Allows lens to move forward
  • 76.
    SUPRACHOROIDAL HEMORRHAGE  non-expulsivesuprachoroidal hemorrhage  rapidly developing posterior mass  produce angle-closure glaucoma without pupillary block.  most often seen after filtering operations in aphakic eyes
  • 77.
    POSTERIOR SEGMENT INFLAMMATORY DISEASE Posterior scleritis - increased IOP in 12–46%  Mechanisms ⚫ increased viscosity of the aqueous humor ⚫ inflammation of the outflow channels ⚫ obstruction of the trabecular meshwork by inflammatory cells and debris ⚫ PAS ⚫ Neovascularization ⚫ Elevated episcleral venous pressure ⚫ also be associated with choroidal effusion ⚫ secondary angle-closure glaucoma without pupillary block ⚫ swelling and anterior rotation of the ciliary body
  • 78.
    CLINICAL FEATURES ⚫ Shallowanterior chamber both centrally and peripherally, ⚫ partial to total angle closure ⚫ sectorial or circumferential choroidal effusion ⚫ IOP - normal, high, or even low depending on the rate of aqueous hum Treatment ⚫ Medical management - systemic non-steroidal anti-inflammatory agents - topical cycloplegic agents - topical and systemic corticosteroids - control IOP 99
  • 79.
    CENTRAL RETINAL VEINOCCLUSION  Vein occlusion interferes with the venous drainage of the uveal tract  swelling and anterior rotation of the ciliary body.  transudation of fluid into the choroid, retina, and vitreous.  Medical treatment  Laser gonioplasty  Pupillary block - laser iridectomy  If ischemia - retinal ablation after the anterior chamber deepens 100
  • 80.
    SCLERAL BUCKLING PROCEDURE Ocular pain, nausea, vomiting, and chemosis.  Examination ⚫ shallow anterior chamber both centrally and peripherally ⚫ corneal edema ⚫ total angle closure ⚫ Intraocular pressure - 25–50 mmHg ⚫ serous or bloody choroidal detachment 101
  • 81.
    MECHANISM  displaces thelens, iris and ciliary body  encircling band - temporary interference with the venous drainage of the uveal tract  swelling and anterior rotation of the ciliary body and accumulation of supraciliary and suprachoroidal fluid.  buckle may directly compress one or more vortex veins, leading to vascular congestion and angle-closure glaucoma.. 102
  • 82.
    PANRETINAL PHOTOCOAGULATION  Oftenfollowed by a shallow anterior chamber and angle  Asymptomatic  Examination ⚫ corneal epithelial edema ⚫ shallow anterior chamber both centrally and peripherally ⚫ myopic shift in refraction ⚫ choroidal detachment ⚫ IOP in the range of 20–50 mmHg ⚫ partial to total angle closure. 103
  • 83.
     Anterior chamber-deepens spontaneously over a few days to a few weeks  Mechanism ⚫ interference with the venous drainage of the uveal tract ⚫ leading to choroidal detachment ⚫ swelling and anterior rotation of the ciliary body.  Medical therapy 104
  • 84.
    SECONDARY ANGLE CLOSURE WITHPUPILLARY BLOCK Lens-induced angle closure
  • 85.
    PHACOMORPHIC GLAUCOMA  Abnormallens either compromises the lens–iris channel (pupillary block) or mechanically pushes the peripheral iris forward into the angle structures.  intumescent cataracts - crowd the anterior chamber  swelling, dislocation or subluxation –laser iridotomy 106
  • 86.
    Intumescent and swollenlens  Increased pupillary block - develop slowly with an age- related cataract or rapidly with a traumatic, swollen cataract.  Unilateral and resembles PACG  Definitive treatment - cataract extraction.  Iridotomy 107
  • 87.
    ECTOPIA LENTIS : Displacementof lens from its normal anatomical position Forward displacement Iris bombe Shallowing of the anterior chamber angle Pupillary block Secondary angle closure. 109
  • 88.
  • 89.
    TREATMENT  Long termtreatment with miotic agents to prevent forward movement of lens.  Treatment of choice to relieve pupillary block : ⚫ Two laser iridotomies (180° apart) pupillary block  Definitive t/m: lensectomy  Lens extraction- Indication: ⚫ to restore vision ⚫ to reduce risk of recurrence of pupillary block 111
  • 90.
    APHAKIC OR PSEUDOPHAKIC ANGLE-CLOSURE GLAUCOMA  Extensive adhesions of the iris to the vitreous face - produce pupillary block and secondary angle- closure glaucoma  Iridectomy is not patent, occluded, or omitted  Adherence of the iris to an intraocular lens (IOL) 112
  • 91.
     With anteriorchamber lenses the optic may form a ball valve type seal over the pupil while the haptic covers the iridectomy.  Iridectomies spaced far enough apart to prevent the haptics from occluding the openings 113
  • 92.
    MICROSPHEROPHAKIA  Congenital  Sphericalor globular lens  Often familial  May occur as an isolated condition  Or as part of either Weill-Marchesani or Marfan syndrome.  Can cause ectopia lentis and subsequent pupillary block and 114 ACG lens (arrow) is trapped anteriorly by pupil, resulting in iris bombe and dramatic shallowing of AC
  • 93.
    TREATMENT 115  Cycloplegia ⚫ tightenzonule, flatten lens, and pull it posteriorly, breaking pupillary block  Miotics may worses the condition by ⚫ Rotating ciliary body forward ⚫ loosening the zonule ⚫ Allowing lens to become more globular
  • 94.
    References 116 # Becker-Shaffer's Diagnosisand Therapy of the Glaucomas; 8th Ed. # American Academy of Ophthalmology BCSC. Section 10; 2015-2016 # Shields Textbook of Glaucoma; 6th Ed. # Yanoff and Duker Ophthalmology 5th Ed

Editor's Notes

  • #6 1. Iridocorneal Endothelial Syndrome (ICE) syndrome is a unique ophthalmic disorder that involves an irregular corneal endothelium that can lead to varying degrees of corneal edema, iris atrophy, and secondary angle-closure glaucoma. ICE syndrome is a group of disorders with three clinical variants: Chandler Syndrome Essential / Progressive Iris Atrophy Iris Nevus / Cogan-Reese Syndrome 2. PPMD is a subtype of congenital hereditary corneal dystrophies, which often manifest as bilateral, non-inflammatory corneal opacities that may result in corneal edema of the stroma and degradation directly affecting vision. Due to abnormal developmental differentiation, the endothelial layer transforms into cells similar to stratified, squamous epithelium, thus causing an abnormal basement membrane and thickening of Descemets membrane. 3. Epithelial downgrowth occurs when non-keratinized stratified squamous epithelial cells from the conjunctiva or cornea migrate through a wound and proliferate onto a variety of intraocular structures. Typically, the epithelium grows as a sheet, proliferating over the cornea, iris, trabecular meshwork, ciliary body, crystalline/artificial lens, vitreous body, and/or retina