UVEITIC GLAUCOMA TARIQ ALASBALI, MD. POAG JUVENILE PDS PXF HEMOLYTIC PHACOLYTIC INFLAMMATORY ↑ EVP PUPILLARY BLOCK PLATEAU IRIS WITHOUT WITH PUPILLARY BLOCK PUPILLARY BLOCK PHACOMOROHIC ECTOPIA LENTIS APHAKIC PSEUDOPHAKIC INFLAMMATORY PS AQ MISSDIRECTION SUBRETINAL MASS PUSHING AXIAL SHALLOWING •CHOROIDAL EFFUSION •CHOROIDAL HE •AQ MISSDIRECTION •ROP •PHPV •CHOROIDAL MASS PERIPH SHALLOWING IRIS CYST CB CYST CB SWELLING SULFA PRP CB INFLAMMATION CB TUMOUR PULLING PAS FORMATION NVG INFLAMMATION TRAUMA TUMOUR RELATED MEMBRANEGROWTH ICE EPITH DOWNGROWTH FIBROUS INGROWTH Uveitis Classifications Anatomic Classification Duration Classification Uveitis Classifications I) Anatomical Classification: • Anterior • Intermediate (Pars planitis 85%, MS, sarcoid, TB, lyme, toxoplasmosis, toxocariasis, syphilis, IBD (children) lymphoma, Eale’s) • Posterior • Panuveitis (ant + intermediate + post) Anatomical Classification: Q1: Which form of ocular inflammation (anatomical classification) most frequently produces an IOP elevation? A1: Anterior uveitis (chronic >>> acute) Even glaucomas that result from other types of ocular inflammation are usually the consequence of secondary involvement of the anterior uveal tract. Q2. What are typical IOPs in anterior uveitis? Q2. What are typical IOPs in anterior uveitis? A2. LOW secondary to CB shut down +/increased uveoscleral outflow Uveitis Classifications II) Duration Classification: Acute: Usually anterior uveitis Moderate ocular pain Blurred vision Sudden onset Photophobia IOP often LOWER than other eye Sub-acute: Often minimal symptoms often undetected till significant complications Chronic: longer than 3 months Most likely to have ↑ IOP Acute Anterior Uveitis • 0.2% cumulative lifetime incidence in general population • HLA-B27 positive – 50% of cases in white patients (Lancet 1973; 2: 944) – Younger age onset (median early 30s) (AJO 1995; 120:351) – Male > female (AJO 1995; 120:351) – Unilat or unilat alternating > bilat (AJO 1995; 120:351) BEHÇET’S DISEASE Idiopathic multisystem disease More common in men Occurs in 3rd - 4th decade Associated with HLA-B5 BEHÇET’S DISEASE Incidance: 1/100, 000 prevalence in USA 670/100,000 in Japan BD is most prevalent (and more virulent) in the Mediterranean region, Middle East, and Far East, with an estimated prevalence of 1 case per 10,000 persons BEHÇET’S DISEASE Aetiology Unknown Various bacteria and viruses suggested No good evidence to suggest any of them Tumour necrosis factor (TNF) thought to be important BEHÇET’S DISEASE Systemic Involvement Oral aphthous ulceration – 100% Genital ulceration – 90% BEHÇET’S DISEASE Systemic Involvement Skin lesions – 80% Erythema Nodosum Acneiform Uveitis 70% (inflam. of iris, ciliary body or choroid) BEHÇET’S DISEASE Systemic Involvement CNS involvement – strokes Major vessels SVC obstruction Increased skin response to trauma BEHÇET’S DISEASE Ocular Features Acute iritis Pain, redness & VA Flare Inflammatory cells in anterior chamber KPs Recurrent hypopyon (Fluid level of WBC) BEHÇET’S DISEASE Ocular Features Marked inflammation of the eye Retinal vasculitis and haemorrhage Occlusive periphlebitis (venous sheathing & occlusion) Cataract or glaucoma BEHÇET’S DISEASE diagnosis International criteria published in 1990 require Oral ulcers 3 X /1 year + Any 2 of the following: 1. 2. 3. 4. Recurrent genital ulcers eye lesions Skin lesions Positive pathergy test 2mm plus papule developing over 24-48 hrs after oblique insertion of a 20 gauge needle into skin. Sarcoidosis • • • • • • o o o Multisystem inflammatory disorder Unknown origin Young adults Black Histopathology: noncaseating granulomas Systemic involvement: Hilar lymphadenopathy, Peripheral lymphadenopathy, Cutaneous lesions • 38-50% have ocular involvement (AJO 1978; 86:648 & Jpn J Ophthalmol 1992; 36:452) Sarcoidosis – Anterior Uveitis • Most common ocular manifestation = chronic granulomatous uveitis • Mutton fat KPs (15%) (AJO 1978; 86:648) • Bilateral > unilateral • Iris nodules (11.4-35%) (Ophthalmology 1986; 93: 511) • AC angle nodules (49%) (Ophthalmology 1986; 93: 511) • CB nodules (42%) (Ophthalmology 1986; 93: 511) Sarcoidosis – Anterior Uveitis • • • Glaucoma in 11% with ocular sarcoid (AJO 1978; 86:648) Glaucoma in 34% with ocular sarcoid (Jpn J Ophthalmol 2002;46:556-62 ) Most common mechanism of glaucoma : - obstruction of TM with inflammatory debris or nodules (Ann NY Acad Sci 1976; 278:445) Other mechanisms: Inflammatory cell infiltration around the inner and outer walls of Schlemm’s canal Iris bombe with PAS formation NVI and NVA Posner Schlossman Syndrome Fuch’s heterochromic iritis Presentation Acute BOV, haloes, pain. Recurrent episodes Asymptommatic. May have mild BOV Cells Mild inflammation In AC, anterior vitreous KPs Fine, few, may be stellate Small white stellate KPs, scattered diffusely Iris Heterochromia ( diff stromal atrophy) Absence of posterior synechiae. Fine abnormal blood vessels on gonio Other features Cataract. Posner Schlossman Syndrome Presentation Acute BOV, haloes, pain. Recurrent episodes Cells Mild inflammation KPs Fine, few. May be stellate Iris Other features Fuch’s heterochromic iritis Features • Described in 1948 by Posner and Asymptommatic. May Schlossman have mild BOV • “Glaucomatocylitic crisis” characterised by self-limited recurrent episodes of markedly elevated IOP with mild AC In AC, anterior vitreous inflammation •IOP elevation out of proportion to degree of AC inflammation Small white stellate KPs, scattered diffusely •Usually in adults 20-50 yrs Heterochromia ( diff stromal atrophy) Absence of posterior synechiae. Fine abnormal blood vessels on gonio •Previously thought to be idiopathic, but postulated aetiologies include oAbnormal vascular process Cataract. oAutonomic defect oInfective: HSV, CMV Posner Schlossman Syndrome Fuch’s heterochromic iritis Presentation Acute BOV, haloes, pain. Recurrent episodes Asymptommatic. May have mild BOV Cells Low grade In AC, anterior vitreous KPs Fine, few (sometimes sentinel only) Iris Other features Features •Chronic unilateral (bilateral in 10%) iridocyclitis •Classic triad of o Iris heterochromia o KPs o Cataract Small white stellate KPs, scattered diffusely •Low grade inflammation which does not usu req Rx Heterochromia (diffuse stromal atrophy) •Postulated aetiology Absence of posterior o Adrenergic dysfunction synechiae. o Infective cause: link Fine abnormal blood between ocular vessels on gonio toxoplasmosis and FHI o Immunologic theories Cataract. JIA Monoarticular or pauciarticular or polyarticular. F>M RAF –ve ,ANA,HLA-B27. The most common systemic disease associated with uveitis in children. Iridocyclitis in 30% of pauciarticular. Arthritis then uveitis. Under treatment by ophthalmologists → PS + PAS formation → closed angle glaucoma Glaucoma===>14 -27% of JRA. Uveitis Masqueraders (i.e. cells in the AC with ↑ IOP but not uveitis) Infection (chronic endophthalmitis) Tumors (lymphoma, melanoma) Acute angle closure Neovascular glaucoma Secondary reaction to intraocular FB GLAUCOMA ASSOCIATED WITH UVEITIS First reported by: Joseph Beer in -------- 1813 Desmans in -------- 1821 Mackenzie in -------- 1830 Glaucoma Associated with Uveitis 391 eyes F/U median 55 months • Etiology of uveitis: Incidence Types • Topographic • 6.6% at 1 year Difference non-significant • 11.2% at 4 years [P>0.05] • 22.7% at 10 years Conclusion: 1. Presence of glaucoma was associated with an increasing risk of visual loss. 2. The incidence of glaucoma increased with time and similar among different types of uveitis. Neri P. J Glaucoma 2004;13:461-65 Secondary Glaucoma in Uveitis Patients Clinical Entry Uveitis Patients HTLV – 1 uveitis 194 Vogt-Koyanagi-Harada’s disease 107 Ocular toxoplasmosis 85 Sarcoidosis 71 Behcet’s disease 55 Herpetic anterior uveitis 22 HLA-B27-related acute anterior uvietis 21 Posner-Scholossman syndrome 10 Others 92 Idiopathic uveitis 442 TOTAL 1099 Secondary Glaucoma % Affected eyes (A) 17.7 9.7 7.7 6.5 5.0 2.0 1.9 0.9 8.4 40.2 100 260 214 95 129 96 23 25 10 116 636 1604 Eyes (B) 42 35 11 44 20 7 5 10 23 96 293 B/A x 100 (%) 16.2 16.4 11.6 34.1 20.8 30.4 20.0 100* 16.1 15.0 18.3 *HTLV-I: human T-lymphotropic virus type1. HLA: human leukocyte antigen Takahashi T et al. Jpn J Ophthalmol 2002;46:556-62 Glaucoma Associated with Uveitis 25% of uvetic patients: Ocular hypentensive 5-19% of uveitic patients: Develop S.G. Risk factors for elevated IOP in uveitis patients 1. 2. 3. 4. Chronicity Age Corticosteroids Activity Herbert H et al. J. Glaucoma 2004;13:96-99 JIA, and ANA positive uveitis without evidence of arthritis. seqandary glaucoma in children with uveitis Sijssens et al. Ophthalmology 2006;113:853-9 PATHOGENESIS A. Biochemical and Cellular Changes in Aqueous Composition Proteins B. 1.Direct Involvement of the TM Inflammatory CellsEffects on the TM C. 2.Corticosteroids ProstaglandinsChanges in the AC Angle D. 3.Morphologic 4. Inflammatory Mediators (Cytokines) & Toxic Agents PATHOGENESIS A. Biochemical and Cellular Changes in Aqueous uveitis Composition Normal aqueous content is 1% of permeability of blood-aqueous barrier (non-specific) that in the serum 1. Proteins proteins in the aqueous (resembles undiluted serum) Persistent Affects IOP Indirectly Directly Post synechiae & PAS Aqueous sludging, impeding outflow PATHOGENESIS A. Biochemical and Cellular Changes in Aqueous Composition 2. Inflammatory Cells Affects IOP Indirectly Directly By releasing inflammatory mediators, Infiltrate TM and SC causing altering TM cells size, function and mechanical blockage extra-cellular matrix composition. PATHOGENESIS A. Biochemical and Cellular Changes in Aqueous Composition 3. Prostaglandins Affects IOP Prostaglandins E1 & 2 Prostaglandins F2 α IOP IOP PATHOGENESIS A. Biochemical and Cellular Changes in Aqueous Composition 4. Inflammatory Mediators (Cytokines) & Toxic Agents Interleukin-1 Conventional root PATHOGENESIS B. Direct Inflammation of the TM Posner-sehlossman Syndrome Fuchs’ Uveitis Herpetic Keratouveitis PATHOGENESIS Affects IOP C. Effect of Corticosteroids on the TM Increase the aqueous production 35% of normal population, moderate responders Reduction of aqueous outflow BY 4-6% high responders (>15mmHg) 50% or more of POAG population, high responders 1. 2. 3. Alteration in cell size Cytoskeletal organization Extra-cellular matrix deposition Weireb RN et al. Invest Ophthalmol Vis Sci 1985;26:170-5 Levin et Invest al. AmOphthalmol J OphtalmolVis 2002;133:196-202 Veda JDS, et al. Sci 2003;44:4772-9 Velota et al. Curr Opn Ophthalmol 2004;15:136-140 Incidence of steroid responsiveness High(%) Moderate(%) Non(%) 5 35 60 Pts With POAG 90 10 0 Siblings of pts with POAG 30 50 20 Offspring of pts with POAG 25 70 5 General Population PATHOGENESIS D. Morphologic Changes in the Anterior Chamber Angle Open Angle Uveitic Glaucoma • • • • Mechanical blockage to outflow pathways Chronic inflammatory damage to outflow pathways Trabeculitis Steroid-induced PATHOGENESIS D. Morphologic Changes in the Anterior Chamber Angle Angle Closure Uveitic Glaucoma Uveitic Glaucoma Management Evaluation Proper Diagnosis Proper Diagnosis History & Symptoms Visual function (perimetry) Slit-lamp: Etiology clues Gonioscopy: Classification Fundus biomicroscopy: Clues, C/D, NFL UBM: Iridocorneal angle, Ciliary body Uveitis Work Up • CBC + differential • HLA • ESR + CRP • ACE, lysozyme • CXR +/- CT chest • FTA Abs + VDRL • TB skin test • Titers: toxocariasis, toxoplasmosis, lyme Management Control Inflammation: Undertreating uveitis with corticosteroids to minimize IOP elevation at the expense of good control of inflammation is A false economy Management Medical therapy: Beta-blockers CA inhibitors Adrenergic agonists Prostaglandin analogues? Miotics - Avoid Q3: What glaucoma drops have been associated with uveitis? A3: Brimonidine Metipranolol prostaglandin analogues (AJO 2000; 130:287) (AJO 1997; 123:843) (Surv Ophthalmol 2002; 47 (suppl 1): S219) Management Surgical: Laser therapy - Laser iridotomy (pupillary block) - ALT – ineffective (avoid it) Filtering surgery - Trabeculectomy with antimetabolite - Non-penetrating glaucoma surgery - Tube surgery - Goniotomy Cyclodestructive procedures Management Surgical: Trabeculectomy with anti metabolites Up to now is the procedure of choice Success rates variable (30%-78% after 5 years) Hypotony & cataract formation were significant complications. Towler HMA et al. Ophthalmology 2000;107:1822-28 Ceballos EM et al. J Glaucoma 2002;11:189-196 Tube Surgery in Uveitic Glaucoma * Ahmad Glaucoma Valve : (14 eyes, 21 eyes) Success Rates ------ 57% to 94% at 1 year Mata AD et al Ophthalmology 1999;11:2168-72 * Molteno Implant: (40 eyes) - Success Rates: ------ 87% at 5 years ------ 77 % at 10 years - Corneal decompensation ------- 27% Ceballos EM J. Glaucoma 2002; 11:189-96 Cyclophotocoagulation in Uveitic Glaucoma Should be used with caution in patients with uveitis. Already inflammed ciliary body • • • Exacerbate the inflammation Higher risk of profound hypotony Visual loss and phthysis bulbi is a significant risk. Rate of hypotony in uveitic eyes was 19% Murphy CC et al. Br J Ophthalmol 2003;87:1252-7 Aside…DDx Krukenberg Spindle • PDS – – – – – • • • • Young Myopic Male 10% have glaucoma ↑ risk RD Trauma Iris infarction (e.g. zoster, ACG) Tumor Uveitis سأل الممكن المستحيل :أين تقيم ؟ ف أجابه في أحالم العاجز
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