UVEITIC GLAUCOMA SIVATEJA CHALLA

LAYOUTINTRODUCTIONHISTORYEPIDEMIOLOGYCLASSIFICATIONPATHOPHYSIOLOGYEVALUATIONSPECIFIC TYPESINVESTIGATIONSTREATMENT

INTRODUCTION Raised intraocular pressure (IOP) is a common accompaniment of inflammatory conditions of the eye.

When IOP elevation in the setting of uveitis is temporary and does not damage the optic nerve, the term uveitis-related ocular hypertension is most appropriate.

Uveitic “glaucoma” must be reserved for cases of uveitis in which elevated IOP is associated with optic nerve damage and visual field changes.

HISTORY In 1813 , Joseph Beer first reported the association of uveitis and glaucoma, describing it as arthritic iritis.

In 1891,Priestley Smith  first modern classification of uveitic glaucoma

EPIDEMIOLOGY 10% patients with uveits Occurs in 3 rd to 4 th decade of life. Females > males Anterior uveitis, older age at presentation, and chronic inflammation are all related to a higher prevalence of uveitic glaucoma Certain types like JIA, sarcoidosis, FHI , herpes simplex keratouveitis are associated with higher prevalence

UNILATERAL GLAUCOMA SHOULD RAISE THE SUSPICION OF AN INFLAMMATORY GLAUCOMA

INDIAN SCENARIO…2650 glaucomatous eyes579 eyes (21.84%) – secondary glaucoma47 eyes (8%) uveitic glaucoma90% of cases followed anterior uveitis

Ritu Gadia, Ramanjit Sihota,Tanuj Dada,Viney Gupta. Current profile of secondary glaucoma. Indian J Ophthalmol. 2008 Jul-Aug; 56(4): 285–289

CLASSIFICATION Anatomical Pathological Etiological Clinical

ANATOMICAL CLASSIFICATION

Anterior Intermediate Posterior PanuveitisFuchs’

heterochromic uveitis

Sarcoidosis Toxoplasmosis Tuberculosis

Posner Schlossman syndrome

Tuberculosis Acute retinal necrosis

Sarcoidosis

Infective uveitis

Lyme’s disease Behcet’s disease

Arthritis associated

uveitis

Vogt-Koyanagi-Harada

Deepankur Mahajan, Pradeep Venkatesh, S.P. Garg ; Uveitis and glaucoma: a critical review : Journal of Current Glaucoma Practise, September December 2011; 5(3): 14-30

PATHOLOGICAL CLASSIFICATION

Non granulomato

us uveitis

Granulomatous

Uveitis

ETIOLOGICAL CLASSIFICATION

InfectiousHerpes zosterVaricella zosterRubella

Idiopathic

SystemicSarcoidosisTuberculosis

AutoimmuneJIASarcoidosis

CLINICAL CLASSIFICATIONInflammatory

ocular hypertension syndromes

(IOHS)

Acute uveitic angle closure

Corticosteriod induced ocular HTN/ glaucoma

Chronic, mixed mechanism

ocular hypertension

glaucoma

1.INFLAMMATORY OCULAR HYPERTENSION SYNDROME Trabeculitis The IOP elevation in these syndromes parallels the course of the inflammation. CAUSES: herpetic anterior uveitis, cytomegalovirus infection, sarcoidosis, toxoplasmosis, syphilis, and Posner Schlossman syndrome

2.ACUTE UVEITIC ANGLE CLOSURE

↑ IOP occurs with or soon after the onset of inflammation but may take longer to resolve than the inflammation.

MECHANISMS : Pupillary block : post synechiae and pupillary membrane iris bombe and angle closure Non pupillary block : iris lens diaphragm moves forward due to choroidal effusion

Eg: VKH , Sympathetic ophthalmia

3.CORTICOSTERIOD INDUCED OCULAR HTN/ GLAUCOMA

Corticosteroid-induced IOP elevation tends to occur days to weeks after the onset of uveitis and initiation of treatment with corticosteroids.

4. CHRONIC, MIXED-MECHANISM OCULAR HTN/GLAUCOMA

IOP ↑ occurs months to years after the onset of inflammation

Chronic closed angle: Angle closure by the “pulling” mechanism” D/T PAS formation or of vascular membranes such as in FHI and other forms of chronic uveitis.

Open angle: In spite of an open angle, there is increased outflow resistance due to chronic damage to the trabecular meshwork.

PATHOPHYSIOLOGY Imbalance between aqueous production and resistance to aqueous outflow from inflammation

Cellular and biochemical

changes

Morphological changes

in angle

CELLULAR AND BIOCHEMICAL CHANGES

Inflamatory cells, proteins, debris, or fibrin liberated from a disrupted blood-aqueous barrier precipitates on TM and leads to mechanical obstruction

INC release of proteins from BAB leads to increased aqueous viscocity

Cytokines from inf cells L/T NVZ of angle

O2 free radicals may cause scarring and membrane formation over TM

MORPHOLOGICAL CHANGES IN ANGLE

Posterior synechiae

Inflammatory pupillary membrane

Iris bombe and Angle closure

PAS and Angle closure

EVALUATIONDetailed

History and systemic

examination

Medication history

Thorough ocular

examination

Tailored investigatio

ns

SLIT LAMP EXAMINATION ANTERIOR SEGMENT

Measure IOP, check lens for cataract changes Fundus look for…

disc changes

retinitis

vascular sheathing

CME

exudates and scars

SPECIFIC TYPES A. FUCHS HETEROCHROMIC UVEITIS B. POSNER-SCHLOSSMAN SYNDROME C. JUVENILE IDIOPATHIC ARTHRITIS D. HERPETIC UVEITIS

A. FUCHS HETEROCHROMIC UVEITIS

TRIAD 90% U/L 3rd-4th decade, both sexes equally Chronic

CLINICAL FEATURES

Low grade iridocyclitis Without synechiaeSmall stellate KPsIris- patchy loss of endothelium, hypo chromia, grey-white nodulesPSCIncreased IOP 13–59%

ASSOCIATIONS

Rubella virus Toxocariasis Toxoplasmosis

INVESTIGATIONS

GONIOSCOPY- vessels in angles

FFA- iris ischemia, NVZ, leakage

MANAGEMENT

Treatment reserved for cataract, Glaucoma and vitreous opacities

Aggressive steroids for the inflammation are not indicated.

Glaucoma should be detected and treated early

Medical management may initially suffice, but eventually patients go on to needing surgical intervention.

Trabeculectomy with MMC, and Glaucoma Valve implants are options.

B. POSNER-SCHLOSSMAN SYNDROME

glaucomatocyclitic crisis, 1948 by Posner and Schlossman 20-60 yrs., unilateral. Recurrent episodes of mild , non granulomatous anterior uveitis with markedly elevated IOP.

Inflammatory changes in the TM and ↑ aqueous humor production secondary to augmented levels of prostaglandins. DECREASED AQUEOUS OUTFLOW FACILITY

MECHANISM

CLINICAL FEATURES

Acute attack :Minimal ocular discomfortBlurring of vision O/Ecorneal epithelial edemamild ciliary flushdilated or sluggishly reactive pupilnonpigmented KP’S on the central and inferior corneaIOP 40-60 mm HgPAS AND PS ABSENT

ASSOCIATIONS

HSV virus CMV virus Ulcerative colitis

MANAGEMENT

Prognosis is usually good.

Controlling inflammation and IOP raise

Inflammation by topical NSAIDS

IOP reduction by aqueous suppressants

Prophylactic therapy does not prevent recurrences and treatment should be given only during acute attack

C. JUVENILE IDIOPATHIC ARTHRITIS

Prevalence of glucoma- 14-27%autoimmune disease typically affecting children <16 years and lasts more than six months Bilateral, non granulomatous, asymptomatic AU, usually preceded by arthritis. Usually they will be asymptomatic and eye looks quiet, so any child with pauci articular arthritis should be referred to ophthalmologistCheck for IOP, cells and flare, disc changes.

Usually open angles, but in later stages pupillary block, secondary angle-closure type, as a result of the formation of posterior synechiae

ANA usually positive RA factor usually negative HLA B 27 positive

INVESTIGATIONS

MANAGEMENT-step ladder approachAchieve remission and continue treatment

Topical steroids predmet 1% hourly and cyclopent 1% TID

↓Change to less potent steroid if IOP

reduces ↓

If steroids fails oral NSAIDS can be tried ↓

If fail, give immune suppressants like oral MTX

GLAUCOMA

Topical beta blockers+CAI, oral CAI If not reducing TRAB+MMC should be done Goniotomy can also be tried

D. HERPETIC UVEITIS

Secondary glaucoma is the most common complication in patients with herpetic uveitis.

28-45% of patients with HSV keratouveitis develop transient ↑ IOP, Secondary glaucoma 10%-54%

Due to inflammation of trabecular meshwork similar to PSS

MECHANISM

Synechiae formationDisciform keratitis, ulcerHypopyon / hyphaema / fibrin depositionDiffuse / sectoral iris atrophy

CLINICAL FEATURES MANAGEM

ENTTACKLE INFECTION INFLAMMATION AND GLAUCOMA

Topical trifluorothymidine , corticosteroids , and cycloplegics

Anti glaucoma agents that ↓ aqueous production.

In patients with several episodes of keratouveitis in a year, oral acyclovir 400 mg bid for a year or more may decrease the recurrences

INVESTIGATIONS Systemic investigations focussing on arthritis, infections, mucosa or skin lesions and cough should be conducted. Non-invasive :Serology- ESR, ACE, Lysozyme, electrolytes, quantiferon goldSkin testsX-ray, MRI, CT scan, Gallium scan

Invasive :Biopsy- conjunctival, vitreous, chorioretinalAnterior chamber paracentesis

TREATMENT AIMS :CONTROL INTRA OCULAR INFLAMMATIONCONTROL IOPTREAT UNDERLYING SYSTEMIC DISEASE

Uveitis is to be treated firstPrimary reason for increased IOPRelieve associated pain and synechiae

CHALLENGES OF TREATING UVEITIC GLAUCOMA Pilocarpine avoided due to increase in spasm and inflammation Prostaglandin analogs would further exacerbate inflammation in cases where mechanism involves PG Fibrinous membrane formation –further clogs the meshwork, hastens drainage Trabeculectomy surgery- production of secondary aqueous, release of more inflammatory mediators, increase inflammation

TREATMENT OF INFLAMMATION

1st line topical / peri ocular /intra vitreal /oral

Decrease photophobia/pain Break or prevent formation of PS

CORTICOSTEROIDS

CYCLOPLEGICS

If corticosteroids are failing then we can use immune suppressants

CONTROL IOP

1St line topical beta blockers. CAI can be combined. Alpha agonist like brimonidine can be added. if desired IOP not achieved then oral CAI can be usedOral or intra venous hyperosmotic agents can also be usedPG analogues are relatively contraindicated,Miotics like pilocar are contraindicated.

MEDICAL METHODS

LPI If pupillary block and iris bombe has formed leading to secondary angle closure then LPI has to be done

TIPSperform on the most convex portion of the iris, and not very peripherally. some times, there may be loculation of aqueous, due to fibrin membranes behind the iris, and in such situations more than one PI may be neededDo large PI, as small PIs tend to get blocked with fibrin / or blood.

Reserved for eyes unresponsive to medical management

some eyes with extensive angle synechiae, or trabecular damage due to long standing uveitis, medical management becomes ineffective and surgical intervention becomes necessary.

Try to perfrom surgery on quiet eye

Pre op steroids can be started

SURGICAL METHODS

Trabeculectomy with antimetabolites and aqueous drainage devices have been successfully used.

Active uveitis, inflammation that is difficult to control, younger age, and history of prior trabeculectomy are all associated with high risk for failure of filtering surgery and an aqueous drainage device is preferable in these patients.

TRABECULECTOMYAfter maximal medical has failedMaximal success with antimetabolites

Uveitic eyes are particularly at risk for postoperative hypotony scleral flap must be sutured tightlyIf hypotony asso with AC shallowing cycloplegia can help move the lens-iris diaphragm posteriorly.Use topical corticosteroids carefully and taper in 6-8 weeks

AQUEOUS DRAINAGE DEVICES Useful in cases with significant conjunctival scarring and cases with failed trab

Ahmed valve is widely used

SUMMARYGlaucoma is seen in 10% of pts with uveitisMechanisms may be of open angle or angle closureCareful history and follow up can be doneMost resolve with topical anti inflammatory agents and medical methodsIf not then surgery has to planned

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