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Inflammatory Glaucoma Inflammatory Glaucoma
Dr.Ashraful HuqDr.Ashraful Huq FCPSFCPS
Eye Specialist & SurgeonEye Specialist & Surgeon Bangladesh Eye Hospital Ltd.Bangladesh Eye Hospital Ltd.
[email protected]@gmail.com
Definition Definition
Inflammatory glaucoma is a condition in whichInflammatory glaucoma is a condition in whichocular inflammation causes -ocular inflammation causes - a persistent or recurrent IOP elevationa persistent or recurrent IOP elevation resulting in progressive optic nerve cuppingresulting in progressive optic nerve cupping with corresponding neuro retinal rim loss with corresponding neuro retinal rim loss and/ or development of typical,perimetric, and/ or development of typical,perimetric,
glaucomatous field defect.glaucomatous field defect.
It presents a diagnostic & therapeutic challenge.It presents a diagnostic & therapeutic challenge.
MajorMajor ocular inflammation associated ocular inflammation associated with secondary glaucomawith secondary glaucoma
Posner-Schlossman syndromePosner-Schlossman syndrome Fuch’s Heterochromic IridocyclitisFuch’s Heterochromic Iridocyclitis Juvenile Rheumatiod ArthritisJuvenile Rheumatiod Arthritis SarcoidosisSarcoidosis Herpes Simplex Kerato-uveitisHerpes Simplex Kerato-uveitis Vericella Zoster IridocyclitisVericella Zoster Iridocyclitis Syphilis Syphilis Vogt-Koyanagi-Harada SyndromeVogt-Koyanagi-Harada Syndrome Toxoplasma RetinitisToxoplasma Retinitis Scleritis & EpiscleritisScleritis & Episcleritis
Diagnostic dilemmas Diagnostic dilemmas
Fluctuation of IOPFluctuation of IOP Ciliary body shutdown Ciliary body shutdown Uncertain mechanism of raised IOP Uncertain mechanism of raised IOP Assessment of glaucomatous damage Assessment of glaucomatous damage
Presence of iris vesselsPresence of iris vessels
Classification Classification
Angle-closure with pupillary blockAngle-closure with pupillary block Angle-closure without pupillary blockAngle-closure without pupillary block Open angleOpen angle Posner-Schlossman syndromePosner-Schlossman syndrome
Secondary angle closure with Secondary angle closure with pupillary blockpupillary block
Pathogenesis-Pathogenesis-
Posterior synechiae → 360° iridolenticular Posterior synechiae → 360° iridolenticular
adhesion(seclusio pupillae) → Iris bombe adhesion(seclusio pupillae) → Iris bombe → shallow anterior chamber and → shallow anterior chamber and apposition of the iris to the trabeculum & apposition of the iris to the trabeculum & peripheral cornea → iridocorneal contact peripheral cornea → iridocorneal contact becomes permanent → development of becomes permanent → development of PAS.PAS.
Findings Findings
Slit lamp bio-microscopy - Slit lamp bio-microscopy - Seclusio pupillaeSeclusio pupillae Iris bombeIris bombe Shallow A/C Shallow A/C Gonioscopy – Gonioscopy – Angle closure from irido-trabecular contactAngle closure from irido-trabecular contact Indentation gonioscopy – Indentation gonioscopy – Extent of appositionExtent of apposition
Management Management
Prevention of posterior synechiae & Prevention of posterior synechiae & seclusio pupillae - seclusio pupillae -
Atropine 1%Atropine 1% Tropicamide 1%Tropicamide 1% Mydriatics.Mydriatics. Prevention of synechial angle closure - Prevention of synechial angle closure - Intensive topical steroids Intensive topical steroids Sub-Tenon triamcinolone acetonide.Sub-Tenon triamcinolone acetonide.
Management Management (continued)(continued)
Lowering of IOP – Lowering of IOP –
Topical aqueous suppressant : beta-Topical aqueous suppressant : beta-blocker, CAI , Hyper osmotic agents.blocker, CAI , Hyper osmotic agents.
Surgery – Surgery –
Laser iridotomyLaser iridotomy
Surgical iridectomy.Surgical iridectomy.
Secondary angle closure without Secondary angle closure without pupillary blockpupillary block
Pathogenesis- Pathogenesis-
Chronic anterior uveitis →deposition and Chronic anterior uveitis →deposition and contraction of inflammatory debris in the contraction of inflammatory debris in the angle → pulling of peripheral iris over the angle → pulling of peripheral iris over the trabeculum → gradual & progressive trabeculum → gradual & progressive synechial angle closure.synechial angle closure.
Risk factors Risk factors
Eyes with pre-existing narrow angleEyes with pre-existing narrow angle
Eyes with granulomatous inflammation Eyes with granulomatous inflammation with inflammatory nodules in the anglewith inflammatory nodules in the angle
Findings Findings
Deep A/CDeep A/C Extensive angle closure by PAS on Extensive angle closure by PAS on
gonioscopygonioscopy Raised IOPRaised IOP Optic nerve head changeOptic nerve head change
Management Management
Prevention – Prevention –
Reconstitution of A/CReconstitution of A/C
Good medical control of pre existing Good medical control of pre existing uveitisuveitis
Observation in mild uveitisObservation in mild uveitis
Management Management (continued)(continued)
Medical management -Medical management -
Topical aqueous suppressant : beta-Topical aqueous suppressant : beta-blocker, CAI, Hyperosmotic agents.blocker, CAI, Hyperosmotic agents.
Invasive procedure – Invasive procedure –
Trabeculectomy with anti metabolite, Trabeculectomy with anti metabolite, Trabeculo dialysis, Trabeculo dialysis,
Artificial drainage shunts,Artificial drainage shunts,
Cyclo destructive procedure.Cyclo destructive procedure.
Inflammatory open angle glaucomaInflammatory open angle glaucoma
Pathogenesis - Pathogenesis - Trabecular obstruction by inflammatory Trabecular obstruction by inflammatory
cells and debris causing increased cells and debris causing increased aqueous viscosity.aqueous viscosity.
Acute trabeculitis causing inflammation Acute trabeculitis causing inflammation and edema of trabecular meshwork → and edema of trabecular meshwork → reduction in meshwork pore size reduction in meshwork pore size →Glaucoma. →Glaucoma.
Pathogenesis – Pathogenesis – (continued)(continued)
Hypersecretion by Prostaglandins.Hypersecretion by Prostaglandins. Trabecular scarring/sclerosis secondary Trabecular scarring/sclerosis secondary
to chronic trabeculitis in chronic anterior to chronic trabeculitis in chronic anterior uveitis.uveitis.
Clinical features Clinical features
Raised IOPRaised IOP Flares and cellsFlares and cells Posterior synechiaePosterior synechiae Keratic precipitates (KP)Keratic precipitates (KP) Irregular small pupilIrregular small pupil Mashed potato like Mashed potato like
membrane in the membrane in the trabeculumtrabeculum
Management Management
IOP comes down to normal once uveitis is IOP comes down to normal once uveitis is cured. cured.
Topical steroids are to be applied.Topical steroids are to be applied.
Posner-Schlossman SyndromePosner-Schlossman Syndrome
Also called glaucomatocyclitic crisisAlso called glaucomatocyclitic crisis RecurrentRecurrent UnilateralUnilateral Acute secondary open angle glaucoma Acute secondary open angle glaucoma
associated with mild anterior uveitisassociated with mild anterior uveitis Herpes simplex virus may play a Herpes simplex virus may play a
pathogenic rolepathogenic role
Posner-Schlossman Syndrome Posner-Schlossman Syndrome (continued)(continued)
Rare condition Rare condition Affecting young adultsAffecting young adults 40% of whom are HLA-Bw54 positive40% of whom are HLA-Bw54 positive Male > FemaleMale > Female 50% patients have bilateral involvement at 50% patients have bilateral involvement at
different time.different time. A significant percentage will develop A significant percentage will develop
chronic open-angle glaucoma.chronic open-angle glaucoma.
►►Presentation –Presentation –
mild discomfortmild discomfort
haloes around lightshaloes around lights
slight blurring of visionslight blurring of vision
►►Gonioscopy – Gonioscopy –
Open angle.Open angle.
► ►Slit-lamp Slit-lamp
biomicroscopy – biomicroscopy –
corneal epithelial corneal epithelial oedema,oedema,
High IOP (40-80 High IOP (40-80 mmHg),mmHg),
Few aqueous cells,Few aqueous cells,
Fine white central Fine white central keratic precipitates.keratic precipitates.
Management Management
During acute attack- Topical steroid, During acute attack- Topical steroid, Aqueous suppressant.Aqueous suppressant.
Oral non-steroidal anti-inflammatory Oral non-steroidal anti-inflammatory agents(indomethacin).agents(indomethacin).
Fuchs’ uveitis syndromeFuchs’ uveitis syndrome
Idiopathic, painlessIdiopathic, painless Chronic, low-grade iridocyclitis with Chronic, low-grade iridocyclitis with
heterochromia,due to iris stromal atrophyheterochromia,due to iris stromal atrophy CataractCataract The typical age of onset is 20 - 40 years of The typical age of onset is 20 - 40 years of
ageage Men and women affected equallyMen and women affected equally It is typically unilateral, but in 13% of the It is typically unilateral, but in 13% of the
cases it has presented bilaterallycases it has presented bilaterally
Findings Findings
Slit lamp bio-microscopy – Slit lamp bio-microscopy –
A. small ,round or stellete gray-white A. small ,round or stellete gray-white
scattered KP. scattered KP.
B.Faint flare & few cells,no synechiae. B.Faint flare & few cells,no synechiae.
C.Diffuse iris stromal C.Diffuse iris stromal
atrophy,Heterochromia. atrophy,Heterochromia.
D. Rubeosis,enlarged pupil, vitritis.D. Rubeosis,enlarged pupil, vitritis.
Gonioscopy – Gonioscopy –
A. Normal angle A. Normal angle
B. Neo-vascularization B. Neo-vascularization
C. Occationally an abnormal C. Occationally an abnormal
membrane over the angle membrane over the angle
D. Small,non confluent, irregular D. Small,non confluent, irregular
PAS.PAS.
Management Management
Topical glaucoma medication.Topical glaucoma medication.
Invasive procedure with anti-metabolite.Invasive procedure with anti-metabolite.
Points to remember in medical Points to remember in medical treatmenttreatment
Steroids are absolutely necessary.Steroids are absolutely necessary. Treat the inflammation first and the IOP Treat the inflammation first and the IOP
secondarily.secondarily. Strong cycloplegia is necessary. Strong cycloplegia is necessary. Avoid pilocarpine and other miotics –as it induce Avoid pilocarpine and other miotics –as it induce
ciliary spasm and increase inflammation.ciliary spasm and increase inflammation. Avoid the prostaglandin analog –Avoid the prostaglandin analog – as in any inflammatory condition, there will as in any inflammatory condition, there will
already be copious amounts of prostaglandins in already be copious amounts of prostaglandins in the anterior chamber.the anterior chamber.
Thank you
