Inflammatory Glaucoma

1. Inflammatory GlaucomaInflammatory Glaucoma
Dr.Ashraful HuqDr.Ashraful Huq
FCPSFCPS
Eye Specialist & SurgeonEye Specialist & Surgeon
Bangladesh Eye Hospital Ltd.Bangladesh Eye Hospital Ltd.
dr.ashraf.ridoy@gmail.comdr.ashraf.ridoy@gmail.com

2. DefinitionDefinition
Inflammatory glaucoma is a condition in whichInflammatory glaucoma is a condition in which
ocular 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 losswith 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.

3. MajorMajor ocular inflammation associatedocular 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
 SyphilisSyphilis
 Vogt-Koyanagi-Harada SyndromeVogt-Koyanagi-Harada Syndrome
 Toxoplasma RetinitisToxoplasma Retinitis
 Scleritis & EpiscleritisScleritis & Episcleritis

4. Diagnostic dilemmasDiagnostic dilemmas
 Fluctuation of IOPFluctuation of IOP
 Ciliary body shutdownCiliary body shutdown
 Uncertain mechanism of raised IOPUncertain mechanism of raised IOP
 Assessment of glaucomatous damageAssessment of glaucomatous damage
 Presence of iris vesselsPresence of iris vessels

5. ClassificationClassification
 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

6. Secondary angle closure withSecondary angle closure with
pupillary blockpupillary block
Pathogenesis-Pathogenesis-
Posterior synechiae → 360° iridolenticularPosterior synechiae → 360° iridolenticular
adhesion(seclusio pupillae) → Iris bombeadhesion(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 contactperipheral cornea → iridocorneal contact
becomes permanent → development ofbecomes permanent → development of
PAS.PAS.

8. FindingsFindings
 Slit lamp bio-microscopy -Slit lamp bio-microscopy -
Seclusio pupillaeSeclusio pupillae
Iris bombeIris bombe
Shallow A/CShallow A/C
 Gonioscopy –Gonioscopy –
Angle closure from irido-trabecular contactAngle closure from irido-trabecular contact
 Indentation gonioscopy –Indentation gonioscopy –
Extent of appositionExtent of apposition

9. ManagementManagement
 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 steroidsIntensive topical steroids
Sub-Tenon triamcinolone acetonide.Sub-Tenon triamcinolone acetonide.

10. ManagementManagement (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.

11. Secondary angle closure withoutSecondary angle closure without
pupillary blockpupillary block
Pathogenesis-Pathogenesis-
Chronic anterior uveitis →deposition andChronic anterior uveitis →deposition and
contraction of inflammatory debris in thecontraction of inflammatory debris in the
angle → pulling of peripheral iris over theangle → pulling of peripheral iris over the
trabeculum → gradual & progressivetrabeculum → gradual & progressive
synechial angle closure.synechial angle closure.

12. Risk factorsRisk factors
 Eyes with pre-existing narrow angleEyes with pre-existing narrow angle
 Eyes with granulomatous inflammationEyes with granulomatous inflammation
with inflammatory nodules in the anglewith inflammatory nodules in the angle

13. FindingsFindings
 Deep A/CDeep A/C
 Extensive angle closure by PAS onExtensive angle closure by PAS on
gonioscopygonioscopy
 Raised IOPRaised IOP
 Optic nerve head changeOptic nerve head change

14. ManagementManagement
 Prevention –Prevention –
Reconstitution of A/CReconstitution of A/C
Good medical control of pre existingGood medical control of pre existing
uveitisuveitis
 Observation in mild uveitisObservation in mild uveitis

15. ManagementManagement (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.

16. Inflammatory open angle glaucomaInflammatory open angle glaucoma
Pathogenesis -Pathogenesis -
 Trabecular obstruction by inflammatoryTrabecular obstruction by inflammatory
cells and debris causing increasedcells and debris causing increased
aqueous viscosity.aqueous viscosity.
 Acute trabeculitis causing inflammationAcute trabeculitis causing inflammation
and edema of trabecular meshwork →and edema of trabecular meshwork →
reduction in meshwork pore sizereduction in meshwork pore size
→Glaucoma.→Glaucoma.

17. Pathogenesis –Pathogenesis – (continued)(continued)
 Hypersecretion by Prostaglandins.Hypersecretion by Prostaglandins.
 Trabecular scarring/sclerosis secondaryTrabecular scarring/sclerosis secondary
to chronic trabeculitis in chronic anteriorto chronic trabeculitis in chronic anterior
uveitis.uveitis.

18. Clinical featuresClinical 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 likeMashed potato like
membrane in themembrane in the
trabeculumtrabeculum

19. ManagementManagement
 IOP comes down to normal once uveitis isIOP comes down to normal once uveitis is
cured.cured.
 Topical steroids are to be applied.Topical steroids are to be applied.

20. Posner-Schlossman SyndromePosner-Schlossman Syndrome
 Also called glaucomatocyclitic crisisAlso called glaucomatocyclitic crisis
 RecurrentRecurrent
 UnilateralUnilateral
 Acute secondary open angle glaucomaAcute secondary open angle glaucoma
associated with mild anterior uveitisassociated with mild anterior uveitis
 Herpes simplex virus may play aHerpes simplex virus may play a
pathogenic rolepathogenic role

21. Posner-Schlossman SyndromePosner-Schlossman Syndrome
(continued)(continued)
 Rare conditionRare 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 at50% patients have bilateral involvement at
different time.different time.
 A significant percentage will developA significant percentage will develop
chronic open-angle glaucoma.chronic open-angle glaucoma.

22. ►►Presentation –Presentation –
mild discomfortmild discomfort
haloes around lightshaloes around lights
slight blurring of visionslight blurring of vision
►►Gonioscopy –Gonioscopy –
Open angle.Open angle.
►►Slit-lampSlit-lamp
biomicroscopy –biomicroscopy –
corneal epithelialcorneal epithelial
oedema,oedema,
High IOP (40-80High IOP (40-80
mmHg),mmHg),
Few aqueous cells,Few aqueous cells,
Fine white centralFine white central
keratic precipitates.keratic precipitates.

23. ManagementManagement
 During acute attack- Topical steroid,During acute attack- Topical steroid,
Aqueous suppressant.Aqueous suppressant.
 Oral non-steroidal anti-inflammatoryOral non-steroidal anti-inflammatory
agents(indomethacin).agents(indomethacin).

24. Fuchs’ uveitis syndromeFuchs’ uveitis syndrome
 Idiopathic, painlessIdiopathic, painless
 Chronic, low-grade iridocyclitis withChronic, 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 ofThe 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 theIt is typically unilateral, but in 13% of the
cases it has presented bilaterallycases it has presented bilaterally

25. FindingsFindings
 Slit lamp bio-microscopy –Slit lamp bio-microscopy –
A. small ,round or stellete gray-whiteA. 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 stromalC.Diffuse iris stromal
atrophy,Heterochromia.atrophy,Heterochromia.
D. Rubeosis,enlarged pupil, vitritis.D. Rubeosis,enlarged pupil, vitritis.

26.  Gonioscopy –Gonioscopy –
A. Normal angleA. Normal angle
B. Neo-vascularizationB. Neo-vascularization
C. Occationally an abnormalC. Occationally an abnormal
membrane over the anglemembrane over the angle
D. Small,non confluent, irregularD. Small,non confluent, irregular
PAS.PAS.

27. ManagementManagement
 Topical glaucoma medication.Topical glaucoma medication.
 Invasive procedure with anti-metabolite.Invasive procedure with anti-metabolite.

28. Points to remember in medicalPoints to remember in medical
treatmenttreatment
 Steroids are absolutely necessary.Steroids are absolutely necessary.
 Treat the inflammation first and the IOPTreat the inflammation first and the IOP
secondarily.secondarily.
 Strong cycloplegia is necessary.Strong cycloplegia is necessary.
 Avoid pilocarpine and other miotics –as it induceAvoid 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 willas in any inflammatory condition, there will
already be copious amounts of prostaglandins inalready be copious amounts of prostaglandins in
the anterior chamber.the anterior chamber.

29. Thank you