Uveitic glaucoma, Dr. Janhvi Mehta,Dr. Rita Dhamankar

1. Uveitic glaucoma
Presenter- Dr. Janhvi Mehta
Moderator- Dr. Rita Dhamankar

2. Index
 Case presentation
 Definition
 History
 Epidemiology
 Age at presentation
 Sex preponderance
 Pathogenesis
 Classification
 Clinical features
 Investigations
 Specific diseases
 Differential diagnosis
 Management

3. Case presentation
 Mrs BM, 45yr female
 16th sept 2011
 C/O LE BOV for distance and near since 1 month
 H/O LE trauma with wooden stick in 2006
 H/O glasses since 5 yrs (not using since 1 yr)
 No H/O systemic illness

4. examination
RE LE
BCVA 6/9,N6 BCVA 6/36, N36
AS- cornea clear AS- ep. microcystic edema
PACD =1/2 CT(grade II) VH grade 0, cells ++
Pupil- irregular PAS at 3 o’
clock, and 6-8 o’ clock
Pupil- 360˚ posterior
synechiae, iris bombe
Lens- Early NS Lens- Early NS
Fundus – CDR- 0.7 : 1 Fundus- Hazy view
IOP- 11 mmHg IOP- 39 mmHg

6. Management
 LE YAG peripheral iridotomy done on same day
 LE Gatifloxacin-Dexamethasone combination e/d
QID for 1 week
 LE Timolol maleate 0.5% e/d BD for 1 week

7. After 1 week
 LE – BCVA 6/36, N18
 LE patent PI
 IOP RE- 10mmHg; LE-34mmHg
 Started on brimonidine tartrate+timolol maleate
combination e/d BD
 Gonioscopy- PTM SL
PTM PTM SL SL
PTM SL

8. 1 month follow up
 IOP – RE 8mmHg ; LE 22mmHg
 Impression- secondary glaucoma post uveitis

9. After 2 months
 LE pain
 IOP- LE 32mmHg
 AC shows no cells / Flare , only old KP’s
 Management- added LE Brinzolamide e/d BD

10. After 2 months
 c/o LE redness , pain, watering since 5-7 days
 O/E – RE healed uveitis with posterior synechiae with
complicated cataract
 LE- circumciliary congestion,
old pigmented KPs,
Cells 1+
360˚PAS
PI patent
IOP- 30mmHg
 Management- prednisolone acetate e/d QID
Homatropine e/d BD
Continue antiglaucoma medication

11. Investigations
 Mantoux test – negative
 ESR- normal
 CCT- RE- 460μm
LE- 447μm
 Fundus : normal sized disc with a c/d 0.9
 Diagnosis – active nongranulomatous uveitis with
secondary glaucoma with cataract
 Advised LE cataract surgery with trabeculectomy with
MMC

12. Further management
 Prenisolone acetate 1% e/d in tapering doses
 Injection 5-FU s/c post operatively
 Timolol maleate 0.5% e/d BD

13. Last visit
RE LE
BCVA 6/18,N6 BCVA 6/9, N6
AS- pigmented old KP AS- few pigmented old KP
Post. synechiae Diffuse shallow bleb
Lens- NS2 Lens- PCIOL
Fundus – CDR- 0.7 : 1 Fundus – CDR 0.9 : 1
IOP- 12 mmHg IOP- 12 mmHg

14. Definition
Elevated
IOP
uveitis
Glaucomatous
optic nerve
damage
Visual field
defects

15. History
 1st reported by Joseph Beer 1813
 Priestly Smith 1891- modern classification of UG
 20% of uveitic patients have glaucoma
 More common in chronic cases

16. Epidemiology
 INDIAN SCENARIO
 2650 glaucomatous eyes
 579 eyes (21.84%) – secondary glaucoma
 47 eyes (8%) uveitic glaucoma
 90% 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

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

18. Study Anterior Intermediate Posterior panuveitis
Merayo
Lloves J
et al
67% 5% 14% 14%
Merayo Lloves J, Power WJ, Rodriguez A et al. secondary
glaucoma in patients with uveitis. Ophthalmologica 1999;
213(5): 300-04

19. Age at presentation
 3rd to 4th decade
 With increasing age there is imbalance in trabecular
meshwork function and inflammatory load
 Mean age – 41.1 yrs
 10%- 41-60yrs; 9%- 21-40yrs
 Prevalence in children- 5% - 13.5%
Ritu Gadia, Ramanjit Sihota,Tanuj Dada,Viney Gupta. Current profile of
secondary glaucoma. Indian J Ophthalmol. 2008 Jul-Aug; 56(4): 285–289
Kanski JJ , Shun Shin GA. Systemic uveitis syndrome in childhood: an
analysis of 340 cases. Ophthalmology 1984:91:1247-52

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

21. Pathogenesis
 Various mechanisms
 Imbalance between aqueous production and
resistance to aqueous outflow from inflammation
Cellular and
biochemical changes
Morphological changes in
angle

22. Cellular and Biochemical changes
 Inflammatory cells-
 PMNs and macrophages increase IOP by:-
 Mechanical obliteration
 Cytotoxic
 Proinflammatory cells
 Proteins:-
 Increased permeability of blood aqueous barrier leads to
nonspecific transudation of protein
 Increased aqueous viscosity
 Reduced outflow
 Chronic flare

23. Cellular and Biochemical changes
 Inflammatory mediators and toxic agents:-
 Cytokines-
 Secreted by macrophages and lymphocytes
 Promote neovascularization
 Oxygen free radicals might damage outflow pathway

24. Morphological changes
 Usually open angle glaucoma
 Mechanical obstruction
 Increased viscosity
 Mediators causing constriction of trabecular
endothelium
 Trabeculitis
 Chronic cases
 Prolonged use of corticosteroids

25. Morphological changes
 Angle closure glaucoma- secondary
 Posterior synechiae and iris bombe
 Peripheral anterior synechiae
 Ciliary body rotates forward

26. Classification
 Anatomical
 Pathological
 Etiological

27. Anterior Intermediate Posterior Panuveitis
Fuchs’
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
DeepankurMahajan, Pradeep Venkatesh, S.P. Garg ; Uveitis and
glaucoma: a critical review : Journal of Current Glaucoma Practise,
September December 2011; 5(3): 14-30

28. Pathological classification
Non
granulomatous
uveitis
Granulomatous
Uveitis

29. Etiological classification
 Infectious
 Herpes
 Varicella zoster
 Rubella
 Autoimmune
 JIA
 Sarcoidosis
 Systemic
 Sarcoidosis
 Tuberculosis
 Idiopathic

30. Signs and symptoms
 Blurring Of Vision
 Pain
 Redness
 IOP elevation
 Corneal edema
 Photophobia and coloured halos

31. Investigations
 Noninvasive
 Serology- ESR, ACE, Lysozyme, electrolytes,
quantiferon gold
 Skin tests
 Xray, MRI, CT scan, Gallium scan
 Invasive
 Biopsy- conjunctival, vitreous, chorioretinal
 Anterior chamber paracentesis

32. Investigations
 Scanning laser ophthalmoscopy-
Optic nerve head
 Ultrasound biomicroscopy-angle
and ciliary body
 Laser flare photometry

33. Uveitis associated glaucoma
 Fuchs’ heterochromic uveitis
 Posner Schlossman syndrome
 Juvenile idiopathic arthritis
 Herpetic uveitis
 Sarcoidosis
 Syphilis

34. Fuchs’ Heterochromic Uveitis
 Ernst Fuchs, 1906
 Anterior uveitis , heterochromia, cataract
 90% U/L
 3rd-4th decade, both sexes equally
 Chronic

35. Clinical features
 Low grade iridocyclitis
 Without synechiae
 Small stellate KPs
 Fine filaments on endothelium
 Iris- patchy loss of endothelium,
hypochromia, grey-white nodules
 PSC
 Increased IOP - 13–59%
Liesegang TJ: Clinical features and prognosis in Fuchs’ uveitis
syndrome, Arch Ophthalmol 100:1622, 1982.
Velilla S, et al: Fuchs’ heterochromic iridocyclitis: a review of 26
cases, Ocul Immunol Inflamm 9:169, 2001.

36. Associations
 Rubella virus
 Virus and antibodies found in aqueous of FHU patients
 Incidence in the United States has significantly
declined since the advent of rubella vaccination
program.
 Toxocariasis and Toxoplasmosis antibodies also found
Birnbaum AD, et al: Epidemiologic relationship
between Fuchs’ heterochromic iridocyclitis and the
United States rubella vaccination program, Am J
Ophthalmol 144:424, 2007

37. Investigations
 Gonioscopy
 Vessels in angles
 Fluorescein angiography of the iris
 demonstrates ischemia, leakage, neovascularization,
and delayed filling of the vessels.
Areas of non
perfusion
leakage

38. Management
 Poorly responsive to corticosteroid therapy
 Aqueous suppressants
 Surgery- filtration surgery with anti metabolites

39. Posner- Schlossman syndrome
 Glaucomatocyclitic crisis
 1948, Posner and Schlossman
 20-60yrs, U/L
 Mild anterior uveitis with very high IOP
 Discomfort, blurring of vision, haloes
 PG level in aqueous

40. Clinical features
 mild ciliary flush
 a dilated or sluggishly
reactive pupil
 There may be Post syn
 corneal epithelial edema
 IOP - 40–60 mmHg
 open angles
 faint flare
 fine keratic precipitates

41. Pathogenesis
 Immunogenetic- HLA-Bw54
 Viral infection- herpes simplex and cytomegalovirus
 GI disease like ulcerative colitis
 Allergy
 Vascular cause
 PGI, oral indomethacin, s.c. polyphloretin

42. Investigations
 Fluoroscein angiography of iris
leakage
Areas of
non
perfusion

43. Management
 Topical NSAID
 Topical steroid
 Oral NSAID or CAI

44. Juvenile Idiopathic Arthritis
 Prevalence- 14-27%
 Persistent low grade intraocular
inflammation
 Young girls
 Mono/Pauciarticular involvement
 Glaucoma – posterior synechiae/
pupillary block or trabeculitis
Kanski JJ, Shun-Shin GA. Systemic uveitis syndromes in childhood: an
analysis of 340 cases. Ophthalmology. 1984; 91:1247—52
Key SN 3rd, Kimura SJ. Iridocyclitis associated with juvenile
rheumatoid arthritis. Am J Ophthalmol. 1975;80:425--9

45. Investigations
 Antinuclear- antibody test
 Rheumatoid factor- usually negative
 Systemic investigations

46. Management
 Topical steroids and cycloplegics
 Regional injection steroids
 Systemic steroids
 Oral NSAIDs
 Immunomodulatory therapy- Methotrexate
 Glaucoma- BB/ Sympathomimetics, CAI, MMC Trab
 Modified goniotomy- Trabeculodialysis Not done any
more

47. Herpetic uveitis
 Secondary glaucoma 10%-54%
 Acute rise in IOP, active iridocyclitis
 U/L
 Herpes simplex, Herpes Zoster, Varicella Zoster
Karbassi M, Raizman MB, Schuman JS. Herpes zoster
ophthalmicus. Surv Ophthalmol. 1992;36:395--410

48. Clinical features
 Synechiae formation
 Disciform keratitis, ulcer
 Hypopyon / hyphaema / fibrin deposition
 Diffuse / sectoral iris atrophy

49. Management
 Systemic antivirals
 Topical steroids and cycloplegics
 IOP- aqueous humour suppressants
 Trabeculectomy with anti metabolites
 Tube shunt surgery- active inflammation

50. Sarcoidosis
 Multisystem granulomatous disease
 Lungs , skin, eyes
 10% develop raised IOP
 Pathogenesis
 Swelling of trabecular meshwork
 Mechanical obstruction
 PAS
 Posterior synechiae
 Neovascular glaucoma
Mutton fat
KP’s

51. Signs
 Conjunctival granuloma
 Anterior uveitis – 22%
 Posterior- vitritis,
intermediate/ panuveitis,
choroidal nodules, CME
 ‘Candle wax dripping’ and
‘punched out lesions’

52. Investigations
 Serum ACE levels- elevated
 Lysozyme levels- elevated
 Hypercalcaemia
 Chest X-ray
 Gallium scan
 PFT

53. Management
 Tube shunt procedures with anti metabolites

54. Syphilis
 Congenital/ Acquired
 Secondary open angle glaucoma in active
inflammatory phases
 Gonioscopy- peripheral anterior synechiae, irregular
pigmentation of TM, presence of endothelial
membrane
 Poor response to medication
 Filtration surgery with drainage valve implantation/
anti metabolites

55. Differential diagnosis
Inflammatory ocular hypertension syndrome(IOHS)
 Elevated IOP for a short duration in uveitis
 More common
 No optic nerve damage or visual field defects
 Raised IOP due to inflammation
 IOP falls after treatment with topical steroids

56. Differential diagnosis
Steroid induced glaucoma
 Instillation of steroids in greater frequency, higher
dose, over a longer period
 Emulate picture of POAG
 Transient raised IOP after instillation- steroid
responders
 Discontinue drug/ weaker alternative

57. Differential diagnosis
Uveitis-glaucoma-hyphaema syndrome
 Presence of iris supported and AC IOLS
 Recurrent raised IOP, uveitis and hyphaema after
cataract surgery
 Extreme blurring, iris chaffing due to IOL haptic

58. Principle of Management
 Manage inflammation first
 Steroids and antiglaucoma help
 Removal of IOL

59. Need to treat primary cause
 Uveitis is to be treated first
 Primary reason for increased IOP
 Relieve associated pain and synechiae

60. Management of inflammation
 Topical / systemic NSAIDs
 Topical / periocular/ systemic corticosteroids
 Systemic immunosuppresants
 Mydriatics/ cycloplegics
 Antimicrobials

61. 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

62. Management of UG
 Medical
 Beta blockers
 Carbonic anhydrase inhibitors
 Systemic CAI
 i.v hyperosmotic agents
 PG analogs

63. Beta blockers
 1st drug of choice
 Reduce aqueous humour production
 Doesn’t alter pupil size
 Timolol- no systemic contraindication
 Metipranolol- avoided not available

64. Carbonic anhydrase inhibitors
 Reduce aqueous production
 Oral, intravenous, topical
 Dorzolamide- prolonged corneal edema
 Systemic- short term in acute high IOP

65. Hyperosmotic agents
 Intravenous route
 Acute rise in IOP
 Secondary angle closure glaucoma with pupillary
block
 Reduce vitreous volume

66. Prostaglandin analogs
 Initially thought to increase CME and exacerbation of
inflammation
 Used with caution
 Bimoprost, latanoprost, travoprost

67. Rho-kinase inhibitors
 Relaxes trabecular meshwork :-
 Increasing aqueous outflow
 Increasing blood flow to optic disc
 Protecting health of ganglion cells
 Antifibrotic agent post glaucoma surgery
 These drugs are in the pipeline & will be available in
future
Jamie Lynne Metzinger, Olga Ceron, C. Stephen Foster Recent
Advances in Uveitic Glaucoma; Glaucoma Now – Issue No 3, 2013
Challa P, Arnold JJ. Rho-kinase inhibitors offer a new approach in the
treatment of glaucoma. Expert Opinion in Investigational Drugs, 2013

68. Surgical
 Trabeculoplasty
 Laser iridotomy
 Trabeculectomy
 Non penetrating glaucoma surgery
 Drainage devices
 Cycloablation

69. Trabeculoplasty
 ALT/ SLT
 Argon laser trabeculoplasty not preferred – IOP not
under control due to angle alterations
 SLT- 532nm Q switched Nd- YAG laser
 Target pigmented cells in TM
 Low power
 Ultra short duration
 Minimal collateral thermal damage
 Maintain structural integrity
Realini T. Selective laser trabeculoplasty: a review.
J Glaucoma. 2008;17:497--502

70. Laser Iridotomy
 Argon / Nd YAG laser
 Iris bombe or angle closure due to pupillary block
 Generally- 3 bursts of 3-6 mJ

71. Trabeculectomy
 In phakic uveitic glaucoma patients
 After maximal medical and laser therapy has failed
 Maximal success with antimetabolites

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

73. Trabeculodialysis/ Goniotomy
 Children and young adults
 Success rate- 56% to 75 % over 2.5-8 years
 Goniotomy – children with refractory glaucoma in
chronic uveitis
 Now used less frequently

74. Drainage devices
 Developed due to low long term
success rate and repeated
trabeculectomies
 AGV-
 cumulative success rate (3-
30months)- 80% and 66%
 Short term success-68% - 95%
 Long term success – 50%-87%

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

76. Non penetrating glaucoma
surgery
 Indication- Mechanical obstruction of trabecular
meshwork with significant PAS
 Success rate- 66.7%-90%
 Complications- hypotony, choroidal effusion,
hyphaema, cataract
 Close post operative monitoring required

77. Cycloablation
 Nd- YAG laser cyclophotocoagulation,
cyclocryotherapy and ultrasonic cycloablation
 Destroys ciliary epithelium
 Induces uveitis
 May result in pthisis in an already compromised
ciliary body

78. Future direction
 Drug delivery implants- Flucinolone acetonide
implant
 4 fold greater risk of raised IOP
 Vs systemic- 23% vs 6% (2 yrs follow up)
 Implantable devices with radiofrequency transceiver:
in vivo model study

79. Thank you