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
5.
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
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
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
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
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
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
Incidently only secondary glaucoma where there is a female preponderance
Interleukines, Cytokines, arachidonic acid metabolites, oxygen metabolites- escalate the inflammatory process
Granulomatous>non granulomatous
AIDS, VKH, pars planitis
8.9%, 45.4% incidence of OHT
Granulomatous leading cause of uveitic glaucoma
Affectic the hypochromic eye.
angioneurotic edema, eczema, urticarial contact dermatitis, asthma, rhinitis, food allergies and intolerance to aspirin.
based on the demonstration of segmental iris ischemia on fluorescein angiography. Vasculature incompetence could be associated with a release of prostaglandins, inflammation, and a subsequent rise in intraocular pressure.
(a prostaglandin antagonist) have been shown to lower intraocular pressures during attacks, further supporting this theory
Due to inflammation of trabecular meshwork, swelling and obstruction of inflammatory cell and debris
Yellow, millet seed nodules
Under check for IOP
Decrease ciliary spasm, reduce inflammation, reduce chances of posterior synechiae
Causes granulomatous uveitis
Alteration of ion transport mechanism in ciliary epithelium