presentation on Inflamatory glaucoma all you need to know about Inflamatory glaucoma by Judith Wokwen

1. INFLAMATORY
GLAUCOMA

2. PRESENTED
BY
JUDITH WOKWEN

3. COURSE OUTLINE
 Brief review of aqueous production and flow
 Brief review of anterior chamber angle
 Introduction
 Definitions
 Signs/symptoms
 classification
 Pathogenesis
 Management

4. AQUEOUS PRODUCTION AND OUT FLOW

5. ANTERIOR CHAMBER ANGLE

6. INTRODUCTION
Glaucoma is an ocular disease characterized by
elevated intraocular pressure(IOP) optic nerve
cupping with or without visual field loss.
several types of Glaucoma exist with their different
causes and pathophysiology.

7. Definitions
Inflammatory glaucoma is a condition in which ocular
inflammation causes a persistent or recurrent increase in
intraocular pressure (IOP), resulting in anatomical and
physiological changes. There maybe progressive optic
nerve cupping with corresponding retinal nerve fiber loss
and visual field defect. Mostly associated with uveitis
(uveitic glaucoma ).
Uveitis is inflammation of uveal tissue (iris, ciliary body
and choroid). It is characterised by presence of cells or
cellular aggregates that are sometimes visible in the
chambers during examinations.

8. SYMPTOMS
• Cloudy vision [in some cases]
• Pains (sudden and severe)
• Photophobia
• Colored haloes,
• Braw ache.
• Nausea /vomiting

9. SIGNS
• Decrease VA
• IOP may or may not be elevated
• Ciliary congestion (ciliary injection)
• Corneal: odema, kerathopathy [bullae] ,
stroma scaring, KPs
• Anterior chamber: shallow , cells, hypopion.
• Anterior / Posterior Synaechia
• Optic Nerve Cupping and destruction of
Retina Nerve fibres

10. • Iris: They may be neovascularization of iris,
posterior synechia, peripheral anterior
synechia, iris bombe.
• Pupils: may be mild dilated or moderately
dilated, reacts sluggishly to light, or fixed.
• Lens: Iris pigments on anterior capsule,
posterior sub capsular opacity.
• Fundus :+/- glaucomatous changes of optic
nerve, retinitis, macular oedema.

11. CLASSIFICATION
1) Angle- closure with pupillary block : when there is
360 degree posterior synaechia]
2) Angle closure without pupillary block: [protein cell
and exudates can migrate during the inflammatory
process into the anterior chamber angle, causing
blockage of the angle]
3) Open angle: Here, there is trabeculitis causing
resistance to aqueous drainage thus accumulation
of fluid leading to destruction of the optic nerve
and retinal nerve fibres

12. PATHOGENESIS
Angle –closure with pupillary block
• It occurs when inflammatory cells and
proteins in aqueous humour, forms
adhesion between iris and lens forming
posterior synechia .
• Posterior synechia obstruct aqueous flow
from the posterior to anterior chamber.

13. • Pressure in the posterior chamber is
increased producing anterior bowing of
the peripheral iris(iris bombe)
• Resulting in shallowing of anterior
chamber.
• Inflamed iris easily sticks to the
trabeculum and the iridocorneal contact.
• This may be permanent with development
of peripheral anterior synechia

14. Posterior synechia

15. Peripheral anterior synechia

16. Angle-closure glaucoma without
papillary block
 Chronic anterior uveitis causes the
deposition of inflammatory cell and
debris in the angle.
.

17. Angle closure without pupillary block

18. Open- angle glaucoma
1. In acute anterior uveitis the IOP is
usually normal or sub normal.
It may be steroid induced or caused
by combination of other machanisms; .
 There may be ciliary short down. But
most commonly as acute inflammation
subsides, the cilliary body function
returns.

19.  Trabecular obstruction; proteins,
fibrin, debris from inflamed iris
blood vessel enter aqueous
humour and anterior chamber
and disrupt the aqueous flow.
 Acute trabeculitis: Cytotoxic
agents from inflammatory cells
further causes oedema of
trabecular meshwork.

22. 2 . In chronic anterior uveitis there is
trabecular scarring and/or sclerosis
secondary to chronic trabeculitis.
.

23. • Pathogenesis of elevated IOP may be
uncertain because multiple mechanisms
may be involved such as steroid
responders.
• Assessment of glaucomatous damage
may be disturbed by small pupil or
opacity in the media. Poor visual acuity
may affect accurate results
• Iris vessels may give diagnostic confusion
(NVG).

24. MANAGEMENT OF INFLAMMATORY
GLAUCOMA
Identify the cause and treat
Medical therapy of elevated IOP and
making sure you assess for steroid
induce ocular hypertension.
Surgical therapy

25. IDENTIFICATION, CAUSE AND TREATMENT
 History taking
Slit lamp examination
Fundoscopy examination
Gionoscopy examination
Laboratory examinations e.g. ESR,TOXO,
ASLO tests

26. MEDICAL THERAPY
1. CORTICOTERIODS
e.g. prednisolone, tablets, frakidex, eye
drops and ointment, flucon eye drop,
maxidex oint and eye drop, etc reduced
inflammation

27. 2. CYCLOPLEGICS e.g Atropine,
mydriaticum.They reduce photophobia
and pains [ciliary spasms]. They should
be used with caution.
3. BETA BLOCKERS eg Timolol, Timosol,
carteol.

28. 4. CARBONIC ANHYDRASE INHIBITORS e.g.
Acetazolamide (diamox ) reduces aqueous
humour production and increases uveosclera
outflow
5. ALPHA 2 AGONIST e.g. Brimonidine eye
drop

29. 6. PROSTAGLANDINS e.g. Travatans,
Increases outflow throw uveal
pathway and ciliary muscle
Site effect may worsen inflammation
and increase risk of macular oedema
in uveitis
7. HYPEROSMOTIC AGENTS eg mannitol

30. SURGICAL THERAPY
 Iridotomy is done in eyes with papillary-
block angle closure glaucoma with uveitis.
The hole can become ocluded .
 Surgical iridectomy can be done to prevent
pupilary block.
 Trabeculectomy..
 Cyclodistructive procedure [cyclocryo]

31. Thanks For Your Kind Attention
END!!!