AQUEOUS HUMOR PRODUCTION

 Aqueous humor is produced by the ciliary

body

 It is formed in two steps

1. Formation of plasma filtrate within the

stroma of the ciliary body
2. Formation of aqueous from the filtrate
across the blood- aqueous barrier
 Angle of the anterior
chamber plays an important
role in process of aqueous
drainage

 Structures- root of iris,

anterior most part of ciliary
body, scleral spur ,
trabecular meshwork,
Schwalbe’s line

 Structures in the angle can

be visualized clinically by a
goinioscopes
TRABECULAR MESHWORK

SCHLEMM’S CANAL

COLLECTOR CHANNELS

AQUEOUS VEINS

EPISCLERAL VEINS
 Determined by the balance between the rate
of aqueous secretion and aqueous outflow

 Aqueous outflow is related to resistance

encountered in the outflow channels and to
the level of episcleral venous presssure

 Normal IOP is 11-21 mm Hg

 Goldmann applanation tomometry

 Digital tonometry
 Methods of measuring IOP

 Schiotz tonometry (indentation tonometry)

 Intraocular pressure
 Gonioscopy
 Visual field examination
 Optical coherence tomography of nerve fibre
layer and optic nerve head
 Fundus photography
 Itis a diverse group of disorder in which
there is a progressive and characteristic
optic neuropathy which is associated with
visual field loss as the damage progresses
and in which IOP is usually a key modifying
factor
Progressive ocular damage occurs

Raised intraocular pressure

Retinal ganglion cell death

characteristic optic disc appearance

and visual field defect
 GLAUCOMATOUS OPTIC DISC
NORMAL DISC
OPEN ANGLE CLOSED ANGLE
PRIMARY GLAUCOMA SECONDARY GLAUCOMA

Can be open angle or closed angle Can be open angle or closed angle

Raised IOP Raised IOP

Characteristic optic disc changes Characteristic optic disc changes

Characteristic visual field changes Characteristic visual field changes

Absence of underlying cause Presence of underlying cause

Usually bilateral Usually unilateral

 It is a group of disorders in which rise of IOP
is associated with some primary ocular or
systemic diseases
 Secondary glaucoma can be open angle and
closed angle
 Can be classified on the basis of site of aqueous outflow
obstruction

- PRE TRABECULAR (membrane covering the angle)

 Neovascular tissue
 Iridocorneal endothelial syndrome
 Epithelial ingrowth

- TRABECULAR (clogging up of meshwork)

• Pigementary glaucoma
• Red cell glaucoma
• Ghost cell glaucoma
• Phacolytic glaucoma
• Pseudoexfoliation glaucoma
• Angle recession glaucoma
 SOAG

 POST TRABECULAR (raised episcleral venous

pressure)

• Carotid cavernous fistula

• Sturge – Weber syndrome
• Obstrucation of the superior vena cava
WITH PUPILLARY BLOCK WITHOUT PUPILLARY BLOCK
 Isdue to impairment of aqueous outflow
secondary to apposition between the
peripheral iris and the trabeculum
 WITH PUPILLARY BLOCK
• Seclusio pupillae (360 degree ring posterior
synechiae)
• Subluxated lens
• Phacomorphic glaucoma
• Aphakic pupillary block (vitreous)
 SACG

 WITHOUT PUPILLARY BLOCK

• Neovascular glaucoma (peripheral anterior
synechiae)
• Posterior segment tumors
• Retinopathy of prematurity
• Malignant glaucoma
 Raised IOP due to some disorder of the lens

 Phacomorphic glaucoma
 Phacolytic glaucoma
 Acute secondary angle closure glaucoma

 Isdue to swollen (intumescent) lens or

anterior subluxation or dislocation of lens

 Pupillary block glaucoma

 PHACOMORPHIC GLAUCOMA

 Lens is swollen

 Itpushes the iris forward and obliterates the

angle

 Formation of iris bombe and pupillary block

 PHACOMORPHIC GLAUCOMA

 Severe pain
 Redness (circumcorneal congestion)
 Very high IOP
 Systemic symptoms due to
increased intraocular pressure
 Shallow anterior chamber
 Dilated pupil
 Diminuition of vision
 LENS IS CATARACTOUS AND
SWOLLEN
 FELLOW EYE- DEEP AC AND OPEN
ANGLE
 PHACOMORPHIC GLAUCOMA

 Treatment should be immediate

 Topical steroids to reduce inflammation
 Measures to control IOP
- Intravenous mannitol
- Systemic acetazolamide
- Topical betablockers
 Cataract extraction with PCIOL once the eye
becomes quite
 Lensprotein glaucoma
 Occurs with a hypermature cataract

 PATHOGENESIS- Trabecular obstruction is

caused by high molecular weight proteins
that has leaked through a intact capsule into
the aqueous humor
 PHACOLYTIC GLAUCOMA

 Pain
 Redness
 Impaired vision due to cataract and
edema
 Raised intraocular pressure
 Corneal edema
 Aqueous contains white lens
particles (pseudohypopyon)
 HYPERMATURE CATARACT
 DEEP ANTERIOR CHAMBER WITH
OPEN ANGLE
 PHACOLYTIC GLAUCOMA

 Control of IOP
 Steroids to decrease inflammation
 Antiglaucoma agents to drecrease intraocular
pressure
 Extraction of cataract
 Secondary open angle glaucoma
 Due to blockage of trabecular meshwork due
to lens particles floating in aqueous either
due to trauma or planned extracapsular
cataract extraction
 Chronic open angle glaucoma
 Grey white fibrillary extracellular material
composed of protein core surrounded by GAG
produced by abnormal basement membranes
of ageing epithelial cells in trabeculum, lens
capsule , iris and ciliary body
 This material is deposited on the anterior
lens capsule, zonules, cilliary body, iris ,
trabeculum , vitreous and conjunctiva
 Medical treatment
 Laser treatment- trabeculoplasty
 trabeculectomy
 PATHOGENESIS
- Occurs as a result of iris noevascularization
(rubeosis iridis)
- CAUSE IS SEVERE , DIFFUSE AND CHRONIC
RETINAL ISCHAEMIA
 RETINAL ISCHAEMIA

PRODUCTION OF VASCULAR ENDOTHELIAL

GROWHT FACTOR (VEGF)

CAUSES NEOVASCULARIZATION OF IRIS,ANGLE

OF ANTERIOR CHAMBER AND PROLIFERATIVE
RETINOPATHY

INITIALLY OPEN ANGLE AND LATER WHEN THE

MEMBRANE CONTRACTS CAUSES SECONDARY
ANGLE CLOSURE GLAUCOMA
 Ischaemic CRVO

 Diabetes mellitus

 CRAO, ocular ischaemic syndrome

 Intraoculartumors, long standing RD and

chronic intraocular inflammation
 Rubeosisiridis
 Secondary open angle glaucoma
 Secondary synechial angle closure glaucoma
 NVG

 Stage of iris neovascularization

 Usually start at the pupillary margin
 NNVG

 Neovascular tissue proliferates across the

face of the angle

 Formation of the fibrovascular membrane at

the angle
 NVG

 Contraction of the fibrovascular tissue with

pulling of the peripheral iris over the
trabeculum

 Raised IOP
 Pain
 Redness
 Diminuition of vision
 Very high IOP
 Iris neovascularization
 Open or closed angles depending on the
stage
 Panretinal photocoagulation (prevents further
neovascularization)

 Medical therapy for control of IOP

 Filtration surgery (trabeculectomy with anti

metabolites)

 Artificial filtration shunt

 Intravitreal Anti – VEGF injection

 Enucleation in cases refractory to other treatment

 Acute inflammation of the anterior uveal
tract is associated with secondary rise in IOP
causing secondary open angle glaucoma due
to

- trabecular clogging by inflammatory cells,

exudates ,
- trabeculitis
 Following iridocyclitis IOP rises due to

- Angle closure glaucoma with pupillary block

posterior synechiae 360 degree (seclusio
pupillae)

Increased pressured in posterior chamber

with anterior bowing of the peripheral iris
(iris bombe)

Shallowing of the AC with apposition of the iris

TM and peripheral cornea with Peripheral anterior
synechiae formation
 Angle closure glaucoma without pupillary block

Chronic anterior uveitis with deposition of

inflammatory cells and debris in the angle

Subsequent organization and contraction pulls

the peripheral iris over the trabeculum causing
synechial angle closure

Raised IOP
 Control of inflammation with topical steroids
 Antiglaucoma agents- beta blockers (first line)
 In severe cases- systemic acetazolamide
 Topical CAI
 PG analogues and miotics are contraindicated
 Laser iridotomy or surgical iridotomy to restablish
communication between the posterior and anterior
chamber
 Trabeculectomy in cases not respond to medical
treatment after control of inlammation
 Hyphema
 Angle recession glaucoma
 Maybe associated with IOP elevation due to
trabecular blockage by red blood cells

 Secondary hemorrhage is more severe than

primary bleed and may develop within 3-5
days of initial injury
 HYPHEMA

 Head end elevation

 Antiglaucoma agents- beta blocker, topical
and systemic CAI
 Avoid prostaglandin analogues and miotics
 Topical steroids
 Mydriatics- eg: atropine
 Surgical evacuation- if persistently high IOP
not responding to medical treatment
 Rupture of the face of the ciliary body ( that
portion which lies between the iris root and
the scleral spur) due to blunt trauma

 Secondary trabecular damage occurs which

leads to increased risk of glaucoma
 ANGLE RECESSION GLAUCOMA

 Medical treatment- beta blockers, alpha

agonist, topical CAIs
 Trabeculectomy with adjunctive
antimetabolites
 Artificial shunts
 Bilateral condition
 Liberation of pigment granules
from the pigment epithelium and
deposition throughout the
anterior segment
 Excessive posterior bowing of the
mid peripheral portion of the iris
leads to mechanical rubbing of
the posterior pigment layer of
the iris against lens zonules
 This pigment obstructs the TM
leading to glaucoma
 Medical management
 Laser iridotomy
 Trabeculectomy
 Rare
 Dueto anterior rotation of the ciliary
processes and iris root leading to aqueous
misdirection and aqueous is forced
backwards into the vitreous
 MALIGNANT GLAUCOMA

 High IOP
 Occurs after trabeculectomy/ intraocular
surgery most commonly
 Absent bleb
 MALIGNANT GLAUCOMA

 Mydriatics (atropine 1%) dilate the ciliary

ring and pulls lens posteriorly
 Intravenous mannitol
 Nd:YAG laser to disrupt the anterior hyaloid
face and disrupts the vitreous volume in the
pseudophakic eyes
 Pars plana vitrectomy