GLAUCOMA

Ajeesh Kumar.R
Optometrist
THQH Nileswaram
What is Glaucoma?
❖ Glaucoma is a neurodegenerative disease of the optic nerve
(optic neuropathy) and is characterised by the progressive,
irreversible loss of retinal ganglion cells resulting in irreversible
visual impairment and eventual blindness.
❖ Glaucoma is not a single disease process, but a group of
disorders characterized by a progressive optic neuropathy
Why is it important for us?
➔ Glaucoma may leads to irreversible visual impairment and
blindness
➔ Optometrists have the clinical skills, diagnostic equipment
and resources most likely to detect new glaucoma cases and
at a younger patient age
➔ Since many glaucoma patients have little to no symptoms,
the only way to detect glaucoma is through eye exams
➔ Once diagnosed, glaucoma can be successfully managed
and treated
➔ Early detection can prevent visual impairment and blindness
Types of Glaucoma
Glaucoma

Congenital Acquired

Primary Secondary

Open-Angle Angle-Closure
History taking
● Age
● Race
● Symptoms
● Visual symptoms
● Refractive status
● Previous ophthalmic history
● Family history
● Past and present medical history
Risk factors for developing glaucoma
● Increased Intraocular pressure
● Older age
● Higher risk if OHT and Central corneal thickness
(CCT) <555 µm and lower in eyes with high CCT
(>588 µm)
● Greater Cup/disc (C/D) ratio
● Central corneal thickness is low
● The higher the Pattern standard deviation (PSD)
value the greater the risk
Examination
● Visual acuity
● Pupils
● Colour vision assessment
● Slit lamp examination
● Tonometry and pachymetry
● Gonioscopy
● Optic disc examination
● Visual field assessment
● OCT -RNFL analysis
Causes
● Congenital glaucoma- Anterior segment developmental
anomalies especially in angle of anterior chamber (Eg.
Axenfeld’s syndrome, Rieger’s syndrome)
● POAG- Exact cause unknown
● PACG- obstruction of aqueous outflow by occlusion of
the trabecular meshwork by the peripheral iris
(iridotrabecular contact)
Congenital
Glaucoma
Congenital Glaucoma
● Caused by abnormalities in the trabecular meshwork and
anterior chamber angle
● Defects in the aqueous outflow causes an increase in IOP, which
causes rapid expansion of the eyeball
● Classic “triad” of symptoms (photophobia, epiphora and
blepharospasm) occurs due to rapid expansion of the child’s eye
causing corneal enlargement, horizontal or oblique breaks in
Descemet's membrane (Haab striae) and subsequent corneal
edema and opacification.
Congenital Glaucoma
● True congenital glaucoma (40%) in which IOP is elevated during
intrauterine life
● Infantile glaucoma (55%) which manifests prior to age 3
● Juvenile glaucoma, the least common, in which IOP rises between
3 and 16 years of age
● Secondary congenital glaucoma is associated with a variety of
ocular and systemic syndromes and aphakia
Signs & Symptoms
⦿ Watering
⦿ Photophobia
⦿ Blepharospasm
⦿ High IOP
⦿ Corneal oedema
⦿ Corneal enlargement and buphthalmos
⦿ Haab's striae- Tears and breaks in
Descemet's membrane
⦿ Thin and blue sclera
⦿ Iridodonesis
⦿ Deep Anterior chamber
Treatment
● Goniotomy- Under direct gonioscopic visualization, an incision
is made at the midpoint of the trabecular meshwork
● Trabeculotomy- if corneal clouding prevents an adequate view
of the angle or if repeated goniotomy has failed
● Trabeculectomy
● Combined trabeculotomy and trabeculectomy (CTT)- If
Schlemm’s canal could not be cannulated or prior
trabeculotomy failed
● When trabeculectomy fails or is not a desirable option, then
the other filtering operations like glaucoma drainage device
(GDD) surgery or cyclodestructive procedures
 Primary Open
Angle Glaucoma
Primary Open Angle Glaucoma
● Also known as Chronic Simple Glaucoma
● Most common form of glaucoma
● Exact cause unknown
● The rise in lOP occurs due to decrease in the aqueous
outflow, due to age related changes in the structures of
anterior chamber angle
● The disease is usually asymptomatic, until it has
caused a significant loss of visual field
POAG- risk factors
● Ocular hypertension
● Family history
● Age, risk increases with increasing age
● Race, more common in black people than in whites
● Myopes
● Central corneal thickness, apart from causing
underestimation of IOP, reduced CCT is being considered
as an independent risk factor for POAG
● diabetics
● smoking
Signs & Symptoms
● No symptoms in early stages
● Mild pain and Headache
● Delayed dark adaptation
● Frequent change of glasses
● High IOP
● Field defects
● Optic disc cupping
Ocular Hypertension
● Normal eye pressure is between 11
and 21 mmHg
● Normal IOP varies with time of day
(diurnal variation)
● A variation in IOP of over 5 mm Hg
(Schiotz) is suspicious and over 8 mm
of Hg is diagnostic of glaucoma
● Elevated eye pressure with no other
symptoms is ocular hypertension
● The risk of glaucoma is greater in eyes
with OHT and CCT <555 µm and lower
in eyes with high CCT (>588 µm)
POAG - early optic disc changes
● Vertically oval cup due to selective loss of
neural rim tissue in the inferior and superior
poles
● Asymmetry of the cups. A difference of
more than 0.2 between two eyes is
significant
● Large cup, with cup to disc ratio >0:4
(normal cup size is 0.3 to 0.4)
● Splinter haemorrhages present on or near
the optic disc margin
● Atrophy and defects of retinal nerve fibre
layer (RNFL)
ISNT rule
● The normal neuroretinal rim is
usually broadest in the inferior rim,
followed by the superior and nasal
rims, and thinnest in the temporal
disc region
● This pattern of rim width is known
as the ISNT rule (inferior ≥ superior
≥ nasal ≥ temporal).
● Any violation of the ISNT rule can
be seen as a sign of glaucomatous
neuropathy
POAG - late optic disc changes
● Marked cupping (cup size 0.7 to 0.9),
excavation may even reach the disc
margin
● Thinning of neuro-retinal rim
● Nasal shifting of retinal vessels
● Pulsations of the retinal arterioles may
be seen at the disc margin
● Glaucomatous optic atrophy- As the
damage progresses, all the neural
tissue of the disc is destroyed and the
optic nerve head appears white and
very deep
POAG - Visual field changes
● Visual field defects appear only
after about 40% of axons have
been damaged
● defects are initially observed in
Bjerrum's area (10-20 degrees
from fixation)
● defects correlate with optic disc
changes
POAG - Optical coherence tomography
● OCT helps in early detection
and monitoring of structural
glaucomatous damage
● OCT can directly measure and
quantify RNFL thickness by
calculating the area between
the internal limiting membrane
and RNFL border
● OCT also automatically
outlines the optic nerve head,
optic cup, and disc borders
POAG- Treatment
❖ Medical
➢ Prostaglandin analogues: Latanoprost, Travoprost,
Bimatoprost, Tafluprost etc.
➢ Topical beta blockers: Timolol, Betaxolol etc.
➢ alpha2 adrenergic agonists: Epinephrine, Brimonidine etc.
➢ Carbonic Anhydrase Inhibitors: Acetazolamide (systemic)
Dorzolamide (topical)
➢ Parasympathomimetics: Pilocarpine
➢ Hyperosmolic agents: mannitol

❖ Laser trabeculoplasty, if medical therapy fails

➢ using argon laser (ALT) or diode laser (DLT)
❖ Trabeculectomy, if glaucoma uncontrolled despite maximal
medical therapy and laser trabeculoplasty.
Normal Tension Glaucoma
⦿ Also called low-tension glaucoma
⦿ Evidence of glaucomatous optic disc and/or visual field
changes with a pressure consistently below 21 mm Hg
⦿ Abnormal sensitivity of the disc to intraocular pressure
because of vascular or mechanical abnormalities at the
ONH
⦿ Treatment: Medications that reduce IOP and increase blood
flow to the ONH are favored
 Primary Angle
Closure Glaucoma
PACG- risk factors
⦿ Age, risk increases with age
⦿ Females are more prone to get PACG
⦿ Family history
⦿ Hypermetropic eyes with shallow anterior chamber
⦿ Short Eyes with narrow angle of anterior chamber
Signs and symptoms
⦿ Severe Pain & Sudden blurring of vision
⦿ Hazy Cornea
⦿ Ciliary congestion
⦿ Eye extremely sensitive to light
⦿ Coloured Halos around lights
⦿ Nausea and/or vomiting
⦿ Pupil is semi dilated, vertically oval and fixed
⦿ High IOP
⦿ Shallow Anterior chamber
Angle closure mechanism
⦿ Rise in IOP occurs due to blockage of the aqueous humour
outflow by closure of a narrower angle of the anterior
chamber
Angle evaluation
● The oblique flashlight test
allows rapid estimation of
the depth of the anterior
chamber of the eye without
gonioscopy
● Angle grading can be done
using slit lamp
● Gonioscopy allows direct
view of anterior chamber
angle
Oblique flashlight test
Van Herick technique
● This technique compares the
depth of the peripheral
anterior chamber with the
cornea thickness (CT)
● Narrow beam is projected at
60° to the patient's temporal
and nasal cornea
● Grade 4- ACD ≥ CT
Grade 3-ACD ½ CT
Grade 2- ACD ¼ CT
Grade 1- ACD <¼ CT
Grade 0- angle is closed
Gonioscopy
Emsley-Fincham stenopaeic test
⦿ Used to differentiate between halos due cornea and halo
due to lens
⦿ A stenopaic slit is moved in front of the eye. The coloured
halo due to immature cataract will break
PACG- Treatment
⦿ It is essentially surgical. However, medical therapy is
instituted as an emergency to control IOP before surgery
⦿ Laser iridotomy
⦿ Peripheral Iridectomy
⦿ Trabeculectomy (filtration surgery)
Secondary Glaucomas
Secondary Glaucoma
● Lens-induced (phacogenic) glaucomas
● Inflammatory glaucoma (glaucoma due to intraocular
inflammation).
● Pigmentary glaucoma
● Neovascular glaucoma
● Glaucomas associated with iridocorneal endothelial syndromes
● Pseudoexfoliative glaucoma
● Glaucomas associated with intraocular haemorrhage
● Steroid-induced glaucoma
● Traumatic glaucoma
● Glaucoma-in-aphakia
● Glaucoma associated with intraocular tumours
Lens-induced (phacogenic) glaucomas
● Phacomorphic glaucoma- due to swollen lens
● Phacotopic glaucoma- due to anterior lens displacement
● Phacolytic Glaucoma (Lens Protein Glaucoma)- trabecular
meshwork is clogged by the lens proteins
● Lens particle glaucoma- trabecular meshwork is blocked by the
lens particles floating in the aqueous humour.
● Phacoanaphylactic glaucoma- acute inflammatory reaction due
to antigen (Lens protein)-antibody reaction
Glaucomas due to Uveitis
● Acute open-angle glaucoma mainly due to trabecular clogging
by inflammatory cells, exudates and turbid aqueous humour
● Angle-closure glaucoma due to pupillary block by synechiae or
occlusio pupillae
Neovascular glaucoma
● Due to neovascularization of iris and the angle of anterior
chamber
● Neovascularization of iris (rubeosis iridis) develops following
retinal ischaemia, which is a common feature of:
○ Proliferative diabetic retinopathy
○ Central retinal vein occlusion
○ Sickle-cell retinopathy
○ Eales' disease
Glaucoma Drainage Devices
● Devices designed to divert aqueous humor
from the anterior chamber to an external
reservoir
● Currently many devices are available
● Used in patients with severe uncontrolled
glaucoma, who have failed previous
glaucoma surgery
● Commonly used in the management of
congenital and developmental glaucomas
● Also used in secondary glaucoma and also
in open angle glaucoma
Absolute glaucoma
Absolute glaucoma
● Final or end stage of glaucoma with uncontrolled pressure and
painful blind eye
● Symptoms include severe eye pain, stony hard eye, watering,
lost pupillary reflex and total loss of vision
● Treatment is focused on reducing the pain, maintaining vision in
the fellow eye, psychological and other support, helping the
patient to keep the affected eye comfortable, reasonable
cosmetic appearance etc.
● Treatments include topical steroids, topical atropine,
cyclocryotherapy, cyclodiathermy, retrobulbar injection of
alcohol, enucleation, radiotherapy, laser/cryotherapy and
cyclophotocoagulation
Useful tips to patients
● Detect it before it steals the vision
● Know your family history
● Protect your eyes from injury
● Taking medicine? Talk with your eye doctor
● Eat well to see well
● Maintain a healthy body weight
● Keep away from bad habits
● Exercise... but carefully
● Avoid head-down positions
● Sleep in the right position
● Protect your eyes from sunlight
Thank you..