CATARACT SURGERY

Aiswarya Sebastian
4
1.Couching

2.Intracapsular cataract extraction (ICCE)

3.Extracapsular cataract extraction (ECCE)

• Conventional extracapsular cataract extraction (ECCE)
• Manual small incision cataract surgery (SICS)
• Phacoemulsification
• Femtosecond laser assisted cataract surgery (FLACS)
ECCE
• Major portion of ant capsule with
epithelium,nucleus,cortex
removed
• Posterior capsule intact

INDICATIONS

All type of adulthood as well as

childhood cataract unless c/I i.e
markedly subluxated or dislocated lens
ECCE ICCE

• All ages • >40 yrs

• Posterior chamber IOL can be implanted • Cannot be implanted
• Not seen • Post op vitreous related problem –
herniation in ant chamber , pupillary block
, vitreous touch syndrome seen
• Low incidence • post op complications like endopthalmitis
, cystoid macular edema , retinal
detachment seen

• Post op astigmatism is less

• Prognosis of subsequent glaucoma
filtering or corneal transplantation is
much improved comp to ICCE
• Incidence of rubeosis in diabetes is
reduced
Conventional manual sics Phacoemulsification

Sutureless Sutureless

Machine dependency

Use of phaco energy inside

eye
 Conventional ECCE
• Superior rectus suture – fix eye in downward gaze
• Fornix based conjunctival flap – to expose limbus
• Partial thickness groove 10 to 2 O ‘clock
• Entry into ant chamber
• Injection of viscoelastic substance – 2%methylcellulose or 1%sodium hyaluronate
• Anterior capsulotomy –
Any of the following method can
be used
1. Can openers technique
2 Envelope technique / linear capsulotomy

3. Continuous circular capsulorrexhis (CCC)

• Removal of ant capsule – Kelman Mcpherson foreceps
• Completion of corneoscleral section
• Hydrodissection – BSS is injected under periph part of ant capsule
separation of corticonuclear mass from capsule
• Removal of nucleus
1. Pressure and counter pressure method
2. Irrigating wire vectis technique
• Aspiration of cortex – two way irrigation and aspiration cannula
• Implantation of IOL
• Closure if incision – 3 to 5 interrupted suture or continuous 10-0 nylon suture
• Removal of viscoelastic substance
• Reposition of conjunctival flap
• Subconjunctival inj dexamethasone 0.25ml & gentamicin 0.5 ml
• Packing of eye
Conventional ECCS demerits

• Long incision
• Multiple sutures are required
• High risk of vitreous prolapse , intraoperative hard eye & expulsive choroidal haemorrhage
• High incidence of post operative astigmatism
• Post operative suture related problem like irrigation and suture abscess
• Post operative wound related problem such as wound leak , shallowing of ant chamber &
iris prolapse
• needs suture removal during which infection occurs
Manual small incision cataract surgery (SICS)

• Superior rectus suture

• Fornix based conjunctival flap
• Haemostasis – achieved by applying gentle and just adequate wet field
cautery
• Sclerocorneal tunnel incision –self
Sealing
1.External scleral incision
2. Sclerocorneal tunnel –using crescent knife extending 1-1.5 mm into clear cornea
3.Internal corneal incision – made with the help of sharp 3.2mm angled keratome
• Side port entry – 1.5 mm valvular corneal incision made at 9 0 ‘clock position .
Helps in aspiration of subincisional cortex and deepening the anterior chamber at the end
of surgery
• Ant capsulotomy : can opener / envelope / CCC
• Hydrodissection – sep of corticonuclear mass from post capsule
• Nuclear management
*prolapse of nucleus into ant chamber
*delivery of nucleus outside thu corneoscleral tunnel
-irrigating wire vectis method
-Blumenthal’s technique
-phacosandwich tech
-phacofracture tech
-fishhook tech
• Aspiration of cortex
• IOL implantation
• Removal of viscoelastic material
• Wound closure
PHACOEMULSIFICATION

• Side portal entry – filling ant chamber with OVD for stabilization of globe & for using sinskey
hook/chopper
• Self sealing clear corneal incision
• CCC after filling ant chamber with OVD
• Hydrodissection and hydrodelineation
• Nucleus removal – commonly used tech
1. Divide and conquer – 4 quadrant nucleotomy
2.Stop and chop tech – 2 quadrant nucleotomy
3.Direct phaco chop technique – nucleus held with phaco probe vaccum & chopped directly
with help of chopper
• Aspiration of cortex
• Foldable IOL implantation with injector system
• Removal of OVD
• Wound closure
Phacoemulsification SICS
• Cannot deal with hard cataract • Universal applicability – all type of
cataract incl hard cataract
• Learning curve is painful for both surgeons • Easier to learn
and patients
• Machine dependent • Not machine dependent
• Complication – nuclear drop • Complic like nuclear drop into vitreous
cavity is less
• High cost • Cost effective
• Post op congestion minimal • Conjunctival congestion persists for 5-7
• Less corneal complic days at the site of conjunctival flap
• Post op astigmatism less • Mild tenderness
• Quick visual rehabilitation • Post op hyphema
• Surg indused astigmatism more
• Delayed visual rehabilitation
Complications of cataract surgery

Preoperative
• Anxiety
• Allergic conjunctivitis
• d/t local anesthesia like retrobulbar haemorrhage
Operative
• Superior rectus muscle laceration
• Excessive bleeding
• Incision rel complic like button holing of anterior wall of tunnel
• Injury to cornea , iris and lens
• Posterior capsular rupture
• Zonular dehiscence
• Vitreous prolapse and loss
Early post operative
• Hyphaema
• Iris prolapse
• Striate keratopathy
• Shallow anterior chamber
• Post op ant uveitis
Late operative complications
• Cystoid macular edema
• Pseudophakic bullous keratopathy
• Retinal detachment
• After cataract / posterior capsule opacification
IOL related problems
• UGH syndrome – uveitis ,glaucoma,hyphaema
• Malpositions of IOL
• Pupillary capture of IOL
• Toxic anterior segment syndrome
 SENILE CATARACT-
AETIOPATHOGENESIS

BY ABEL JOBY ELIAS

ROLL NO:1
WHAT IS CATARACT ?
 Cataract refers to the development of any opacity
in the lens.
SENILE CATARACT

 Age related cataract

 Commonest type of aquired cataract above 50 yrs
of age
 Usually bilateral, but almost always one eye is
affected earlier than the other.
Senile cataract occurs in two forms:
Cortical senile cataract (Soft cataract)
Nuclear senile cataract (Hard cataract)

Cortical senile cataract may start as:

Cunieform (Most common)
Cupuliform(Posterior subcapsular cataract)
 ETIOLOGY
RISK FACTORS
1.Age: Usually occurs above 50 yrs of age
If it occurs before 45 yrs of age, it is termed as pre senile cataract
By age of 70 yrs, over 90% of individual develop senile cataract

2. Sex: Both males and females are affected equally

3. Heredity: Plays a considerable role in incidence,onset and

maturation of cataract in different families.
 4. Ultraviolet irradiations: More exposure to UV irradiation from
sunlight implicated for early onset and maturation of senile
cataract
 5.Dietary factors: Diet deficient in certain proteins,amino
acids,vitamis like riboflavin,Vit E,Vit C
 6.Dehydrational crisis: An association with prior episode of severe
dehydrational crisis due to diarrhoea, cholera, etc.
 7.Smoking : Associated with an increase in the frequency of
nuclear cataract. Smoking causes accumulation of pigmented
molecules-3-hydroxykynurenine and chromophores, which lead to
yellowing. Cyanates in smoke causes carbamylation and protein
denaturation.
 CAUSES OF PRE-SENILE CATARACT
Common causes are:
1. Heredity: Cataractous changes may occur at an earlier age in
successive generations.
2. Diabetes mellitus: Occurs earlier in diabetics.
Nuclear cataract is more common

3. Myotonic dystrophy: Associated with posterior subcapsular

Christmas tree cataract is typically seen
4. Atopic dermatitis: Associated with pre-senile cataract in 10%
of the
cases.
Syn and co-cataractogenic factors

 Cataract is the result of multiple subthreshold cataractogenic

stresses. Age is one of these cataractogenic stresses and that
superimposition of other toxic stresses on the ageing lens may
accelerate the rate of cataract formation.
 The elimination of one or more cataractogenic stresses may
delay the cataract formation.
MECHANISM OF LOSS OF TRANSPARENCY

1. Cortical senile cataract

 2. Nuclear senile cataract:
 the usual degenerative changes are intensification of the
age-related nuclear sclerosis associated with
dehydration and compaction of the nucleus resulting in a
hard cataract.
 It is accompanied by a significant increase in water
insoluble proteins. However, the total protein content and
distribution of cations remain normal.
 There may or may not be associated deposition of
pigment urochrome and/or melanin derived from amino
acids in the lens.
 STAGES OF MATURATION

Maturation of the cortical type of senile cataract

 1. Stage of lamellar separation: The earliest senile change is

demarcation of cortical fibres owing to their separation by fluid.
 Can be demonstrated by slit-lamp examination only
 These changes are reversible.
2. Stage of incipient cataract: Two types of senile cortical cataracts can be seen
Cuneiform senile cortical cataract:
 Wedge-shaped opacities with clear areas in between.
 These extend from equator towards centre and in early stages can only be
demonstrated after dilatation of the pupil.
 They are first seen in the lower nasal quadrant.
 These opacities are present both in anterior and posterior cortex and their
apices slowly progress towards the pupil.
 On oblique illumination these present a typical radial spoke-like pattern of
greyish white opacities
 On distant direct ophthalmoscopy, these opacities appear as dark lines against
the red fundal glow.
 Since the cuneiform cataract starts at periphery and extends centrally, the
visual disturbances are noted at a comparatively late stage.
 b. Cupuliform senile cortical cataract :Here a saucer-shaped
opacity develops just below the capsule usually in the central
part of posterior cortex (posterior subcapsular cataract), which
gradually extends outwards.
 There is usually a definite demarcation between the cataract
and the surrounding clear cortex.
 Cupuliform cataract lies right in the pathway of the axial rays
and thus causes an early loss of visual acuity.
 3. Immature senile cataract : In this stage, opacification
progresses further. The cuneiform or cupuliform patterns can be
recognised till the advanced stage of ISC when opacification
becomes more diffuse and irregular.
 The lens appears greyish white but clear cortex is still present
and so iris shadow is visible.

At this stage, lens may become swollen due to continued
hydration. This condition is called 'intumescent cataract.
Intumescence may persist even in the next stage of maturation.
Due to swollen lens anterior chamber becomes shallow.
4. Mature senile cataract (MSC): In this stage, opacification
becomes complete, i.e., whole of the cortex is involved. Lens
becomes pearly white in colour. Such a cataract is also labelled
as 'ripe cataract

5. Hypermature senile cataract (HMSC): When the mature

cataract is left in situ, the stage of hypermaturity sets in.
The hypermature cataract may occur in any of the two forms:

a. Morgagnian hypermature cataract: After maturity the whole

cortex liquefies and the lens is converted into a bag of milky
fluid. The small brownish nucleus settles at the bottom, altering
its position with change in the position of the head. Such a
cataract is called Morgagnian cataract
 b. Sclerotic type hypermature cataract: Sometimes after the
stage of maturity, the cortex becomes disintegrated and the
lens becomes shrunken due to leakage of water.
 The anterior capsule is wrinkled and thickened due to
proliferationof anterior cells and a dense white capsular
cataract may be formed in the pupillary area.
 Due to shrinkage of lens, anterior chamber becomes deep and
iris becomes tremulous (iridodonesis).
MATURATION OF NUCLEAR CATARACT
 Progressive nuclear sclerotic process renders the lens
inelastic and hard, decreases its ability to accommodate and
obstructs the light rays. These changes begin centrally and
spread slowly peripherally almost up to the capsule when it
becomes mature; however, a very thin layer of clear cortex
may remain unaffected.
 The nucleus may become diffusely cloudy (greyish) or tinted
(yellow to black) due to deposition of pigments. In practice,
the commonly observed pigmented nuclear cataracts are
either amber, brown (cataracta brunescens) or black
(cataracta nigra) and rarely reddish (cataracta rubra) in colour
Senile cataract
Clinical features

Presented By:
Abel John Zachariah
Roll No: 02
Table of contents
01
Symptoms

02

Signs

45
01 Symptoms

46
47
1.Glare.

One of the earliest visual disturbance with the cataract is glare or intolerance of bright
light; such as direct sunlight or the headlights of an oncoming motor vehicle. The amount
of glare or dazzle will vary with the location and size of the opacity, being most common
with posterior subcapsular and cortical cataract.

2. Uniocular diplopia or polyopia (i.e. doubling or trebling of objects).

One of the early symptoms. It occurs due to irregular refraction by the lens owing to
variable refractive index as a result of cataractous process, seen commonly with incipient
stage of cortical category (spoke or cuneiform).

48
3. Coloured halos around light.

These may be perceived by some patients owing to breaking of white light in coloured
spectrum due to irregular refractive index being more common in nuclear cataract.
4. Poor colour discrimination

It occurs especially at blue end of visible light spectrum, occurs due to progressive
yellowing or browning of the lens.

49
5. Black spots in front of eyes.

Stationary black spots may be perceived by some patients.

6. Image blur, and misty vision.

Loss of ability to see objects in bright sunlight, blinded by light of oncoming headlamps
when driving at night. This occurs due to loss of contrast sensitivity and also due to the
fact that constriction of pupil in bright light cuts off the peripheral vision from non
cataractous part of the lens.

50
7. Deterioration of vision.
It is painless and gradually progressive in nature.
•Patients with central opacities have early loss of vision. These patients see better when pupil is dilated
due to dim light in the evening (day blindness).
• In patients with peripheral opacities visual loss is delayed and the vision improves in bright light when
pupil is contracted.
•In patients with nuclear sclerosis, distant vision deteriorates due to progressive index myopia. Such
patients may be able to read without presbyopic glasses. This improvement in near vision is referred to
as 'second sight’.
•As opacificalion progresses, vision steadily diminishes, until only perception of light and accurate
projection of light rays remains in the stage of mature cataract.
• Gradual progressive loss of vision followed by rapid deterioration may occur during stage of
intumescent cataract.
51
02 Signs

52
53
1.Visual acuity.
Depending upon the location and maturation of cataract, the visual acuity may range from
6/9 to just PL+

2. Test for iris shadow.

When an oblique beam of light is thrown on the pupil, a crescentic shadow of pupillary
margin of the iris will be formed on the greyish opacity of the lens as long as clear cortex
is present between the opacity and the pupillary margin. No iris shadow will be formed if
the lens is completely transparent or opaque.
Hence, presence of iris shadow is a sign of immature cataract.

54
3. Colour of lens

Depending upon the type

of cataract, colour of the !ens is as below:
• Nuclear cataract: Amber, brown, black or reddish
• lmma ture senile cataract: Greyish white
• Mature senile cataract: Pearly white
• Morgagnian hypermature senile cataract: Milky white
• Sclerotic HMSC: Dirty white with hyper white spots.

4. Morphology of cataractous lens

Best seen with slit lamp examination using direct illumination and in optical section of t.he lens with fully
dilated pupil. Three main types of cataracts are seen:
● Cortical cataract(CC)
● Posterior subscapular cataract(PSC)
● Nuclear cataract(NO)

55
Grading of cataract.

These cataracts are graded by Lens

opacity classification system (LOCS)
III,using a reference
set of standard photographs as below

● PSC: P1 - P5
● CC: C1 - C5
● NO and colour: NO1 - NO5 and
NC1 - NC5

56
5. Distant direct ophthalmoscopic examination.

A reddish yellow fundal glow is observed in the absence of any opacity in the media. Partial cataractous
lens shows black shadow against the red glow in the area of cataract. Complete cataractous lens does not
even reveal red glow.

6. Refraction/ retinoscopy

It may reveal myopia in patients with nuclear sclerosis and hypermetropia (index) in patients with cortical
cataract during incipient and immature stage.

57
Thanks!

58
INVESTIGATION OF
SENILE CATARACT
ABIN KOSHY IYPE
ROLL NO:3
19TH BATCH
PREOPERATIVE EVALUATION
1.General medical examination of the patient –
DIABETES MELLITUS
HYPERTENSION
CARDIAC PROBLEMS
OBSTRUCTIVE LUNG DISORDERS
EXCLUDE ANY SOURCE OF INFECTION LIKE
URNARY TRACT INFECTIONS,SEPTIC GUMS,ETC
OCULAR EXAMINATION
1.VISUAL STATUS ASSESSMENT
VISUAL ACUITY
PERCEPTION OF LIGHT[PL]
PERCEPTION OF LIGHT RAYS[PR]
LASER INTERFEROMETRY[LI]
POTENTIAL ACUITY METER[PAM] TEST
2.PUPIL
Light reactions AND Relative afferent pupillary
defect[RAPD]
Ability of the pupil to dilate adequately before surgery
3.ANTERIOR SEGMENT EVALUATION
CORNEA –Scarring, endothelial status
KERATIC PRECIPITATES
POSTERIOR SYNECHIAE
PSEUDOEXFOLIATION
IRIDODONOSIS
PIGMENTS OVER ANTERIOR LENS CAPSULE
4.INTRAOCULAR PRESSURE[IOP]
5.EXAMINATION OF LIDS,CONJUNCTIVA AND LACRIMAL
APPARATUS
1.Conjunctival infections
2.Lacrimal sac infections
3.Conjunctival swab culture and sensitivity
4.Lacrimal syringing
6.FUNDUS EXAMINATION
7. MACULAR FUNCTION TEST
Two-light discrimination test
Maddox rod test
Colour perception
Entoptic visualisation
8.OBJECTIVE TEST FOR EVALUATING RETINA
Electroretinogram[ERG]
Electrooculogram[EOG]
Visually evoked response[VER]
9.KERATOMETRY AND BIOMETRY
to evaluate power of IOL.
 MANAGEMENT OF CATARACT
A.NON SURGICAL MEASURES

1.Treatment of cause of cataract

Adequate control of DM
Removal of cataractogenic drugs like corticosteroids,phenothiazines,etc.
Removal of irradiation [IR or X rays]
Early and adequate treatment of ocular disease
2.Measures to delay progression
Topical preparartions containg iodine salts of Ca and K are given
Bid to delay progression
3.Measures to improve vision in presence of incipient or immature
cataract
Prescription of glasses refractive status
Arrangement of illumination [peripheral opacities]
Use of dark googles[central opacities]
Mydriatics-5%phenyl ephrine {1 drop Bid }
 B.SURGICAL MANAGEMENT
1.VISUAL IMPROVEMENT
2.MEDICAL INDICATIONS
Lens –induced glaucoma
Phacoanaphylactic endoopthalmitis
Retinal diseases like diabetic retionopathy or retinal
dettachments.
3.COSMETIC INDICATIONS
 PREOPERATIVE MEDICATIONS AND
PREPERATIONS
1.CONSENT
2.SCRUB BATH,CARE OF HAIR AND MARKING OF THE EYE
3.PREOPERATIVE ANTIBIOTICS AND DISINFECTANTS
Topical antibiotics like 0.3%moxifloxacin or gatifloxacin
Povidone-Iodine {10%}
Povidone-iodine{5%}
4.IOP Lowering
5.Mydriasis
 TYPES OF SURGERY

1. INTRACAPSULAR CATARACT EXCISION[ICCE]

2.EXTRACAPSULAR CATARACT EXCISION[ECCE]
3. SMALL INCISION CATARACT SURGERY[SICS]
4.PHACOEMULSIFICATION
INTRACAPSULAR CATARACT EXTRACTION
• In this technique, the entire cataractous lens along with the
intact capsule is removed.
• Weak and degenerated zonules are a pre-requisite for this
method.
• Widely employed for about 100 years over the world (1880-
1980).
• At present the only indication of ICCE is markedly
subluxated and dislocated lens.
 EXTRACAPSULAR CATARACT EXTRACTION

• In these techniques, major portion of anterior

capsule with epithelium, nucleus and cortex are
removed; leaving behind the intact posterior capsule.
• CONTRAINDICATION:The only absolute
contraindication for ECCE is markedly subluxated or
dislocated lens.
 Advantage of ECCE over ICCE
1.ECCE is a universal operation and can be performed at all ages,
except when zonules are not intact; whereas ICCE cannot be performed
below 40 years of age.
2. Posterior chamber IOL can be implanted after ECCE, while it cannot
be implanted after ICCE.
3. Postoperative vitreous related problems (such as herniation in anterior
chamber, pupillary block and vitreous touch syndrome) associated with
ICCE are not seen after ECCE.
4. Incidence of postoperative complications such as endophthalmitis,
cystoid macular oedema and retinal detachment are much less after
ECCE as compared to that after ICCE.
5. Postoperative astigmatism is less with ECCE techniques, as the
incision is smaller.
6. Prognosis for subsequent glaucoma filtering or corneal transplantation
(if required) is much improved with ECCE.
7. Incidence of secondary rubeosis in diabetics is reduced after ECCE.
 DEMERITS OF CONVENTIONAL ECCE OVER
SICS
• Long incision (10 to 12 mm).

• Multiple sutures are required.

• Open chamber surgery with high risk of vitreous
prolapse, operative hard eye and expulsive choroidal
haemorrhage.
• High incidence of postoperative astigmatism.
• Postoperative suture-related problems like irritation and
suture abscess etc.
• Postoperative wound-related problems such as wound
leak, shallowing of anterior chamber and iris prolapse.
• Needs suture removal, during which infection may occur.
 MERITS OF MANUAL SICS OVER
PHACOEMULSIFICATION
1. Universal applicability i.e., all types of cataracts including hard
cataracts (grade IV and V) can be operated by this technique.
2. Learning curve. This procedure is much easier to learn as compared
to phacoemulsification.
3. Not machine dependent. The biggest advantage of manual SICS is
that it is not machine dependent and thus can be practised anywhere.
4. Less surgical complications. Disastrous complication like nuclear drop
into vitreous cavity is much less than phacoemulsification technique.
5. Operating time in manual SICS is less than that of
phacoemulsification, especially in hard cataract. Therefore, it is ideal for
mass surgery.
6. Cost effective. With manual SICS, the expenses are vastly reduced as
compared to considerable expenses in acquiring and maintaining phaco
machine
 DEMERITS OF MANUAL SICS OVER
PHACOEMULSIFICATION
1.Conjunctival congestion for 5-7days
2.Mild tenderness
3.Postoperative hyphema
4.Surgical induced astigmatism
5.Delayed visual rehabilitation
 Merits of phacoemulsification over manual
SICS
1.Topical anaesthesia may be sufficient for phacoemulsification in expert
hands.
2. Postoperative congestion is minimal after phacoemulsification, as
phaco is usually performed through a clear corneal incision.
3. Small incision. The chief advantage of phacoemulsification over
manual SICS is that it can be performed through a smaller (3.2 mm)
incision.
4. Less corneal complications. Phacoemulsification can be performed in
the posterior chamber without prolapsing the nucleus into the anterior
chamber, thereby minimising the risk of corneal complications.
5. Visual rehabilitation is comparatively quicker in phacoemulsification as
compared to manual SICS.
6. Postoperative astigmatism is comparatively less when foldable IOLs
are implanted through a smaller incision (3.2 mm).
 DEMERITS OF PHACOEMULSIFICATION
OVER MANUAL SICS
1.Learning curve for phacoemulsification is more painful both for the
surgeons and patients.
2. Complications encountered during phacoem- ulsification like nuclear
drop are unforgiving.
3. Machine dependent. This procedure is solely machine dependent and
in the event of an unfortunate machine failure in the middle of surgery
one has to shift to conventional ECCE.
4. High cost. Cost of this technique is very high because of expensive
machine, accessories and maintenance.
5. Limitations. It is very difficult to deal with hard cataracts (grade IV and
V) with this technique, and also there is high risk of serious corneal
complications due to more use of phaco energy in such cases.
AQUEOUS HUMOUR DYNAMICS
By : Amal Uthuanganakath
RollNo:12
AQUEOUS HUMOUR( PRODUCTION, CIRCULATION &
DRAINAGE)
-UVEA
-PARS PLICATA
-PARS PLANA

ThePhoto by PhotoAuthor is licensed under

CCYYSA.

ThePhoto by PhotoAuthor is licensed under CCYYSA.

 Na+,Cl-,HCO3-

GLUCOSE,H20,AMINOACIDS
AQEOUS HUMOUR:
The aqueous humour is a clear watery fluid filling the anterior chamber (0.25
mL) and posterior chamber (0.06 mL) of the eyeball.

Functions of aqueous humour are:-

• Maintenance of a proper intraocular pressure.

• Metabolic and nutritional role.
• Optical function: It maintains optical transparency.
• Clearing function. Aqueous humour serves as a mechanism to clear blood,
macrophages, remnants of lens and products of inflammation from anterior
chamber. Act as a lymph within the eyeball.
AQEOUS HUMOUR PRODUCTION:
■ Aqueous humour is derived from plasma within the capillary network of ciliary
processes. The normal aqueous production rate is 2.3 µL/min. The three
mechanisms are: Ultrafiltration, Active secretion and diffusion.
1. Ultrafiltration:-
First of all, by ultrafiltration, most of the plasma substances pass out from the
capillary wall and loose connective tissue. Thus, the plasma filtrate (dialysate)
accumulates behind the pigmented and non-pigmented epithelium of ciliary
processes.
2. Active secretion:-
• Active transport is brought about by Na+-K+ activated ATPase pump, calcium
and voltage gated ion channels and carbonic anhydrase enzyme system
• Substances that are actively transported include sodium, chlorides, potassium,
ascorbic acid, amino acids and bicarbonates.
3. Diffusion.
Active transport of the substances across the nonpigmented ciliary epithelium
results in an osmotic gradient leading to the movement of other plasma
constituents into the posterior chamber by ultrafiltration and diffusion.
Sodium is primarily responsible for the movement of water along with glucose
into the posterior chamber.
DRAINAGE:
-Resistance to aqueous
outflow (drainage). From
clinical point of view, this
is the most important
factor. Most of the
resistance to aqueous
outflow is at the level of
trabecular meshwork
and Jc tissue.

-Maintains the normal

IOP= 12-20 mmhg.
 GLAUCOMA-
PRIMARY OPEN ANGLE GLAUCOMA
■ Glaucoma is a group of progressive
optic neuropathies that have in
common a slow progressive
degeneration of retinal ganglion cells
and their axons, resulting in a distinct
appearance of the optic disk and a
concomitant pattern of visual loss.
■ Raised IOP is the common risk factor
of Glaucoma.
 A. Predisposing and Risk factors
1.Raised IOP
2.Family history- 10% in siblings and 4% in offsprings of patients with
POAG.
Responsible genes: MYOC, Optineurin(OPTN), WDR 36.
3.Age: Increases with increasing age.
4.Race:Black>White
5.Myopes
6.Diabetics
7. Smoking
8.High BP
9.Thyrotoxicosis
B. Pathogenesis of raised IOP:
lt is certain that rise in lOP occurs due to decrease in the aqueous
outflow facility, Such changes are caused by age related:
• Thickening and sclerosis of trabecular meshwork with faulty collagen
tissue.
• Narrowing of intertrabecular spaces.
• Deposition of amorphous material in the juxtacanalicular space.
• Collapse of Schlemm's canal and absence of giant vacuoles in the
cells lining it.
C. Pathogenesis of glaucomatous optic neuropathy
■ It has now been recognized that progressive optic neuropathy results from
the death of retinal ganglion cells (RGCs) in a typical pattern which results in
characteristic optic disc appearance and specific visual field defects.
A. Primary insults
I. Raised intraocular pressure (Mechanical theory):
Raised IOP-> Mechanical stretch on lamina cribrosa -> Axonal deformation and
ishchemia.
II. Pressure independent factors( Vascular insufficiency theory):
i. Failure of autoregulatory mechanism of blood flow:- Once the autoregulatory
mechanisms are compromised, blood flow may not be adequate beyond some
critical range of IOP (which may be raised or in normal range).
 iii. Systemic hypolension, particularly nocturnal dips in patients
with night time administration of antihypertensive drugs, has been
implicated for low vascular perfusion of optic nerve head resulting
in TG and progression of damage in POAG.
iv. Other factors such as acute blood loss and abnormal
coagulability profile have also been associated with NTG.

ii. Vasospasm is another mechanism affecting vascular perfusion of

optic nerve head. This hypothesis gets credence from the
convincing association between NTG and vasospastic disorders
(migranous headache and Raynaud's phenomenon).
B. Secondary insults (Excitotoxicity theory)
Neuronal degeneration is believed to be driven by toxic factors such as
glutamate (excitatory toxin), oxygen-free radicals, or nitric oxide which are
released when RGCs undergo death due to p1imary insults. In this way,
the secondary insult leads to continued damage-mediated apoptosis,
even after the primary insult has been controlled.
APHAKIA
Akshay Shaju
Roll No : 05
 APHAKIA
1. Aphakia literally means absence of crystalline lens.
2. From an ophthalmological point of view, aphakia is the
absence of lens in the pupillary area.
Causes of Aphakia:
● Congenital absence of lens. Usually rare.
● Surgical aphakia occuring after removal of lens.
● Aphakia due to absorption of lens matter - sometimes seen
in children after any trauma.
● Traumatic extrusion of lens.
● Posterior dislocation of lens in vitreous causes optical
aphakia.
Optics in Aphakia:
● Hypermetropia of high degree.
● The total power of eye reduces from +60 D to +44 D.
● Anterior focal point becomes 23.2mm in front of the cornea
(Normal : 15.7mm) .
● Posterior focal point is around 31mm behind the cornea,
i.e. around 7mm behind the eyeball (The AP length of
eyeball ~ 24mm).
● Accomodation power is lost fully.
Clinical features:
● Symptoms
a. Defective vision - due to high degree of hypermetropia and loss of
accomodation.
b. Erythropsia and cyanopsia, i.e. seeing red and blue images. This occurs
due to the excessive entry of ultraviolet rays and infrared rays in the
absence of crystalline lens.
● Signs (anterior to posterior)
a. Limbal/corneal scar is seen in case of surgical aphakia.
b. Deep anterior chamber.
c. Iridodonesis - tremulousness of the iris can be demonstrated due to loss of
support of the lens.
d. Jet Black pupil.
e. Purkinje’s Image Test shows only 2 images (normally 4 images are seen).
f. Fundus examination reveals a small hypermetropic disc.
g. Retinoscopy and autorefractometry shows high hypermetropia.
 TREATMENT:
● SPECTACLES
○ Spectacles should be prescribed with about + 10D lens for correction of
aphakia.
○ It should also include correction for surgical astigmatism and + 3-4D for
near vision as there is loss of accomodation.
○ Nowadays, spectacles are not preferred for use in aphakia due to its many
disadvantages.
 Disadvantages of using
spectacles in Aphakia:
● The images are magnified for about 30%. So it is not useful in unilateral
aphakia as it causes diplopia.
● Field of vision is limited.
● Spherical and chromatic abberations of thick lenses.
● Roving ring Scotoma ( Jack in the box phenomenon).
● Prismatic effect of thick lenses.
● High power lenses are cosmetically less acceptable.
CONTACT LENSES:
Advantages over spectacles:

● Produces less magnification.

● Wider and better field of vision.
● Eliminates prismatic effect and abberations of thick glasses.
● Cosmetically more acceptable.
● Better suited for uniocular aphakia.

Disadvantages:

● Costly
● More care is required in usage of contact lenses - may not be suitable for use in young children and
elderly.
● Corneal complications may be associated.
Intraocular Lens Implantation:
● This is the preferred method nowadays.
○ Primary IOL implantation occurs during cataract surgery.
○ Secondary IOL implantation is done in already aphakic patients.
● The lens can be implanted in the capsular bag or in the anterior chamber.
● It eliminates most of the disadvantages associated with the use of spectacles
or contact lenses.
● Disadvantages includes the complications associated with surgery.
Refractive surgery:
● This is a newly emerging treatment for aphakia.
○ Keratophakia
■ A lenticule prepared from the donor cornea is placed within the lamellae
of the patient's cornea.
○ Epikeratophakia
■ A lenticule prepared from the donor cornea is stitched to the patient's
cornea after removing the epithelium.
○ Hyperopic LASIK
■ Maybe tried in cases where secondary IOL can't be implanted.
THANK YOU!
pseudophakia
BY: ALAN.C.PHILIP
ROLL NO. : 6
definition

 The condition of aphakia when corrected with

an intraocular lens implant (IOL) is referred to as
pseudophakia or artephakia.
Refractive status of psudophakic
eye
 Depends upon the power of the IOL implanted.

 Emmetropia

 Consecutive Myopia

 Consecutive Hypermetropia

 Surgically induced Astigmatism

 Signs of pseudophakia
 Surgical scar may be seen near the limbus.
 Anterior chamber is slightly deeper than normal.
 Mild iridodonesis of iris may be demonstrated.
 Purkinje image test shows four images.
 Pupil is blackish in colour but when light is thrown in pupillary area
shining reflexes are observed.
 Presence of !OL is confirmed on slitlamp examination after dilating the
pupil
 Visual status and refraction will vary depending upon the power of lOL
implanted as described above.
management

 Spectacles for near vision alone (in pseudophakia with

emmetropia) or as bifocal/ progressive glasses for both distance
and near vision (in pseudophakia with consecutive refractive error)
are required.
 LASIK or Advanced surface ablation (ASA) may be required in
case of consecutive refractive error.
 lntraocular lens (IOL) exchange or pigiback IOL is required when
the consecutive refractive error is large.
THANK YOU
Primary open angle glaucoma -
Clinical features

Ameesha Susan Mathew

13
Symptoms
Asymptomatic: Thus, periodic eye examination is necessary
after middle age.
Non- specific symptoms:
1. Headache and eye ache
2. Difficulty in reading and close work
3. Delayed dark adaptation
4. Scotoma
5. Significant loss of vision and blindness
Signs

1. Anterior segment signs

● Slit lamp biomicroscopy: normal anterior segment
● Late stages, pupil reflex becomes sluggish, cornea: slight
haze.
● A low (<555 um) central corneal thickness is a significant
factor.
2. Intraocular -pressure changes

● Repeated observations of IOP ( every 3-4 hour), for 24 hours is

required during initial stage(Diurnal variation test).
● IOP falls during evening in most cases.
● A variation in IOP of over 5 mm Hg (Schiotz) is suspicious
and over 8 mm of Hg is diagnostic of Glaucoma.
● In later stages, IOP is permanently raised above 21 mm of
Hg and ranges between 30-45 mm of Hg.
● Morning rise in IOP- 20% of cases
● Afternoon rise in IOP- 25% of cases
● Biphasic rise in IOP- 55% of cases
3. Glaucomatous optic nerve head changes
a) Examination techniques: Careful fundus examination. Best technique being
stereoscopic view of optic disc with contact or non contact lenses on slit lamp
biomicroscopic examination.
Non contact lenses (+78D or + 90D) are more convenient.
b)Recording and documentation techniques: Serial hand drawing, optic disc
imaging, photography
Optic disc imaging techniques include
● Confocal scanning laser tomography
● Optical Coherence Tomography
● Scanning laser polarimetry i.e Nerve Fiber Analyser(NFA).
Glaucomatous changes in the optic disc
a) Early glaucomatous changes should be suspected to exist if fundus
examination reveals one or more of the following signs:
1.Vertically oval cup due to selective loss of neural rim tissue in the inferior and
superior poles.
2.Asymmetry of the cups
A difference of more than 0.2 between two eyes is significant.
3.Large cup, i.e., 0.6 or more (normal cup size is 0.3 to 0.4) may occur due to
concentric expansion.
4.Splinter haemorrhages present on or near the optic disc margin.
5.Pallor areas on the disc.
6.Atrophy of retinal nerve fibre layer (RNFL) which may be seen with red free
light.
B. Advanced glaucomatous changes in the optic disc
● 1. Marked cupping ( cup size 0.7 to 0.9), excavation may even reach the disc
margin, the sides are steep and not shelving (c.f. deep physiological cup)
which are well-delineated on OCT examination.
● 2. Thinning of neuroretinal rim which occurs in advanced cases is seen as
a crescentric shadow adjacent to the disc margin. Normally, the thickest to
thinnest parts of the neuroretinal rim of the optic disc are inferior, superior,
nasal and temporal (ISNT rule). Any variation from this helps to detect
glaucoma. Notching of the rim specially up to disc margin is pathognomic
3.Nasal shifting of retinal vessels which have the appearance of being broken
off at the margin is an important sign (Bayonetting sign). When the edges
overhang, the course of the vessels as they climb the sides of the cup is hidden.
4.Pulsations of the retinal arterioles may be seen at the disc margin (a
pathognomic sign of glaucoma), when IOP is very high.
5.Lamellar dot sign the pores in the lamina cribrosa
are slit-shaped and are visible up to the margin of the disc.
C)Glaucomatous Optic Atrophy
As the damage progresses, all the neural tissue of the disc is destroyed and the
optic nerve head appears white and deeply excavated.
Pathophysiology of disc changes. Both mechanical and vascular factors play a
role in the cupping of the disc.
Mechanical effect of raised IOP forces the lamina cribrosa backwards and
squeezes the nerve fibres within its meshes to disturb axoplasmic flow.
Vascular factors contribute in ischaemic atrophy of the nerve fibres without
corresponding increase of supporting glial tissue. As a result, large caverns or
lacunae are formed (cavernous optic atrophy).
4) Visual Field Defects
Only after 40% of axons have been damaged.
Anatomical basis of field defects. For better understanding of the actual field
defects, it is mandatory to have a knowledge of their anatomical basis.
Superior and inferior arcuate fibres occupy superior and inferior temporal aspects
of optic head. Most sensitive to glaucomatous damage.
Macular fibres are most resistant to glaucomatous damage.
Nomenclature of glaucomatous field defects. Visual field defects in glaucoma
are initially observed in Bjerrum’s area (10–25 degree from fixation) and correlate
with optic disc changes. The natural history of the progressive glaucomatous field
loss, more or less, takes the following sequence:
1.Isopter contraction. Mild generalised constriction of central as well as
peripheral field. Limited diagnostic value.
2.Baring of blind spot. Baring of the blind spot means exclusion of the blind
spot from the central field due to inward curve of the outer boundary of 30° central
field.Limited diagnostic value.
● 3. Small wing-shaped paracentral scotoma :earliest clinically significant
field defect.
Below or above the blind spot in Bjerrum’s area (an arcuate area extending
above and below the blind spot between 10° and 20°of fixation point).
● 4. Seidel’s scotoma: paracentral scotoma + blind spot, sickle-shaped
scotoma.
● 5. Arcuate or Bjerrum’s scotoma: It is formed at a later stage by the
extension of Seidel’s scotoma in an area either above or below the fixation
point to reach the horizontal line. Damage to the adjacent fibres causes a
peripheral breakthrough.
● 6. Ring or double arcuate scotoma. It develops when the two arcuate
scotomas join together.
● 7. Roenne’s central nasal step. It is created when the two arcuate scotomas
run in different arcs and meet to form a sharp right-angled defect at the
horizontal meridian.
● 8. Peripheral field defects. These appear sometimes at an early stage and
sometimes only late in the disease.
The peripheral nasal step of Roenne’s results from unequal contraction of the
peripheral isopter.
9. Advanced glaucomatous field defects. The visual field loss gradually
spreads centrally as well as peripherally, and eventually only a small island of
central vision (tubular vision) and an accompanying temporal island are left.
AFTER CATARACT
Aleena Ann Binoy
Roll No:7
◦ Also known as posterior capsule opacification or secondary
cataract.
◦ It is the opacity that persist or develops after extracapsular lens
extraction.
◦ Rate varies with age of patient , the surgeon , surgical technique
,type of IOL , duration of surgery
◦ Higher rates ~20% seen in younger individuals
Causes

◦ Residual opaque lens matter may persist as after

cataract , surrounded by fibrin or blood .
◦ Proliferative type develop from left out anterior
epithelial cells in capsular bag.
Clinical types

◦ Thin posterior capsule opacification

◦ Dense PCO or membranous after cataract
◦ Soemmering’s ring- thick ring of after cataract behind
iris between 2 layers of capsule
◦ Elschnig’s pearls – vacuolated subcapsular epithelial
cells are clustered like soap bubbles along posterior
capsule
Treatment

◦ YAG-laser capsulotomy is the best treatment for thin

and centrally located cataract
◦ Discission with cystitome or ziegler knife in case of thick
cataract
◦ Soemmering’s ring after cataract with clean central
posterior capsule – no treatment needed
THANK YOU
 PRIMARY OPEN ANGLE
GLAUCOMA- MANAGEMENT

ANEENA VARGHESE V
 Approach to treatment of
POAG
1. Record of Baseline data and grading of severity of glaucoma

2. Identification of target intraocular pressure

3. Initiation of medical therapy

4. Monitoring of medical therapy

 1. Record of Baseline data and grading of severity
of glaucoma

• Baseline data should include:

• Grading
• visual acuity

• slitlamp examination of anterior

segment

• tonometry (preferably with

applanation tonometer)

• measurement of central corneal

thickness,

• optic disc evaluation (preferably

with fundus photography)

• gonioscopy and visual field charting

2. Identification of target intraocular pressure
• From the baseline evaluation data a ‘target pressure’ (below which glaucomatous damage
is not likely to progress) should be identified for each patient.

• Depending upon the severity of glaucomatous damage, American Academy of

Ophthalmologists (AAO) suggested to calculate target IOP by reducing the baseline IOP
by:

In mild glaucomatous damage : 30%

In advanced glaucomatous damage : 40%

In ocular hypertension: 20%

3. Initiationof medical therapy
• Monotherapy

Initiated using topical prostaglandins (latanoprost, bimatoprost or travoprost)

or topical beta blocker (0.5% timorous or betaxolol)

IOP checked after 15 days. If drug choosen is ineffective or intolerable it

should be replaced by drug of second choice

• Combination topical therapy

If one drug is not effective, then a combination of two drugs

- one which decreases aqueous production (timolol or other beta blocker, or

brimonidine or dorzolamide)

-other drug which increases aqueous outflow (latanoprost or brimonidine or

pilocarpine)
 4. Monitoring of therapy
• most essential on regular follow-up.

• by disc changes and field changes and tonometry

 Laser trabeculoplasty
• done using argon laser (ALT), or diode laser (DLT) and selective laser trabeculoplasty (SLT).

• Indications :

IOP is uncontrolled despite maximal tolerated medical therapy.

as primary therapy where there is non-compliance to medical therapy.

• Technique and role of argon (ALT) or diode laser trabeculoplasty (DLT) in POAG.

It has an additive effect to medical therapy.

Its hypotensive effect is caused by increasing outflow facility, possibly by producing collagen
shrinkage on the inner aspect of the trabecular meshwork and opening the intratrabecular
spaces.

It has been shown to lower IOP by 8–10 mm of Hg in patients on medical therapy and by 12–
16 mm in patients who are not receiving medical treatment.
• Treatment regime usually employed consists of 50 spots on the anterior half of the
trabecular meshwork over 180°.

• Complications:

Transient acute rise of IOP, which can be prevented by pretreatment with

apraclonidine (an alpha agonist) and/or acetazolamide

Transient inflammation which can be lessened by use of topical steroids for

3–4 days.

Other complications seen less commonly are haemorrhage, uveitis,

peripheral anterior synechiae and reduced accommodation.
 Selective laser trabeculoplasty (SLT)

• based on the principle of selective photothermolysis, targets selectively pigmented

trabecular meshwork (TM) cells without causing thermal or collateral damage to
non-pigmented cells or structures unlike ALT or DLT.

• SLT is performed using Q-switched frequency doubled 532 nm Nd:YAG laser with
a pulse duration of 3 ms, a spot size of 400 microns and energy setting of 0.8 mJ.

• Pressure lowering effect of SLT is similar to ALT with the advantage of not causing
scarring and damage to TM. Further, SLT can be used in patients treated with ALT.
 Surgical therapy
Indications

1. Uncontrolled glaucoma despite maximal medical therapy and laser trabeculoplasty.

2. Noncompliance of medical therapy and nonavailability of ALT/SLT.

3. Failure of medical therapy and unsuitable for ALT either due to lack of cooperation or
inability to visualize the trabeculum.

4. Eyes with advanced disease, i.e., having very high IOP, advanced cupping and
advanced field loss should be treated with filtration surgery as primary line of
management.
 Types of surgery

• Surgical treatment of POAG primarily consists of a fistulizing (filtration) surgery which provides
a new channel for aqueous outflow and successfully controls the IOP (below 21 mm of Hg).

• Filtration operations can be grouped as below:

• A. External filteration surgery

1. Free-filtering operations (Full thickness fistula).These are no longer performed

nowadays, because of high rate of postoperative complications.

2. Guarded filtering surgery (Partial thickness fistula e.g., trabeculectomy).

3. Non-penetrating filtration surgery e.g., deep sclerectomy and viscocanalostomy.

B. Internal filteration surgery

also called as canalbased procedure, are newer techniques that restore filteration through Schlemm’s
canal. These are designed to keep the normal anatomy and to be conjunctival bleb free; and thus
reducing the risk of long-term endophthalmitis and ocular hypotomy.

These procedure includes:

1. Canaloplasty, i.e., dilatation and circumferential, traction of canal using 10–0 prolene
suture.

2. Trabectome involves an ab interno microcautery that ablates the trabecular meshwork

and inner wall of Schlemm’s canal.

3. iStent, is a titanium micro device that is placed inside the Schlemm’s canal. It allows the
aqueous humor to flow directly into the canal bypassing the trabecular meshwork.
 Trabeculectomy
Indications:

1. Primary angle-closure glaucoma with peripheral anterior synechial involving more

than 270° angle or where PI and medical treatment fail.

2. Primary open-angle glaucoma not controlled with medical treatment.

3. Congenital and developmental glaucomas where trabeculotomy and goniotomy fail.

4. Secondary glaucomas where medical therapy is not effective.

Mechanisms of filtration

1. A new channel (fistula) is created around the margin of scleral flap, through which
aqueous flows from anterior chamber into the subconjunctival space.

2. If the tissue is dissected posterior to the scleral spur, a cyclodialysis may be produced
leading to increased uveoscleral outflow.

3. When trabeculectomy was introduced, it was thought that aqueous flows through the cut
ends of Schlemm’s canal. However, now it is established that this mechanism has a
negligible role.
Surgical technique:

1. Initial steps of anaesthesia, cleansing, draping, exposure of eyeball and fixation with
superior rectus suture are similar to cataract operation.

2. Conjunctival flap: A fornix-based or timbal-based conjunctival flap is fashioned and

the underlying sclera is exposed. The Tenon’s capsule is cleared away using a Tooke’s
knife, and haemostasis is achieved with cautery.

3. Scleral flap: A partial thickness (usually half) limbal-based scleral flap of 5 mm × 5

mm size is reflected down towards the cornea.
4. Excision of trabecular tissue: A narrow strip (4 mm × 2 mm) of the exposed deeper sclera
near the cornea containing the canal of Schlemm and trabecular meshwork is excised.

5. Peripheral iridectomy is performed at 12 O’clock position with de Wecker’s scissors.

6. Closure. The scleral flap is replaced and 10-0 nylon sutures are applied. Then the
conjunctival flap is reposited and sutured with two interrupted sutures (in case of fornix
based flap) or continuous suture (in case of limbal-based flap).

7. Subconjunctival injections of dexamethasone and gentamicin are given.

8. Patching. Eye is patched with a sterile eye pad and sticking plaster or a bandage.
 Complications

• postoperative shallow anterior chamber

• hyphaema

• iritis

• cataract due to accidental injury to the lens

• endophthalmitis (not very common).

 Sutureless trabeculectomy

1. Initial steps, and

2. Conjuctival flap fashioning is similar to conventional trabeculectomy.

3. Sclero-corneal valvular tunnel, 4 mm × 4 mm in size, is made by first making 4 mm

partial thickness scleral groove about 2.5 mm away from the superior limbus with the
help of a razor blade fragment

A 4 mm wide sclero-corneal tunnel which extends about 1.5 mm in the clear cornea is
then made with the help of a crescent knife.
4. Entry into the anterior chamber is made with the help of a sharp 3.2 mm angled
keratome.

5. Punching of posterior lip of the anterior chamber entry site is then performed with the
help of a Kelly’s punch to make a sclerostomy of about 2 mm × 2 mm in size.

6. Peripheral iridectomy is performed at 12 O’clock position with the help of de

Wecker’s or Vanna’s scissors.

7. Closure. Anterior chamber is filled with balanced salt solution (BSS) or air to close
the valvular sclero-corneal tunnel incision. Conjunctival flap is reposited and anchored
with wet-field cautery.
PRIMARY ANGLE
CLOSURE

ANGEL ROSE ROSHAN A

 PRIMARY ANGLE CLOSURE DISEASE
• Apposition of peripheral iris against the trabecular
meshwork resulting in obstruction of aqueous outflow by
closure of an already narrow angle of the anterior chamber
• The condition is not associated with any other ocular and
systemic abnormalities
• Primary angle closure glaucoma – optic disc and visual field
changes are present
 EPIDEMIOLOGY
As per International Society Of Geographical and
Epidemiological Ophthalmology (ISGEO):
a) For every 10 occludable angles (PAC suspects) seen there is
only one case of PACG
b) Chronic PACG (asymptomatic) is more common than acute
PACG (symptomatic) (3:1)
c) There is great ethnic variability in the prevalence of PACG
d) Major cause of world glaucoma blindness is PACG
 ETIOPATHOGENESIS
PREDISPOSING RISK FACTORS

A. DEMOGRAPHIC RISK FACTORS

1) Age – PACG with pupillary block occurs with greatest

frequency in 6th and 7th decades of life
2) Gender – male to female ratio 1:3
3) Race – In Asians, it presents in 5th to 6th decade and
accounts for 50% of primary adult glaucomas in this ethnic
group
B. ANATOMICAL AND OCULAR RISK FACTORS

Hypermetropic eyes with shallow anterior chamber and short axial

length
1) Eyes in which iris-lens diaphragm is placed anteriorly
2) Eyes with narrow angle of anterior chamber, which may be due
to:
- small eyeball
- relatively large size of the lens and smaller
diameter of the cornea
- bigger size of the ciliary body
- more anterior insertion of the iris on the ciliary body
4) Plateau iris configuration
5) Heredity – most cases are sporadic in nature
shallow anterior chamber and narrow angles
have been reported as more common in
first degree relatives of the patient
 PATHOMECHANISM OF
RISE IN INTRAOCULAR PRESSURE

PUPILLARY BLOCK MECHANISM

PLATEAU IRIS CONFIGURATION AND SYNDROME
PHACOMORPHIC MECHANISM
PUPILLARY BLOCK MECHANISM
Responsible for rise in IOP in 70% of the predisposed patients

PRECIPITATING FACTORS
a) Physiological mydriasis
b) Pharmacological mydriasis
c) Pharmacological miosis
d) Valsalva manoeuvre
MECHANISM OF RISE IN IOP AFTER MYDRIASIS
• Mid dilatation of the pupil which increases the amount of
apposition between iris and anteriorly placed lens with a
considerable pressure resulting in relative pupil block
• The aqueous collects in the posterior chamber and pushes the
peripheral flaccid iris anteriorly (iris bombe)
• Resulting in appositional angle closure due to iridocorneal
contact
• Eventually there occurs rise in IOP which is transient to begin
with
• But slowly the appositional angle closure is converted into
synechial angle closure (due to formation of peripheral
anterior synechiae)
A. RELATIVE PUPIL BLOCK

B. IRIS BOMBE FORMATION

C. APPOSITIONAL ANGLE CLOSURE

 MECHANISM OF RISE IN IOP AFTER MIOSIS
• Drugs that constrict pupil are reported to increase pupillary
block
• These drugs contract the ciliary muscles allowing the zonules
to relax and the lens to move forward
• So it is advisable to avoid miotics in the prevention of PACG
in predisposed eyes
PLATEAU IRIS CONFIGURATION AND SYNDROME
• Responsible for 10% atypical cases of acute angle closure
glaucoma
• This is atypical in the patients that have normal central
anterior chamber depth, flat iris plane and minimal pupillary
block
• Anterior chamber angle is closed by a pushing mechanism
because of the anterior positioned ciliary processes displacing
the peripheral iris anteriorly
• Such a situation is called plateau iris configuration
• Plateau iris syndrome – when acute angle closure glaucoma
occurs either spontaneously or after pharmacological dilation
in spite of patent iridotomy
• ISGEO CLASSIFICATION (based on natural history, IOP
measurements, gonioscopy, disc and visual field evaluation)
a) Primary angle closure suspect (PACS)
b) Primary angle closure (PAC)
c) Primary angle closure glaucoma (PACG)

• TRADITIONAL CLINICAL CLASSIFICATION (based on clinical

presenting symptoms)
a) Latent primary angle closure glaucoma
b) Sub acute primary angle closure glaucoma
c) Acute primary angle closure glaucoma
d) Chronic primary angle closure glaucoma
 PRIMARY ANGLE CLOSURE SUSPECT
SYMPTOMS – absent at this stage

PRESENTING SITUATIONS for diagnosis include:

a) Suspicious clinical signs on routine ocular examination in
patients coming for some other complaints
b) Fellow eye of the patients presenting with acute attack of
PAC
c) Glaucoma screening programme
 CLINICAL SIGNS

1. ECLIPSE SIGN
• Indicates decreased axial
anterior chamber depth
• Elicited by shining a penlight
across the anterior chamber
from the temporal side and
noting a shadow on the
nasal side
2. SLIT LAMP BIOMICROSCOPIC SIGNS include:
• Decreased axial anterior chamber depth
• Convex shaped iris lens diaphragm
• Close proximity of the iris to cornea in the periphery

3. VAN HERICK SLIT LAMP GRADING OF THE ANGLE

• Peripheral anterior chamber depth (PACD) is compared to the adjacent
corneal thickness (CT) and is graded as follows:
a) Grade 4 (wide open angle) – PACD=3/4 TO 1 CT
b) Grade 3 (mild narrow angle) – PACD=1/4 TO 1/2 CT
c) Grade 2 (moderate narrow angle) – PACD=1/4 CT
d) Grade 1 (extremely narrow angle) – PACD<1/4 CT
e) Grade 0 (closed angle) – PACD=Nil
DIAGNOSTIC TESTS
• IOP measurement
• Gonioscopy
• Ultrasonic biomicroscopy
• Anterior segment OCT
• Optic disc evaluation
• Visual field analysis
DIAGNOSTIC CRITERIA for PAC suspect
• Gonioscopy should reveal irido-trabecular contact in greater
than 270 degree angle and no PAS
• IOP should be normal
• Optic disc should show no glaucomatous changes
• Visual fields should be normal
 MANAGEMENT
PROVOCATIVE TESTS (designed to precipitate closure of the angle)
1. Prone darkroom test
• Baseline IOP recorded
• Patient made to lie prone in a darkroom for 1 hour
• He must remain awake so that the pupils remain dilated
• IOP again measured after 1 hour
• Increase in IOP > 8 mm Hg – diagnostic of PAC suspect
2. Mydriatic provocative test
• In this test either a weak mydriatic (0.5% tropicamide) or
simultaneously a mydriatic and miotic (10% phenylephrine and 2%
pilocarpine) are used to produce a mid dilated pupil
• Pressure rise > 8 mm Hg – positive
• Not used nowadays

INFERENCE FROM PROVOCATIVE TESTS

• Positive – angle is capable of spontaneous closure
• Negative – patient should be warned of possible symptoms of an
acute attack of PAC
 TREATMENT
• Periodic follow up and educate the patient about the symptoms
of the disease
• Prophylactic laser iridotomy
more than 270 degree of oppositional iridotrabecular contact is
seen on gonioscopy ( in the fellow eye of patients with PACG)
• If untreated risk of conversion to PACG during the next 5 years is
50%
PACG
BY: ANITA JOSE.C
 PRIMARY ANGLE CLOSURE(PAC)

Features of Pac include:

• Elevated IOP and or Peripheral anterior synechiae (PAS) present.
• Gonioscopy reveals irido-trabecular contact > 270 degree angle.
• Optic disc and visual fields are normal,
Acute primary angle-closure:
• An attack of acute rise in IOP may occur in these patients due to pupillary block causing
a sudden closure of the angle.
• It’s a sight threatening emergency
Precipitating factors :
• Physiological mydriasis
• Physiological swallowing of anterior chamber
• Pharmacological mydriasis
Clinical features include:
Symptoms:
• Pain : Acute attack of sever pain in the eye radiating along the 5 th nerve
• Nausea, vomiting, prostrations associated with pain.
• Rapidly progressive impairment of vision, photophobia, redness and lacrimation.
• Colored halos around light.
• Past history
 Signs of acute PAC
• Lids may be edematous
• Conjunctiva is chemosed and congested, (both conjunctival and scleral vessels are
congested)
• Cornea becomes edematous and insensitive
• Shallow anterior chamber
• Angle of anterior chamber is completely closed (Sheffer grade 0)
• Iris may be discolored
• Pupil is semi dilated, vertically oval and fixed. It is non-reactive to both light and
accommodation
• IOP is markedly elevated ( 40-70 mmHg)
• Optic disc is edematous and hyperemic
• Other eye : shallow anterior chamber and an occludable angle.
 Differential diagnosis

1. From other causes of red eye; Acute conjunctivitis and acute iridocyclitis
2. From acute secondary glaucomas such as : Phacomorphic glaucoma, phacolytic
glaucoma, neovascular glaucoma
 MANAGEMENT

A. Immediate medical therapy to lower IOP

B. Definitive treatment
C. Prophylaxis of the fellow eye
D. Long time glaucoma surveillance and IOP management of both eyes
 IMMEDIATE MEDICAL THERAPY TO
LOWER IOP
1. Systemic Hyperosmotic agents given initially (> 40mmHg)
- i.v mannitol ( 1gm/kg body weight) – preferred in nausea and vomiting
- Oral hyperosmotics like glycerol 1gm/kg.b.w of 5% solution in lemon juice
(contraindicated in Diabetes mellitus)
2. Systemic carbonic anhydrase inhibitors : acetazolamide 500 mg followed by
250 mg tablet t.i.d
3. Topical anti-glaucoma drugs given immediately:
- Beta blockers- 05% timolol / 0.5% betaxolol
- Alpha adrenergic agonist , brimonidine 0.1-0.2%
- Prostaglandin analogues , latanoprost 0.005%
- Pilocarpine 2% Q.I.D should be started after 1 hr of treatment ( when IOP is
lowered)
 Immediate medical therapy to lower
IOP
4. Compressive gonioscopy with a 4 mirror goniolens – relieves pupil block and
determines if the trabecular block is reversible
5. Topical steroids –prednisolone acetate 1% or dexamethasone eye drops q.i.d
6. Analgesics and antiemetic
DEFINITIVE THERAPY

1.Laser peripheral iridotomy (LPI)

• Gonioscopy should be done as soon as the eye is clear
• LPI is done when PAS are seen in <270° angle
• It reestablishes communication between posterior and anterior chamber.
• It bypasses the pupillary block and relieves the crowding of the angle.
• LPI done with YAG LASER OR Argon last and is always preferred over
surgical iridotomy.
 Definitive therapy

2. Filtration surgery – Trabeculectomy

• Done when IOP is not controlled with the max medical therapy
• Goniscopy reveal PAS > 270 °
• Or when peripheral iridotomy is not effective
3. Clear lens extraction : by phacoemulsification with IOL implantation is
recommended in presence of phacomorphic etiology
TRABECULECTOMY - MECHANISM

1. A new channel is created around the scleral flap , through which aqueous
flows from anterior chamber into the subconjunctival space
2. If the tissue is dissected posterior to the scleral spur, a cyclodialysis may be
produced leading to increased uveoscelarl outflow
 Surgical technique of trabeculectomy
1. Initial steps of anaesthesia, cleansing, draping, exposure of eyeball and fixation
with superior rectus suture
2. Conjunctival flap: A fornix based conjunctival flap is fashioned and the
underlying sclera is exposed. The tenon’s capsule is cleared away using a
Tooke’s knife and hemostasis is achieved with cautery
3. Scleral flap ; A partial thickness limbal based scleral flap of 5mm × 5mm size is
reflected down towards cornea
4. Excision of trabecular tissue : A narrow strip ( 4mm × 2mm )of the exposed
deeper sclera near the cornea containing the canal of Schlemm an trabecular
meshwork is excised.
5. Peripheral iriditomy is performed at 12 O’ clock position with de Wecker’s scissors
6. Sub – conjunctival injections of dexamethasone and gentamicin are given
7. Patching
C. Prophylactic treatment in the normal fellow eye : Prophylactic laser iridotomy or surgical
peripheral iridectomy should be performed on the fellow asymptomatic eye as well
D. Long term glaucoma surveillance and IOP management in both eyes
• Eyes treated with PI may develop PACG at any time, so should be treated as and when
required
• Filtration surgery needs to be repeated with antimetabolites
 Fate of acute PAC
1. Post surgical acute PAC : raised IOP after unsuccessful (LPI) , treated by
trabeculectomy.
2. Treated case of acute PAC , the eye usually quitens after some time.
3. Spontaneous angle reopening ; occurs rarely but LPI needs to be done
4. Ciliary body shutdown : Temporary cessation of aqueous humor secretion due
to ischemic damage to ciliary epithelium.
Treatment includes :
• Topical steroids to reduce inflammation
• LPI performed when cornea becomes clear
• IOP monitored regularly
• Trabeculectomy done in constant rise of IOP
5. Vogt’s triad :
• Glaukomfleken( anterior sub capsular lenticular opacity)
• Patches of iris atrophy
• Slightly dilated non reacting pupil ( sphincter atrophy)
 PRIMARY ANGLE CLOSURE GLAUCOMA
Pathogenesis : PACG occurs due to gradual synechial closure of the angle of anterior
chamber .
Clinical features:
• Constantly raised IOP
• Eyeball remains white and painless
• Optic disk shows glaucomatous cupping
• Visual field defects
• Gonioscopy reveals >270° with PAS
Clinical Diagnostic impression : Angle is abnormal in function (elevated IOP) and structure (PAS
+)
TREATMENT
• Laser iridotomy alone or with medical therapy
• Trabeculectomy
• Prophylactic laser iridotomy in fellow eye must be performed
 Absolute Primary Angle Closure
Glaucoma
 PACG if untreated gradually progresses into the final phase
Clinical Features
• Painful blind eye
• Peri-limbal reddish blue zone( dilated anterior ciliary veins)
• Caput medusa
• Cornea slowly becomes hazy and develops bullous keratopathy or filamentary keratitis
• Very shallow anterior chamber
• Iris becomes atrophic
• Pupil becomes fixed and dilated and gives a greenish hue
• Optic disc shows glaucomatous optic atrophy
• High IOP, eyeball is stony hard
 Management of absolute glaucoma

1. Retrobulbar alcohol injection given to relieve pain – First, 1ml of 2% xylocaine is given
followed after 5-10minutes by 1ml of 80% alcohol. It destroys the ciliary ganglion.
2. Destruction of secretory ciliary epithelium to reduce IOP by cyclocryotherapy or
cyclophotocoagulation.
• Anaestesia
• Lids separation
• Cryoapplication: Cryo is applied with a retinal probe placed 3mm from the limbus .
• Freezing at -80°C for 1 minute is done.
3. Enucleation of the eyeball
COMPLICATIONS

1. Corneal ulceration – prolonged epithelial edema and insensitivity

2. Staphyloma formation : Due to high IOP , sclera becomes thin and atrophic
and bulges out resulting in a ciliary or equatorial staphyloma
3. Atrophic bulbi
THANKYOU
ANTERIOR UVEITIS
ANJANA BABU , ROLL NO. 18
 UVEAL TISSUE CONSTITUTES THE MIDDLE VASCULAR COAT OF EYEBALL
 IRIS , CILIARY BODY , CHOROID
UVEITIS

 INFLAMMATION OF UVEAL TISSUE but clinically asso adjacent strs

 ANATOMICAL CLASSIFICATION :
 1. ANTERIOR UVEITIS – Iris up to pars plicata of ciliary body.
Subdivided into –
 A] IRITIS - IRIS
 B]IRIDOCYCLITIS-IRIS AND PARS PLICATA EQUALLY INVOLVED
 C]ANTERIOR CYCLITIS- PARS PLICATA
 2.INTERMEDIATE UVEITIS
 3. POSTERIOR UVEITIS
 4.PANUVEITIS
 CLINICAL CLASSIFICATION:
 1. ACUTE –sudden onset , ≤3 m

 2. CHRONIC –insidious asymptomatic onset , >3 m

 3. RECURRENT –repeated episode separated by inactive periods
>3m
 PATHOLOGICAL CLASSIFICATION :
 1.SUPPURATIVE
 2.NON SUPPURATIVE –granulomatous / nongranulomatous
 ETIOLOGICAL CLASSIFICATION :
 1.INFECTIVE
 2. IMMUNE RELATED
 3.TOXIC
 4.TRAUMATIC
 5.ASSO WITH NON INFECTIVE SYSTEMIC DISEASES
 6.IDIOPATHIC
ETIOLOGY 1. INFECTIVE UVEITIS
1. EXOGENOUS
INFECTION –
• PENETRATING
2.SECONDARY INFECTION-
INJURIES
SPREAD FROM
• PERF OF CORNEAL
NEIGHBOURING STRS
ULCER
• AFTER INTRAOCULAR
• ACUTE PURULENT
OPERATIONS 3.ENDOGENOUS –
CONJUNCTIVITIS
• KERATITIS BLOODSTREAM
ACUTE IRIDOCYCLITIS
• SCLERITIS
OF SUPPURATIVE
• RETINITIS
NATURE
• ORBITAL CELLULITIS
• ORBITAL
ENDOPHALMITIS/PANO
THROMBOPHLEBITIS
PTHALMITIS
TYPES OF INFECTIOUS UVEITIS

 1.BACTERIAL –granulomatous
[tb,leprotic,syphilitic,brucellosis,pyogenic-step,staph,pneumo,gono]
 2.VIRAL- herpes simplex, zoster,CMV
 3.FUNGAL-rare- systemic
aspergillosis,candidiasis,blastomycosis,histoplasmosis
 PARASITIC-toxoplasmosis,amoebiasis,toxocariasis
 RICKETTSIAL- scrub typhus,epidemic typhus
2. IMMUNE RELATED [MOST COMMON CLINICALLY]
1.MICROBIAL ALLERGY –
INFN. Ab BLOOD Uveal tissue Ab secondary infn

allergic rn
eg: TB[used to be the mc cause of uveitis]
2.ANAPHYLACTIC UVEITIS-
Serum sickness , angioneurotic edema- systemic anaphylactic rns
3.ATOPIC –
Allergens –seasonal iritis-pollens , dander ,dust ,egg albumin, beef
proteins
4.AUTOIMMUNE-
RA , SLE, Reiter’s , wegener’s granulomatosis
5.HLA associated
3.TOXIC UVEITIS

 Endotoxic- autotoxins , microbial toxins[pnumo , gono]

 Endocular- blind patients, long standing retinal detachment
 Exogenous –irritant chemical substances-miotics, cytotoxic drugs
CLINICAL FEATURES - SYMPTOMS

ACUTE ant uveitis –

• Pain-dull aching
CHRONIC uveitis –
throbbing , worsen
Eye maybe white with
@night,refer to forehead
minimal symptoms
and scalp[CN5]
• Photophobia And
Blepharospasm
• Redness[circumcorneal
congestion]
Irritated
• Lacrimation sensory
• Defective vision fibres of
CN5
MOTOR
FIBRES OF
CN7
SIGNS-SLIT LAMP BIOMICROSCOPY
 A]LID EDEMA – usually mild , may accompany a severe attack of AAU
 B. CIRCUMCORNEAL CONGESTION

Marked –A iridocyclitis
Minimal-chronic
 3.CORNEAL SIGNS –
1.CORNEAL EDEMA –due to toxic endothelitis
[infl of corneal endothelium] & raised iop

2.KERATIC PRECIPITATES –proteinaceous cellular deposits

at back of cornea

3.POSTERIOR CORNEAL OPACITY-

long standing iridocyclitis
MUTTON FAT KP -
GRANULOMATOUS-
LARGE,THICK,FLUFFY,GREASY APPEARENCE

SMALL AND MEDIUM KPS –

NON GRANULOMATOUS
SMALL,DISCRETE,DIRTY WHITE ARRANGED IRREGULARLY

FINE KPS –
STELLATE KPS , COVER ENTIRE ENOTHELIUM-
Endothelial dusting
Seen in fuch’s heterochromic iridocyclitis
Herpitic iridocyclitis , CMV retinitis

OLD KPS – Sign of healed uveitis-KPs shrink/fade/pigmented/irreg/

old mutton fat –ground glass [hyalinization]
 D. ANTERIOR CHAMBER SIGNS –
1. AQUEOUS CELLS – Early feature , cells counted using slit lamp and graded
2. AQUEOUS FLARE –Leakage of protein particles to
aq h from damaged blood vessels –
seen suspended and moving dust particles
 3. HYPOPYON- thick and heavy exudate settle in lower part of ant
chamber[sterile pus]

 Dense immobile HP-slow to abrorb due to high fibrin content[ HLA B27]
 Hypopyon in behcet’s syn has minimal fibrin , shifts with head position , quick to
absorb
 Hemorrhagic HP-herpitic , trauma , rubeosis iridis
 4. Changes in depth and shape of anterior chamber-
May occur due to synechiae formation –
Deep and irreg in post synechiae
Funnel shaped in annular synechiae with iris bombe

5.Changes in angle of ant

chamber-
Gonioscopic examination
Active stage-cellular
deposits
Chronic stage-peripheral
ant synechiae
 E. IRIS SIGNS
1.LOSS OF NORMAL PATTERN –
edema and water logging in active phase
atrophic changes in chronic phase
2.CHANGES IN COLOUR –
muddy in active phase
hyperpigmented/depigmented in healed stage
3.IRIS NODULES –typically in granulomatous uveitis
 KOEPPE ‘S nodules –
pupillary border ;
may initiate post synechiae
 BUSACCA’S nodules –
 near collarette, large ,less common
4.POSTERIOR SYNECHIAE-
Adhesions btw post surface of iris and ant capsule of lens due to organisation of fibrin
rich exudates

ANNULAR PS –
360 adhesion –ring-
prevent aq h from PC
to AC –Inc IOP-
Seclusio pupillae –
push iris anteriorly-IRIS
BOMBE TOTAL PS –
SEGMENTAL PS –
Plastering pf total
Adhesion at some
surface –rare-deepening
points
of ant chamber
5. NEOVASCULARISATION OF IRIS [ RUBEOSIS IRIDIS ]
Chronic iridocyclitis
Fuch’s heterochromic iridocyclitis
F. Pupillary signs
1.NARROW PUPIL –
Acute iridocyclitis due to irritation of splincter pupillae by toxins , iris edema , engorged
radial vessels of iris

2.IRREGULAR PUPIL SHAPE –

Segmental post syn

3.ECTROPION PUPILLAE –
Evertion of pupillary margin dur to contraction of fibrinous exudates on ant surface of
iris

4.PUPILLARY REACTION –
Sluggish/absent due to edema and hyperemia of iris which hamoers movement

5.OCCLUSIO PUPILLAE –
When pupil completely occlude due to organisation of exudates across entire
pupillary area
G.CHANGES IN LENS –
1.PIGMENT DISPERSAL –
On ant capsule of lens is almost universal in ant uveitis

2.EXUDATES deposited on lens

3.COMPLICATED CATARACT –
Persistant iridocyclitis- early stage- polychromatic luster/bread crump
appearance of early post subcapsular opacities . In the presence of
synechiae ,complicated cataract progress to maturity
H. CHANGES IN VITREOUS AND RETINA
1.EXUDATES AND INFLAMMATORY CELLS- ACUTE
2.CYSTOID MACULAR EDEMA [CME]- CHRONIC

I. CHANGES IN IOP –
Normal
Increased – secondary glaucoma
Decreased – acute iridocyclitis
SIGNS
1. LID EDEMA
2. CIRCUMCORNEAL CONGESTION
3. CORNEAL SIGNS
 Corneal edema
 Keratic precipitates
 Posterior corneal opacity
4. ANTERIOR CHAMBER SIGNS
 Aqueous cells
 Aqueous flare
 Hypopyon
 Depth &shape
 Angle of ant chamber
4. IRIS SIGNS
 Loss of normal pattern
 Change in colour
 Iris nodules
 Posterior synechiae
 Neovascularisation
5. PUPILLARY SIGNS
 Narrow pupil
 Irregular pupil shape
 Ectropion pupillae
 Pupillary reaction
 Occlusio pupillae
6. LENS
 Pigment dispersal
 Exudates
 Complicated cataract
7. VITREOUS AND RETINA
 Exudates and inflammatory cells
 Cystoid macular edema
8.IOP
DIFF BTW granulomatous and
nongranulomatous uveitis
COMPLICATIONS OF
ANTERIOR UVEITIS

ANJU THOMAS

10/11/2024 245
1. COMLICATED CATARACT

– as a result of persistant iridocyclitis

- Typical features : polychromatic luster and breadcrumb appearance of
the early posterior subcapsular opacities

10/11/2024 246
2. SECONDARY ANGLE CLOSURE GLAUCOMA

It is most commonly seen in recurrent cases of Anterior uveitis

Due to Annular/ Ring Synechiae ( 360 degree adhesion between the rim of the
iris to the nterior capsule of the lens)

Aqueous cannot travel from posterior to anterior chamber

Aqueous pushes the iris forward, narrowing the angle of anterior chamber

Secondary Angle Closure Glaucoma

10/11/2024 247
3. CYCLITIC MEMBRANE

Exudates leak behind the lens

Covers the ciliary process and posterior surface of the lens

No aqueous secretion

Decreased IOP

10/11/2024 248
4. Choroiditis
5. Band Shaped Keratopathy : Calcium deposits in the Bowmans Layer of
cornea is seen
6. Papillitis : In severe cases of iridocyclitis, there is inflammation of the optic
disc

10/11/2024 249
7. PHTHSIS BULBI

-It is the final stage end result of any form of chronic uveitis in which the eye
becomes soft, shrunken and atrophic.
3 STAGES:
a) Stage of atrophic bulbi without shrinkage

Due to continued inflammation and loss of nutritional support, there is loss of

function of ocular tissues.
Shape of globe is maintained.
Vision is completely lost. Lens becomes cataractous. Retina develops atrophic
changes.
10/11/2024 250
b) Stage of atrophic bulbi with shrinkage
It occurs due to continued ciliary body dysfunction.
Cornea becomes edematous and vascularised. Anterior chamber is collapsed.
Eyeball becomes smaller and square shaped.

c) Atrophic bulbi with disorganization

IOP is markedly lowered.
Size of eyeball is markedly decreased.
Cornea becomes sclera like.

10/11/2024 251
INVESTIGATIONS

10/11/2024 252
1. HAEMATOLOGICAL INVESTIGATIONS
TLC – information about inflammatory response of the body
ESR – to ascertain existence of any chronic inflammatory condition in the body
Blood Sugar – to rule out diabetes mellitus
Blood uric acid levels – in patients suspected of having gout
HLA Typing – HLA B-27 : for ankylosing spondylitis and Reiter disease
- HLA A-25 : for birdshot chorioretinopathy

10/11/2024 253
2. URINE EXAMINATION : for WBCs, pus cells, RBCs and culture to rule out urinary
tract infections.
3. RADIOLOGICAL INVESTIGATIONS :
X-rays of chest, paranasal sinuses, sacroiliac joints and lumbar spine
CT Scan of thorax for suspected sarcoidosis cases
MRI Scan of head for suspected sarcoidosis, demyelination and lymphoma

10/11/2024 254
TREATMENT
a) Non Specific Treatment
b) Specific Treatment

10/11/2024 255
NON SPECIFIC TREATMENT
a) LOCAL THERAPY

(I) CYCLOPLEGIC DRUGS : 1% atropine sulphate

: 2% homatropine
: 1% cyclopentolate
MODE OF ACTION : Relaxes the ciliary muscle and relieves pain
: Breaks any posterior synechiae formed
: Prevents formation of posterior synechiae
10/11/2024 256
• (II) CORTICOSTEROIDS : Prednisolone
: Dexamethasone
: Betamethasone
MODE OF ACTION : Reduce inflammation by their anti-inflammatory effect
: Special use in allergic type of uveitis due to anti-allergic
property
: Reduce fibrosis due to anti-fibrotic activity

10/11/2024 257
b) SYSTEMIC THERAPY

(I) COTICOSTEROIDS
Systemic corticosteroids are indicated for intractable anterior uveitis resistant to
topical therapy
(II) NSAIDs : Aspirin
: Can be used where systemic corticosteroids are containdicated
(III) IMMUNOSUPPRESSIVE DRUGS
: Should be used only in desperate and extremely serious cases of
uveitis in which vigorous use of steroids have failed to resolve the inflammation and
there is imminent danger of blindness

10/11/2024 258
C) PHYSICAL MEASURES
(I) Hot fomentation
(II) Dark Goggles

10/11/2024 259
SPECIFIC TREATMENT OF THE CAUSE
- Non specific treatment is very effective and controls uveal inflammation in
most cases, but does not cure the disease resulting in relapses.Therefore,
efforts must be made to treat the underlying cause.
(I) Anti tubercular drugs for underlying Kochs disease
(II) Adequate treatment for syphilis toxoplasmosis etc must be carried out
when detected

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