Ophthalmology

1. GLAUCOMA
Dr. Mohd Najmussadiq khan
M S (Ophth) DiSSO (ESASO)

2.  Glaucoma is a disorder in which IOP is
sufficiently raised to cause damage vision
 Normal IOP IS {12 – 21 or 15 – 22 } mmHg

3. HISTOPHYSIOLOGY OF AQUEOUS
 A.C = anterior chamber .
 P.C = posterior chamber .
 The IOP is determined by the rate of aqueous
production by the ciliary epithelium {secretion of
ultrafiltration } and the resistance to outflow of
aqueous from the eye.Aqueous is a clear fluid that
fills anterior and posterior chamber .
Aqueous is composed of :
 Water , proteins , electrolytes , other components
found in plasma are found in aqueous with different
concentrations .
 Aqueous volume is 125 ml .Rate of formation is 1
ml / minute {as tears aqueous is formed through
blood aqueous barrier (BAB )}.

4. AQUEOUS FORMATION AND FLOW :
 Water and other substance form the aqueous either
by passive diffusion from ciliary body or active by
secretion from ciliary epithelium ---- posterior
chamber ---- pupil ------ anterior chamber ----
trabecular meshwork ----- canal of Schlemm ----
aqueous veins and collecting channels --- venous
system.
 Small amount of aqueous leaves the eye through
uveal vessels and sclera {uveoscleral flow }

7. NORMAL IOP SHOWS PHYSIOLOGICAL VARIATION
{2 – 5 MMHG } DUE TO :
 Change in respiration .
 Change in heart rate .
 Change in pupillary diameter .
 Change in arterial blood pressure {ABP}.
 Diurnal variation .{morning more than night }.
Factors affecting IOP:
 ABP drugs PH CNS effect change in
intraocular vessels.

8. CLINICAL EVALUATION OF A CASE OF
GLAUCOMA

9. 1.Measurement of IOP diagnostic tests :
Digital .
 Tonometry {indentation , applanation and
pneumotonometry

18. 2.Gonioscopy :Its used to measure the angle of A.C
by contact lens and a prism .This method is very
important for differentiation between open angle
glaucoma and angle closure glaucoma . Goldmann
single and three mirror gonioscope
 Direct gonioscopy with goniolens like-
Koeppe,Barkan,Thorpe
 Indirect gonioscopy with gonioprisms like-
Goldmann single and three mirror gonioscope &
Zeiss four mirror gonioscope

24. ANGLE STRUCTURE

26. 3.Ophthalmoscopy :
 Direct visualization of optic disc is the most
important test in diagnosing glaucoma .
4.Measurement of visual acuity
5.Anterior segment examination on slit lamp
6.Perimetry :For functions in peripheral and central
fields related to optic nerve atrophy present in
glaucoma .Its important for detecting open angle
glaucoma .Now a days it is done by automated
perimeter

27. PERIMETRY

28. 7.PROVOCATIVE TESTS :
These test are done for high risk patients :
 If IOP is very high .
 If pressure difference between 2 eyes > 5 mmHg {normal difference
2 – 4mmHg }.
 Diurnal variation {> 4 mmHg between morning and evening }.
These tests are :
 a- Water drinking test :Measuring IOP after the patient drinks 1
liter of water on empty stomach (POAG)
 b- Dark room test :Patient sites in dark room { without sleeping }for
1 hours arise of > 8mmHg suggests angle closure glaucoma .
 c- Prone position test :Patient lies in prone position – rise of >
8mmHg – angle closure glaucoma
 { tests b & c --- +ve results –confirm by gonioscopy }.
 d-Prone-dark room test
 e-mydriatic provocative tese(0.5% tropicamide)
 f-mapistones(2%pilocarpine-10%phenylephrine) test
 g- Steroid response test :increase IOP --- after taking steroids 4
times daily for 6 weeks

29. CLASSIFICATION OF GLAUCOMA :
I-Primary glaucoma {unknown cause }:
 Open angle glaucoma {simple glaucoma }.
 Angle closure glaucoma { narrowing angle glaucoma }:
 Pupillary block .{iris bombe}.
 Ciliary body block .
 Peripheral iris block .
II-Congenital glaucoma :
1- Primary congenital glaucoma :
2- Glaucoma associated with ocular disorder :
 Mesodermal dysgenesis .
 Posterior polymorphous corneal dystrophy .
 Aniridia .
 Microphthalmous .
3- Glaucoma associated with systemic disorders :
 Phacomatosis - hereditary multiple hamartomas as:
Neurofibromatosis , Sturge Dimitri Weber syndrome ,
Von Hippel- Lindau s disease .
 Lens dislocation {Marfan's syndrome and Homocystinuria }.
 Congenital infection {Rubella and syphilis }.

30. CONGENITAL GLAUCOMA {BUPHTHALMOS }
 Etiology :Autosomal {recessive and dominant
}inheritance .Failure of development of angle structure or
presence of a cellular membrane called Barkans
membrane which obstructs the aqueous outflow.2/3 are
males and 2/3 are bilateral .40% cases are true
congenital and 50% cases are infantile.
 clinically :defects interfere with drainage of aqueous ----
increase IOP .
 defects include :iridodysgenesis , iris hypoplasia ,
isolated trabeculodysgenesis , unsplitted Mesodermal
tissue at the angle .

31. SYMPTOMS & SIGNS-
 Lacrimation {earliest and most constant }.
 Photophobia , Blepharospasm , blue sclera .
 Enlargement of eyeball .
 Deep A.C .,iris atrophy and tremulousness
 Edema and opacity of cornea .Large
cornea(megalocornea>11.5mm) with horizontal
curvilinear lines k/a Haabs striae due to breaks in
the descements membrane.sensations are
diminished.
 Optic disc cupping but it may regress when IOP is
normalised quickly
 Lens is flattened and backward displaced.there
may be subluxation
 IOP usually neither marked nor acute
 Eye becomes myopic

33. BUPHTHALMOS :
 Infantile congenital glaucoma marked by increased
intraocular fluid with enlargement of eye ball
{autosomal recessive inheritance }

34. Diagnosis (examination under general
anaesthesia)
 corneal diameter
 Gonioscopy
 IOP
 Fundus exam .
D/D :
 Mega cornea
 2ry glaucoma
 traumatic corneal haze

35. TREATMENT :SURGERY {MIOTICS AS PREOPERATIVE
MEDICATION }
 Goniotomy : surgical opening of canal of Schlemm
{removing abnormal structure } .An arcuate incision
incision is made with a special knife halfway between iris
and schwalbes line.

36.  Goniopunture : a puncture is made through the whole
thickness of trabecular region in the subconjuctival
space. If the fail or not possible because of corneal haze
.
 Trabeculectomy excision of part of trabecular
meshwork
 Trabeculotomy incision through trabecular meshwork
.A fine metal probe is passed into the schlemms canal
and is then swept into the anterior chamber.
 Prognosis :Untreated cases --- blindness .Most cases
of infantile congenital glaucoma are discovered in 3rd
month of life.Goniotomy controls IOP in 70 – 80 % of
cases

38. PRIMARY ANGLE CLOSURE GLAUCOMA :
 Definition :It’s a condition in which IOP increase
because the outflow of aqueous humor from the
anterior chamber is mechanically impaired by
contact of the iris with the trabecular drainage
meshwork and peripheral cornea ----- decrease angle
of A.C .
 Females are more affected [F:M---3:1], Age incidence
40 – 45 Y.
 Usually bilateral {2nd eye involved after 1 year}.
Predisposing factors:
 Nervous anxious persons . Small eyeball { in
hyperopies }.
 Family history . Females more affected .
 Age: with increase age lens become large ---- A.C get
shallower and it s angle narrower .
 Thick iris --- may narrow A.C angle .

39. PRECIPITATING FACTOR ;
 Iris remains in contact with trabecular meshwork ---
adhesions result --- defect in aqueous outflow .
 Anterior displacement of peripheral part of iris ---- block the
exit of aqueous flow through trabecular meshwork .
 Anterior displacement of lens ---- iris adheres to lens ----
physiological pupillary block---- accumulation of aqueous in
posterior chamber ---- iris bombe { forward bulging of non –
adherent part of iris }-----impaired aqueous drainage.
 Relative pupillary block --- by increase size of lens with
increase age .
 Plateau iris – a rare condition where the iris is flat rather
than normally convex ---iris close to trabecular meshwork
 Congestion of ciliary body { in menses emotional
disturbance , endocrinal causes }------ it leads to increase
aqueous secretion and narrowing of A.C angle .

42. PATHOLOGY :
 Increase IOP --- vascular strangulation ----edema
and congestion of iris and ciliary processes -------
atrophy {late }.
 Increase IOP--- corneal edema --- loose epithelium
----epithelial bullae {bullous keratopathy}.
 Increase IOP---degeneration of nerve fibers and
loss of substance of optic disc – visual field defects.

43. GRADING OF A.C ANGLE BY GONIOSCOPY
(SCHAFFERS CLASSIFICATIO )

44. SCHAFFERS CLASSIFICATION
 Grade IV --- wide open (35-450),can not be
occluded .
 Structure visible are Schwalbe s line , trabecular
meshwork , scleral spur , ciliary body band,
Schlemm canal.
 Grade III --- open angle (20-350), can not be
occluded . Structure visible are
Schwalbe s line , trabecular meshwork , scleral
spur .
 Grade II ---- moderately narrow angle (10-200),
Potentially can be occluded .Structure visible are
Schwalbe s line , trabecular meshwork.
 Grade I ---- extremely narrow angle(<100)
.Complete occlusion only Schwalbes line visible.
 Grade zero—nothing visible

45. VAN HERICK SLIT LAMP GRADING OF THE
ANGLE
 Grade 4- PAC>Full corneal thickness
 Grade 3-PAC=1/2-1/4 corneal thickness
 Grade 2-PAC=1/4 corneal thickness
 Grade 1-PAC=<1/4 corneal thickness

47. CLINICAL PICTURE :
 1.Prodromal stage :Intermittent attacks of raised
IOP without congestion -----eye remains white brow
ache , headache , blurring of vision { occasionally
}.There may be transient sudden rise in IOP upto 40
or 60 mmhg.
 2.Constant instability stage :The intermittency of
prodromal attacks is replaced by regularity.Haloes
around light because of corneal edema .headache
.slight ciliary congestion .
 3.Acute congestive stage :Acute onset of pain
radiating along 5th cranial nerve , severe temporal
headache , haloes around light , redness , marked
diminution of vision , nausea , vomiting , malaise to
be different from acute

48. SIGNS
 Vision – C.F or H.M or even P.L.
 Eyelids edematous with narrow palpebral aperture
 Conjunctiva shows -----edema , redness and marked ciliary
congestion .
 Cornea --- edema , opacity , insensitive .
 A.C ---- very shallow , cells & increase protein but no Kps
 Gonioscopy shows marked narrowing of the angle with or
without anterior synechiae.
 Pupil ---- mid-dilated non reactive , oval .
 Iris --- edema , dilated b.v , atrophy , congested and iris
bombe .
 Lens --- white fine superficial opacities {glaukom flecken }.
 Fundus --- can not be examined due to corneal edema .It
shows hyperaemic disc with small haemorrhages and central
retinal artey pulsation.No cupping
 IOP--- continues to increase – hard stony eye .
 The fellow eye usually has a shallow anterior chamber and a
narrow angle.

49. ACUTE CONGESTIVE STAGE

56.  4.Chronic stage (creeping angle closure)
the patient never have a severe acute congestive
attacks but intermittent periods of increase
IOP.Symptoms may be absent There’s less
increase in IOP {less than previous stage}.Iris
gradually occludes the trabecular meshwork with
time and peripheral anterior synechiae develops
.Shallow A.C .Visual field loss .Cupping of the optic
disc and visual field defects may develop.
 5. Stage of absolute glaucoma:painfull blind eye
with no PL.The limbus is surrounded by dilated
anterior cilliary veins.Cornea is cloudy and
insensitive with bullous or filamentary
keratopathy.Anterior chamber is shallow,iris having
atrophic patches,dilated fixed pupil,disc having
deep cupping and optic atrophy.The eye is stony
hard.

57. Complication :
 Peripheral anterior synechiae --- damage to
drainage system .
 Cataract . Atrophy of retina and
optic nerve .
 Staphyloma Atrophic bulbi(ciliary body
atrophy)
Diagnosis :-History – tonometry- gonioscopy - slit
lamp- provocative test .
D/D:
 Acute iritis : normal IOP , constricted pupil , slight
reduced vision , Keratic precipitate .
 Acute conjunctivitis : conjunctival { not ciliary
}injection , normal pupil , normal vision , clear
normal cornea , normal IOP.

59. TREATMENT :
 Angle closure glaucoma is to be treated by surgery
.Before surgery do your best to reduce IOP by
medical means :
Medical therapy :
 Prodromal stage treated by Pilocarpine drops .

60. ACUTE STAGE {EMERGENCY CASE }:
 I.V mannitol 20% {hypertonic agent }.
 Oral glycerol {glycerine }1 ml / kg .Both act as hypertonic
or osmotic agents --- making blood hypertonic ---drawing fluid
form the eye --- decrease IOP.
 Isosorbide orally for diabetic patient & urea 1-2gm/kg
 Pilocarpine drops 4% every 5 min (drop every minute).
 Pilocarpine constricts the pupil ---- pulls the iris away from
{posteriorly}trabecular meshwork ---- reestablished aqueous
outflow .
 Acetazolamide 250 – 500 mg IV or orally
[Diamox].Acetazolamide {carbonic anhydrase inhibitor }---
decrease production of aqueous .
 Beta blockers { timolol } locally 0.25 -0.5 % ---- decrease
aqueous production .
 Steroid-antibiotic e.d. for congestion
 Analgesics and sedatives
 When IOP is controlled ----give Pilocarpine 1% only .

61. SURGERY TREATMENT :
 The kind of surgery depended upon :Degree of
damage to trabecular meshwork .Way of
regulation of IOP.
 Peripheral iridectomy :Its indicated when IOP
controlled by Pilocarpine and when peripheral
anterior synechiae dose not exceed 1/3 of iris .Its
performed by surgery or ARGON/Nd-YAG LASER .
 Trabeculectomy :Its indicated if there’s complete
closure of angle of A.C so that IOP is not controlled
by Pilocarpine and when peripheral anterior
synechiae exceeds 1/3 of iris .
 Prophylactic treatment in other eye { If not
affected }:
 Topical Pilocarpine 1% & Peripheral iridectomy .

63. TREATMENT OF ABSOLUTE GLAUCOMA :
 Enucleation { excision } of the eye { after a
written consent from the patient } if the eye is
blind and painful .
 Retrobulbar alcohol injection to destroy ciliary
ganglion , it gives relief up to 6 months only .
 Cyclocryotherapy

64. PRIMARY OPEN ANGLE GLAUCOMA
(CHRONIC SIMPLE GLAUCOMA)
Definition
 Primary open angle glaucoma (POAG) is a chronic
progressive condition with characteristic changes at the
optic disc (glaucomatous excavation), visual field
changes related to the disc changes. In most patients,
the IOP is above the normal range (i.e. over 21 mmHg)
at some time of the day, usually being highest in the
morning. In addition, there is a gonioscopically open
angle and, in those eyes with elevated IOP, a reduced
facility of outflow.
Prevalence and natural history
 Common in 5th-6th decade ,equal in both
sexes,multifactorial inheritence with 5-20%family
history. Disease is to progress, leading to irreversible
blindness.

65. RISK FACTORS FOR THE DEVELOPMENT OF POAG
 Height of the IOP - the greater the IOP the greater the risk
 Large vertical cup/disc ratio (indicating reduced neuroretinal rim
area/volume)
 Cup/disc (C/D) ratio asymmetry >0.2
 Previous history of disc haemorrhage
 Retinal nerve fibre layer defect in the absence of morphometric
optic nerve headchanges
 Thinner than average central corneal thickness (note excimer
laser procedures on thecornea can result in artifactually lowered
IOPs on measurement)
 Systemic risk factors like diabetes,thyroid
disorders,cardiovascular abnormalities,ptc
nontasters,corticosteroid responsivness
 Increasing age
 Family history
 Individuals of black African or Caribbean origin
 Positive family history in a first degree relative
 High myopia,retinal vein occlusion,fuchs endothelial
dystrophy,retinal detachment,retinitis pigmentosa etc.

66. Pathogenesis
 Increase resistance of the drainage channels in justracanalicular
trabecular meshwork or endothelial linning of schlemm canal.
Risk factors for blindness in POAG
 Advanced disease at presentation
 Sub-optimal intraocular pressure control
 Individuals of black African or Caribbean origin
 Low socio-economic group (because of late presentation)
Symtoms
 Painless progressive loss of vision with mild headache or eyeache
 Increasing difficulty for near vision with frequent change of presbyopic
glasses due to pressure on ciliary muscle.
 History of visual field problem
Signs
 visual acuity may remain good till late.
 Clear cornea with normal anterior chamber depth.
 Pupllary reaction normal till late
 Increased iop with diurnal variation
 Cupping of the optic disc

67. DIAGNOSIS
 Raised intraocular tention-- more than 21 mm hg
with diurnal variation less in the evening.
 Cupping of the optic disc--(c:d ratio >0.3) which
starts in the inferotemporal quadrant,bayonetting
sign which is the double angulation of the blood
vessels,thinning of the neuroretinal rim,nasalization
of vessels,splinter haemorrhage at disc,baring of
circumlinear vessels,and in late stage total cupping
with laminar dot sign.

72. GLAUCOMATOUS VISUAL FIELD DEFECTS
 Small peripheral Isopter contraction
 Baring of blind spot
 Angio scotoma above and below the blind spot due to
shadow of large retinal vessels
 Isolated paracentral scotoma in arcuate or bjerrum area
 Seidels scotoma which is sickle shaped involving blind
spot
 Arcuate and double arcuate(ring)scotoma
 Roenne nasal step in which the arcuate defects may
not proceed at same rate in upper and lower portion.
 Generalised constriction of the peripheral field leading
to tubular vision
 Lastly only a paracentral island of vision persists
 Ultimately no perception of light

76. d/d of ring scotoma
 high myopia
 aphakic spectacles
 retinitis pigmentosa
 panretinal photocoagulation
d/d of tubular vision
 retinitis pigmentosa
 high myopia
 central retinal artery occlusion with sparing of
cilioretinal artery

77. INVESTIGATIONS IN POAG
 Diurnal iop variation
 Gonioscopy for angle
 Tonography for aqueous out flow
 Water drinking provocative test-1 lit. Water is
drinked and iop taken every 15 min for 1 hr.If rise in
iop >8 mmhg then significant
 Slit lamp examination
 Perimetry and scotometry

78. GLAUCOMA WITHOUT FIELD LOSS DETECTED ON
STANDARD AUTOMATED “WHITE ON WHITE”
PERIMETRY (SAP)
 The discovery that a significant number of the optic
nerve fibres can be damaged before any change is
detectable in visual function by SAP has lead to the
concept of "glaucoma without field loss" or “pre-
perimetric glaucoma”. However other
psychophysical tests such as frequency doubled
perimetry (FDP) and blue on yellow perimetry
(SWAP) have consistently shown that defects in
visual function are present before any defect can be
detected by SAP.

79. CONCEPTS IN GLAUCOMA MANAGEMENT
 The overall aim of glaucoma management is to prevent
significant visual impairment within the patient’s lifetime.
This will be achieved by a process of monitoring visual
function with medical and/or surgical intervention when
appropriate. Treatment may, therefore, not always be
necessary to achieve this objective. Management of POAG
for an individual patient is helped by defining a "target IOP"
for a particular eye
 The "target" IOP should be considered as the "optimum"
IOP for the eye .
 measurement error which may be equipment and/or
patient/operator related
 diurnal variation
 compliance with medication
 timing of medication in relation to clinic times

80. MONITORING THE PATIENT WITH POAG
 examination of the anterior segment with a slit-
lamp, at least one IOP measurement, and
gonioscopy. A careful stereoscopic disc assessment
through the dilated pupil and drawing (which may
be usefully supplemented by disc photography +/or
digital computerised scanning of the disc/nerve
fibre layer assessment) and visual field analysis
completes the pre-treatment picture. Some patients
will benefit from a number of pre-treatment IOP
measurements and 2-3

81. Optic disc assessment
 It may be possible to identify progression by anatomical
change in the optic nerve head by comparing current and
previous appearances.Disc haemorrhages are a good
indicator that disease progression is occurring.
Visual field analysis.--The interpretation of sequential visual
fields depends upon a number of factors:-
 the disease process itself may induce fluctuation
 the varying ability of the patient to perform the test with time
 the nature of the test (and the skill of the technician)
 the development of any coexisting disease (e.g. cataract, age
related macular degeneration anddiabetic retinopathy).
 The identification of deterioration in a visual field generally
requires several visual fields. Automated perimeters allow for
repeated fields to be subjected to computer-assisted analysis
to detect significant changes

82. MANAGEMENT OF THE PATIENT WHO
DEMONSTRATES PROGRESSION
 In most circumstances, this will involve a change in
management, particularly if it is considered that an
alternative strategy will result in a lower IOP.
 Individual circumstances will dictate the action to be
taken.
 Some eyes will continue to lose visual function
despite lowering the IOP below the population
mean by surgery.

83. NORMAL TENSION GLAUCOMA
 Apart from the finding of an IOP that does not exceed 21
mmHg, this form of open angle glaucoma may be
indistinguishable from its higher pressure variant.
 It has been shown that central corneal thickness (CCT)
may be thinner in some NTG patients compared with
normal controls. This suggests that true IOP may be
greater than measured IOP in some individuals with
NTG.
 As with POAG, it is important to be sure that the visual
function and the optic disc appearance equates with a
diagnosis of glaucoma, as the differential diagnosis may
include space occupying intracranial lesions. Where
doubt exists, the appropriate investigations should be
performed.

84. THE TREATMENT OF PRIMARY OPEN
ANGLE GLAUCOMA
 Pilocarpine e.d.(2-4%) qid iop is lowered by increased
aqueous outflow due to ciliary muscle contraction.
 Systemic side effects include
bradycardia,salivation,diarroea,abdominal
cramps,increased prespiration and glandular
ecretion,bronchospasm.
 Ocular side effects include ciliary muscle spasm leading
to browache and induced myopia,decreased visual
acuity due to miosis,altered visual fields,retinal
detachment due to vitreoretinal traction,lens opacities by
cholinestrase inhibitors,iris cyst,permanant
miosis,decreased night vision.
 The miotic effect of pilocarpine is useful in PACG while
strong miotics may cause incearsed pupillary block.

85.  Beta blockers e.d.
 Timolol maleate(0.25-0.55) e. d.. bd - it lowers iop
by decreasing aqueous production. Systemic side
effects include
bradiacardia,hypotention,arrhythmias(beta
1block)and bronchospasm(beta 2 block),mental
depression,sexual impotence,heart block fatigue
confision,disorientation.ocular side effects are
superficial punctuate keratitis,reduced corneal
sensation,reduced tear secretion.
 Betaxolol(0.5%)e.d.-it is beta 1 blocker with little
effect on cardiopulmonary system
 Levobunolol (0.5%) e.d. –as effective as timolol but
less side effects

86.  Epinephrine (0.5-2%)e.d. bd-it reduces aqueous
production due to alpha adrenergic vasoconstriction
and increased out flow by beta adrenergic
effect.dipvefrine 0.1% is a pro drug with 17 times
more corneal penetration and less side effects.the
side effects rae increased
b.p.,tachycardia,arrhythmias,tremor,ocular
irritation,increased acg,hyperaemia,conjuctival
pigmentation,black cornea ,mydriasis,cystoids
macular edema,NLD obstruction,punctal
stenosis,blepharoconjuntivitis.
 Topical carbonic anhydrase inhibitor-like
dorzolamide,brinzolamide

87.  Latanoprost(0.005%) which is a prostaglandin
analogue which increases uveoscleral out flow by
over 100%.
Systemic treatment
 Tab acetazolamide 250 mg qid which is the
carbonic anhydrase inhibitor and lowers aqueous
production by 50 – 60% at the level of secretory
epithelium of the ciliary body.Its systemic side
effects include malaise,fatigue,anorexia ,weight
loss,depression,loss of libido,git irritation
,cramps,diarrhoea,paraesthesia,renal
stones,stevens-johnson syndrome and blood
dyscrasias while ocular side effects are dry
eye,transient acute myopia etc.

89. LASER SURGERIES
Argon laser trabeculoplasty-
 the laser burns are given in the trabecular meshwork to
open inter trabecular spaces but there is a progressive
diminution of the effect of ALT with time in some
patients and control can be lost quickly.
 Patients who have had this treatment should therefore
be monitored more frequently than would otherwise be
indicated.
 If subsequent drainage surgery is required, a history of
ALT may increase the chance of surgical failure

91. Yag laser iridotomy.
 Laser iridotomy may have a role in the absence of
symptoms of intermittent angle closure but is only
likely to lower the IOP in an eye with an open but
narrow drainage angle where there is some iris-
trabecular contact.
Cyclodiode laser.
 In certain patients, usually those in whom other
modalities of therapy have failed, partial
cycloablative therapy with trans-scleral (or
endoscopic) diode laser may be indicated.

92. SURGERY
 Full thickness surgeries like scheies thermosclero
surgery,elliots sclerocorneal trephine,iridenclesis
etc
 Partial thickness surgeries like trabeculectomy
 Newer surgeries like trabeculectomy with anti
metabolites(mitomicin-c),trabeculectomy with
molteno or krupin-denver or ahmed valve.

95. TRABECULECTOMY
 Those eyes at risk of later failure due to scarring of
the drainage bleb should be considered for
antimetabolite supplementation.
 Risk actors for late failure include previous ocular
surgery, a long pre-operative history using certain
topical medications, black African or Caribbean
origin, pre-existing uveitis and diabetes mellitus
(particularly with retinopathy).

103. TRABECULECTOMY

112. Glaucoma in the presence of cataract.
 For the patient with glaucoma controlled on a simple topical
edication regimen who requires cataract surgery, cataract
extraction with implant can be performed with continuation of
topical medications as appropriate postoperatively. In some
patients, cataract surgery may be associated with a fall in
IOP.For the patient who requires drainage surgery but who
also has cataract, a combined cataract extraction, implant and
trabeculectomy procedure should be considered.
Phaco-trabeculectomy (in which phacoemulsification and lens
implantation is combined with drainage surgery) has the
convenience to the patient.
Risks of filtering surgery.
 the long-term risk of blebitis and endophthalmitis, which is
greater when antimetabolites are used.
 Non-penetrating surgery such as viscocanalostomy and deep
sclerectomy

113. OCULAR HYPERTENSION
 Ocular hypertension (OHT) is a term reserved for eyes in
which the intraocular pressure (IOP) lies above the
normal population range, the optic nerve and visual field
show no signs of glaucomatous damage, and there is no
ocular co-morbidity.
 Excluded from this definition are eyes with raised IOP
from demonstrable causes such as pseudoexfoliation
and pigment dispersion syndrome.
 Most population studies on the over 40-year age group
indicate that IOPs measured with Goldmann tonometry
are distributed in a manner similar to a normal
distribution (mean approximately 16 mmHg).

114. RISK FACTORS FOR THE DEVELOPMENT OF OH
 Increasing age
 Individuals of black African or Caribbean origin.
 Female gender
 Systemic hypertension
 Current use of oral and/or inhaled corticosteroids
 Diabetes (especially those on insulin)
 Family history of glaucoma

115. MANAGEMENT
 Since elevated IOP is the major risk factor for the
development of glaucomatous visual loss,finding a
"raised" IOP indicates the need for further
investigation and management decisions.
 "Persistent" OHT where raised IOP is a constant
feature.
 Assuming an otherwise normal ocular examination,
discharged and advised to seek periodic (e.g. one
to two yearly) optometric re-examination.

116. PROPHYLACTIC THERAPY
 A decision to treat an eye with ocular hypertension
should be made when the risk factor(s)present in
the patientIndications include the presence of signs
suggestive of early glaucoma or central retinal vein
occlusion in the fellow eye.
If no treatment is decided upon, two options are
available to the ophthalmologist.
 Discharge to the GP with appropriate advice for
follow-up in the community.
 Periodic review in the Hospital Eye service or
managed shared care scheme.

117.  When treating OHT, the aim is to lower the IOP to a level
considered safe for the individual patient, and this should be at
least a 20% reduction.
Treating on IOP without additional risk factors.
 A constant IOP over 35 mmHg merits treatment as at these
levels mechanical damage occurs to the optic nerve head.
 lower level of IOP should be based on perceived risk by the
ophthalmologist and the patient
Treating on raised IOP plus other risk factors.
 The decision to treat should take into account the patient’s life
expectancy and the probability of
 functional visual loss occurring within the patient’s lifetime.
 Eyes that already possess evidence of early glaucomatous
damage such as acquired neuroretinal rim changes consistent
with glaucoma, nerve fibre layer defects or abnormalities on
morphometric, psychophysical or electrodiagnostic tests
probably have POAG and should be treated .

118. SECONDARY GLAUCOMA S

120. III- SECONDARY GLAUCOMA :
Open angle glaucoma :
 Uveal tract related :
 Ocular tumors inflammation .
 Phacoanophylactic uveitis A.C epithelization .
 Exfoliation syndrome { translucent deposits more on lens and
pupillary margin }.
 Trauma :
 Hyphema & siderosis from iron foreign body .
 Angel recession {fellows confusion injury }.
 Corneal laceration with iris prolapse in the wound --- P.A
 Miscellaneous :
 Corticosteroid induced glaucoma .
 Increase episcleral venous pressure .
 Alpha chemotropism glaucoma .
 Thyrotrophic exophthalmos .
 Fuchs dystrophy .
 Lens abnormalities { posterior dislocations}.

121. Angle closure glaucoma :
 Intumescent cataracts . Ciliary body tumors .
 Dislocated lens . Flat A.C after trauma .
 Irido-corneo-endothelial syndrome . Retrolental
fibroplasia .
 Persistent hyperplastic primary vitreous . Rubeosis
iridis .
 Ciliary block { anterior displacement of iris-lens
diaphragm }.
Pupillary block :
 Inflammatory adhesion of iris to lens or vitreous in
aphakia .
 Vitreous block { in aphakia }.
 Intraocular lens block .
 Anterior dislocation of lens .

124. GLAUCOMA SECONDARY TO LENS CHANGES
{LENS INDUCE GLAUCOMA }
1.Lens dislocation {posterior type}:
 Mechanism is unknown .
 May be angle recession or trabecular damage by
trauma .
 Anterior type ---lens press iris against posterior chamber
--- break aqueous outflow .
2.Phacogenic {phacomorphic }glaucoma :
 Is the result of 2 causes :
 Spherophakia --- small round lens , it causes pupillary
block ---2ry glaucoma.
 Intumescent cataract ---swelling of lens .Acute rise of
IOP,sec.angle closure type,treated by cataract surgery
and IOL implantataion.

126. 3.Phacolytic glaucoma :
 Leakage of irritant lens material {proteins }through
the capsule leading to obstruction of trabecular
meshwork by proteins or macrophages { it occurs in
hyper-mature cataract }.OAG type,treated by
cataract surgery.


130. 4.Lens particle glaucoma:after extra capsular
cataract extraction or penetrating lens injury due to
obstruction of trabecular meshwork by lens
particles with associated inflammation.treated by
surgical removal of lens particles and irrigation.
5.Phacoanaphylactic glaucoma: always associated
with a latent period during which sensitisation to
lens proteins occurs resulting into typical
granulomatous uveitis.It is treated with topical
steroids and anti glaucoma medications.

131. EXFOLIATIVE SYNDROME { GLAUCOMA CAPSULARE
}:
 Deposits of unknown origin and composition on lens
surface , ciliary processes , zonule , posterior iris surface
, A.C trabecular meshwork .Glaucoma and cataract may
develops . OAG type
 Medical therapy or laser trabeculopalsty

135. PIGMENTARY GLAUCOMA
 sec OAG type occurs in young myopic male.
 Pigment dispersion through out anterior segment with
Krukenbergs spindle over corneal endothelium.
 Gonioscopy shows hyperpigmentataion in the angle with
Sampolesi line.

140. NEOVASCULAR GLAUCOMA
 it is associated with neovascularisation of the
iris(rubeosis iridis) and angle neovascularisation.It is
seen in diabetic retinopathy,CRVO(90 days
glaucoma),sickle cell retinopathy,retinopathy of
prematurity,carotico-cavernous fistula.It can has three
stages
 Preglaucomatous stage(rubeosis iridis)
 Open angle stage(angle NV)
 Angle closure stage(angle fibrovascular membrane
contraction)
 Treatment is difficult and requires pan retinal or gonio
photocoagulation with anti glaucoma surgery.

146. GLAUCOMATO-CYCLITIC CRISIS
(HYPERTENSIVE UVEITIS)—
 also k/a Posner and Schlossmann syndrome.
 It is unilateral disease of middle aged characterised
by recurrent attacks of mild acute iridocyclitis with
marked IOP and coloured halos.
 OAG type.

148. MALIGNANT { CILIARY BLOCK }GLAUCOMA:
 surgery on angle closure glaucoma ---- increase
collection of aqueous behind iris -------lens – iris
diaphragm pushed forward ---increase IOP .
TREATMANT :
 Mydriatic and cycloplegia
 hyperosmotic agent .
 Vitrectomy
 posterior scleroctomy .
 Lens extraction may be needed .

149. TRAUMATIC GLAUCOMA:
 blunt trauma can cause trabecular damage by tear
between horizontal and circular ciliary muscles and after
6 weeks formation of scar in this area giving rise to
block in aqueous outflow and wide looking angle on
gonioscopy k/s angle recession glaucoma.

152. APHAKIC & PSEUDOPHAKIC GLAUCOMA
 Tight suturing,peripheral anterior synechiae,
 pupllary block by vitreous,fibrinous iridocyclitis
 angle block by vitreous,hyphaema,iridocyclitis
 Epithelial or fibrous ingrowth,
 Pupillary block by anterior or posterior IOL
 Prolonged use of corticosteroids
 Treated by anti glaucoma medication.Laser
peripheral iridectomy and trabeculectomy.

154. HYPOTONY :
 IOP is low { < 10 mmHg }soft eye .
Causes :
 Excessive filtration in glaucoma surgery .
 Ciliochoroidal detachment .
 Perforating injury to eye ball or blunt trauma .
 Diabetic coma .
 Atrophy of ciliary body as in uveitis .
 External ophthalmoplagia .
 R.D .
 High myopia .
 General dehydration