glaucoma

1. GLAUCOMA
NUR AINA BINTI AB KADIR

2. CONTENTS
 Primary Angle Closed Glaucoma(PACG)
 Congenital/developmental glaucoma
 Secondary glaucoma

3. Apposition of peripheral iris against the
trabecular meshwork(TM) obstruction of
aqueous outflow by closure of an already
narrow angle of the anterior chamber
PRIMARY ANGLE-CLOSURE
DISEASE

4. Primary angle closure
glaucoma(PACG)
 Epidemiology
 Etiopathogenesis
 Classification
 Clinical profile
 Management

5. Primary angle closure
glaucoma(PACG)
 EPIDEMIOLOGY(International Society of
Geographical and Epidemiological
Ophthalmology (ISGEO)
 Every 10 occludable angles(PAC suspects) seen
there is only one case of PACG
 Chronic PACG(asymptomatic): acute
PACG(symptomatic) = 3:1
 Great ethnic variability in the prevalence of PACG
 Major cause of world glaucoma blindness is
PACG
Ethnic group POAG PACG
Europeans, Africans, Hispanics 5 1
Urban Chinese 1 2
Mongolian 1 3
Indian 1 1

6. Etiopathogenesis
Predisposing risk
factors
Pathogenesis of rise in
IOP

7. Predisposing risk factors
 Demographic risk factor
 Age: PACG + pupillary block6th & 7th decades
 Gender: male to female ratio (1:3)
 Race: South-East Asians, Chinese, Eskimos
(more common)

8. Predisposing risk factors
 Anatomical and ocular risk factors
 Hypermetropic eyes
 Eyes in which iris-lens diaphragm is placed
anteriorly
 Eyes with narrow angle of anterior chamber
 Plateau iris configuration
 Heredity

9. Pathogenesis of rise in IOP
Pupillary block mechanism
Plateau iris configuration& syndrome
Phacomorphic mechanism

10. Pupillary block mechanism
 PRECIPATING FACTORS
 Physiological mydriasis
 Pharmacological mydriasis:
bronchodilators,antidepressant
 Pharmacological miosis: echothiophate,
pilocarpine
 Valsalva manoevure

11. Mechanism of rise in IOP after
mydriasis
 Due to effect of precipitating factorsmid
dilatation of the pupil
 Relative pupil block
 Iris bombe formation
 Appositional angle closure
 High IOP(transient)synechial angle closure

12. Plateau iris configuration and
syndrome
 Anterior chamber angle is closed by pushing
mechanism because of the anterior positioned
ciliary processes displacing the peripheral iris
anteriorly
 Iridotomy
 Syndrome: acute ACG occurs either
spontaneously/ after pharmacological
dilatation, in spite of patent iridotomy
 Treat: miotics, laser peripheral iridoplasty

13. Phacomorphic mechanism
 Acute secondary angle closure glaucoma
caused by the intumescent/other lens
morphological abnormalities
 Ultrasonic biomicroscopy (UBM) and
Anterior,Segment OCT (AS-OCT) acute
primary ACG in predisposed patient
 Base of lens extraction for acute PACG

14. Classification
 ISGEO,based on natural historyPrimary angle closure suspect
(PACS)
Primary angle closure(PAC)
Primary angle closure
glaucoma (PACG)

15. Classification –traditional
clinical
Latent PACG
Subacute(intermittent) PACG
Acute PACG
Chronic PACG

16. Primary Angle-Closure Suspect
(PACS)
 No symptoms
 PRESENTING SITUATIONS
 Suspicious clinical sign, glaucoma screening
programme
 Eclipse sign
 Slit-lamp biomicroscopic signs
 Decreased axial anterior chmaber length
 Convex shaped iris lens diaphragm
 Close proximity of the iris to cornea in the periphery
 Van Herick slit-lamp grading of the angle

17. Primary Angle-Closure Suspect
(PACS)
 Van Herick slit-lamp grading of the angle:
 Grade 4 pacd = ¾ to 1 CT (wide open angle)
 Grade 3 pacd = ¼ to ½ CT (mild narrow)
 Grade 2 pacd = ¼ CT (moderate narrow)
 Grade 1 pacd < ¼ CT (extremely narrow)
 Grade 0 pacd = NIL (closed)

18. Primary Angle-Closure Suspect
(PACS)
 DIAGNOSTIC TEST
 IOP measurements
 Gonioscopy
 Ultrasonic
biomicroscopy
 Anterior segment
OCT
 Optic disc evaluation
 Visual filed analysis
 DIAGNOSTIC
CRITERIA
 Gonioscopy: irido-
trabecular contact
>270’, no peripheral
anterior synechia
 IOP: normal
 Optic disc: no
glaucomatous
change
 Visual fields: normal

19. Management
 Prone dark room (provocative test)
 Dark room, prone position without sleeping 1hour
 IOP >8mmHg ( diagnostic)
 Mydriatic test (O.5% tropicamide)
 produce mid-dilated pupil
 pressure rise > 8mmHg (positive)
 Inferences
 Positive: angle is capable of spontaneous closure
 Negative: presence of occludable angles on
gonioscopy does not rule out the possibility

20. Treatment
 Prophylactic laser iridotomy : >270’ of
oppositional iridotrabecular
contact(gonioscopy) in the fellow eye of all
patients (acute PAC or PACG in one eye)
 Periodic follow up
 Education

21. Primary Angle Closure (PAC)

22. Criteria
 Irido-trabecular contact: >270’
 IOP elevated and/or peripheral anterior
synechiae(PAS) present
 Optic disc: normal
 Visual field: normal

23. Subacute PAC
 Transient rise of IOP (40-50mmhg) may last
minutes- 1-2 hours
 Precipitating factor
 Physiological mydriasis (dark room or
sympathetic response)
 Physiological shallowing of anterior chamber
(lying in prone position)
 Pharmacological mydriasis- fundus examination

24. Symptoms
 Unilateral transient blurring of vision
 Colored halos around light
 accumulation of fluid in corneal epithelium and
corneal lamellae
 Mild headache & brow ache
 due to raised IOP
 In between recurrent attacks
 FREE from symptoms

25.  Signs: eye is white, not congested
 DD: acute purulent conjunctivitis, early
cataractous changes
 Treatment: peripheral laser iridotomy

26. Acute PAC
 Attack of acute rise in IOP in patients with PAC
may occur due to pupillary block sudden
closure of angle
 SYMPTOMS:
 Pain
 Nausea,vomiting, prostrations associated with
pain
 Rapidly progressive impairment of vision,
redness, photophobia, lacrimation
 Past history

27. Signs
 Lids: oedematous
 Conjunctiva: chemosed,congested
 Cornea: oedematous, insensitive
 Anterior chamber: shallow
 Angle: completely closed
 Iris: discolored
 Pupil: semidilated,vertically oval & fixed
 IOP: markedly elevated
 Optic disc: oedematous, hyperamic
 Fellow eye: shallow anterior chamber,
occludable angle

28. Differential Diagnosis
 Other causes of acute red eye
 Acute conjunctivitis
 Acute iridocyclitis
 Acute secondary glaucomas
 Phacomorphic glaucoma
 Acute neovascular glaucoma
 Glaucomatocyclitic crisis

29. Management
IMMEDIATE MEDICAL THERAPY TO LOWER IOP
 Systemic hyperosmotic agent (IOP 40mmHg)
 Intravenous mannitol (1gm/kg)
 Oral hyperosmotics (glycerol)
 Systemic carbonic anyhydrase inhibitor
 Acetazolamide 500 mg IV
 Topical antiglaucoma drugs
 Beta blocker(timolol), PG analogues
 Analgesics and antiemetic
 Topical steroid

30. Definitive therapy
 Laser peripheral iriditomy (LPI)
 Filtration surgery
 Clear lens extraction
 PROPHYLACTIC: prophylactic laser iridotomy
should be performed on the fellow
asymptomatic PACS

31. Sequale of acute PAC
 Postsurgical acute PAC
 Successful: normalized IOP
 Failed: high IOP trabeculectomy
 Spontaneous angle reopening: rare
 Ciliary body shutdown: AH production,
ischaemic, similar CF, treatment
 Vogt’s triad
 Glaukomflecken (anterior subcapsular lenticular
opacities)
 Patches of iris atrophy
 Slightly dilated nonreacting pupil

32. Primary Angle-Closure Glaucoma
(PACG)
 Gradual synechiael closure of the angle of
anterior chamber
 Untreated patient of PAC

33. Clinical features
 Subacute and acute PACG
 Similar
 Glaucomatous optic disc changes
 Visual field defect
 Chronic PACG
 IOP remains constantly raised
 Eyeball remains white and no congestion
 Optic disc show galucomatous cupping
 Visual field defect
 Gonioscopy >270 angle closure + PAS

34.  Diagnosis
 Irido-trabecular
contact >270 on
gonioscopy
 PAS are formed
 IOP elevated
 Optic disc show
glaucomatous sign
 Visual field defect
 Treatment
 Laser iriditomy
 Trabeculectomy
 Prophylactic laser
iriditomy

35. Absolute Primary Angle-closure
Glaucoma
 CLINICAL FEATURES
 Painful blind eye with no perception of light
 Perilimbal reddish blue zone
 Caput medusae
 Cornea (bullous keratopathy/filamentary
keratitis)
 Anterior chamber is very shallow
 Iris atrophic
 Pupil fixed, dilated, greenish hue
 Optic disc (optic atrophy)
 High IOP
 Stony hard eyeball

36. Management
Retrobulbar alcohol injection
• Relieve pain
• 1 ml of 2% xylocaine
• After 5-10 min:1ml of 80% alcohol-destroy ciliary ganglion
Destruction of secretory ciliary epithelium
• Lower IOP
• Cyclocryotherapy / cyclophotocoagulation/cyclodiathermy
Enucleation of eyeball
• Painful blind eye+malignant growth

37. Complications
Corneal
ulceration
• Prolonged epithelial edema & insensitivity
• Perforate
Staphyloma
formation
• High IOPvery thin sclerabulges out
Atrophic
bulbi
• Ciliary body degenerates, IOP falls
• Eyeball shrinks

38. CONGENITAL/DEVELOPMENTAL
GLAUCOMAS
 Types
 Pathogenesis
 Clinical features
 Examination(evaluation)
 Differential diagnosis
 Treatment

39. TYPES
Primary developmental/ congenital
glaucoma
DG with associated congenital ocular
anomalies
DG with associated systemic
anomalies

40. Primary developmental/ congenital
glaucoma
 Abnormal high IOP d/t developmental anomaly
of the angle of the anterior chamber
 NOT associated with ocular/systemic anomalyNewborn
40%
• True CG,IOP raised during intrauterine life
• Born with ocular enlargement
Infantile
55%
• Manifest prior to the child’s 3rd birthday
Juvenile
5%
• After 3 year but before adulthood
• Aka juvenile POAG(10-35y/o)
• 35%: myopes

41. Prevalence & genetic pattern
 Sporadic occurrence (90%)
 Autosomal recessive inheritance with
incomplete penetrance (10%)
 Loci linked with PCG : 2p21(GLC3A),
1p36(GLC3B), and 14q24(GLC3C)
 Sex linkage ,>65% are boys
 Bilateral occurrence (70%) , asymmetric
 1:10 000 births

42. Pathogenesis
 Maldevelopment, from neural crest derived cells,
of trabeculum including the iridotrabecular junction
(trabeculodysgenesis)
 Absence of angle recess with iris insertion
 Flat iris insertion (commoner) : iris insert flatly &
abruptly into the thickened trabeculum either at or
anterior to scleral spur (more often) or posterior,
often possible to visualize a portion of ciliary &
scleral spur.
 Concave iris insertion: superficial iris tissue
sweeps over the iridotrabecular junction & the
trabeculum obsecure the scleral spur, ciliary
body

43. Clinical features
 Lacrimation, photophobia, blepharospasm
 Corneal signs
 Corneal oedema
 Corneal enlargements
 Tears and breaks in Descemet’s
membrane(Haab’s striae)
 Sclera: thin, appears blue
 Anterior chamber: deep
 Iris: iridodonesis, atrophic patches in late
stages

44. Clinical features
 Lens: flat, stretching of zonules, subluxate
backward
 IOP: increased
 Axial myopia

45. Examination(evaluation)
 Measurement of IOP with Schiotz/preferably
hand held Perkin’s applanation tonometer
 Measurement of corneal diameter by callipers
 Slit-lamp examination: portable slit-lamp
 Ophthalmoscopy: optic disc
 Gonioscopic examination of angle of anterior
chamber

46. Differential diagnosis
 Cloudy cornea
 Large cornea
 Lacrimation: congenital nasolacrimal duct
blockage
 Photophobia
 Raised IOP in infants
 Optic disc changes

47. Treatment
 MEDICAL TREATMENT
 Hyperosmotic agents, acetazolamide, beta-
blocker
 Miotics- not used
 Alpha-2 agonist(brimonidine): CNS depression
CI

48. Treatment
 SURGICAL TREATMENT
 INCISIONAL ANGLE SURGERY
 Goniotomy
 Trabeculotomy
 FILTERATION SURGERY
 Trabeculectomy
 Combined trabeculectomy & trabeculectomy with
antimetabolites
 GLAUCOMA DRAINAGE DEVICES (GDD)

49. Goniotomy
 Barkan’s goniotomy knife
 Through the limbus of temporal side
 Anterior chamber to the nasal part
 Incision: midway between root of the iris and
Schwalbe’s ring(75’)

50. Trabeculotomy
 Corneal clouding prevents visualisation of the
angle/failed goniotomy
 Canal of Schlemm is exposed at about 12
o’clock position by a vertical scleral incision 
conjunctival flap & partial thickness scleral flap
 Lower prong of Harm’s trabeculotome is
passed along the Schlemm’s canal on one
side and the upper prong is used as guide
 Rotate break the inner wall over one quarter
of the canal

51. DG with associated congenital
ocular anomalies

52. Glaucoma associated with
iridodysgenosis
 Glaucoma associated with:
 Aniridia-50%
 Familial iris hypoplasia
 Congenital ectropion uvea
 Congenital microcornea
 Congenital nanophthalmos

53. Glaucoma associated with
iridocorneal dysgenesis
 Posterior embryotoxon: prominent Schwalbe’s
ring
 Axenfeld-Rieger syndrome
 Axenfeld anomaly: post. Embryotoxon with
attachment of strands of peripheral iris tissue.
 Rieger anomaly:post. Embryotoxon, iris stomal
hypoplasia, ectropion uveal corectopia, full
thickness iris defect
 Rieger syndrome: Rieger anomaly+dental
anomalies (hypodentia/microdental), facial
anomalies(maxillary hypoplasia),other
anomalies(hypospadias)

54. Glaucoma associated with
iridocorneal dysgenesis
 Peter’s anomaly: central cornea opacity with/
without irido-corneal/lenticulocorneal
adhesions
 Combined Rieger’s syndrome & Peter’s
anomaly

55. DG with associated systemic
anomalies
 Glaucoma associated with:
 Chromosomal disorders: trisomy 13-15,18,21,
turner’s syndrome
 Ectopia lentis syndrome: Marfan’s syndrome,
Weil-Marchesani syndrome
 Phakomatosis: Sturge-Weber syndrome(50%),
Von-Recklinghausan’s neurofibromatosis(25%)
 Metabolic syndrome:
 Lowe’s syndrome(oculo-cerebrorenal sydndrome)
 Hurler’s syndrome(mucopolysaccharidosis)
 Zellweger syndrome(hepato-cerebral renal syndrome)

56.  Group of disorders
 High IOP + primary ocular/systemic
disease
SECONDARY GLAUCOMAS

57. Classifications
 Mechanism of rise
in IOP
 Secondary OAG
 Pretrabecular
membrane
 Trabecular clogging
 oedema&scarring
 Post-trabecular
elevated episcleral
venous pressure
 Secondary ACG
 +/- pupil block
 Causative primary
disease
 Lens induced
(phacogenic)
glaucomas
 Inflammatory
glaucoma
 Pigmentary
glaucoma
 Steroid induced
 Trumatic glaucoma

58. Lens-induced (phacogenic)
glaucomas
 IOP raised 2’ to some disorder of lens
 Classifications :
 Lens-induced 2’ angle closure glaucoma
 Phacomorphic glaucoma (swollen lens)
 Phacotopic glaucoma (ant. lens displacement)
 Lens-induced 2’ open angle glaucoma
 Phacolytic glaucoma
 Lens particle glaucoma
 Phacoanaphylactic glaucoma

59. Phacomorphic Glaucoma
 Causes :
 Intumescent lens – swollen cataractous lens (rapid
maturation of cataract or traumatic rupture of capsule
 Ant. subluxation/dislocation of the lens &
spherophakia congenital smaller, more spherical optic
lens cause for phacotopic glaucoma
 Pathogenesis :
 Swollen len pushes iris forward & obliterates the angle
 Further increase iridolenticular contact (pupillary block
& iris bombe)

60.  Clinical presentation
 As in acute
congestive glaucoma
with features of
primary angle
closure glaucoma
 Lens is always
cataractous &
swollen
 Treatment :
 Medical treatment –
IV mannitol, systemic
acetazolamide &
topical BB
 Surgical – laser
iridotomy (breaking
closure-angle attack)
 Cataract extraction
with implantation of
PCIOL

61. Phacolytic glaucoma (Lens protein
glaucoma)
 Pathogenesis
 Trabecular meshwork is clogged by lens protein,
macrophages which have phagocytosed lens
protein & inflammatory debris
 Leakage of lens proteins occurs through intact
capsule in hypermature cataractous lens
 CLINICAL FEATURES
 Features of acute congestive glaucoma
 Pseudohypopyon
 Open ant. Chamber (gonioscopy)
 MANAGEMENT: Extraction of hypermature
cataractous lens

62. Lens particle glaucoma
 Pathogenesis
 Trabecular meshwork
is blocked by lens
particles floating in
aqueous humour
 After
accidental/planned
ECCE (Extracapsular
Cataract Extraction)
or following traumatic
rupture of lens
 Clinical features:
 Symptoms of acute
rise in IOP assoc.
lens particles in
anterior chamber
 Treatment:
 Irrigation-aspiration of
lens particles from
ant. chamber

63. Phacoantigenic glaucoma
 Fulminating acute inflammatory reaction due to Ag-Ab
reaction
 Same mechanism & management with acute inflammatory
glaucoma
 Typical finding – granulomatous inflammation in involved eye
after it goes surgical trauma
 Pathogenesis :
 There is preceding distruption of lens capsule by ECCE,
penetrating injury or leaks of protein from capsule
 Trabecular meshwork is clogged by both inflammatory cells &
lens particles
 Management :
 Treatment of iridocylitis (streroid & cycloplegics)
 Irrigation-aspiration of lens matter from ant. Chamber

64. Glaucoma due to uveitis
 IOP raised because of iricocyclitis or even due
to keratitis and scleritis
 Types :
 Non specific inflammatory glaucoma
 Open angle inflammatory glaucoma (acute/chronic)
 Angle closure inflammatory glaucoma
 Specific hypertensive uveitis syndromes
 Fuchs’ uveitis syndrome
 Glaucomatocyclitic crisis

65. Acute OAIG
C/F :
• Features of acute iridocylitis + increased IOP + open angle of
ant. Chamber
• Returns to normal after acute episode of inflammation
Management :
• Treat iridocylitis
• Medical therapy to lower IOP (hyperosmotic agents,
acetazolamide, BB)
Mechanism
• Trabecular clogging, trabecular edema and prostaglandin-
induced rise in IOP

66. Chronic OIAG
Mechanism
• Chronic trabeculitis and trabecular scarring
C/F
• Raised IOP, open angle, no active inflammation
• Signs of prev episode of uveitis present
• Glaucomatous disc changes & field defects
Treatments
• Medical therapy – topical BB , CAI & alpha agonist (avoid
pilocarpine & PGs)
• Trabeculectomy
• Cyclodestructive procedure (cycloiodide)

67. Angle closure inflammatory
glaucoma
PAS are formed causing synechiae angle closure
Mechanism :
• 2’ angle closure with pupil block (due to annular synechiae or acclusio pupillae –
iris bombe)
• 2’ angle closure without pupil block (organization of inflammatory debris in the
angle causing pulling of iris over the trabeculum during contraction – gradual &
progressive synechiae angle closure + increased IOP)
C/F :
• Raised IOP, seclusion papillae, iris bombe, shallow ant. Chamber
Management
• Prophylaxis (treat acute iridocylitis – local steroids & atropine)
• Curative – medical therapy to reduced IOP, surgical or laser iridotomy in pupil block
without angle closure and filtration surgery in presence of angle closure

68. References
 Comprehensive Opthalmology, 6th Edition, AK
Khurana, New Age International publisher,
page 219-256
 Googles images
 Any questions?