AAC

Sx
- IOP (30-70)
- Acute eye pain
- Headache, n/v
- Acute VA drop, halos
- Ciliary injection

Ddx
- Phacomorphic/anterior lens dislocation(ectopia lentis)/phacolytic
- Uveitic glaucoma
- NVG
- Malignant glaucoma
- Posterior segment pathology
- Possner Schossman syndrome

Hx
- Gender, age
- Symptoms and duration of painful red eye
Predisposing factors
- Anti-cholinergic medication (flu med, antitussive)
- Dense cataract
- Previous attack (Uveitis, PSS, intermittent PACG)
- Recent ocular surgery
- Refractive error, hypermetropia
- Trauma
- Retinal vascular disease (CRVO, PDMR), new vessels formation
Medical hx
- Renal failure
- Asthma
- COPD
- Arrythmia, heart disease
- DM, HT
- Allergy, allergy to sulphonamides (indapamide, Topiramite)

O/E
- VA
- IOP
- Slit lamp
o Diffuse ciliary injection
o Cornea edema
o Shallow AC (unequal AC depth)
o AC activity, ACC, KP
o Iris bombe / PS / pupil block
o Fixed, mid dilated irregular pupil
o NVI
 o Hypermature/swollen cataract
o Lens instability
o Glaucomflecken
- Gonioscopy (if corneal edema/IOP controlled)
o Narrow angle
o PAS
o NV of angle
o <Post PI goni+/- indentation>
 Differentiate synechiae vs appositional closure
 Any degree of PAS
- Fundus
o Posterior pushing mechanism (e.g. Choroidal mass)
o Vertical cup to disc ratio
o Disc colour
o Retinal rim integrity
o Retinal pathology
Ix
- RFT
- B scan (if no fundal view)
- UBM (if angle status not verified by goni)
o Ciliary body / peripheral choroid abnormalities

Acute elevated IOP

- AC status
Shallow AC
1) Phacomorphic (hypermature cat)
2) PACG (peripheral iridocorneal touch + pupil block + central AC maintained)
3) Malignant glaucoma
- recent ocular surgery
- After excluding pupil block / supra choroidal haemorrhage
Deep AC
1) NVI
a. NVG
2) No NVI
a. Uveitic glaucoma (marked AC activity)
b. PS syndrome (mild AC activity)

IOP control
1) Systemic IOP lowering med
2) Topical anti glaucoma med
3) ALPI (APAC & acute phacomorphic angle closure)
Check IOP few hours later
IOP controlled
- Phacomorphic  early cat extraction
- APAC  BE laser PI  early cat
- NVG and PSS  OPD FU + treat underlying pathology
IOP not controlled
 - IV mannitol 20% 200ml over ½ hour
- ALPI x APAC / acute phacomorphic
- AC paracentesis / early drainage (TBx + MMC)

Medication

ALPI
Contraction Burns
- Long duration
- Low power
- Large spot size
Angle closure
4 anatomical position
- Lens Phacomorphic
- Posterior chamber (pupillary block)
- Ciliary body (plateau iris)  younger/can closure in spite of patient PI
o Med/PI/ALPI/treb/drainage
- Posterior to lens (malignant glaucoma)

PACG
RFs
- Asians
- Ocular biometrics
- Age (increase after 40, increase lens thickness)
- Women (2-3x)
- Family history (ABCC5 gene, reduced ACD)
- Hyperopia
o If ACG in high myopia  secondary mechanisms:
o Microspherophakia, plateau iris, phacomorphic (NS)

Plateau Iris syndrome

- Atypical configuration of AC angle
- Anteriorly positioned ciliary processes  push peripheral iris forward  narrow AC
angle
- Dilation of pupil  further compromise (as peripheral iris bunches up + obstruct)
- “Double hump” sign on goni / USG
- AC appear deeper/flat iris plane  but shallow angle recess
Mx
- LPI to remove any component of pupillary block
- Long term miotic
- ALPI
<Secondary angle closure with pupillary block>

Phacomorphic
- Lens intumescenece (swelling) pp pupillary block
- Cholinergic/miotic agent  minimal role as they may further narrow the angle
Ectopia lentis causes
- Pseudoexfoliation*
- Trauma
- Marfan
- Homocysteinuria
- Microspherophakia
- Ehlers Danlos
- Weill Marchesani syndrome
- Sulfite oxidase deficiency

<Secondary closure without pupillary block>

1) Contraction of inflammatory/haemorrhagic/vascular membrane/band/edudate in
the angle  PAS formation
2) Forward displacement of lens/iris interface, often with swelling and anterior rotation
of the ciliary body

NVG
- DR, CRVO, BRVO, OIS, chronic uveitis
- NVI  PAS  fibrovascular membrane  contraction
- PAS end as Schwalbe line
ICE syndrome
- Iris atrophy, secondary angle closure, corneal edema
- Chandler syndrome, essential iris atrophy, Cogen Reese (iris nevus)
- Unilateral, middle aged, women
- Corneal endothelium “beaten bronze” apperanace
- High PAS anterior to Schwalbe line
Tumours
- Posterior segment tumour
o Primary choroidal melanomas
o Ocular metastases
o RB
- Anterior uveal cysts

Inflammation
- Uveitis
Malignant glaucoma
- Post ocular surgery
- Hx of angle closure / PAS
- Uniform flat central and peripheral AC
- Anterior rotation of the ciliary body and posterior misdirection of aqueous
Nonrhegmatogenous RD and uveal effusions
- (Vs rhegmatogenous RD  subretinal fluid can escape through the tear_
- Nonrhegmatogenous  fluid accumulate  SOL in vitreous
Epithelial and fibrous ingrowth
Trauma
Retinal surgery, retinal vascular disease
Nanopthalmos
Persistent fetal vasculature, ROP
- Contracting retrolental tissue
Flat AC
- Can form PAS
Flat AC from postop / filtering sugery with leak
Drug induced
- Topiramate (epilepsy)
o Acute myopic shift + acute bilateral angle closure
o Choroidal effusion?
<Clinical evaluation>

Hx
- Pain, redness, halos, vision
- DM/cardiac/pulmonary/HT/hypotension/sleep apnea/Raynaud/migraine/renal
stones/pregnancy

Refraction
- Hyperopia  ACG, smaller optic disc
- Myopia  optic nerve head morphology, pigment dispersion

External adnexae
- Tuberous sclerosis (Bourneville syndrome)
o Ash leaf sign, adenoma sebaceum  VH/NV/RD  glaucoma
- Type 1 NF  subcutaneous plexiform neuromas
- Juvenile xanthogranuloma  yellow/orange papules
- Oculodermal melanocytosis
Raised episcleral venous pressure
- Sturge weber syndrome  port wine stain
- Klippel Trenaunay weber syndrome  cutaneous hemangiomas
- Orbital varices
- AV fistula
- Superior vena cava syndrome
- Carotid cavernous, dural cavernous, AV fistula
- TED

Pupils
- Size
- Pupillary response, RAPD
- Corectopia, ectropion uveae, pupillary abnormalities
- Colour vision/EOM/CN  nonglaucoma vs glaucomatous optic neuropathy

Conjunc
- Conj hyperemia (prostaglandin, sympathomimetics)
- Allergic reaction to alpha adrenergic
- Filtering bleb

Episclera and sclera

- Dilated episcleral vessles  elevated EVP
- Sturge weber, AV fistula, TED

Cornea
- Breaks in DM (Haab striae) in developmental glaucoma
- PEE (medication toxicity)
- Microcystic epithelial edema (acute elevated IOP)
Others
- Krukenberg spindle (pigmentary glaucoma)
 - Exfoliative material (pseudoexfoliation)
- KP (uveitic glaucoma)
- Irregular and vesicular lesions (posterior polymorphous dystrophy)
- Beaten bronze appearance (ICE)
- Large posterior embryotoxon (Axenfeld Rieger syndrome)
Pachymetry
AC
- Deep centrally, shallow peripherally (iris bombe and plateau iris)
- Flat (aqueous misdirection and other posterior pushing mechanism)
- Irregular iris surface contour
o Iris masses, choroidal effusions, trauma
- Cells, RBS, pigment
Iris
- Heterochromia
- Iris atrophy
- Transillumination defects (PSX at margin, PDS in mid spoke like)
- Ectropion uveae
- Corectopia
- Nevi
- Nodules
- Exfoliative material
- Evidence of trauma
- NV

Lens
- Phacodonesis
- Pseudoexfoliation
- Subluxation
- Dislocation
Fundus
- Cells, hemorrhage, ghost cells
- Optic nerve head
- Hemorrhage/effusion/masses/retinovascular occlusions, DR, RD
Goni
- Normally light reflected from the angle undergoes total internal reflection at the tear
air interface (46 degree)
- Direct (Koeppe), mirrored indirect (Goldmann / Zeiss)
- Schwalbe line, TM, scleral spur, ciliary body
Corneal light wedge (parallelepiped) technique
- To determine the position of Schwalbe line
- Exact junction of cornea and TM
- Narrow slit beam  2 linear reflections meet at Schwalbe line
Othres
- PAS
Shaffer and Spaeth systems
- Grade 4 (45), Grade 3 (20-45), Grade 2 (20), Grade 1 (10), Slit (<10)
Trauma
 - Angle recession (tear between longitudinal and circular muscles of ciliary body)
- Cyclodialysis (separation of ciliary body and scleral spur)
- Iridodialysis (tear in root of iris)
- Trabecular damage

Optic nerve
- Neural tissue, glial tissue, connective tissue, blood vessels
- 1.2 million axons of retinal ganglion cells
Intraorbital optic nerve
- Anterior ON (retinal surface to retrolaminar region)
- Posterior ON (
- Diameter 1.5mm  expands to 3-4mm immediately upon exiting the globe
o Due to axonal myelination, glial tissue, beginning of leptomeninges
RGCs
- Magnocellular neurons (M cells)
- Parvocellular neurons (P cells)
- Koniocellular neurons (Bistratified cells)

Anterior ON 4 layers
- Nerve fiber  continuous with NFL of retina
- Prelaminar
- Laminar  continuous with sclera, composed of lamina cribrosa
- Retrolaminar  beginning of axonal myelination
Connective tissue density within the lamina
- Lesser superiorly and inferiorly (vs temporal and nasal)
Blood supply
- Ophthalmic artery (via 1-5 posterior ciliary arteries)
- Posterior ciliary arteries  medial and lateral group  short posterior ciliary arteries
 supply peripapillary choroid and anterior optic nerve
- Circle of Zinn-Haller (non continuous arterial circle)
Central retinal artery
- Has few intraneural branches (occ small branch within the retrolaminar region 
may anastomose with the pial system

Recurrent retinal arterioles (central retinal artery)  NFL

Short posterior ciliary arteries, circle of Zinn  prelaminar and laminar
Retrolaminar  short posterior ciliary artiers + pail arterial branches (CRA)

Glaucomatous optic neuropathy

- Loss of axons, vessles, glial cells
- Start at: lamina cribrosa
- More pronounced in the superior and inferior poles of the optic nerve head

Early cupping in infants/children

- Cupping a/w expansion of entire scleral ring

ON head examination
 - Tissue between cup and disc marign = neuroretinal rim
- Large disc  large cup (0.7 ratio may be normal for a large ON)

Changes of glaucomatous optic neuropathy

- Enlargement of cup
- Focal rim thinning
- Superficial disc hemorrhage
- Nerve fiber layer loss
- Asymmetry of cupping
- Beta zone of peripapillary atrophy
Generalized
- Large cup
- Progressive cup enlargement
- Asymmetry of cups (and CDR of >-0.2)
Focal
- Notching of rim
- Vertical elongation of cups
- Cupping to rim margin
- NFL hemorrhage
- NFL loss
Less specific
- Nasal displacement of vessels
- Barring of circumlinear vessels
- PPA
- Exposed lamina cribrosa  acquired optic disc pit
ISNT rule thinning (inferior thickest)

Peripaillary atrophy 2 types

- Alpha zone (irregular RPE hypo or hyperpigmentation)
- Beta zone *glaucoma* (atriophy of RPE and choriocapillaris)
o Atrophy area corresponds to neuroretinal rim thinning

Ddx of cupping
- Congenital pits
- Coloboma
- Morning glory syndrome
- Arteritic ischemic neuropathy
- Compressive optic neuropathy
- Myopic
-

OCT
Confocal
Scanning laser polarimeter

Visual field/perimetry
- Central 24 and 30 programs
 - Humphrey 24-2 and 30-2

Pattern
- Arcuate scotom
- Nasal step
- Paracentral scotoma
- Altitudinal defect
- Generalised depression (rare)
- Temporal wedge (rare)
<Open-angle glaucoma>

Diagnosis
- Optic nerve head appearance
- VF testing
- RNFL
RFs
- IOPs
- Older age
- Age
- Race (Blacks)
- Thin central corneal thickness
- Family history
- Myopia
Associated disorders
- DM
- HT for older patients
- Lower ocular perfusion pressure / overtreatment of HT
- Retinal vein occlusion  NV of angle
Others
- Sleep apnea
- Thyroid
- Hypercholesterol
- Migraine
- Low CSF pressure
- Corneal hysteresis
- Raynaud

Normal tension glaucoma

RFs
- Vasospastic disorders (migraine, Raynaud)
- Ischemic vascular disease
- Autoimmune
- Sleep apnea
- Systemic hypotension
- Coagulopathies
More optic disc hemorrahge than POAG
2 groups based on ON appereance
- Senile sclerotic group (shallow pale sloping of rim)
- Focal ischemic group (deep focal notching of rim)
VF defect
- More focal, deeper, closer to fixation
- Dense paracentral scotoma (shotgun appearance)
DDx
- Congenital (coloboma, optic nerve pit, myopitc disc)
- Physiological cupping due to a large scleral canal
- ON drusen
 - Compressive lesions of optic nerve and chiasm
- Anterior ischemic ON
- Posterior ischemic ON
- Toxic/nutritional optic neuropathy (vitB12def)

Glaucoma suspect
- Suspicious ON / NFL appearance BUT no VF defect, or
- VF defect suggestive of glaucoma BUT no ON abnormality

Ocular hypertension
- Elevated IOP BUT no ON, RNFL, or VF abnormalities
- RFs for progression
o Age
o IOP
o Thinner corneas
o Larger cup disc ratio at baseline
o Higher pattern standard devation on perimetry

<Secondary Open Angle Glaucoma>

Pseudoexfoliation
- LOX1
- ** old age >50-70
- Pseudoexfoliative material in anterior lens capule (Bulls eye)
- Deposits in pupillary margin + ?TID
- Sampaolesi line
- Fibrillar material in TM  impede outflow

Pigment dispersion syndrome

- Zonular fibrs rub posterior iris pigment epithelium  release pigment
- Posterior bowing of iris with “reverse pupillary block” configuration
- Concave iris  greater contact with zonular fibers  release pigments
- Krukenberg spindle, spokelike iris transillumination defects
- Uniform pigmentation of TM
- Pigment in lens capsule (zentmayer ring, scheie stripe)
- Young/middle aged myopic men
- Wide fluctuation in IOPs

Lens induced (phacolytic, lens particle, phacoantigenic)

Phacolytic
- Mature/hypermature  leak lens protein  obstruct TM
Lens particle
- Retention of lens material after cataract extraction
- Ocular trauma
Phacoantigenic
- Rare, sensitized to lens protein
 - AC reaction, KPs

Intraocular tumours

Inflammatory / uveitic
- KPs
- PAS / PS
- Avoid miotic agent
o May exacerbate inflammation + formation of PS

Glaucomatocyclitic crisis (Posner Schlossman syndrome)

- KPs, low grade AC inflammation, unilateral
- Middle aged
- IOP range 40-50mmHg
- Etiology: HSV, autoimmune
- Recurrent attacks
- No evidence that topical NSAID or corticosteroids help prevent attacks

Fuchs heterochromic uveitis/iridocyclitis

- Unilateral, young to middle age
- Iris heterochromia, low grade AC inflammation, PSC
- Heterochromia  due to loss of iris pigment
- Fine vessels in TM (no fibrous membrane, no PAS)
- Steroid no use

Elevated Episcleral venous pressure

- AV malformation, fistula, sturge weber
- Carotid cavernous sinus (hx of trauma)
- Venous obstruction(retrobulbar tumour, TED)
- Superior vena cava syndrome
- Idiopathic
Blood in Schlemm canal*

Trauma and surgery

- Inflammation, hyphema, angle recession, lens subluxation

Traumatic hyphema

Hemolytic and ghost cell glaucoma (post VH)

- Hemolytic -> Hb laden macrophages block TM
- Ghost cells -> degenerated RBCs obstruct the TM

Blunt trauma, angle recession glaucoma

- Tear between the longitudinal and circular fibres of the ciliary body
- Widening of ciliary body band
- Torn iris process
 - White glistening scleral spur
- Irregular and dark pigmentation in angle
- PAS at border of recession

Uveitis glaucoma hyphema syndrome

Schwartz syndrome
- RRD

Drugs
- Steroid
o Less: fluorometholone, loteprednol
o More: prednisolone, dexamethasone
- Dilating drops
o Pseudoexfoliation, pigment dispersion
Glaucoma

Eyedrops

Betoptic beta 1- asthma COPD

Trusopt vs Azopt
- Trusopt is way more irritative **

Timolol + alphagan P (combigan)

Timolol + azopt (Azarga)  cheaper, less preservative

Alphagan P + Azopt (Simbrinza)  much cheaper

Xalatan vs Lumigan
- Xalatan cheaper, less blepharoconjunctivitis
- Lumigan more powerful

Xalacom vs Duotrav (Travatan + timolol – travatal effect/SE in between, but expensive)

PGE overuse  paradoxical increase in IOP

- Half-life over 24hrs

Change Daily to OM

First line: timolol and xalatan

PAOG  timolol
NTG  not timolol first line (poor IOP lowering profile)

Single eye  more timolol

Timolol screen MG
Timolol less local side effect

Alphagan P  prone to hypersensitivity in 30-40%, delayed, follicular conjunctivitis

(redness, not much itch)  borderline high IOP
Combination drop  less hypersensitivity

Rechallenge

Alphagan P  TDS to have neuroprotective effect

Ganfort no preservative

Tapcom S (Tafluprost, timolol)

>2 glaucoma med  add lubricant

Fridge  more tolerable

Alphagan P  CNS depression (CI in breast feed), lethargy

Punctal occlusion  reduce systemic absorption

<Glaucoma>

- Thinned RNFL and narrowed neuroretinal rim

- Often with deformation of optic nerve head (ONH) (cupping)

How is it diagnosed
Incidental vs presentation
Presenting s/s: IOP, CDR, OCT
Where was it diagnosed

Alert
VA at presentation
Uncertain hx
Pale disc
Diagnosis based on OCT
?Dx in private

VA, IOP, VF, OCT

Disc morphology  to establish diagnosis

- Increased CDR, disc h’age (poor prognostic factor), nasalization of vessels
- Disobey ISNT

OCT signal strength at least 7

DDx on increased CDR
ADOA
Compressive ON  post compression still red rim
Ischemic ON
Traumatic ON
LHON
Post optic neuritis

VA, IOP, VF, OCT, EDS

Neuropathy
Retinopathy

Generalised thinning  bilateral optic neuropathy

- Hx of bilateral optic neuritis
- VF can recover

Thinning of RNFL
- ADEM
- MS
- TB meningitis
- Optic neuritis

** OCT only confirms RNFL defect, not necessarily glaucoma

Myopic
VF: relaiability

** VF defect may not be glaucoma

Disc OCT VF correlation

EDS
RP sine pigment

Red flags
- Age younger than 50
- VA less than 20/40 or rapid progression
- Disc with rim pallor
- RAPD / VA loss out of proportion
- Color vision asym impaired
- Vertically aligned visual field defect
- Mismatch between the degree of cupping and degree of VF loss
0.5 cup but 10 degree VF remaining
<2. Type of glaucoma>

Primary vs secondary
Angle closure vs open angle
Baseline/max IOP
Hx of uveitis/steroid/ocular surgery

Stage
Pre-perimetric (VF normal, OCT picked up)
Mild
Moderate
Severe
Advanced

24-4
- MD
- Pattern deviation map
- Proximity to fixation

Staging  set IOP target

+  20
++  < 18 etc

NTG baseline  IOP target 20-30% lowering

OHT if IOP >30  start med

Staging
MD 0
1-6
12
18
>18

IOP as quick guide to med change before next VF

But if next VF no progression (even if IOP not lowered enough to target)  not need change
med

Progression: - <0.5MD per year

Average -0.8 to -1
Fast progressor -2
Blindness = -33MD

More VF initially for progression rate

Progressive VF every 2-3 months *** if poor control/progression
Age, life expectancy

Pachymetry x 1 for CCC

Monitoring

OCT thinning (early stage glaucoma)

- Blindness  45-48 um  floor effect

VF 24-2  worsen  central vision remaining  VF 10-2 for central VF monitoring

Monitor VA only (very late stage)

Suprathreshold test
Manual: Aimark/Goldman

Macula ganglion cell complex analysis *** GCC

- Thinning from macula first
- Explains why some present with VF defect before OCT RNFL finding

Suspicious disc
But OCT normal  OCT in 1 year  if both OCT normal  GCC
Or  directly GCC
Before discharge

GCC still worth it in myopia

Red disease
- Myopic  double hump have temporal shift
- False positive picture
o Can do a macula ganglion cell complex analysis
Hyperope
- Nasal shift, can still red

TPA
Progression analysis

Spectralis  for dense cat patients

NTG target

Pigment dispersion, floppy  pilo

OHT
5 year untreated OHT  8.8% of developing POAG
Treated  5.5% risk
Take into account of RFs
OHT calculator  individualized risk

OHT
SLT and MLT
(baseline IOP low – good, virgin eye – not med  good response)

Monotherapy  still high  then consider SLT

Collaborative NTG study

NTG: allow 1 or 2 times IOP spikes higher than 21
True NTG profile  18-22 range (high normal side)
Median IOP 16

See if NCT and GAT match in previous visits

Use both peri-start med to see