1
Q
What are the causes of heterochromia?
A
HETEROCHROMIA
H - Horner syndrome (congenital/acquired)
E - eye trauma/surgery
T - Tumours - iris melanoma
E - Endocrine/waardenburg (congenital)
R - raised IOP - congenital glaucoma
O - ocular melanocytosis / nevus of ota
C - Chronic uveitis - Fuch’s, HZV, HSV
H - Hemosiderosis / Siderosis
R - Rash / vascular syndromes (Sturge-Weber)
O - Operations/iatrogenic
M - Medications - prostaglandins - browning of iris
I - ICE syndrome/iris atrophy
A - Atrophy
2
Q
What is the difference between direct and indirect gonioscopes?
A
Direct: Erect and direct view of angle structures - patient needs to be in supine position (in theatre)
Indirect: Inverted and reversed view of angle structures, dynamic gonioscopy possible.
Direct: Koeppe, Barkan, Swan-Jacob, Richardson
Indirect: Goldmann, Zeiss, Posner, Sussman
3
Q
Which visual field progression analysis is useful for earlier detection?
A
Event analysis (STATPAC) - compared current field to baseline –> progression flagged if 3 adjacent points worsen significantly
4
Q
What is the Humphrey Visual Field Index (VFI)
A
Global index that summarises patients visual field status as a percentage of normal age-adjusted visual field
VFI of 100% –> normal visual field
VFI of 0% –> perimetrically blind visual field
5
Q
Is VFI more or less affected by media changes and cataract compared to mean deviation (MD)?
A
VFI - less affected by media changes and cataract –> reflective of percentage of remaining of retinal ganglion cells
6
Q
When is goniotomy considered in congenital glaucoma? When is trabeculectomy considered?
A
Goniotomy - clear corneas
Trabeculectomy: If unclear corneas
7
Q
Whats the difference between primary congenital glaucoma and primary juvenile glaucoma?
A
Primary juvenile glaucoma if diagnosed > 5 years
8
Q
What are the 3 factors which are considered in angle closure disease?
A
- Iridotrabecular contact (ITC)
- Raised IOP / PAS
- Optic neuropathy
9
Q
What is the difference in classification between PACS, PAC, and PACG?
A
PACS: >180 degrees of iridotrabecular contact
PAC: >180 degrees of iridotrabecular contact + raised IOP/PAS
PACG: PAC with optic nerve damage / field defect
10
Q
What is the difference between PACS and PACS plus?
A
PACS: >180 degree of iridotrabecular contact
PACS plus (ZAP trial) : vulnerable adults, FH of angle closure, high hypermetropia (+6D), diabetes/other condition requiring dilation, lives remotely, medication with anti-cholinergic action (anti-depressants)
11
Q
What is the treatment difference between PACS and PACS plus?
A
PACS -
PACS plus: PI
12
Q
What is the difference in treatment for PAC and PACG?
A
PAC: Clear lens extraction or PI
PACG: Clear lens extraction or PI +/- medical +/- surgical
13
Q
What are the type of glaucoma visual field defects seen (8)
A
- Nasal step obeying horizontal meridian
- Temporal wedge defect
- Arcuate defect (with peripheral breakthrough)
- Paracentral defect 10-20 degrees from blindspot
- Generalised constriction (tunnel vision)
- Temporal sparing severe visual field loss
- Total loss of field
14
Q
What is the difference between plateau iris configuration and plateau iris syndrome?
A
The ciliary processes are anteriorly positioned and bulky.
They push the peripheral iris root forward toward the trabecular meshwork. This creates a flat (“plateau”) iris plane with a sharp angulation at the root — causing angle crowding.
Plateau Iris Configuration:
Anatomical predisposition to narrow angle (seen before laser PI); not necessarily causing closure yet.
Plateau Iris Syndrome: Persistent narrow angle after a patent peripheral iridotomy — due to ciliary body anatomy (no pupillary block)
15
Q
What are the findings of plateau iris syndrome?
A
Deep central AC, shallow peripheral AC
Gonioscopy: Double hump sign
16
Q
What is the treatment of plateau iris syndrome?
A
PI then…
Argon laser peripheral iridoplasty –> causes cicatricial contraction of peripheral iris stroma to tighten iris and widen angular approach.
Pilocarpine
17
Q
What are the main causes of generalised depression in visual field testing (3)
A
- Pilocarpine or anything causing pupillary diameter < 2.5mm
- Cataract
- Incorrect use of corrective lens
18
Q
Whats the difference between ALT and SLT?
A
19
Q
What are the associated conditions with aniridia?
A
20% - Wilms tumour
WAGR syndrome: Wilms tumour, aniridia, GU abnormalities, Reduced IQ.
20
Q
What ocular conditions do patients with aniridia develop?
A
ANIR
Angle closure glaucoma (chronic)50-75% patients
Nystagmus
Iimbal stem cell deficiency
Retinal hypoplasia : foveal and optic nerve
21
Q
What are the risk factors for aqueous misdirection?
A
SPAM
S - Short axial length, nanophthalmos, uveal effusion syndrome
P - Post procedure - trabs, tubes, cataract, iridectomy, Pi
A - Angle closure
M : Miotic therapy (rare)
22
Q
What is the pathophysiology behind angle recession glaucoma?
A
Usually caused by blunt trauma
1. The globe compresses anteroposteriorly (front to back).
2. This causes sudden expansion equatorially (sideways).
3. Force stretches the iris root and ciliary body, causing a tear between the longitudinal and circular muscle fibres of the ciliary body.
4. This creates a widened ciliary body band visible on gonioscopy — that’s angle recession.
Angle recession –> deepened AC angle due to split.
23
Q
What are the clinical features of angle recession glaucoma?
A
Gonioscopy: Widened ciliary body band (>180 degrees) compared to other eye
Asymmetry in AC depth
24
Q
What is the difference between cyclodialysis and angle recession?
A
Angle recession: Tear within the ciliary body separating circular and longitudinal fibres –> widened ciliary body band on gonioscopy
Cyclodialysis: Tear between ciliary body and scleral spur –> new hole between AC and suprachoroidal space –> hypotony.
25
What's the difference between ghost cell glaucoma and haemolytic glaucoma?
Ghost cell glaucoma: Closely associated with vitreous haemorrhage - ghost cells visible within 1 month of vitreous haemorrhage - tan coloured blood cells
Haemolytic glaucoma: Haemoglobin-laden macrophages block trabecular outflow channels after traumatic hyphaema
26
What are the conservative measures to manage bleb leak? (5)
1. Pressure patching
2. Bandage contact lens
3. Temporarily tapering topical steroids
4. Cyanoacrylate tissue adhesive or autologous fibrin glue
5. Injection of autologous blood inside/around bleb
27
What are the risk factors of pigment dispersion syndrome?
1. Myopia
2. 20-40
3. Caucasian males
4. High intensity Exercise - exercise induced pigment release
28
What is the mechanism behind pigment dispersion syndrome?
The iris is posteriorly concave (bowed backwards).
During pupil movement (especially with exercise or dilation), the iris rubs against the lens zonules.
This mechanical friction releases pigment granules from the posterior surface of the iris --> clogging up trabecular meshwork and other ocular surfaces --> raised IOP.
29
What are the ocular findings of pigment dispersion syndrome?
PIGMENTZ
P - Pigment reversal sign (darker super angle) or Sampaolesi line
I - Iris bowing posteriorly seen on AS OCT - more common in myopes
G - Gonioscopy shows homogenous 360 degree pigmentation
M - More pigmentation on corneal endothelium - Krukenberg's spindle
E - Egger's line - pigment dispersion on anterior hyaloidocapsular ligament
N - Near radial iris transillumination defects
T - Thin retina - lattice degeneration
Z - Zentmayer's line (Scheie's line) - pathognomonic - pigment on zonular attachments at lens equator and posterior capsule
30
What is the treatment of pigment dispersion syndrome?
1. ALT/SLT with low settings (>50% failure by 5 years)
2. Topical drops
3. Surgery (trabeculectomy/tube) similar success rate but higher complication rate - hypotensive maculopathy
31
What is the pathophysiology of pseudoexfoliation syndrome? PXF
The pseudoexfoliative material is produced by abnormal basement membranes of anterior segment epithelial cells (lens epithelium, iris, ciliary body).
The material is deposited in the pupillary border, anterior lens capsule, zonules, and trabecular meshwork.
Mechanical blockage and trabecular damage by this material → elevated IOP and glaucomatous optic neuropathy.
32
What are the clinical features of pseudoexfoliation?
3-EXFOLIATE
3 - 3 zone pattern on anterior lens capsule : clear central disc (constant iris rubbing), intermediate granular zone of pseudoexfoliate material, clear peripheral zone
E - Endothelium deposition (can resemble PDS)
X - 10 x increase glaucoma risk
F - Females > Males, Scandanavian
O - Open angle glaucoma
L - Line - sampaolesi line due to irregular pigment deposition in angle
I - Iridodonesis/phacodonesis due to weak zonules
A - Atrophic iris - fails to dilate
T - Transillumination defects of iris peripupillary
E - Elderly
33
What are the complications of PXF?
1. Secondary open angle glaucoma
2. Zonular instability - small pupil and weak zones during cataract surgery
3. Ectopia lentis
4. Corneal decompensation (rare)
34
Why would you prefer using prostoglandin analogues than b-blockers in normal tension glaucoma?
Nocturnal dips in optic nerve head perfusion --> PGAs have better IOP control at night, B-blockers can reduce blood flow at night
35
What is the mechanism of aqueous misdirection?
aqueous humor is misdirected posteriorly into or behind the vitreous into the retrolental space, causing forward displacement of the lens–iris diaphragm and shallow anterior chamber with raised intraocular pressure (IOP).
36
What is the management of aqueous misdirection (medical, surgical)
Medical:
1. Intensive cycloplegic therapy (atropine)
2. Systemic + topical IOP drops
3. Ensure patient PI before commencing treatment
Laser:
1. YAG disruption of posterior capsule (if pseudophakic)
2. Trans-scleral cyclodiode photocoaguluation of ciliary body in one quadrant --> to rotate the ciliary body.
Surgical:
1. Pseudophakic: PPV + posterior capsulotomy
2. Phakic: Cataract + PPV + posterior capsulotomy --> hyaloidotomy can be attempted through patent PI
37
When is valved drainage devices used? When is non-valved drainage devices used typically?
Valved: Eyes at high risk of hypotony: Uveitic, neovascular, post-vitrectomy
Non valved: Advanced glaucoma
38
What are the other secondary causes of congenital glaucoma?
1. Anterior segment dysgenesis: Axenfeld-Rieger, Peter's anomaly
2. Aniridia
3. Phakomatoses (Sturge-Weber)
4. Connective tissue disease (Marfan, homocysteinuria, Weill-Marchesani)
5. Tumour related
39
What are the clinical features of congenital glaucoma? (7)
1. Photophobia
2. Watery eyes
3. Blepharospasm
4. Buphthalmos (enlargement of globe)
5. Megalocornea
6. Haab striae (breaks in Descemets)
7. > 0.3 cup to disc ratio or >0.2 difference in both eyes
40
What treatments should be avoided / used with caution in congenital glaucoma?
1. a2 agonists (brimonidine) < 2yo due to potential CNS depression/drowsiness
2. CAI - lethargy, decreased appetite, impaired growth
41
What is the management of hyphaema? Monitoring?
High risk - admit
Conservative: Bed rest, globe protection
Medical: Topical steroids, cycloplegia, treat high IOP
Surgical: AC paracentesis +/- washout or trabeculectomy if medical treatment fails
Monitoring
1. Gonioscopy on resolution
2. Annual IOP checks due to risk of angle recession glaucoma
42
What is the difference in Sampoelsis line in PXF vs PDS?
PDS: thick homogenous line
PXF: patchy like
43
What is the IOP response after SLT short and long term for a patient with PXF?
Short term: profound initial IOP reduction as it reduces mechanical blockage of TM meshwork by PXF material
Long term: Less sustained over long term, requiring repeat laser or surgery earlier.
44
What is the definitive treatment of a late, leaking hypotonic bleb?
Surgical bleb revision with conjunctival advancement flap --> to achieve mechanical closure and prevent risk of endophthalmitis
45
What are the systemic and ocular features of sturge weber syndrome?
FACE SWS
F - **Facial port wine stain (naevus flammaus) **--> Capillary malformation in distribution of V1 (ophthalmic division) of trigeminal nerve which ay extend to V2. *Important because V1 involvement = high glaucoma risk*
A - Angiomas (CNS leptomeningeal) - vascular malformations causing epilepsy, hemiparesis, developmental delay
C - Choroidal haemangioma (episcleral + ciliary body haemangioma) --> **not retinal haemangioma like in Tuberous sclerosis**
E - Elevated episcleral venous pressure --> late onset glaucoma in teenagers/adults
S - Secondary glaucoma - infants --> angle maldevelopment --> elevated IOP
W - Weakness due to stroke
S - So many haemangiomas --> episcleral, ciliary body, choroidal.
46
What is the treatment pathway of a patient with POAG/COAG newly diagnosed?
1. Offer 360 SLT (except those with PDS)
2. Offer generic PGA whilst waiting/ additional treatment required
Then
Second class of drops
47
What is the definition of normal tension glaucoma (NTG)?
Open angle glaucoma with glaucomatous ONG + VF despite IOP <21mmHg, diagnosis of exclusion
48
What are the risk factors of NTG? (normal tension glaucoma)
1. Elderly Japanese female
2. Thin CCT
3. Low BP
4. Vasospasm
5. Migraine
6. Raynaud's
7. Myopia
8. Family History
49
What are the differentiating clinical features of normal tension glaucoma vs POAG?
1. More likely to have disc haemorrhages and acquired optic disc pits
2. Cup may be larger and shallower (saucerisation)
3. VF defects in superior hemifield (superonasal)
4. Generalised depression is less marked than high-tension POAG
50
What is the difference in mechanism between pupillary block and iris plataeu mechanisms for acute angle closure?
**Pupillary block:
Aqueous cannot move freely from posterior chamber to anterior chamber because the lens and iris are in close apposition --> Pressure builds behind the iris --> Iris bows forward (iris bombe) --> Angle closes circumferentially.
**Plateau Iris**
Ciliary body is anteriorly rotated and enlarged --> Peripheral iris is pushed forward despite a deep central anterior chamber --> Angle closes because the peripheral iris is crowded, not because of iris bombe.
Caused by structural anatomy of ciliary processes.
51
What is the difference in mechanism risk factors between pupillary block and iris plataeu mechanisms for acute angle closure?
**Pupillary Block
**
Older age
Hypermetropia
Thick crystalline lens
Cataract progression
Narrow anterior chamber overall
Female sex
Asian ethnicity
Family history of angle closure
**Plateau Iris
**Younger patients
Females
Normal or shallow refractive error
Large or anteriorly positioned ciliary processes
Often discovered after peripheral iridotomy because the angle still remains narrow
52
What is the difference in ocular findings between pupillary block and iris plateau angle closure?
Pupillary Block
Shallow anterior chamber centrally and peripherally
Iris bombe (convex bowing)
Responds very well to laser peripheral iridotomy (LPI) which equalises pressure between chambers
Plateau Iris
Deep central anterior chamber but shallow periphery
Flat looking iris plane that rises sharply at the periphery (the “double hump sign” on indentation gonioscopy)
No iris bombe
LPI does not open the angle because mechanism is not pupillary block
53
What is acute crisis AAC management?
1. Medical STAT: Aqueous suppressants, IV acetazolamide, topical beta blocker, alpha agonist
2. Inflammation: Topical steroids hourly to control inflammaiton
3. Break block: Pilocarpine 2% to both eyes, but only when IOP <40mmHg to avoid iris ischaemia
4. Definitive : YAG PI performed on both eyes once cornea is clear and IOP controlled
54
What are the mechanisms for secondary glaucoma?
CLOSE UPT
Ciliary body rotation: plateau iris, cysts, uveal effusion
Lens associated: Phacomorphic,
Obstruction at pupil: pupillary block, PAS from uveitis
Synechiae: ICE syndromes, chronic uveitis, seclusio pupillae
Effusion: Choroidal effusions, malignant glaucoma
Uveal ischaemia: NVG
P: Post-operative/Pigmentary: post trab
T: Trauma: Angle recession (TM tear) or ghost cell obstruction (from vitreous haemorrhage)
55
What are the main complications associated with MIGS? (3)
1. Endothelial cell loss: Due to malpositioned stent of anterior chamber device contact
2. Stent erosion: with subconjunctival devices like XEN, conjunctival erosion over implant --> infection risk
3. Hyphaema: Bleeding occurs intra and post-operatively
56
What are the clinical features of iridocorneal syndrome?
ICE CAPI
I: Iris abnormalities - iris pigmented nodules (Cogan-Reese), iris atrophy (essential iris atrophy)
C: Corneal oedema (chandlers) and guttata
E: Endothelial beaten metal appearance/hammered siliver
C: Contraction membrane over angle --> PAS
A: Angle signs: PAS extend to schwalbe's line
P: Pupil distortion: corectopia, pseudopolycoria
i: Inflammation absent - white eye glaucoma, no uveitis
57
What is the pathophysiology behind iridocorneal syndrome?
The corneal endothelium proliferates and migrates across the angle and iris.
These abnormal endothelial cells form a “membrane” on the posterior cornea → contracts → causes:
Progressive PAS (peripheral anterior synechiae)
Iris distortion (corectopia, holes)
Secondary angle-closure glaucoma
Thought to be triggered by HSV infection
58
What are the differentials for ICE syndrome?
PPMD: Bilateral and mild iris findings, vesicular endothelial changes
Axenfeld-Reiger syndrome: Bilateral and present from birth
Uveitis PAS: Usually bilateral with redness, KPs and cells
Congenital iridodysgenesis: Bilateral, congenital, absent endothelium findings
59
What is the management of iridocorneal syndrome? (ICE)
1. Medical IOP lowering
2. Sugery (trabeculectomy +/- tube +/- cyclodestruction)
60
What are the general features suggestive of compressive neuropathy over glaucoma?
1. Positive visual symptoms
2. Unexplained VA reduction
3. Reduced colour vision
4. RAPD
5. Optic disc pallor
6. VF defect observing vertical midline
7. Mismatch between optic disc and VF defect
61
What are the two trabeculectomy approaches?
Fornix based and limbal based
Fornix based: Higher incidence of wound leaks since edge of wound as at limbus. More diffuse and lower blebs since subconjunctival scar is anterior to scleral flap.
Limbal based: More focal and elevated blebs since scar is posterior to sclceral flap --> less prone to leaks but more difficult to do due to poorer exposure
62
What is the management of secondary angle closure glaucoma from topiramate?
Topical atropine, hypotensive agents
Oral acetazolamide may worsen ciliary body oedema.
63
Which glaucoma conditions is SLT contraindicated? (3)
1. ICE syndrome
2. Neovascular
3. Uveitic glaucoma
64
When does phaco-anaphylactic uveitis commonly occur?
Within first 2 weeks after truama / cataract surgery with retained lens fragments
65
Differentials of shallow AC after trabeculectomy?
66
What are the differentiating signs of blebitis and bleb related endophthalmitis? (3)
1. More severe clinical findings (pain/redness/inflammation)
2. Decreased visual acuity
3. Vitritis
67
What is the management of bleb-related endophthalmitis? (7)
1. Microbial swab
2. Tap and inject (Vancomycin 1-2mg and amikacin 0.4mg)
3. Iodine in conjunctival sac
4. Topical Abx hourly
5. Oral Abx
6. Topical steroid / oral / IV steroid started next day
7. Bleb revision when infectious phase over
68
What is the classification of angle recession?
Low risk: <90degrees extent of angle recession
Moderate risk: 90-180 degrees of angle recession
High risk: > 180 degrees of angle recession
69
What are the features for Fuchs heterochromic iridocyclitis?
FUCHS
F - Fine transillumination defects
U - Unusual iris - atrophy, nodules, abnormal vessels
C - Cataract (posterior cortical, subcapsular)
H - Heterochromia (bluer iris)
S - Stellate KPs
70
What are the features of POSNER SCHLOSMAN syndrome?
POSNER
P - Pure eye (white)
O - Open angle
S - Some flare
N - No synechiae or peripheral anterior synechiae
E - Elevated IOP (40-80mmHg)
R - Rarely cells / KPs
71
What are the distinguishing features between Posner Schlossman syndrome and Fuch's heterochromic iridocyclitis? (4)
Fuchs has
1. No sex bias
2. Chrnoic low grade inflammation that does not respond to steroids
3. Associated with less elevations of IOP
4. Associated with rubella virus, Posner schlossman associated with HSV
72
Which MIGs devices enhance aqueous flow into Schlemm's?
Which MIGs devices shunt outflow into subconjunctival space?
Which MIGs devices bypass trabecular meshwork?
Schlemms: OMNI
Subconjunctival: Preserflo, Xen
TM bypass: istent, hydrus
73
What is uveal effusion syndrome?
Accumulation of fluid in suprachoroidal space --> choroidal and exudative retinal detachment without any evidence of inflammation or neoplasm
74
What are the risk factors for uveal effusion syndrome?
1. Nanophthalmos (axial length <20mm)
2. Thickened sclera with decreased scleral permeability
3. Middle-aged males more affected
75
What is the management of uveal effusion syndrome?
Nanophthalmic: Sclerostomy
Non-nanophthalmic: Vitrectomy
76
What is the difference in iris transillumination between PXF and PDS?
PXF: peripupillary
PDS: mid-periphery
77
What are the uses of pilocarpine (5)
78
What are the side effects of pilocarpine?
1. Brow ache
2. Accomodative spasm (myopic shift)
3. Reduced night vision
4. Anterior uveitis
5. CMO (aphakia)
6. Miosis induced crowding --> worsens angle
7. Retinal detachment (aphakia, high myopes)
79
Table of IOP lowering drops
80
What is the indication of mitomycin C in ophthalmology? (4)
1. Glaucoma filtration surgery --> reduce post-op scarring and improve bleb survival
2. Pterygium surgery - reduce recurrence rate
3. Ocular surface neoplasia (OSSN) --> topical chemo agent
4. Refractive surgery --> reduces haze after PRK (high myopes)
81
What are the investigations of a patient with congenital glaucoma?
**examination under anaesthesia
**Pressure: IOP, gonioscopy
Posterior: Optic disc
Other: corneal diameter, pachymetry, axial length
82
What is the management of congenital glaucoma?
Medical - temporary before surgery
1. CAIs
2. Caution with beta blocks (bradycardia, hypotension, apnoea
3. Alpha-2 agonists contraindicated - CNS depression
4. Prostaglandin analogues - limited rule as usually ineffective
5. Miotics - avoided as can worsen inflammation
Surgical:
1. Goniotomy - clear cornea (incise TM directly with ab interno approach)
2. Trabeculotomy - cloudy cornea (ab externo approach to access schlemm's canal via sclera and open TM
83
What are the differentials of congenital glaucoma?
1. Congenital NLDO : Watering only, no photophobia or conrela changes
2. Megalocornea: Large cornea with normal IOP
3. Keratitis: Red, painful eye
4. Metabolic disorders (mucopolysaccharidosis) - corneal clouding
5. Birth trauma: Corneal oedema, multi-layered retinal haemorrhages
84
What is the difference between goniotomy and trabeculotomy?
Goniotomy: opens trabecular meshwork internally --> performed when cornea clear
Trabeculotomy: opens Schlemms canal externally --> performed when cornea cloudy
85
What are the differentials of a patient with pseudoexfoliation syndrome?
1. Pigment dispersion syndrome
2. Uvietic glaucoma with fibrin deposits
3. Glassbowers cataract: true exfoliation
4. Amyloidosis with ocular involvement
86
What are the risk factors for patients with pseudoexfoliation syndrome? (5)
Demographics
1. Females > 60 living in Scandanavia / Mediterranean
Genetic
LOXL1 genetic mutations
Environment
UV light exposure
87
What are the investigations of a patient with pseudoexfoliation?
History: Geographical factors
Slit lamp examination (5Ps)
- Pupillary border and anterior lens capsular deposits with clear intermediate zone
- Pigment in AC and on endothelium
- Peripupillary transillumination defects
- Phacodenesis
- Poor pupillary dilation
- Fundus disc analysis (CD ratio)
Gonioscopy
- Open angle with pigment deposition (Sampaolesi line)
IOP assessment: Goldmann tonometry
OCT RNFL/HVF for glaucoma detection
Anterior segment OCT/UBM for assessment of zonular integrity
Systemic
- Cardiovascular evaluation - IHD and aortic aneurysm
- Genetic testing for LOXL1 mutations
88
What is the management of a patient with pseudoexfoliation syndrome?
Medical glaucoma management
- Prostaglandin analogues
- Adjuncts: Beta blockers, alpha-agonists, carbonic anhydrase inhibitors
- Avoid cholinergics due to potential for pupillary block
Laser
SLT: more effective in PXF than POAG but linked to post-operative IOP spikes
Surgical
- Trabeculectomy or glaucoma drainage device --> higher complication rate but similar success as POAG
- Cataract surgery considerations
89
What is the management strategies of cataract surgery in a patient with PXF?
Preoperative assessment
Slit lamp examination: assess zonular integrity (phacodenesis), pupillary dilation (PXF patients have sphincter fibrosis), Glacuoma status (prone to post IOP spikes)
Biometry: Use Kane or Barrett Universal II which is more accurate in eyes with lens subluxation
Informed consent: increased risk of zonular dialysis, vitreous loss, nucleus drop, further surgeries.
Intraoperative management : minimise stress on zonules
PUPIL
1. Pupil expansion devices: Iris hooks, Malyguin rings,
2. Healon GV (high cohesive viscoelastic) for viscodilation
CAPSULOREXIS: larger rexis (5.5-6mm)
HYDRODISSECTION: avoid hydrodissection or very gentle, do hydrodilineation
PHACO: vertical chop - less forces on zonules, reduced fluidic parameters
CAPSULE: Consider capsular tension ring, capsular hooks
Post-operative management: Manage IOP spikes and inflammation
- consider acetazolamide due to raised IOP due to retained OVD or pigment release
- Use more potent or more frequent steroid to prevent inflammation
- Monitor for capsular phimosis syndrome - late onset IOL-bag complex dislocation
90
What are the differentials of a patient with pigment dispersion syndrome?
1. Psuedoexfoliation
2. Pigmentation post-surgery or trauma - iris chafing
3. Guttata from Fuch's
4. Chandlers syndrome: ICE spectrum with corneal endothelial changes
91
What are the investigations of a patient with pigment dispersion syndrome?
Slit lamp examination: Krukenberg spindle, iris defects, lens zonules
Gonioscopy: assess trabecular pigmentation (chocolate-brown band) and wide open angle
IOP: Goldmann tonometry
OCT RNFL/HVFF: assess evidence of pigmentary glaucoma
Imaging: Anterior segment OCT to confirm posterior iris bowing
92
What are the management strategies for a patient with pigment dispersion syndrome?
Conservative: observation if asymptommatic and IOP normal
Medical: anti-glaucoma drops, avoid medications that excessively dilate the pupil
Laser:
SLT: pigmentary glaucoma present
Argon laser peripheral iridoplasty: To reduce iris concavity
Surgical
- MIGS, Trabeculectomy --> higher risk of post operative hypotonus maculopathy
93
What are the risk factors for physiological cupping?
African descent
Myopes: Larger, tilted discs
94
What are the features of physiological cupping?
Symmetrical discs, healthy neuroretinal rims, no notching
Scans: No RNFL defects, no IOP changes, normal visual fields
95
How would you evaluate a bleb?
B – Bleb height & extent ?overhanging bleb
L – Leak (Seidel test) ⭐
E – Epithelial / vascularity
B – Blebitis
S – Shape (diffuse vs flat vs cystic)
A – Anterior chamber depth
F – Function (IOP) ⭐
E – Encapsulation
👍 Good / functioning bleb
Diffuse
Low to moderate elevation
Minimal vascularity ⭐
Translucent
Microcystic appearance
❌ Failing / failed bleb
Flat
Localised
Increased vascularity ⭐
Thickened / scarred conjunctiva
96
What are the signs of an overfiltering bleb?
⚠️ Overfiltering bleb
Very thin
Cystic
Avascular
May be leaking
97
How would you manage an encapsulated bleb?
Dome-shaped, tense bleb
Often vascular
Elevated IOP despite bleb presence
Usually occurs 2–6 weeks post-op
⭐Medical
1. Restart patient on IOP lowering drops,
2. Digital massage to encourage drainage
Surgical
1. Bleb needling with 5FU
2. Bleb revision
98
What is the difference in signs/risks/ management of a leaky bleb vs an overfiltering bleb?
Leaky bleb signs:
Positive Seidel test ⭐
Thin, avascular bleb
Conjunctival defect or microhole
Low IOP (may be normal early)
Shallow AC (if significant leak)
Risks:
Bleb-associated endophthalmitis 🚨
Hypotony
Choroidal effusions
Overfiltering bleb signs:
Low IOP (<5–6 mmHg) ⭐
Diffuse, often avascular bleb
Shallow anterior chamber
Hypotony maculopathy: Choroidal folds
Risks:
Choroidal effusion
Hypotony maculopathy
Cataract
**Management of leaky bleb**
Conservative (small / early leak)
BCL, stop steroids, Abx (infection prophylaxis)
🟡 Intermediate
Autologous blood injection
Tissue glue (cyanoacrylate)
Compression patching
🔴 Surgical (persistent / large leak)
Conjunctival resuturing / advancement ⭐
Bleb revision
Patch graft if needed
Management of overfiltering bleb
Conservative (early / mild)
Cycloplegics (e.g. atropine) ⭐
Increase steroids (reduce inflammation → improve sealing)
Pressure patching
🟡 Intermediate
Viscoelastic injection into AC
Autologous blood injection into bleb to enhance healing
🔴 Surgical (persistent hypotony)
Resuture scleral flap ⭐
Compression sutures
Bleb revision
Conjunctival advancement
Amniotic membrane graft
99
What are the clinical signs of a patient with blebitis?
1. Milky, white opaque bleb fillled with purulent material with some discharge
2. Diffuse ciliary and conjunctival congestion
3. Check Siedel's positivity
WHITE on RED appearance
100
What are the investigations of a patient with blebitis?
Ophthalmology
-Siedel's test
- Conjunctival swab: streptococcus, staphylococcus, gram-negative bacilli
B scan - check for vitreous opacities
If signs of endophthalmitis - AC tap / vitreous tap and inject
101
What are the differentials of a patient with blebitis?
ITCC
I: Infectious bleb related endophthalmitis
T: Toxic conjunctivitis
C: Cystic bleb with no infection (sterile inflammation)
C: Conjunctival wound dehiscence
102
What are the risk factors of a patient with blebitis?
Patient factors
- poor wound healing/immunosuppresion (diabetes, previous radio)
- Contact lens use
Environmental factors
- trauma to area
Surgical factors
- Use of antimetabolites
- Poor surgical technique (inferior bleb or bleb leak)
- Thin avascular cystic blebs
103
What is the management of a patient with blebitis?
Medical
- Arrange admission
- Conjunctival swabs
- Povidoiodiine in conjunctival sac
- Hourly moxifloxacin
- 400mg Moxifloxacin oral for 10 days / Oral Ciprofloxacin 750mg BD
- Topical steroids QDS from next day
- Cycloplegia
Surgical
- AC washout / tap and inject
- Urgent PPV if HM vision (EVS study)
- Bleb revision or removal
104
What are the main complications of trabeculectomy?
Intraoperative
- Damage to scleral flap
- Damage to conjunctival flap
- Vitreous loss
Post operative - Early
- Hypotony
- Post operative high pressure
- Endophthalmitis
Post operative (Late)
- Filtration failure due to subconjunctival fibrosis - encapsulated cyst --> treat with bleb needling
- Leaky bleb - treat with autologous blood injection, BCL, bleb revision, compression sutures
- Infection - blebitis / endophthalmitis
- Visual wipeout / visual loss
- Ptosis: commoner with SR traction sutures and in revision surgery where conj has been mobilised from superior fornix
105
What are the clinical features of Fuch's Heterochromic iridocyclitis?
FUCHS SA
F: Fine stellate KPs
U: Unusual iris: Atrophy, nodules, vessels
C: Cataract (posterior subcapsular cataract)
H: Heterochromia + Iris atrophy
S: Synechiae absent
S: Secondary glaucoma
A: Amsler sign (hyphaema) during cataract surgery / paracentisis due to fragile iris vessels
106
What are the differentials of a patient with Fuch's Heterochromic Iridocyclitis ?
1. Possner-Schlossman Syndrome
2. Juvenile idiopathic arthritis related uveitis
3. Herpetic uveitis
4. Tubercular uveitis
107
What are the investigations of a patient with Fuch's Heterochromic iridocyclitis?
General:
Anterior segment findings
IOP measurement
Gonioscopy: detect neovascularisation of angle
108
How would you manage a patient with Fuch's Heterochromic Iridocyclitis?
Conservative: Observiation
Medical:
Uveitis: Mild, often don't need steorids
Glaucoma: Treat as POAG with topicals
Surgical
- Cataract sugery
- Management of amsler sign.
109
What are the causes of Fuch's Heterochromic Iridocyclitis?
Idiopathic
Viral: Rubella, HSV, CMV.
110
What are the clinical features of Posner Schlossman syndrome?
Triad
- Markedly raised IOP
- Mild AC inflammation
- Minimal pain, open angles
111
What are the causes of Possner Schlossman Syndrome?
Associated with CMV
112
What are the causes of a vascular bleb?
1. Early postoperative vascular bleb --> digital massage, increase post-op steroids, needling, 5-FU.
2. Encapsulated bleb (2-6 weeks post op): early trab failure --> needling +/- antimetabolite, surgical revision
3. Late vascular bleb: subconjunctival fibrosis, reduced filtration, bleb failure --> bleb revision, repeat trabeculectomy, tube surgery.
113
What is the differentials of a patient with hyphaema?
1. Trauma
2. NVI: CRVO, PDR, OIS
3. Tumours: Iris melanoma, retinoblastoma
4. Inflammatory: Herpetic uveitis, Fuch's heterochromic
5. Systemic: Sickle cell, anti-coagulation disorders
114
What are the absolute indications for surgery in hyphaema?
1. Uncontrolled raised IOP > 50 for 5 days, >35 for 7 days, >25 sustained in sickle cell disease
2. Corneal blood staining
3. Total hyphaema > 5 days
4. Sickle cell disease --> early surgery due to optic nerve vulnerability and increased trabculitis (avoid acetazolamide)
5. Rebleeding with pressure rise
115
Why does rebleeding occur in patients with hyphaema?
Rebleeding happens because the initial clot that sealed the damaged iris or ciliary body vessels breaks down before stable healing occurs.
116
What are the common early complications of a trabeculectomy with a high IOP with deep AC?
High IOP with shallow AC?
1. Inadequate filtration --> tight scleral flap or obstruction of fistula by iris/ciliary process --> YAG laser to remove obstruction of iris/ciliary process
Shallow AC
1. Suprachoroidal haemorrhage --> surgical drainage
2. Malignant glaucoma (Aqueous misdirection) -- atropine, surgical revision
3. Incomplete iridectomy with pupil block
117
What are the clinical features of acute angle closure glaucoma?
corneal oedema
mid-dilated fixed pupil
shallow anterior chamber
Also:
IOP often >40–60 mmHg
ciliary injection
reduced vision
118
What are the investigations of acute angle closure glaucoma?
Gonioscopy ⭐ (gold standard)
closed angle
PAS
plateau iris configuration
Anterior segment OCT
angle narrowing
iris configuration
Optic nerve assessment
cup:disc ratio
RNFL OCT
visual fields
(if chronic disease suspected)
119
What is the pathophysiology and causes of Axenfeld Reiger syndrome?
Usually autosomal dominant of PITX2 and FOXC1 --> These regulate neural crest migration → abnormal anterior segment development
Axenfeld anomaly: Posterior embryotoxon + iris strands
Rieger anomaly: Iris hypoplasia ± corectopia
Rieger syndrome: Ocular features + systemic abnormalities
120
What are the clinical features of Axenfeld Reiger syndrome?
1. Posterior embryotoxon ⭐ (most common sign)
Prominent anteriorly displaced Schwalbe’s line
white peripheral corneal ring on slit lamp
(Can also be present in normal individuals (~10–15%)
2. Iris strands to Schwalbe’s line
bridging processes from iris to angle structures on gonioscopy
3. Iris hypoplasia ⭐
stromal thinning
corectopia (eccentric pupil)
polycoria (multiple pupil openings)
4. Angle dysgenesis
abnormal trabecular meshwork
anterior iris insertion
peripheral anterior synechiae
Leads to glaucoma risk.
5. Glaucoma ⭐
≈50% of patients
trabeculodysgenesis ± PAS
Systemic features (Rieger syndrome)
- Microdontia (missing small peg teeth)
- maxillary hypoplasia
- umbilical hernia
- cardiac/hearing/skeletal/pituitary abnormalities
121
What are the differentials of a patient with Axenfeld Reiger?
1. Peters anomaly: Central corneal opacity
(Lens–cornea adhesions)
2. ICE syndrome: Unilateral (Adult onset)
Endothelial abnormality
3. Aniridia: PAX6 mutation, Almost absent iris, Foveal hypoplasia
4: Primary congenital glaucoma, Buphthalmos, Haab striae
No iris strands
122
What are the investigations for a patient with Axenfeld Reiger syndrome?
Gonioscopy ⭐: iris strands, anterior iris insertion
PAS, angle dysgenesis
IOP measurement
Optic nerve assessment
disc exam
OCT RNFL
visual fields
Pachymetry
For glaucoma interpretation
Genetic testing: PITX2, FOXC1 mutations
Systemic assessment
Refer: dentistry, paediatrics, genetics, endocrinology (if indicated)
123
What is the management of axenfeld reiger syndrome?
Conservative: Contact lenses, observe
Surgical:
Usually glaucoma management --> require trabeculectomy
glaucoma drainage devices
Angle surgery less effective than in PCG
Consideration of iridoplasty/pupilloplasty, artificial iris implantation
124
What are the pathophysiology/causes of Aniridia?
PAX6 gene
Controls development of:
iris, cornea, lens, retina, optic nerve, anterior chamber angle
So disease affects entire eye
PAX6 + WT1 genes
Associated with:
WAGR syndrome
Wilms tumour
Aniridia
Genitourinary anomalies
Range of intellectual disability
Requires urgent screening
125
What are the ocular features of aniridia?
Iris hypoplasia
Foveal hypoplasia
Optic nerve hypoplasia
Keratopathy
Cataract
Glaucoma
126
What are the differentials of a patient with aniridia?
Aniridia:
ICE syndrome: Unilateral, adult onset, abnormal corneal endothelium
Rieger syndrome: Posterior embryotoxon, corectopia
dental abnormalities
Surgical/traumatic iris loss
127
What are the investigations of a patient with aniridia?
OCT macula: foveal hypoplasia
OCT RNFL: Baseline glaucoma monitoring
Gonioscopy: angle dysgenesis, PAS
IOP measurement
Lifelong monitoring required
Corneal assessment: limbal stem cell deficiency, pannus, vascularisation
Systemic investigations: Renal ultrasound to screen for Wilms tumour
128
What are the indications for a primary tube?
ABAD U CANT BLEB
A: Aphakia/Pseudophakia: ACIOL/vitrectomised eyes
B: Burns/Conjunctival scarring: Trauma/cicatricial
A: Angle closure: Extensive PAS
D:
U: Uveitic glaucoma: Inflammation --> bleb fibrosis
C: Corneal graft
A: Aniridia/anterior segement dysgenesis
N: Neovascular glaucoma: fibrosis
T: Trab failed previously
B: Babies: Paediatric/Congenital glaucoma
L: Lens related glaucoma (aphakic glaucoma)
E: ICE syndrome (progressivve PAS formation)
B: Bandage contact lens wearers, young patients, immunosuppressed patients
129
What are the indications for primary trab?
1. POAG
2. NTG
3. PXF
4. PDS
5. PACG after iridotomy/cataract surgery
PART 2 ORAL
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