1
Q
How is aqueous produced
A
produced from plasma by ciliary epithelium of ciliary body pars plicata, using active and passive secretion.
2
Q
where does the aqueous outflow into
A
-trabecular meshwork 90% has 3 components
uveal meshwork (innermost portion), corneoscleral meshwork (middle portion just behind uveal), juxtacanalicular (cribriform) meshwork (outermost portion)
-Schlemm canal
3
Q
Which part of the trabecular meshwork has greatest resistance to flow of aqueous
A
corneoscleral meshwork
4
Q
What are the three exit routes for aqueous
A
-trabecular outflow (90%) through trabecular meshwork into Schlemm canal and episcleral veins
-uveoscleral drainage (10%) - suprachoroidal space
-iris
5
Q
What kind of variation is seen with IOP
A
Diurnal
Highest in morning, low in afternoon/ evening
6
Q
What is OHT
A
Estimated 4-7% population over 40 years have IOP >21mmHg with open filtration angles and without glaucomatous nerve damage.
7
Q
What percentage of OHT people will develop glaucoma over 10 year period
A
1 in 10 (10%)
8
Q
What did the OHTS study look at
A
Effect of treatment of individuals with OHT (Iop in one eye 34-32) including risks for conversion to glaucoma
9
Q
What were the limitations of the OHTS
A
Study goal was IOP reduction of 20% which may not be sufficient in some people
compliance with medication not measured, so some patients may already have had early glaucomatous nerve damage
10
Q
What conclusions were derived from OHTS based on factors that were significant on multi variate analysis
A
IOP- risk of glaucoma increases as IOP increases
Older Age increases risk of glaucoma
CCT greatest in OHT and CCT <555 microns and lower in eyes CCT >558
Higher the C/D ratio-> greater the risk
Higher the PSD value greater the risk- signifies early glaucoma damage
African racial background associated higher glaucoma risk
Males more likely to convert
Heart disease significant risk factor
Myopia, Diabetes, Family history of glaucoma
11
Q
What were the conclusions of OHTS
A
Early treatment reduces cumulative index of glaucoma
Effect is greatest in high risk individuals
Early treatment of low risk individuals not needed
Individualised assessment of risk is useful and helps guide management
12
Q
What are the genetics of OHT
A
Single nucleotide polymorphism TMC01 associated with conversion to glaucoma in white people people with OHT
13
Q
What is pre perimetric glaucoma
A
refers to glaucomatous damage usually manifested by suspiscious disc and or presence of RNFL defects in which no VF abnormality developed.
14
Q
What field test is used for the purpose of detecting pre perimetric glaucoma
A
standard achromatic automated perimetry
15
Q
What was the rate of OHT conversion to glaucoma in the OHTS
A
9.5% cumulative risk in developing POAG in 5 years. Treatment which aimed to reduce IOP by 20% or more to reach 24mmHg or less reduced this to 4.4%
16
Q
What is the definition of glaucoma
A
a term to describe conditions that have in common a chronic progressive optic neuropathy resulting in characteristic morphologival changes at the ONH and in RNFL. Progressive retinal ganglion cell death and VF loss associated with these changes. IOP key modifiable factor
17
Q
What did the EMGT (early manifest glaucoma trial) show
A
provides prospective natural history data on progression of glaucoma in 3 glaucoma types: high tension glaucoma, normal tension glaucoma, pseudoexfoliative glaucoma using changes in VF and optic disc as end points. Without IOP reduction, the mean rate of change is as follows
HTG -1.31dB/year, NTG -0.36dB/year, PXEG -3.13dB/year
18
Q
What are the features of POAG
A
RNFL thining,
GON damage,
VF loss as damage progresses
Open Anterior chamber angle
Absence of signs of secondary glaucoma/ non glaucoma cause for ON
IOP key modifiable risk factor
19
Q
What is the prevalence of POAG in patients over 70 years old
A
White- 6%
Black- 16%
Asian- 3%
20
Q
What are the risk factors for POAG
A
High IOP, asymmetry of IOP 4mmHg, Age- older, Race- 4x/ common in black people, FH of POAG - 4x sibling risk, 2x to offspring, Diabetes mellitus, Myopia, AntiVEGF therapy- sustained IOP elevation- likely to need glaucoma surgery after 6 IVT, Systemic CCB, Vascular disease- poor ocular perfusion risk factor, translaminar pressure gradient- difference in IOP and orbital CSF pressure increase likelihood of development and glaucoma progression. Large discs more vulnerable. Ocular perfusion pressure- difference betweena rterial BP and IOP shown to increase risk for development and progression of glaucoma. Low OPP increase risk
21
Q
What genetic mutation is associated with POAG
A
POAG associated with 127 loci- MYOC gene mutation- protein myocillin in trabecular meshwork and OPTN gene for optoneurin accepted as causing glaucoma.
22
Q
If a single family member develops glaucoma prior to age 35 years, what are the chances of a mutation in the myocilin gene
A
33%
23
Q
What are the 3 proposed mechanisms for GON and retinal ganglion cell death
A
direct mechanical damage to RNFL fibres at ONH- as they pass through lamina cribrosa
Ischaemic damage- due to compression of blood vessels supplying ONH. Relate to OPP as a risk factor for glaucoma
Common damage pathways- both mechanisms lead to reduction in axoplasmic flow, interference with delivery of nutrients or removal of metabolic products, oxidative injury and initiate immune mediated damage
24
Q
What is the ISNT rule
A
inferior rim broadest, followed by superior, nasal, tempora. High sensitivity for glaucoma 81% but not specific 32% i.e eyes without glaucoma often do not respect the rule
25
What sort of C/D ratio assymetry is significant between both eyes
0.2 or more
26
In which type of glaucoma are large discs more likely to sustain damage and why
NTG- result of larger diameter conferring relative mechanical weakness and greater vulnerability to IOP induced displacement of lamina cribrosa which is thinner in eyes with NTG
27
What is a normal median vertical diameter for non glaucomatous discs in the white population
1.5-1.7mm
28
What are the 4 morphological glaucomatous disc appearances that have been described
-focal ischaemic discs- localised superior/ inferior notches
-myopic discs with glaucoma- tilted (oblique inserted) shallow disc with temporal crescent of PPA with features of glaucomatous damage
-Sclerotic discs- shallow saucerized cup gently sloping NRR, variable PPA and peripheral visual field loss
-Concentrically enlarging discs characterised by fairly uniform NRR thinning associated with diffuse VF loss.
29
What are the correction factors for estimating ODD with the various lenses
Volk 60D- 0.88-1x
Nikon 60D- Around 1.0
Volk 90D- X1.3
Volk 78D- X1.1
Goldmann 3 mirror- X1.27
30
What are some non specific signs of glaucomatous nerve damage
disc haemorrhage
baring of circumlinear blood vessels- sign of early thinning of NRR
Bayonetting- double angulation of blood vessel
Collaterals between 2 veins at disc
Loss of Nasal NRR- moderately advanced damage
Lamina dot sign- advancing glaucoma- grey dot like fenestrations in lamina cribrosa become exposed as NRR recedes.
Sharpened edge/ rim advancing damage
31
What is the difference between alpha PPA and beta PPA
Alpha (outer zone) superificial retinal pigment epithelial changes- larger and more common in glaucomatous eyes
Beta (inner zone) chorioretinal atrophy. Distinct from scleral rim. Beta zone larger and more common in glaucoma risk factor for progression
32
What is the retinal arrangement of the 1.2 million ganglion cells as they go to the ONH
fibres from macula- straight course to ONH (spindle shaped papillomacular bundle)
Fibres from nasal retina- straight course to ONH
Fibres arising temporal to macula- arcuate path around papillomacular bundle to reach ONH. Dont cross horizontal raphe which extends from foveola to temporal retinal periphery which demarcates superior and inferior halves of retina
Arcuate fibres reaching superotemporal and inferotemporal aspect of ONH most vulnerable to glaucomatous damage. Fibres in papillomacular bundle most resistant
33
Within the ONH, how are the retinal fibres arranged as they go into the brain
Fibres from peripheral fundus- deep within RNFL but occupy superficial peripheral portion of ON
Fibres arising near to ON lie superficially within RNFL (near vitreous) but deep central part of ON
34
At what distance from the scleral spur is Angle opening distance measured
500 microns
35
What are some tests used in combination to look for glaucoma
Pachymetry
Stereo disc photography
UBM
OCT anterior segment
AC depth measurement
OCT posterior pole
Confocal scanning laser ophthalmoscopy
Scanning laser polarimetry
36
What are some early VFD in glaucoma
increased response variability in areas with defects and slight asymmetry between 2 eyes. SAP is insensitive in early glaucoma, SWAP is better for early changes
- Small paracentral depressions superonasally- NTG
- Nasal step
- Temporal wedge
- Arcuate defects coalescence of paracentral scotomas
- Ring scotoma superior and inferior arcuate scotoma continuous
37
What are some VFD in End stage glaucoma
small island of central vision accompanied by temporal island. 10-2 pattern helps monitor this.
38
What are the minimal criteria for glaucomatous damage on SAP
- GHT outside normal limits on 2 consecutive occasions.
- Cluster of 3 or more non edge points in a location typically for glaucoma which are depressed on PSD at P< 5% level and one depressed at P<1% level on 2 consecutive occasions
- Corrected PSD that occurs in <5% of normal individuals on 2 consecutive fields
39
What is the staging to determine early, moderate and severe glaucoma loss on field
Early - MD <-6dB
Moderate- MD -6 to -12dB
Severe >-12dB
Any absolute defect 0dB in central 5 degrees is considered severe
40
What does the pattern ERG measure
macular ganglion cell function. Objective measure of retinal function
41
What does the pERG waveform consist of
small negative deflection near 35ms (N35 component), positive deflection near 50ms (P50 component) and positive deflection near 95ms (N95 component). N95 component reduced in glaucoma.
42
What is a reasonable IOP target to aim for when lowering IOP in glaucoma and what study shows this
<18mmHg
Advanced Glaucoma Intervention Study (AGIS)
43
What are the factors of progression risk as found in the EMGT study
magnitude of initial IOP reduction
Height of baseline IOP
Presence of PXF syndrome
Presence of bilateral disease
Worse MD
Older age
44
What did the LIGHT trial show with regards to SLT
SLT reduced progression of visual field rates, improved QoL compared to medications. SLT is now first line for newly diagnosed OHT/ POAG.
SLT group patients less likely to show disease progression and less likely to require trabeculectomy/ phaco IOL 6 years after diagnosis
45
What % reduction of IOP is achieved generally with Phaco IOL
15%
46
What are the features of NTG
IOP consistently equal to or less than 21mmHg on diurnal testing
Signs of optic nerve damage in characteristic glaucomatous pattern
VF loss as damage progresses consistent with nerve appearance
Open AC angle
No features of secondary glaucoma/ non glaucomatous cause for neuropathy
47
What is the pathogenesis of NTG
Similar risk factors as POAG.
Other factors are to do with vascular supply, structural optic nerve anomalies and autoimmune disease. NTG in some patients explained by very low CCT. Overall this is lower compared to POAG. Others have marked nocturnal IOP spikes, sometimes only detected in supine position
48
What are some risk factors for developing NTG
Older age
High female prevalence
Japanese race
FH of POAG. Mutations in OPTN gene
Lower CCT
Abnormal vasoregulation- migraines, Raynauds, other cardiovascular risk factors important
Systemic Hypotension- nocturnal BP dips of >20%. EMGT shows low BP risk factor for NTG patients
OSA
Autoantibody levels higher in NTG
Low serum retinol levels
Translaminar pressure gradient- larger than POAG
Ocular perfusion pressure- lower than POAG
Myopia- greater glaucoma likelihood and progression
TED more common
49
What are the differential diagnoses for NTG
Angle closure
Low CCT
POAG
Previous raised IOP due to ocular trauma/ uveitis/steroid therapy
Spontaneously resolved pigmentary glaucoma
Myopic degeneration, Optic disc drusen
Congenital disc anomalies- disc pit/ coloboma
Neurological lesions
Previous AION
Previous acute optic nerve insult eg hypovolemia, septicaemia, head injury
Inflammatory/ infiltrative/ drug induced can masquerade as NTG
50
What are the differences between visual field defects in NTG vs POAG
Closer to fixation, steeper and more localised. In more than half of these patients, changes are non progressive over 5 years without treatment.
51
What are the indications for neuroimaging in NTG patient
Loss of VA out of proportion to cupping
Loss of colour vision on Ishihara testing
VF not consistent with RNFL dropout
Pallor of NRR of disc
Rapid progression despite normal pressure
52
How is NTG treated
encourage regular exercise. Avoid head stands
Prostaglandins initial tx. Brimonidine has neuroprotective effect in addition to IOP lowering. Topical beta blockers used with caution
SLT- reasonable option
Surgery if progression despite IOP in low teens. Control of systemic vascular disease. Systemic CCB for vasospasm.
Sleep in head up position as IOP higher in flat position than 30 degree head up position. Ginkgo biloba may have benefit
53
What does the term angle closure mean
occlusion of trabecular meshwork by peripheral iris (ITC) obstructing aqueous outflow.
54
Where is the ITC narrowest
superiorly
55
What is the Shaffer method for grading angle width
Grade 0- closed due to ITC
Grade 1 (10 degrees)- very narrow angle only Schwalbe line and top of trabeculum identified
Grade 2 (20 degrees)- angle in which trabeculum but not scleral spur seen
Grade 3 (25-35 degrees)- open angle scleral spur seen
Grade 4 (35-45 degrees)- widest angle, myopia and pseudophakia. CB visualised without lens tilt
56
How to distinguish appositional from synechial angle closure
indentation
57
How is the Spaeth system used to measure angle grading
description of iris insertion, angular approach and peripheral iris curvature
58
How is the Scheie classification used to measure angle grading
angle structures visible and allocates a Roman numeral accordingly. Higher Roman numeral signifies narrower angle
59
What are the features of PACS (primary angle closure suspect)
axial AC depth less than normal- eclipse sign
Gonio shows posterior meshwork ITC in 3 or more quadrants but no PAS
Gonio shows 2 quadrants of ITC and signs of intermittent angle closure like pigment smudging
Normal IOP, optic disc and field
No PAS
Ant Seg OCT shows occludable angle
Risk of developing Angle closure disease in individuals classified as PAC suspects is low
60
What are the features of Primary Angle Closure (PAC)
Gonio shows 3 or more quadrants of ITC associated with raised IOP and or PAS seen on indentation gonioscopy
Normal ON, field
Some classify into ischaemic and non ischaemic. Ischaemic shows evidence of prior IOP elevation like iris change or glaucomflecken
61
What are the features of Primary Angle Closure Glaucoma (PACG)
ITC in 3 or more quadrants with GON
ON damage from episode of severe IOP elevation eg acute angle closure, may not appear as typical glaucoma cupping
62
What are some mechanisms of angle closure
-Relative pupil block
-Non pupillary block- asian patients with plateau iris - not fully resolved by iridotomy
-Lens induced angle closure- intumescent lens, phacomorphic
-Retrolenticular- malignant glaucoma ciliolenticular block
-Combined mechanism
-Reduced aqueous outflow - appositional obstruction by iris, TM degeneration, permanent occlusion of TM By PAS
63
What is plateau iris configuration
flat or only slightly convex central iris plane with normal or slightly shallow central AC depth. Angle recess very narrow with sharp backward iris angulation over anterior positioned and or oriented ciliary processes. 'double hump' sign seen on indentation gonioscopy. Central hump due to underlying central lens supporting iris and peripheral hump from underlying ciliary process
64
What is plateau iris syndrome
persistence of gonioscopic angle closure despite patent iridotomy in patient with morphological plateau iris. Divided into complete form which occlusion of functional TM is present and IOP elevation and incomplete form with occlusion to lesser extent and normal IOP
65
What are the risk factors for angle closure
Age - average 62
Females
Far eastern and indian asians- non pupillary block more significant
Family history- genetic factors
Refraction- hypermetropic eyes.
Shorter AL- Nnanophthalmic eyes <20mm AL high risk
66
What are the signs of Resolved APAC
Early: low IOP (ciliary body shutdown and treatment effect), DM folds if IOP reduced rapidly, ON head congestion ,choroidal folds.
Late: iris atrophy spiral like configuration, glaucomflecken (white foci of necrosis in superficial lens), cataract, posterior synechiae, pale/ glaucomatous optic nerve.
67
What are some provocative tests for PAC
Pharmacological mydriasis- poor discrimnator small risk of APAC in patients without PI
Dark room/ prone provocative test (DRPPT), patient sits in a dark room face down 1 hour without sleeping. IOP checked before and immediately after test. IOP rise 8mmHg or more is significant.
68
Differential diagnosis of acute IOP elevation
lens induced angle closure
malignant glaucoma
NVG
Hypertensive uveitis
Scleritis
PDS/ PXF
Orbital/retro orbital lesions
69
What is the initial treatment for APAC
Lie supine
Diamox 500mg IV if IOP >50 and PO if <50. Contraindication is sulfonamide allergy/angle closure secondary to topiramate/ other sulfonamide derivatives
Apraclonidine 0.5%/ 1%. Timolol 0.5%, Prednisolone 1%. Pilocarpine repeated after 30 mins. Dont repeat if IOP still >40 as ischaemia may compromise action
Analgesia, antiemetic
70
What is the management for treatment resistant APAC
- central corneal indentation with squint hook/ goniolens force aqueous into angle. Epithelial oedema cleared with 50% topical glycerol
- Mannitol 20% 1-2g/kg IV over 1 hour.
- Early PI after corneal oedema cleared with glycerol
- Paracentesis effective but risk of lens damage
- Surgical options PI/ Lens extraction/ Goniosynechiolysis, Trabeculectomy, cyclodiode
71
What were the conclusions from the Zhongshan Angle Closure prevention trial (ZAP)
Laser PI small prophylactic effect over 6 year period, only offered to those with highest risk of developing APAC/ Chronic angle closure glaucoma
72
What are the PACS Plus criteria
symptoms of previous intermittent angle closure
systemic medication with atropine like structure which may provoke pupil block
need for frequent dilations eg diabetes/ AMD
When the health/ occupation of person makes it difficult for them to access care
73
What to do next if there is significant ITC despite iridotomy
Observation (most)
Laser iridoplasty
long term pilocarpine prophylaxis
If symptomatic cataract present, lens extraction opens angle. If IOP elevated by definition PAC is present
74
What is the management of PAC and PACG
Same as PACS but lower threshold for further intervention if angle widening is inadequate after iridotomy if IOP remains elevated
- Trab + MMC an option but may result in malignant glaucoma
- phaco IOL is good option
75
What were the findings of the EAGLE study
clear lens extraction with IOL implantation shows greater efficacy and more cost effective than LPI in patients with PAC + IOP >29 or in patients with PACG
76
What are some causes of secondary open angle glaucoma
pre trabecular- NVG/ ICE syndrome/ epithelial ingrowth
Trabecular- pigmentary glaucoma, red cell glaucoma, ghost cell glaucoma, phacolytic glaucoma, proteins in hypertensive uveitis, PXF material, Trabeculitis or scarring after angle recession
Post trabecular-carotid cavernous fistula, Sturge Weber, SVC obstruction
77
What are some causes of secondary closed angle glaucoma
With pupil block- seclusio pupillae recurrent iridocyclitis, subluxated lens, phacomorphic glaucoma, capsule block syndrome with 360 iris capsule adhesion in pseudophakic eye, aphakic pupillary block, AC IOL without PI
Without pupil block- secondary PAS causes eg NVG/ CAU, ciliochoroidal effusion, posterior segment tumour, malignant glaucoma
78
What is the commonest cause of secondary open angle glaucoma
Psuedoexfolation syndrome (PXS)
79
What is the incidence of glaucoma PXG at diagnosis of PXS and what is the cumulative risk of eyes with PXS needing glaucoma treatment at 5 years
15-30% incidence
60% at 5 years
80
what is the pathogenesis of PXS
PXF material grey white fibrillary substance from abnormal ECM metabolism in ocular/ other tissues. Deposited on lens capsule/ zonules, iris, trabeculum, conjunctiva.
81
What SNP mutation is found in PXS
SNP mutations in LOXL1 gene on chromosome 15 coding for enzyme cross linking tropoelastin and collagen and important for formation /maintenance of elastic fibres and ECM.
82
What plasma and aqueous level is high in PXS
Homocysteine levels and inadequate folate intake may be a risk factor
83
What are the signs of PXS
PXF material on cornea- Krukenburg spindle. Endothelial cell count lower than normal.
AC- PXF material particles seen. Mild aqueous flare from impaired blood aqueous barrier can be seen
Iris- granular PXF material deposits, pupillary ruff loss, patchy transillumination defects at pupil margin,
Anterior lens capsule shows PXF material ( Xmas tree like deposits)
AC angle- patchy trabecular/ schwalbe line hyperpigmentation is common inferiorly, Sampaolesi line anterior to schwalbe line seen. Risk of angle closure due to zonular laxity.
84
What is the prognosis for PXG
Worse than POAG- IOP higher and marked fluctuation. Severe damage may be seen at presentation. Monitor at no later than 6 month intervals
85
What are some systemic manifestations of PXS
High tone hearing loss
Ischaemic cardiovascular/ Cerebrovascular disease, increased risk of pelvic organ prolapse in older women
86
What is the treatment for PXG
Medical -similar to POAG but failure more common
SLT- more effective than POAG with mean reduction 30% after. Significant rise may occur 2 years after SLT
Phaco alone may lower IOP but better control with trabeculectomy. Filtration surgery has similar success to POAG, Trabecular aspiration seems to confer short term benefit
87
What is PDS
Liberation of pigment granules from iris pigment epithelium and deposition throughout the anterior segment. Secondary Pigmentary glaucoma is common. PDS and PG common in males- myopic.
88
What % of patients with PDS develop elevated IOP at 15 years
15
89
What is the pathogenesis of PDS/PG
Pigment shedding precipitated by rubbing of posterior pigment layer of iris against zonules due to posterior bowing of mid peripheral iris. Increased AC pressure relative to posterior chamber due to reverse pupil block. PI flattens the iris and decrease iridozonular contact. Acute IOP elevation due to trabecular obstruction by released melanin granules. Chronic elevation due to pigmentary obstruction of intertrabecular spaces and damage to TM due to denudation ,collapse and sclerosis
90
What signs can be seen in PDS and PG
Krukenberg spindle
AC deep, melanin granules in aqueous
Iris radial spoke like transillumination defects in lighter irides. Partial loss of pupillary ruff
Angle open and mid peripheral iris concavity where iris bows backward. TM heavily pigmented in all 4 quadrants. Pigment may be seen on or anterior to Schwalbe line. Pigment granules on the anterior lens capsule. May be a line Scheie stripe or Zentmayer ring on peripheral surface around zonule insertions
91
What should the follow up be like for PDS/ PG
PDS- yearly
if glaucomatous atrophy present- monitor at 4-6 month intervals as myopia and PDS combination lead to rapid visual function deterioration
92
How to treat PDS/ PG
Lifestyle- excessive exercising cause increased pigment dispersion, reduce this
Medical similar to POAG. Miotics are of benefit as they reduce iridozonular contact and increase aqueous outflow. Can make myopia worse.
SLT- effective careful with power. Treat only 2 quadrants
Laser PI- reverse iris concavity eliminate iridozonular contact.
Filtration surgery- adjunctive antimetabolites improves outcomes. Post op hypotony and suprachoroidal haemorrhage commoner in myopic and younger patients
93
What is the pathogenesis of NVG
Aggressive iris neovascularization (rubeosis) which leads to progressive angle closure and glaucomatous atrophy. Common factor is severe diffuse and chronic retinal ischaemia. Upregulation of Anti VEGF
94
What are the causes of NVG
Ischaemic CRVO- 35 to 50% cases. VA 6/60, RAPD, Extensive dropout on FFA risks. Glaucoma occurs 3 months after onset but intervals 4 weeks to 2 years documented.
Diabetes Mellitus- Risk decreased by PRP.
Arterial retinal vascular disease like CRAO / OIS
Intraocular tumours, longstanding RD, chronic intraocular inflammation
95
What are the clinical signs/ symptoms of NVG
None to severe pain, decreased vision, photophobia, corneal oedema when raised IOP, Advanced disease hypotony may supervene, AC flare/cells/PS/AC haemorrhage may happen. Pupil margin subtle vessels may be seen. NVI grow radially over iris towards angle. IOP can still be normal at this stage. Gonioscopy shows NV tissue proliferating across face of the angle. Cataract common once ischaemia established. GON present
96
What factors predict a poor visual outcome in NVG
Young age
VA <6/60
IOP >35 on presentation
97
How is NVG treated
frequent reviews
Medical treatment for IOP as POAG. Avoid miotics. PRP effective for NV regression. IVT AntiVEGF eg Avastin if fibrovascular angle closure not happened yet. AC injection alternative route for AntiVEGF. RD repair once IOP controlled if TRD involving macula present. Ciliary body ablation Cyclodiode if medical IOP control impossible. Risk of hypotony. Filtration surgery- if VA HM or better. artificial shunt (GDD)/ Trab + MMC/ shunt/ 5-FU. PPV with endolaser if vitreous haemorrhage in CRVO. Enculeation/Evisceration last resort
98
What is the prognosis of NVG
Be realistic with patients. Best outcome blind but comfortable eye. Prevalence of blindness in affected eye varies from 25-50% depending on f/u length. Life expectancy reduced significantly in patients. Good presenting VA useful predictor for long life expectancy
99
What are the commonest causes of secondary inflammatory glaucoma
Fuchs uveitis syndrome
Chronic anterior uveitis associated with JIA
Posterior uveitis affects aqueous outflow pathway and lead to IOP elevation
100
How does angle closure with pupillary block happen in inflammatory glaucoma
360 degree posterior synechiae causing seclusio pupillae and anterior bowing of iris to block angle and raise IOP
101
How does angle closure without pupillary block happen in inflammatory glaucoma
chronic anterior uveitis cause deposition of inflammatory cells and debris in the angle with subsequent organization and contraction pulling peripheral iris over trabeculum leading to gradual progressive synechial angle closure.
Gonio shows PAS with deep AC
102
How does secondary open angle glaucoma happen in acute anterior uveitis
trabecular obstruction by inflammatory cells and debris causing increased aqueous viscosity, due to leakage of protein from inflamed iris blood vessels
Acute trabeculitis involving inflammation and oedema of trabecular meshwork with secondary dimunition of inter trabecular porosity causing reduced outflow facility.
103
What are the causes of acute trabeculitis
herpes zoster
herpes simplex
other viral anterior uveitides
toxoplasma retinitis
104
How does secondary open angle glaucoma happen in chronic anterior uveitis
trabecular scarring and or sclerosis secondary to chronic trabeculitis. Most have some degree of synechial angle closure. Sometimes gelatinous exudate is seen on trabeculum
105
What is the treatment for inflammatory glaucoma
Medical control of IOP- beta blocker first choice. Prostaglandin analogues avoided as promote inflammation. If IOP >35 add PO Diamox. Miotics contraindicated as increase vascular permeability promote PS formation.
Laser PI-if pupil block angle closure, likely to block up and intense steroids needed. Surgical iridectomy may be needed.
Glaucoma surgery once control for at least 3 months achieved. Preop and post op steroid. Consider oral steroid 0.5mg/kg/day. Trab + MMC/ tube is choice.Cyclodiode with caution as may exacerbate inflammation. Risk of profound hypotony
106
What is Posner Schlossman syndrome (PSS)
Recurrent attacks of unilateral acute raised IOP associated with mild AU. Acute trabeculitis evidence of possibly CMV/ H pylori. Risk of chronic IOP elevation.
107
What is the treatment for Posner Schlossman syndrome
topical steroids for inflammation control with aqueous suppressants to lower IOP. Trabeculectomy + MMC may be needed if GON/ progressive field loss
108
What is the pathogenesis of steroid induced glaucoma
increased resistance to outflow of aqueous due to altered ECM function or endothelial cells of TM. Usually occurs 2-4 weeks after commencement of treatment.
109
What are the risk factors for steroid induced glaucoma
Established glaucoma/OHT
FH of glaucoma
High Myopia
Young age/ childhood
CTD - RA
110
What is the treatment for steroid induced glaucoma
Discontinue- IOP becomes normal within days in acute form. Chronic form 1-4 weeks
Less potent steroid drop used eg FML 0.1%, Loteprednol
3% cases- IOP may still be elevated after stopping all drops, seen in patients with FH glaucoma
Persistent IOP elevation maanged with medication/ glaucoma surgery
111
What is Phacolytic glaucoma
Secondary open angle glaucoma associated with hypermature cataract. Trabecular meshwork obstruction caused by high molecular weight lens proteins leaking through intact capsule into aqueous. Macrophage containing lens proteins may contribute.
112
What is the treatment for phacolytic glaucoma
After medical IOP control, proteinaceous material washout from AC, cataract removed. Care taken not to rupture the zonule
113
What is pathogenesis of phacomorphic glaucoma
Acute secondary angle closure glaucoma precipitated by intumescent cataractous lens. Equatorial age related lens growth slackens suspensory ligament causing lens to move anteriorly. Associated AP growth cause increased iridolenticular contact, pupil block and iris bombe
114
What is the treatment for phacomorphic glaucoma
Medical treatment similar to APAC. Miotics omitted as increase iris- lens apposition and shift lens anteriorly. Dilation sometimes help but with caution. Systemic hyperosmotic agents may be more helpful. Laser PI useful but difficult due to corneal oedema/AC depth. Laser iridoplasty useful temporizing measure, cataract extraction helps.
115
A hyphaema involving less than half the anterior chamber is associated with what % incidence of complications and final VA better than 6/18
20%
116
When is the rebleeding risk highest after the first bleed in traumatic hyphaema
3-5 days after initial injury.
117
Why are patients with sickle cell higher risk for complications like IOP elevation after traumatic hyphaema
IOP elevation due to trabecular meshwork obstruction by deformed red cells and vascular occlusions
118
How is traumatic hyphaema treated
Coagulation bloods exclude haemoglobinopathy. Anticoagulants discontinued. NSAID avoided for analgesia. Hospital admission for large hyphaema. Strict bed rest elevated/ semi upright position. Protective eye shield worn.
Topical prostaglandins/ beta blockers/ topical/ systemic CAI depending on IOP. CAI NOT used in sickle cell. Miotics avoided increase pupil block, disrupt blood aqueous barrier. Topical steroids good. Atropine achieve mydriasis reduce secondary haemorrhage. TXA in high risk cases with recurrent bleeding.
119
What are the indications for surgical hyphaema evacuation
Total hyphaema
IOP >50 for 2 days or IOP >35 for 5 days
120
What are the surgical benefits of hyphaema evacuation long term
risk of permanent corneal staining reduced
optic atrophy risk reduced.
Prevent PAS formation and chronic secondary glaucoma. Glaucoma Filtration device may be needed in some cases.
121
What is angle recession glaucoma and what is the mechanism of IOP rise
rupture of face of ciliary body portion between iris root and scleral spur due to blunt trauma
IOP rise secondary to associated trabecular damage rather than from angle recession itself. Risk of glaucoma related to extent of angle recession. If <3 quadrants recessed low risk of angle recession glaucoma
122
What does gonioscopy show in angle recession glaucoma
initially irregular widening of ciliary body band. Longstanding cases recession obscured by fibrosis and angle shows hyperpigmentation
123
How to manage angle recession glaucoma
2 or more quadrants of angle recession should have IOP check yearly
medical treatment is same as for other types of secondary open angle glaucoma. SLT no benefit. Trabeculectomy with MMC effective. Artificial shunt/ cyclodiode considered if trabeculectomy fails
124
What is the pathogenesis of ghost cell glaucoma
trabecular obstruction by degenerate erythrocytes causing raised IOP and rarely glaucoma. 2 weeks after vitreous haemorrhage, haemoglobin leaks from erythrocytes which evolve into ghost cells. They pass through anterior hyaloid defect into AC. These get entrapped within pores of TM, obstruct aqueous outflow.
125
When does ghost cell glaucoma occur (3 scenarios)
Cataract surgery in the context of pre existing VH
VH in aphakic/pseudophakic eye
When cataract surgery complicated by VH and hyphaema.
126
What are the clinical features of ghost cell glaucoma
cornea oedematous if IOP raised
AC ghost cells- reddish brown/ khaki particles in the aqueous. Not confused with leucocytes
127
What is the treatment for ghost cell glaucoma
Medical treatment with aqueous suppressants
Irrigation of AC with washing out of ghost cells if medical therapy fails
PPV- for persistent VH
128
What are the 3 presentations of ICE syndrome and what is the pathogenesis in ICE syndrome
-Chandler syndrome
-Progressive (essential) iris atrophy
-Iris naevus (Cogan Reese) Syndrome
abnormal corneal endothelial cell layer with prediliction for proliferation and migration across AC angle and onto iris surface with progression to glaucoma (50%) and corneal decompensation in a significant proportion. Glaucoma due to TM obstruction by proliferating tissue followed by angle closure secondary to contraction
129
What does PCR testing in ICE syndrome show
Herpes simplex viral DNA- possible viral aetiology
130
What are the features of Chandler syndrome
most common
abnormal corneal endothelial appearance said to resemble hammered silver
present with blurry vision and haloes due to corneal oedema. Iris atrophy absent in 60% rest variable. Corectopia mild- moderate. Glaucoma less severe than the other 2 ICE counterparts
131
What are the features of progressive (essential) iris atrophy
iris changes corectopia (pupil malposition), iris atrophy in early stage, pseudopolycoria (supernumerary false pupil) and broad based PAS extending anteriorly to Schwalbe line. Severe iris atrophy occurs in late stage associated with ectropion uvea and severe glaucoma
132
What are the features of iris naevus (Cogan Reese) syndrome
diffuse naevus covering anterior iris or by iris nodules. Iris atrophy absent in 50% cases and in remaineder mild- moderate. Corectopia may be severe. Appearance may be mimicked by diffuse iris melanoma
133
What is the treatment for ICE syndrome
Medical treatment ineffective
Trab + MMC tried but long term results poor
GDD or cyclodiode may be required
Corneal oedema- 5% NaCl and PKP later on
Poor prognosis long term
134
What are the causes of trabecular block glaucoma associated with intraocular tumours
angle invasion by solid iris melanoma
trabecular infiltration by neoplastic cells originating from iris melanoma
tumour seeding from retinoblastoma invade trabeculum
trabecular blockage by macrophages that have ingested tumour similar to phacolytic glaucoma (melanomalytic glaucoma)
135
What are the causes of secondary angle closure glaucoma associated with intraocular tumours
NVG commonest mechanism with choroidal melanoma/ retinoblastoma
Anterior displacement of iris- lens diaphgram in ciliary body melanoma or large posterior segment tumour
136
What is glaucoma secondary to epithelial ingrowth pathogenesis
rare but complication of anterior segment surgery or trauma when conjunctival/ corneal epithelial cells migrate through wound and proliferate in Anterior segment. IOP elevation by trabecular obstruction by one or more epithelial membrane, secondary PAS angle closure
137
What is iridoschisis
rare condition- both eyes affected in older patient. PAC and PACG in 90%. Intermittent iOP elevation results in iris atrophy severity ranging from stromal atrophy to fibrillar disintegration of anterior layer. Gonio shows occludable angle with PAS. Treat angle closure with Laser PI
138
What are the classification of primary congenital glaucoma
True congenital glaucoma 40% IOP elevated during intrauterine life
Infantile Glaucoma 55% manifests prior to age 3
Juvenile Glaucoma least common- IOP rise between 3-16 years age
139
What is the pathogenesis of primary congenital glaucoma
thought to be due to impaired aqueous outflow due to maldevelopment of anterior chamber angle (trabeculodysgenesis).
140
What mutations play a role in primary congenital glaucoma
Angiopoetin receptor TEK mutations transmitted as autosomal dominant pattern with variable expressivity
CYP1B-1 coding for cytochrome p450 and LTBP2- autosomal recessive
141
What are some signs of primary congenital glaucoma
Watering/ photophobia/ blepharospasm/ corneal haze (localised corneal oedema from raised IOP)/ Buphthalmos large eye due to stretching from raised IOP/ Haab striae (curvilinear healed breaks in DM)/ Corneal scarring and conv/optic disc cupping in infants may regress once IOP normalised
142
What are some examination findings under GA which may suggest primary congenital glaucoma
IOP measured first- 10 to 12 is normal. Optic disc asymmetry or C/D ratio >0.3 is suspiscious. Corneal diameter >12mm prior to age of 1 highly suspiscious. Increased AL measurement. >20.25 mm at 1 month abnormal.
Gonioscopy may reveal trabeculodysgenesis
143
What is the most reliable signs of IOP control after primary congenital glaucoma surgery
stabilisation of AL
144
How is primary congenital glaucoma treated
surgery always required- successful in 80-90% cases. Medication to supplement therapy.
- goniotomy- incision made at midpoint of trabecular meshwork
-trabeculectomy- if corneal clouding prevents view of angle and when repeated goniotomy has failed. Partial thickness scleral flap created and Harms trabeculotome inserted into Schlemm canal rotated into AC
- Modified trabeculotomy
-Tube shunt implant, cyclodiode
145
What are some differentials for congenital cloudy cornea
birth trauma
rubella keratitis (congenital rubella associated with congenital glaucoma)
Metabolic disorders like mucopolysaccharidoses and mucolipidoses
CHED
Sclerocornea
146
What are some differentials for congenital large cornea
megalocornea
high myopia
147
What are some differentials for congenital epiphora
delayed/failed canalization of nasolacrimal duct
lacrimation due to ocular irritation conjunctivitis, aberrant eyelashes, entropion
148
What are some examples of iridocorneal dysgenesis
Posterior embryotoxon
Axenfeld- Rieger syndrome
Peters Anomaly
Aniridia
149
What phacomatoses are associated with glaucoma
Sturge Weber syndrome
NF-1
150
What is posterior embryotoxon
prominent and anteriorly displaced Schwalbe line seen as thin grey white arcuate ridge adjacent to the limbus on inner surface of cornea. One of the features of Axenfeld- Rieger syndrome. Seen in Alagille syndrome with optic disc drusen
151
What is Axenfeld Rieger syndrome
umbrella term for spectrum of disorders featuring bilateral developmental ocular anomalies: Axenfeld anomaly, Rieger anomaly, Rieger syndrome. Caused by defective neural crest cell related processes during fetal development leading to incomplete development of TM or schlemm canal.
152
What are some genes associated with Axenfeld -Rieger syndrome
PITX2
PAX6
FOXC1
RIEG2
153
What is Axenfeld anomaly
posterior embryotoxon with attached strands of peripheral iris best seen with gonioscopy
154
What is Rieger anomaly
manifests with anterior segment appearance similar to ICE
Posterior embryotoxon
Iris stromal hypoplasia
Ectropion uveae
Corectopia and full thickness iris defects
155
What is Rieger syndrome
Rieger anomaly + extraocular malformations related to defective neural crest cells
- Dental anomalies- hypodontia and microdontia
- Facial anomalies maxillary hypoplasia, broad nasal bridge, telecanthus, hypertelorism
- redundant paraumbilical skin, hypospadias, hearing loss, hydrocephalus, cardiac, renal anomalies
156
What is Peter anomaly
Rare but severe condition bilateral due to defective neural crest cell migration during fetal development. Manifestations range from mild to severe.
157
What is the difference between Peter anomaly 1 and Peter anomaly 2
1- cornea affected alone
2- corneal and lens abnormalities
158
What are the clinical features of Peters anomaly
Central corneal opacity variable density
Posterior corneal defect involving posterior stroma, DM, Endothelium with or without iridocorneal or lenticulocorneal adhesions
Glaucoma in 50% due to associated angle anomalies. Prognosis worse than primary congenital glaucoma
Systemic associations craniofacial/ CNS anomalies. Peters plus includes systemic abnormalities
159
What is Aniridia and what genes are associated with it.
What other gene is next to it associated with tumour
rare bilateral condition- life threatening associations. Result of abnormal neuroectodermal development due to mutations in PAX6 gene. PAX6 is adjacent to WT1 mutation which if mutated leads to Wilms tumour
160
What are some features of autosomal dominant aniridia
2/3rd cases no systemic implications. Penetrance is complete (all patients with this genotype will have the phenotype) but expressivity variable
161
What are some features of sporadic aniridia
WARG- Miller syndrome (Wilms tumour, Aniridia, Mental Retardation, GUM anomalies) 1/3rd patients- children with sporadic aniridia have 30% chance of developing Wilms tumour
162
What are some features of Gillespie syndrome
1% cases. Inheritance AR. not caused by PAX6 mutations. Cerebellar ataxia and LD are features
163
What should the screening schedule with abdominal ultrasound in sporadic aniridia be
Abdominal USS every 3 months until 5 years age, every 6 months until 10 years then annually until 16 to detect Wilms tumour or until molecular genetic analysis confirms the absence of WT1 mutation
164
What are the signs in aniridia
typically at birth with nystagmus/ photophobia. Parents may notice absent irides/ large pupils. Variable aniridia from minimal, detectable on retroillumination to total absence. Lids show MGD, Cornea shows tear film instability, dry eye, LSCD cause conjunctivalisation of peripheral cornea. Total corneal central scarring/ vascularization.
Fundus shows foveal/ optic disc hypoplasia/ choroidal coloboma
Gonioscopy shows hypoplastic/ rudimentary frill of iris tissue
Lens changes- cataract/ subluxation
Glaucoma 75% present in late childhood, adolescence
165
What is the mechanism of glaucoma in aniridia
synechial angle closure secondary to contraction of rudimentary iris tissue.
166
How is Aniridia treated
medical treatment inadequate
trabeculectomy + MMC or combined trabeculectomy + trabeculotomy usually fails to control IOP. GDD offer best long term control
Diode laser last resort for IOP control.
Painted CL for artificial pupil. lubricants, cataract surgery, prosthetic iris implants , limbal stem cell transplant, refractive errors, amblyopia squint managed aggressively
167
What is Sturge- Weber syndrome (encephalotrigeminal angiomatosis)
congenital, sporadic phacomatosis. Glaucoma ipsilateral to facial haemangioma develops in 30% and in 60% of these IOP elevation occurs before 2 years result in buphthalmos.
168
What is the pathogenesis of glaucoma in Sturge Weber syndrome
trabeculodysgenesis in infants and raised episcleral venous pressure associated with arteriovenous communication in episcleral haemangioma in older patients
169
What is the treatment for glaucoma in Sturge Weber Syndrome
medical treatment alone inadequate
goniotomy in those with angle anomalies
combined trabeculectomy- trabeculotomy good results in early onset cases. High risk of choroidal effusion and suprachoroidal haemorrhage
170
What are some facts about NF1
Disorder affecting cell growth of neural tissues. Inheritance AD with irregular penetrance, variable expressivity. Glaucoma rare and when present is unilateral and congenital. 50% have ipsilateral plexiform neurofibroma of upper eyelid or facial hemiatrophy. Associated with ectropion uveae
171
How can systemic absorption of drops be minimised
closing eyes for 3 minutes reduce absorption by 50%, enhanced by applying digital pressure over lacrimal sac. Prolongs drug eye contact
172
How do prostaglandin analogue drops work and what is the percentage IOP reduction achieved with this
increase uveoscleral outflow. Achieve 27-35% reduction from baseline.
173
Can using more than one prostaglandin analogue rise IOP
yes
174
What is the first line prostaglandin analogue and what % show no response to this medication
Latanoprost.
5-10% show no response (IOP reduction less than 10%)- may respond to other prostaglandins
175
What is the side effect of bimatoprost
conjunctival hyperaemia. A new 0.01% prep has comparable IOP lowering effect with less hyperaemia.
176
What is Omidenepag 0.002% and what are its indications/ benefits
new selective E- prostanoid sy type 2 agonist used OD. Effective in patients that dont respond to Latanoprost- does not cause periorbitopathy. Hyperaemia in 5%
177
What are some side effects of prostaglandin analogues
conjunctival hyperaemia, eyelash lengthening, thickening, hyperpigmentation. Irreversible iris hyperpigmentation in 1/4 patients at 6 months. Periocular skin hyperpigmentation, periocular atrophy, preoperative PG agent use increase CMO risk after phaco IOL. Can promote HSK growth
Systemic side effects: headache, migraine, malaise, myalgia,, skin rash, mild URI
178
How do topical beta blockers work and what % reduction in IOP is seen with beta blockers
21-27% from baseline.
Decreased aqueous production mediated by effect on ciliary epithelium.
179
What are some side effects of topical beta blockers
risk of BP lowering at night reducing optic disc perfusion worsening glaucoma. Allergy, SPK, Bronchospasm, heart block, bradycardia, heart failure, hypotension, peripheral vascular disease and Raynauds use with caution. Sleep disorders, reduced exercise tolerance, headache, nausea, fatigue, alopecia - reversible
180
What are some advantages of betaxolol
lower hypotensive effect than timolol. Optic nerve blood flow may be increased due to CCB effect. Beta 1 selective so less likely to cause bronchoconstriction
181
What is a known side effect of metipranolol
granulomatous anterior uveitis
182
Which beta blocker has intrinisic sympathomimetic activity
Carteolol
183
How do CAI work and what is the dosing for CAI drops in glaucoma
inhibit aqueous secretion
TDS as monotherapy
BD as adjunctive
184
What are the advantages and side effects of CAI drops
neuroprotective effect
disadvantages- less effective than beta blockers, precipitate corneal decompensation with corneal endothelial dysfunction.
Contraindicated in patients with sulfonamide allergy
185
What are the differences between dorzolamide and brinzolamide in terms of side effects
Dorzolamide- stinging/ transient bitter taste. Allergic blepharoconjunctivitis may occur
Brinzolamide- similar to dorzolamide but less likely to cause stinging and local allergy. Suspension and white residue may be left on eyelids if excess not wiped away
186
How do alpha 2 agonists work
decrease aqueous synthesis via effect on ciliary epithelium and increase uveoscleral outflow
187
What are some benefits and side effects of alpha 2 agonists
neuroprotective effect
Crosses BBB used in caution with young children in whom severe CNS depression and hypotension can occur (contraindicated in <2 yo). May potentiate vascular insufficiency. Not be given with oral MOAI and antidepressants due to risk of hypertensive crisis
188
When is Apraclonidine used
prevent/ treat acute IOP rise following laser surgery on anterior segment. 0.5% used as temporizing measure over several weeks as patient awaits glaucoma surgery. Long term use causes tachyphlaxis
189
How do miotic drops work in glaucoma
they pull the peripheral iris away from the TM opening the angle. They also reduce IOP by contraction of ciliary muscle increasing aqueous ouflow through TM.
190
What are 2 new topical glaucoma drops and how do they work
Latanoprostene bunod 0.024%- reduce IOP significantly. Dual mechanism action. Latanoprost increases outflow via uveoscleral pathway. Butanediol mononitrate undergoes further metabolism to nitric oxide and enhances outflow via TM. Used OD and better than latanoprost.
Rho Kinase inhibitors (ROCK)- increase aqueous outflow via TM. Effective with Latanoprost Rocklatan
191
What are some ocular and systemic side effects of oral CAI
Ocular: choroidal effusion after cataract surgery, angle closure may result
Systemic: paraesthesia, hypokalemia, malaise, low mood, GI symptoms, renal stones, aplastic anaemia
192
How do osmotic agents work in glaucoma
lower IOP by creating an osmotic gradient so water is drawn out from vitreous into blood. Employed when short term IOP reduction is required eg resistant angle closure glaucoma.
193
What are some side effects of osmotic agents in glaucoma
cardiovascular overload due to increased Extracellular volume, urinary retention, headache, backache, nausea, confusion
194
What is the theory of how SLT works and what is the % IOP reduction with it
Not clear but stimulation of TM cell division, macrophage and ECM recruitment.
IOP 10-40% reduction can be expected after 6 months with 25% common.
195
What % of patients will achieve IOP fall in 6 months with 180 degree TM treatment in SLT and how many % will be drop free and at target pressure at 3 years
2/3rd patients fall in IOP
80% drop free and at target pressure
196
What are the types of laser trabeculoplasty
SLT
ALT
Micropulse laser trabeculoplasty (MLT)
197
What are the indications for laser trabeculoplasty (SLT/ALT/MLT)
LTP for both primary and secondary open (primary/ PXF/ pigmentary/ OHT)
Primary therapy
Failure of adherence to drops
Adjunctive treatment to avoid polypharmacy
Intolerance of topical medication including allergy
Failure of medical therapy
198
What are some idnications for diode laser cycloablation
raised IOP in patients with poor vision
Pain relief in blind eye with raised IOP
Uncontrolled secondary glaucoma eg NVG/ Malignant glaucoma
In patients where glaucoma filtration surgery/drainage unlikely to be successful
199
What is the technique of trans scleral cyclophotocoagulation
subtenon/peribulbar
laser settings 1.5-2s and 1500-2000mW, spot size fixed. power adjusted until popping sound heard then reduced to just below that level. 12-24 burns placed posterior to limbus over 360 degrees avoiding neurovascular bundles at 3/9 o clock. (treatment of 1-2 quadrants likely to be enough in eyes with good vision)
more than one treatment session likely to be needed with this
200
What are some complications of cyclodiode ablation
chronic hypotony, phthisis, suprachoroidal haemorrhage, serous retinal detachment
201
What is laser iridoplasty
performed to widen the anterior chamber angle by contraction of peripheral iris away from angle recess. Used to break an episode of acute angle closure but more elective basis. Used in plateau iris syndrome.
202
What are the indications for trabeculectomy
Failure of conservative therapy to achieve low IOP
Progressive deterioration despite seemingly adequate IOP control (including poor adherence to drops)
Primary therapy in advanced disease needing very low target pressure especially younger ones
Patient preference if want drop free
203
What is the benefit of placing the bleb incision at 12 o clock in trabeculectomy
less likelihood of bleb dysaesthesia
204
What are the risk factors for trabeculectomy surgery failure
previous failed trabeculectomy or MIGS
Previous conjunctival/ cataract surgery
Secondary glaucoma (inflammatory/ neovascular/ post trauma)
Demographic: black/ age <65
Patients on topical medication eg sympathomimetics for over 3 years
205
What is more potent 5FU or MMC
MMC
206
What are the causes of shallow AC after trabeculectomy
pupil block
overfiltration
malignant glaucoma
207
What is the pupil block mechanism and shallow AC after trabeculectomy. Signs and treatment
may occur with non patent peripheral PI
Signs: high iOP and flat bleb, negative Seidel test, Iris Bombe with non patent PI
Treatment: YAG PI at iridectomy site/ elsewhere
208
What is the overfiltration mechanism and shallow AC after trabeculectomy. Signs and treatment
insufficient resistance to outflow at the lamellar scleral flap but bleb leakage through inadvertent buttonhole or due to inadequate closure of conj/tenon capsule
signs: low IOP, well formed bleb in scleral flap leak/ flat in bleb leak. Seidel test negative in scleral flap leak but positive in bleb leak. Cornea hypotony- DM folds.
Treat by atropine and observation- prevent PAS. Temporary tamponade of conj- large diameter soft BCL, simmons shell. Definitive treatment with additional conj sutures/place a transconjunctival scleral flap suture. Choroidal detachment rarely requires drainage
209
What is the malignant glaucoma mechanism and shallow AC after trabeculectomy. Signs and treatment
rare but serious complication. anterior rotation of ciliary process and iris root leading to posterior misdirection of aqueous.
Signs: shallow AC/ myopic shift, High IOP absent bleb, negative Seidel test
Treatment: mydriatics (Atropine 1%) dilate ciliary ring and increase distance between ciliary processes and lens equator tightening zonules pulling lens posteriorly. IV mannitol can be used. YAG hyaloidotomy to disrupt anterior hyaloid face. PPV if laser fails.
210
What should a normal functional bleb look like
slightly elevated, relatively avascular, show superficial microcysts which are distended conjunctival goblet cells.
211
How to spot a poorly filtering bleb
increasing IOP + bleb with
1) flat without vascularization
2) Vascularized bleb due to episcleral fibrosis
3) Encapsulated bleb (tenon cyst) localised highly elevated dome shaped fluid filled vacity of hypertrophied tenon capsule with engorged blood vessels
212
What are some extrascleral causes of bleb failure
subconjunctival/episcleral fibrosis with bleb encapsulation
213
What are some scleral causes of bleb failure
overtightening sutures of scleral flap and gradual scarring in scleral bed
214
What are some intraocular causes of bleb failure
uncommon- blockage of sclerostomy by vitreous /blood/uveal tissue or by a variety of membranes derived from surrounding cornea/ sclera
215
How is bleb filtration failure managed- what are the options
ocular digital massage- force outflow through surgical fistula. digital compression via upper lid massage when patient looking down 4-8x/day until bleb stable.
Suture manipulation considered 7-14 days post op if high IOP/flat bleb and deep AC. Releasable sutures can be cut/ released.
Needling of encysted bleb at slit lamp augmented with MMC/FU
Subconj injection of 5-FU in first 7-14 days to suppress episcleral fibrosis- directed away from the fistula.
216
Why does late bleb leakage occur and what are the signs
disintegration of conj overlying sclerostomy- following perioperative application of antimetabolites like MMC. Necrosis of surface epithelium results in transconj drainage of aqueous.
Signs: low IOP, avascular cystic bleb, seidel negative initially with sweating, shallow AC and choroidal detachment in severe cases.
Treatment: depends if sweating or due to hole.
217
What is bleb sweating and how is it treated
sweating: multiple Punctate staining areas on the bleb
Treated by injection of autologous blood into bleb/ compression sutures/ transconjunctival scleral flap, suture or sometimes surgery.
218
What is bleb dysaesthesia
Postop ocular discomfort secondary to tear film disturbance adjacent to the bleb in 5% patients with trab surgery. Younger patients and thin walled nasal positioned bleb are risk factors. key sign is a number of small bubbles adjacent to the bleb seen with fluorescein. Symptoms relieved with topical lubricants but surgical revision may be needed
219
What are the risk factors for blebitis and bleb related endophthalmitis
antimetabolite use
inferior placed bleb
bleb leak
blepharitis/conjunctivitis
220
What are the pathogens commonly causing blebitis and bleb related endophthalmitis
H influenza
Streptococcus
Staphylococcus
Gram negative organisms
Poor visual prognosis overall
221
What is the treatment for blebitis
conj swab
broad spectrum antibiotics eg ofloxacin and cephalosporin
PO Augmentin + Ciprofloxacin for at least 5 days
Role of topical steroids unclear- add when definite response to antibiotics
222
Which structure is preserved in non penetrating glaucoma surgery
internal trabecular meshwork preserved
223
What glaucoma surgery is good when there is a high risk of 'snuffing out' central damage with advanced damage
Non penetrating glaucoma surgery
224
How is MIGS surgery classified
-Surgery that avoids bleb formation by manipulating Schlemm canal/ excision of TM/ bypassing TM or by dilation of canal
-Implants that result in drainage under Tenon capsule + conj leading to bleb formation eg Xen/Preserflo. MMC injected under conj adjacent to implant reduce risk of bleb fibrosis. Bleb needling often required post operatively.
-Surgery that increase aqueous outflow from AC into supraciliary space - MiniJect silicone implant with interconnected hollow spheres- no bleb and no antimetabolite used
225
What are the indications for MIGS
Mild- moderate glaucoma- rate of slow visual field loss and target pressure modest 15-17
In select cases combined with Phaco IOL reduce need for topical medication
226
What are the complications of MIGS
Schlemm canal manipulation- risk of implant malposition/ haemorrhage/infection/corneal decompensation.
Bleb formation- trab complications, malposition and stent erosion seen
Supraciliary implant- risk of endothelial cell loss
Late MIGS failure- increased risk of bleb fibrosis
227
What does the standalone iStent implant study show in terms of % IOP reduction from baseline for upto 5 years post op
30% reduction
228
What does the horizon study of Hydrus Microstent show
stent safe, less likely to result in VF loss, more likely to lower IOP with fewer medications than Phaco IOL alone at 5 years
229
What do GDD do
create a communication between AC and subtenon space via tube attached to posteriorly explanted episcleral reservoir. Some contain pressure sensitive valves for regulation of aqueous flow
230
What are the results of the tube vs trab study
Five years after tube surgery, IOP reduction, rates of surgical failure and visual loss are similar to those in MMC enhanced trab, but more post operative medication needed to control IOP in those receiving a tube
231
What are some examples of GDD's
All silicone tubes
Molteno
Baerveldt
Ahmed- valve
PAUL- valveless
232
What are the indications for GDD
Severe conjunctival scarring precluding accurate dissection of conjunctiva
Uncontrolled glaucoma despite previous trab with adjunctive antimetabolite
Secondary glaucoma- routine trab+/- adjunctive antimetabolite less likely to be successful eg NVG/ aniridia/ ICE/ post trauma
Certain types of congenital glaucoma where conventional procedures failed
233
What are the complications of GDD
Excessive drainage- hypotony, shallow AC, bleb encapsulation- raised IOP 1-6 weeks after aqueous enters footplate (common in Ahmed valve rather than non valved tube)
Malposition with endothelial or lenticular touch.
Tube erosion through sclera/conj
Corneal decompensation
Early drainage fail due to blockage with vitreous/ blood
Double vision due to EOM interference if footplate in superonasal quadrant.
234
Which location placement of the GDD is double vision likely to occur and with which type of GDD is this reduced and why
if footplate in superonasal quadrant.
PAUL tube reduced as not placed under rectus muscles
235
What were the results of the Ahmed Baerveldt comparison (ABC) study
The average preoperative IOP was 30 mmHg) showed an average postoperative IOP of 14.7
mmHg in the Ahmed group and 12.7 mmHg in the Baerveldt
group at 5 years. The long-term success rate in some conditions
such as neovascular glaucoma and ICE syndrome is poor. Adjunctive MMC may enhance the success rate of drainage shunt surgery.
236
Part 2
flashcards
Decks in class (20)
# Cards
-
Exam Techniques68
-
Eyelids183
-
Lacrimal Drainage System41
-
Orbit167
-
Dry Eye34
-
Conjunctiva80
-
Cornea183
-
Corneal and Refractive Surgery49
-
Episclera and Sclera35
-
Lens101
-
Glaucoma236
-
Uveitis191
-
Retinal Vascular Disease147
-
Acquired Macula Disorders163
-
Inherited Retinal Degenerations127
-
Retinal Detachment99
-
Vitreous Opacities10
-
Strabismus201
-
Neuro-ophthalmology352
-
Ocular Tumours164
