Mx Exam Revision Flashcards
1
Q
What is the 1st-choice pharmaceutical treatment for reducing IOP in glaucoma and why?
A
Prostaglandin Analogues [specifically Xalatan]: highest efficacy [30% reduction] and once-daily usage [24hr IOP control] is convenient.
2
Q
List 4 potential side effects of prostaglandin analogues
A
Darker iris
Lash growth
Loss of orbital fat
Red eye [either short term or long term]
3
Q
List 4 different options for prostaglandin analogues, including their dosage percentages
A
Latanaprost [Xalatan 0.005% NOCTE]
Travaprost [Travatan 0.004% NOCTE]
Bimatoprost [Lumigan 0.03% NOCTE]
Tafluprost [Zioptan 0.0015% NOCTE]
** that’s right lumigan is actually 0.03%
4
Q
What alternative prostaglandin can you consider if Xalatan is only achieving a small reduction (IOP redcution <5mmHg)? Why?
A
You could try Lumigan or Travatan.
Lumigan has a different chemical composition and some studies suggest it can have a greater IOP lowering effect. There’s a preservative free lumigan you can use.
Travatan can also be considered as it binds better to PGF2alpha, however the chemical composition is similar to Xalatan so it might not have much greater an effect. Travatan does use polyquad preservative rather than BAK like xalatan, so that’s another benefit.
5
Q
What downside may occur in switching from xalatan to travatan?
A
May have more adverse/side effects
6
Q
Of the 4 mentioned prostaglandin options, which results in the least side effects and least conjunctival hyperaemia?
A
Xalatan.
7
Q
List 3 contraindications for prostaglandin analogues
A
Uveitis
Pregnancy
HSV
8
Q
List 3 prostaglandin analogues to consider for a patient with ocular surface disease or sensitivity to BAK preservative
A
Travaprost [uses an ionic buffered preservative - polyquad]
Tafluprost [preservative free]
Preservative-free Lumigan [specifically the preservative free kind]
9
Q
Aside from PGAs, list 3 other drug classes that can be used to reduce IOP in open angle glaucoma
A
Carbonic Anhydrase Inhibitors
Beta Blockers
Alpha Agonists
10
Q
Which drug class makes the best adjunct to PGAs?
A
CAIs. Because PGAs secondary action promotes the action of CAIs.
11
Q
What is the ideal patient for PGAs?
A
Those with a chronic, non-acute IOP elevation (i.e. POAG and NOT aacg or post-op iop spike)
12
Q
List 2 topical CAI options for reducing IOP
A
Dorzolamide [Trusopt 2% TiD]
Brinzolamide [Azopt 1% BiD]
13
Q
List 4 benefits for topical CAIs
A
Reduces diurnal fluctuation
Good vascular nocturnal profile
Fast effect [1 hr]
Good adjunct to PGAs
14
Q
Which topical CAI has less stinging? Dorzolamide or Brinzolamide? Why?
A
Brinzolamide. It coms in a 10mg/ml suspension which means it has a slower release and therefore less stinging.
15
Q
List 1 contraindication for CAIs
A
Corneal graft/corneal compromise. Topical CAIs can result in corneal deturgescence.
16
Q
Which glaucoma drops are safest to use in the first trimester?
A
Brimonidine [an alpha agonist] may be the safest option for the first trimester. [** it’s also generally the safest drug as it’s a category B1 drop]
17
Q
Which glaucoma drops are safest to use in the second trimester? (3)
A
Brimonidine
Beta blockers [with regular fetal heart rate/growth monitoring]
CAIs [with fetal growth monitoring]
18
Q
Which glaucoma drops are safest to use in the third trimester? (3)
A
Brimonidine [must discontinue late in 3rd trimester to avoid CNS depression in newborns]
Beta blockers
Topical CAIs
**All to be used with caution
19
Q
What are the main risks associated with glaucoma surgery in pregnant patients? (4)
A
the usage of local anaesthetics
post-operative meds
gastro-oeseophageal reflux
increased risk of aortic + vena cava compression in 2nd/3rd trimester
20
Q
Name an alternative to traditional glaucoma surgery that can be safer for pregnant patients. Why? (4)
A
Selective Laser Trabeculectomy (SLT):
- only uses topical anaesthesia
- upright positioning during procedure
- faster rehab
- reduced need for post-op meds [both dosage + duration]
21
Q
When is the ideal time to consider surgery for a pregnant patient?
A
Before their (planned) pregnancy, as a way to manage IOP without having them on drops
22
Q
Does IOP naturally rise or lower during pregnancy? By how much? Why? When is this most pronounced?
A
IOP diminishes by up to 10% during pregnancy, most pronounced in the 3rd trimester. Is attributed to fluctuating hormones [β-human chorionic gonadotropi and progesterone]
23
Q
Is MIGS-iStent safe for pregnant patients?
A
Yeah-ish. About as safe as SLT anyway.
24
Q
List the IOP reduction efficacies, in percentage, for the 4 different drug classes used in primary open angle glaucoma
A
PGAs: 30%
Beta Blockers: 25-30%
Topical CAIs: 20%
Alpha agonists: ~25% ish. Unsure. Expect maybe a 5-6mmhg reduction.
[update on the role of alpha agonists in glaucoma management]
25
Name 3 scenarios where you might consider MIGS-iStent
Pregnancy/Planned pregnancy
Drops not working
Patient about to undergo cataract surgery [can get iStent at same time]
26
When might you consider oral CAI [i.e. Diamox]? (2)
Topical therapy not working
AACG management
27
What effect does Diamox have on IOP?
~50% IOP reduction
28
What dosage of diamox would you use for glaucoma where topical is not working?
250mg Diamox po per day
29
What dosage of diamox would you use as an initial dose for AACG patients?
2x250mg Diamox + 500mg KCl
30
List 3 contraindications to Diamox
Kidney disease
Alergy to sulfa drugs
COPD [get GP advice]
31
Are there any fixed combination drugs containing both a PGA and CAI?
No. Not on the PBS at least. I couldn't find any.
32
Are there any fixed combination drugs containing both a PGA and a beta blocker?
Yes.
Ganfort: Bimataprost + Timolol
Xalacom: Latanaprost + Timolol
33
How would a typical glaucoma treatment pathway look? (4)
Start with PGA1
If PGA1 not working properly (<5mmHg reduction), switch to PGA2
If PGA working but not enough, Add topical CAI
If still not enough, turn CAI into a combo with a beta blocker or alpha agonist
34
Are beta blockers effective at night?
No
35
List 2 options for beta-blockers to reduce IOP
Timolol 0.5% QD [once per day] or BiD
Betaxolol 0.5% sol BiD [safest b-blocker for asthmatics]
https://www.aaopt.org/detail/knowledge-base-article/timoptic-05-bid-or-qd-which-controls-glaucoma-more-effectively - suggests timolol 0.5% BiD is better than qd
36
List 6 contraindications of beta blockers
Low tension glaucoma
Bradycardia (<50bpm)
Asthma/COPD [can use betaxolol with caution]
MG
Diabetes
Depression
37
List the benefit of alpha agonists for glaucoma treatment
Good pulsatile ocular blood flow (POBF) effect. Particularly good for low tension glaucoma, especially when IOP = 14.
(NB: though in NTG, PGAs are still good/should try first, but try Tafluprost, which has a vascular action as well).
38
List 2 glaucoma drops that are good for treating the vascular nature of normal tension glaucoma
Brimonidine
Topical CAIs also good.
**Neuroprotective effect.
39
How was brimonidine postulated to have a neuroprotective effect in normal tension gluacoma?
it was compared to timolol in the LOGTS [Low-Pressure Gluacoma Treatment Study] and was found to result in lower likelihood of having VF progression.
40
List 2 alpha agonist options for treating glaucoma
Alphagan [Brimonidine 0.2% Tid (max) or BiD (adjunct)]
Apraclonidine [Iopidine 0.5% Tid (max) or BiD (adjunct)]
41
Which is the most commonly used alpha agonist?
Alphagan
42
What is the benefit of Apraclonidine?
Large fast IOP lowering which is good for IOP spikes, such as post-surgical IOP spikes (however not on PBS).
43
List 4 contraindications of alpha agonists
Tricyclic antidepressants
MAO inhibitors
Severe cardiovascular disease
Heavy machinery usage.
44
What is the main use for pilocarpine?
Low dose (0.16%) treatment for PDS/PGS, where miosis and reduced iris movement is desired
45
Why is pilocarpine not used much for open angle glaucoma?
too many adverse effects (e.g. CME, angle closure, variable myopia, RD, chol. toxicity, tachycardia, fever)
46
What is the primary IOP management for secondary glaucoma?
Same as POAG really. It depends. Can try Apraclonidine to treat IOP spikes for instance.
Avoid PGAs if secondary to uveitis.
47
What is the first aid treatment for AACG?
1 drop of: BB [timolol] + AA [alphagan] + CAI [trusopt] + pilo 2%. Also steroid drop if inflammation.
Then Oral diamox [2x250mg + 500mgK+] if kidneys ok
48
What is required for the diagnosis of POAG? (4)
NRR loss or RNFL defect
Typical VF defect (repeatable. Need baseline x3 for monitoring)
Open un-occluded angle
IOP >21mmHg (at some stage)
49
How many signs do we need to make a general glaucoma diagnosis? [Graham L.]
3 structural signs of glaucomatous disease that all match with each other
50
List 7 signs on fundus that should make you more suspicious of glaucoma (add +1 to OHTS for each)
Vertical notching
Loss of ISNT (sup/inf thinning)
High CDR (0.7+) + increasing over time [standard disc size]
CDR asymmetry >0.2
Deepening of cup
Drance Haem
Barring of circumlinear vessels
51
What should you do if you see an isolated drance haemorrhage in an otherwise normal patient?
While it is less likely to be glaucoma, you should still monitor every 3 months for the first 2 years. Including baseline visual fields.
Repeated drance haemorrhages that occur in this time are much more suggestive of glaucoma
52
How long does an isolated drance haemorrhage typically last?
about 3 months, sometimes longer. If it lasts longer, it should still be faded and less noticeable on 3 month review.
53
List 6 high ocular risk factors for OAG
Myopia
RVO
Oc injury/sx
Iris degen
Past/present papilloedema
High IOP
54
List 4 low risk factors for OAG
Female
DM
MIgraine
Sleep apnoea
55
List 6 other risk factors for OAG (6)
Fam Hx
African-american
High BP or very low BP
Aggressive BP control
Low CCT
Steroid use [prednisolone - e.g. for COPD]
56
List 9 risk factors for NTG
Age >65yo
Fam Hx
Japanese
High myopia
Aggressive BP control
CV disease
DM
Migraine
Sleep apnoea
57
What are the 5 main factors to consider for the OHTS risk calculator for 5 year prognosis of OAG?
Age
Mean IOP (avg of 2 eyes)
Mean CCT
Mean vertical CDR (avg of 2 eyes)
Pattern Standard Deviation on VF
58
Describe a suggested sequence for performing a glaucoma workup
Slit lamp --> IOP --> Gonio --> Pachymetry --> VF (dilate as doing) --> OCT -->Fundus Lens -->Repeat IOP
59
Why would you perform a gonio on a glaucoma patient?
Check for signs of neovascularisation or secondary glaucoma
60
Describe an early VF defect in glaucoma
MD >/= -6.00dB + one of:
- >/= 3 pts cluster p<5%, with at least 1pt in cluster p<1% on pattern dev plot
- Pattern SD p<0.05
- GHT "outside normal limits"
61
Describe a moderate VF defect in glaucoma
MD -6.01dB to -12.00dB + one of:
-25-50% p<5%, with at least 15-25%p<1% on pattern dev plot
- >/= 1pt in central 5 deg <15dB, but none <0dB
- Only 1 hemifield containing a pt <15dB in central 5deg
62
Describe an advanced VF defect in glaucoma
MD -12.01dB to -20.00dB + one of:
-50-75% p<5%, with at least 25-50% p<1%
- >/= 1pt in central 5 deg <0dB
- Both hemifields containing a pt <15dB in central 5deg
63
Describe a severe VF defect in glaucoma
MD >/= -20.00dB + one of:
>/=75% p<5%, with at least 50% p<1%
- >/= 50% pts in central 5 deg <0dB
- Both hemifields conta`ining >50% of pts <15dB in central 5deg
64
Describe an end-stage VF defect in glaucoma
Unable to perform VF in "worst eye" (due to central scotoma or VA = 6/60)
65
You should advance 1 grade in VF defect for glaucoma if there is a "threat to fixation", what does this refer to?
4 points within central 3 degrees @ 16-25dB
66
When would a threat to fixation make you advance to advanced VF defect?
if 1 point within central 3 degrees @ 0-15dB
67
List 4 signs of PXS
White deposits (GAGs) on ant lens/iris/tm
Iris transillumination at pupil margin
Pigment loss/dispersion from iris collar
Gonio pigment
68
List 3 risk factors for PXS
Often 60-80yo men
Myopia
Scandinavian/Meditteranean
69
How does the prognosis of PXS differ from POAG?
Prognosis is worse than POAG, with faster rates of progression and poorer response
70
List 4 signs of PDS
Backward iris bowing
Pepper pigment deposits on anterior iris, lens capsule, corneal endothelium
Gonio pigment
Possible red eye post exercise
71
Why might a PDS patient acquire a red eye post exercise?
IOP spike (from the pigment)
72
Where are the pigment deposits on the anterior iris located in PDS?
Mostly inferior, due to gravity
73
How does pigment from PDS appear on the corneal endothelium
Appears as "Krukenberg's Spindle" - a vertical line of pigment on the corneal endothelium
74
List 6 risk factors for PDS
M>F
30yo M or Older F
Myopic
African
Concave iris
Flat cornea
75
Is PDS usually unilateral or bilateral?
bilateral
76
Is PXF usually unilateral or bilateral?
unilateral
77
List the 3 main steps for managing a secondary glaucoma like PDS/PXF
Treat underlying disorder
Manage IOP (aq suppress) if long term elevated IOP
Rev 24 hours: if IOP still >/=30 with tx, refer for sx
78
How frequently should you monitor PXS/PDS (no glaucoma)?
4-12 monthly
79
How frequently should you monitor PXG/PDG?
4 monthly
80
List 7 risk factors for PAC
50-70yo
Female
Fam Hx
Fellow eye
Asian
Narrow angle
Forward lens + shallow AC
81
What 3 measurements and values would constitute a forward lens and shallow AC?
Lens vault >/= 0.6 [forward lens]
ACD <2.1 [shallow AC]
AC width <11.7
82
What two tests combined should be used to screen for high risk PAC suspects?
Iris shadow test and VH
83
What is considered a fail on the shadow test?
>33% shadow
84
When a OAG diagnosis is established, and treatment chosen, how should you proceed with follow up?
Follow up in 1 month, then 3 months, then 4 months, then 6 months or 1yr.
85
How many baseline VF tests should you do on the 1 month review for OAG?
2 Visual Fields [making 3 total baseline VFs when adding original VF from month prior].
**NB: patient may feel uncomfortable sitting through 2 VFs, so perhaps schedule the 2nd VF for a week later. This is also good for timing purposes. NB: you should also be doing OCT/photo on this and subsequent visits too. And check IOP.
86
What is required for a PACS diagnosis?
PTM not visible in 2 mirrors
87
What is required for a PAC diagnosis?
PACs [PTM not visible in 2 mirrors] + IIS [Ischemic iris changes]
88
What constitutes Ischemic Iris Changes? List 3 examples.
increased pigment (2+) in sup PTM
iris atrophy
glaucomflecken
89
What is required for a PACG diagnosis?
PAC + NRR loss or RNFL defect
90
How do you manage PACG?
Peripheral laser Iridotomy
91
What is required for an AACG diagnosis
Angle closure with IOP >/= 24mmHg and
2 or more symptoms (pain/nausea/blur) and
2 or more signs (red/corneal oedema/mid-dilated pupil/shallow AC)
92
List 8 indications for a PLI
APAC/PACs/PAC/PACG
Contralateral eye in APAC
2ndary angle closure with pupil block
Plataeu iris configuration/syndrome
Aqueous misdirection
Malignant Glaucoma
Ciliary Block
PDS
93
List 4 contraindications for a PLI?
corneal oedema
ac inflammation
uveitis
very flat ac
94
List the 3 primary combination glaucoma IOP reduction drugs not involving a PGA
Combigan [Brimonidine + timolol]
Cosopt [Dorzolamide + timolol]
Simbrinza [Brimonidine + Brinzolamide]
95
What is the prevalence of glaucoma in siblings of patients?
10.4% [population family study]
96
What is the prevalence of glaucoma in children of patients?
1.1%
97
Which optic nerve disease in a 60yo women could be mimic the appearance of primary open angle glaucoma?
AION: Anterior Ischemic Optic Neuropathy
98
List 4 symptoms of AION
Sudden painless vision loss
TIAs/Amaurosis Fugax
Diplopia
Flashes/flicker/colour scintillations
99
List 4 GCA specific symptoms
HAs [50%]
Tender/swollen temporal artery
Jaw claudication
Scalp tender/pain
100
List 5 ocular signs of AION
Central scotoma
Achromatopsia/Dyschromatopsia
RAPD
Peri-papillary non-perfusion
Optic neuropathy
101
Describe the optic neuropathy that occurs in AION
Disc oedema + pp haem + CWPs OR ...
White pallid disc with mild pp oedema
102
List 6 differentials for AION
NAION
ON inflammation via syphilis, sarcoidosis
Infiltrative optic neuropathies
Anterior orbital lesions with ON compression
Diabetic papillopathy
Open angle glaucoma.
103
What are the 5 steps for GCA Management
.
1. Hospital Emergency ward: referral with mention of your suspicion
2. Urgent blood test: ESR + CRP
3. Systemic Steroid [Prednisolone 60mg qd po]
4. Urgent temporal artery biopsy
5. Low dose maintenance steroid typically for 1-2 days, after which stopping tx can be considered depending on ESR levels. Tx may be lifelong however.
104
How can you differentiate NAION from AION?
Lack of arteritis. Diagnosis of exclusion from AION.
105
List 5 features of NAION
Sudden painless vision loss [6/30]
RAPD
RG defect + red desaturation
VF: altitudinal (inf) or arcuate defect
Unilateral disc oedema
106
Where is unilateral disc oedema most marked in NAION?
superiorly
107
How long after unilateral disc oedema in NAION does optic atrophy ensue?
after 1-2 months
108
List 6 systemic associations with NAION
Arteriorsclerosis
DM
Hypertension
Hyperlipidemia
Anemia
Sleep apnoea
109
How would you manage NAION [4]
Monitor [no effective tx for NAION]
GP referral: check for systemic associations like CV/DM
Review 1 month
Council on risk to contralateral eye
110
What percentage of NAION patients show mild improvement in vision over 3-6 months?
Up to 40%
111
Which 3 classes of glaucoma drugs reduce IOP by reducing aqueous production?
CAIs
Beta Blockers
Alpha agonists
112
Which 2 classes of glaucoma drugs reduce IOP by increasing aqueous outflow? Which pathway does each use?
PGAs - via uveoscleral pathway
Pilocarpine - via uveoscleral pathway indirectly which outweighs reduction in outflow from tm pathway
113
How does angle recession occur?
ocular blunt force trauma can cause shearing forces that tear between the longitudinal and circular fibres of the ciliary muscle, causing the circular fibres to displace posteriorly along the iris root, causing angle recession
114
How does angle recession glaucoma occur?
the ocular blunt force trauma causes damage to trabecular meshwork, making it dysfunctional
115
Which class of glaucoma drop is contrainidcated in angle recession glaucoma? Why?
pilocrapine: causes a pardoxical IOP rise in some
116
Which classes of glaucoma drops are preferred in treating angle-recession glaucoma? [3]
Aqueous suppressants: CAIs, Beta Blockers, Alpha agonists
[*So something like timolol 0.5% QiD is a good choice here]
117
When can angle recession glaucoma occur post trauma?
Can be anytime from days to years later
118
Are argon laser trabeculectomy (ALT) and selective laser trabeculectomy (SLT) effective in treating patients with angle recession glaucoma? When will better responses occur?
Rarely. Better responses will occur when more of the TM is intact on gonio.
119
When max tolerated medical therapy fails to control IOP adequately in angle recession glaucoma, which filtering surgical option is ideal?
Trabeculectomy with antimetabolites
[Mermoud et al, 1994]
[https://glaucomatoday.com/articles/2012-may-june/clinical-approach-to-angle-recession-glaucoma]
120
How often are patients with angle recession typically monitored for development of glaucoma?
yearly, in the absence of other findings.
121
What can early onset angle recession gluacoma present alongside?
Iritis with or without hyphaema
[treat with topical steroids like aau]
122
How many mirrors should be open to PTM on gonio to be safe to dilate?
3 mirrors.
123
List 3 epidemiological risk factors for Optic Neuritis
Typically 20-45yo. F>M [2x]. Caucasian
124
List 5 systemic associations with Optic Neuritis
Infections
Multiple Sclerosis
Tumours/compressive lesions
Vascular diseases
Idiopathic
125
What is the main cause of retrobulbar neuritis?
Multiple Sclerosis
126
How often does multiple sclerosis cause retrobulbar neuritis?
75%
127
List 4 ocular signs of retrobulbar neuritis
RAPD
Orbital pain/pain with eye movement
Acute vision loss
Brightness/CV defects
128
After how many weeks of untreated retrobulbar neuritis, might a patient experience mild disc oedema? Why?
1-2 weeks. Due to axoplasmic stasis (doesn't always happen)
129
After how many weeks of untreated retrobulbar neuritis, might a patient experience RNFL loss on OCT?
6-8 weeks
130
After how long of retrobulbar neuritis, might a patient experience optic atrophy?
3-6 months
131
What are the 2 main causes of papillitis?
GCA [beware bilateral spread]
MS
132
How does the presentation of papilitis differ from retrobulbar neuritis?
There's also disc oedema [mostly swelling, few retinal haems]
133
Is neuroretinitis usually associated with multiple sclerosis?
No
134
What are the 2 main causes of neuroretinitis?
infectious
inflammatory
135
Is orbital pain always present in neuroretinitis?
No. It's actually not as common compared to retro/papilitis
136
Can neuroretinitis present with a macula wing/star exudate?
Yes.
137
List 5 differential diagnosis for optic neuritis
Ischemic optic neuropathy
Acute papilloedema
Severe systemic hypertension
ON compression (tumour)
Intracranial mass
138
How do you perform the photostress test?
Hold light 2-3cm from patient's eye [other eye occluded] for 10 seconds, then remove light.
-- Ask patient to read line of best VA after central scotoma has disappeared. Time how long it takes to read at least 2/3rd of the line of their best VA.
139
What is an abnormal photostress test?
>50 seconds = abnormal.
140
List what possible tests you can do for a patient with suspected optic neuritis (9)
VA
Screening [confrontation/HH/pupils/red cap
Lid ax/FAT: if lid protosis or ptosis present
Refraction/Ret
IOP
Ocular health
VIsual fields: 30-2?
Photostress test
OCT: check RNFL thinning
141
What eye movement condition is MS associated with? What percentage of patients may acquire this? Explain the condition.
~30% of MS patients may have INO [Internuclear Ophthalmoplegia]. INO: sluggish or absent contralateral adduction.
142
What type of evidence do you need to diagnose MS?
evidence of CNS damage that is "disseminated in time and space"
143
What tests are required for diagnosing multiple sclerosis (2)
MRI scans: for lesions
CSF-specific marker: needs lumbar puncture
144
Other than MS testing, what other referred tests might be considered in a patient with optic neuritis? (list 5)
CBC
ESR
ACE level
FTA-ABS
Chest x-ray or CT.
145
Should blood pressure be checked in a patient with optic neuritis?
yes
146
How often should you review a patient with optic neuritis?
Review 4-6 weeks after presentation, and then every 3-6 months thereafter
147
What is CDMS and who should patients at high risk of this be referred to?
Clinically Definitive Multiple Sclerosis. High risk patients should be referred to a neurologist for evaluation and mx of possible MS.
148
How can we treat MS? Does this improve final outcome?
IV Methyl pred. Hastens recovery but doesn't improve final outcome
149
Why don't we use oral pred for MS?
Oral pred increases the rate of recurrence of MS
150
What is the NHMRC target IOP for Ocular Hypertension (OHT)?
-20% or =24mmHg [whichever is less]
151
When would be an appropriate time to start treatment for OHT prior to seeing evidence of any glaucomatous damage?
There is no real consensus on the minimum IOP threshold for this. But generally IOPs >24* with a normal CCT is a good guide.
**In these cases, diurnal IOP should ideally be measured as well
152
At what time of day is IOP normally highest?
For most normal eyes the pressure is highest in the early morning between 6am and 8am.
153
At what time of day is IOP normally lowest?
Afternoon
154
Why does IOP vary throughout the day?
hormonal fluctuation
155
With what type of CCT value is IOP overestimated?
Thicker CCTs
156
Normal CCT value
555
157
What is the NHMRC target IOP for Early OAG?
-20% or = 18mmHg, whichever is less
158
What is the NHMRC target IOP for OAG [starting point] and Moderate OAG?
-25% or = 18mmHg, whichever is less
159
Should you write the target pressure in the management section of sunix/optomate for someone you have begun treating for glaucoma?
Yes, you should
160
What is the NHMRC target IOP for Advanced OAG [or high risk early/mod OAG]?
-30% or =12mmHg, whichever is less
161
What is the NHMRC target IOP for LTG [MD
-30% or =12mmHg, whichever is less
162
Describe the surgical treatment pathway for OAG (4)
SLT/MIGs --> Filtering sx + antimiotic --> aqueous shunt or cyclodestructive sx --> low vision care
163
Define papilloedema
bilateral optic disc swelling secondary to elevated intracranial pressure
164
List 3 potential causes of papilloedema
Intracranial tumour
Malignant hypertension [must always check for this]
Idiopathic intracranial hypertension
165
Define Malignant Hypertension
Diastolic blood pressure >120mmHg
166
What should you suspect if a young person presents with malignant hypertension?
Kidney failure.
167
How do you manage malignant hypertension? [and even if not malignant but DBP >110]
Immediate referral to ICU/emergency department for cardiac monitoring, urine analysis, and neurological status assessment.
168
What are 6 potential symptoms of elevated ICP associated with papilloedema?
Severe headaches
Nausea
Vomiting
Slight blur
Diplopia
Pulse-like ringing sound in ears
169
What are 4 additional tests you can do for a patient with papilloedema?
Blood pressure
VF [check for stroke/signs of cortical VF loss]
Refer to neuro for MRI + Lumbar puncture
170
What are 5 indications for urgent hospital referal in patients with papilloedema
Recent onset [within 1-2 months] with unusual headaches
Transient vision loss [<1min complete blackout]
EOM abnormality - diplopia
new related VF loss
Other new neuro problems like muscular paralysis, palsy, cognition issues
171
How can you treat pseudotumour cerebri? [3]
Weight loss +/- spinal tap
Oral diamox 250-500mg BiD for progressive vision loss on monitoring
Shunt surgery if still progressing on diamox
172
What is considered normotensive blood pressure?
<140/90
173
What is considered borerline high blood pressure?
140/90 - 160/95
174
What is considered primary hypertension?
>160/95
175
What percentage of hypertensive cases are secondary to a renal or endocrine condition?
5%
176
List 8 systemic risk factors for hypertension/hypertensive retinopathy
duration of high bp
heart disease
atherosclerosis
diabetes
smoking
high cholesterol
overweight
fatty/sugary diet
177
How does grade 1 [minimal] hypertensive retinopathy present on fundus examination? [Keith-Wagener-Barker Classification]
Mild general retinal arteriolar narrowing [reduced AVR]
178
How does grade 2 [mild] hypertensive retinopathy present on fundus examination? (2)
Focal arteriolar narrowing + AV nipping
Potential "copper wiring" of arteriolar walls
179
How does grade 3 [moderate] hypertensive retinopathy present on fundus examination? (3)
G2 + any of the following:
Retinal Haems (mostly flame)
Exudates
CWPs
180
How does grade 4 [severe] hypertensive retinopathy present on fundus examination?
Severe G3 + OD swelling [a marker of "malignant" hypertension]
181
T/F: The increasing severity of hypertensive retinopathy makes it more likely that it is secondary to other issues
True
182
Rank the 4 most important fundus signs for detecting early hypertension
1. Focal arteriolar constriction
2. Vein occlusions
3. Banking {particularly with shunt vessels]
4. Atherosclerotic signs
183
When would you refer a hypertension suspect to the GP for blood pressure and systemic workup?
GP referral when signs of recent origin seen: haems, CWPs, papilloedema, RVO
(NB: also do ophthalm referral if needed)
184
What percentage of strokes are ischaemic vs haemorrhagic?
Ischemic: 80%
Haemorrhagic: 20%
185
Over what age do most strokes occur?
50 years old.
186
List 4 systemic risk factors for stroke
Uncontrolled hypertension
Diabetes
prior attacks/TIAs
Atheerosclerosis
187
List 2 lifestyle risk factors for stroke
sedentary lifestyle
smoking
188
In what time period do major stroke events often occur following TIA?. How long after do the patients continue to be a high risk for stroke?
Within the first week. High risk within next 2 years.
189
Describe a transient ischemic attack (TIA)
Temporary blockage of blood flow causing a visual blackout typically lasting a few minutes
190
On what side would a visual blackout occur in a patient with carotid stenosis?
ipsilateral side
191
What are 4 potential ocular signs of carotid insufficiency?
Venous Stasis Retinopathy (i.e. type 1 non-ischemic CRVO)
Ocular Ischemic Syndrome
Asymmetric Cataract
Dilated conj/scleral vessels
192
What are 3 atherosclerotic signs of carotid insufficiency?
BRAO [old or recent]
Hollenhorst plaque [cholesterol]
Fisher plug [fibrin]
193
How can visual signs of stroke manifest?
Depends on where the stroke occurs
194
List 6 possible visual manifestations of stroke
Hemianopia
Diplopia/EOM palsy
CN5 palsy [loss of sensation to one side of face]
CN7/Bell's palsy
Nystagmus/gaze palsy
Visual processing/visual memory issues
195
How can you manage carotid insufficiency? (3)
Refer to GP for stroke workup.
Anticoagulant therapy (e.g. aspirin daily)
carotid endarterectomy (surgical removal of a plaque)
196
If you see ocular signs of carotid insufficiency, what should you ask the patient?
Any temporary visual blackouts in the past? When did they occur?
197
How long after a stroke do you need to wait before the patient can safely undergo elective surgery (e.g. cataract surgery). Why?
3 months post stroke. To avoid increased risk of adverse cardiovascular events.
[Jorgensen et al. 2014]
198
List 8 differentials for "localised areas of no vision"
BRVO
RD
DR
Pre-retinal haem
AMD
Vitritis
Ret infection
Vit haem
199
What should you do if a patient presents with localised area of no vision and you suspect posterior pathology but the angle is not open on gonio?
Same day referral to the ophthalmologist so you can deal with the narrow anterior chamber and the presenting problem today.
200
What does sectoral retinal hemorrhaging and painless positive scotoma most likely indicate?
BRVO
201
Where are flame haemorrhages localised in the retina?
GCL and RNFL
202
Where are dot/blot haemorrhages localised in the retina?
INL and OPL
203
List 6 potential retinal signs of BRVO
Dilated veins/Banking
Tortous veins
Haems [typically flame]
CWPs
Ret oedema/thickening
Vit haem
204
What type of ocular issues lead to positive scotomas? [i.e. area of black]
retinal problems like RVOs, haemorrhages
205
What type of ocular issues lead to negative scotomas?
[i.e. area of blank]
optic nerve or posterior visual pahway disease [glauc/on glioma/optic neuritis, etc]
206
Should you refer a patient with BRVO and no macular involvement? Explain
Non-urgent referral to GP and Retinal specialist. The retinal specialist can perform fluorescein angiography after the haemorrhage has cleared enough, to assess the level of capillary damage and non-perfusion. GP is for systemic workup.
207
How long do the haemorrhages in BRVO typically take to clear up enough so that adequate fluorescein angiography can be performed by the ophthalmologist?
Somewhere around 6-12 weeks usually. During your 2nd [8wks]/3rd [12wks] review you can assess this and decide if it's appropriate to refer to ophthalm now.
208
How should you monitor a BRVO?
Monthly review for 3 months to check for development of neovasc or any macula oedema, and then review every 3 months until resolution.
209
Within what time period do BRVOs typically resolve?
Within 6-12 months.
210
What are 2 treatment options for macula oedema in BRVO patients?
aVegF [1st choice]
Laser photocoagulation [grid]
211
What are the 3 factors contributing to thrombosis and subsequent vein occlusions [known as Virchow's Triad]
Vessel damage
Venous Stasis
Hypercoagulability
212
List 5 systemic or lifestyle risk factors for RVO
Hypertension
DM
Hyperlipidemia
Smoking
Renal Disease
213
How can glaucoma be a risk factor for CRVO?
can cause compression + backward bowing of the lamina cribrosa, which can lead to pinching of axons and blockage of axonal flow
214
What percentage of CRVO are ischemic vs non-ischemic?
Ischemic: 20%
Non-ischemic: 80%
215
What type of vision loss is ischemic CRVO best characterised by?
Painless marked vision loss within hours to days resulting in very poor VA (e.g. 6/60)
216
What type of vision loss is non-ischemic CRVO best characterised by
painless less obvious vision loss ocurring within days to weeks resulting in slightly reduced VA (e.g. 6/7.5-6/9.5)
217
What features of CRVO can indicate that it's ischemic? (4)
CWPs
Marked vision loss
RAPD (is worse with increasing ischemia)
Macula oedema >600 um
218
List 5 differentials for CRVO
Severe DR
Ocular Ischemic Syndrome
Retinitis
Coats Disease
Benign Intracranial Hypertension
219
What is the prognosis of untreated non-ischemic CRVO
10-20% improve but around 35-50% get worse
220
How should you manage CRVO?
More urgent referral of all new cases to GP and retinal specialist. Should be within a week.
221
What is rubeosis?
Neovascular glaucoma (a secondary angle closure like glaucoma) that develops around 90 days following CRVO in 50% of cases due to increased vegF as a result of retinal ischemia.
Ret ischemia --> increased vegF --> Iris neovasc --> Neovascular glaucoma/ACG.
222
How often should you monitor patients with ischemic CRVO? What test should you perform each time on review?
Monitor monthly for 6 months (checking for development of iris neovasc, so perform gonio each time)
223
When should you review non-ischemic CRVO (without mac oedema)?
Review in 4-6 weeks to monitor for oedema and/or ischemia or prn if vision deteriorates
224
Provide 2 options for treating macula oedema associated with CRVO
AvegF
IV Triamcinolone
225
How often should you review clinically significant macula oedema?
Monthly review for OCT and tx response for 1st 4 months, then quarterly until resolution.
226
What is the criteria to diagnose CSMO (Clinically Significant Macula Oedema)? [3]
Ret thickening within 500um of centre of fovea
Lipid exudate within 500um of centre of fovea
Ret thickening >1500um, which is within <1500um of centre of fovea
227
What is the average normal macula thickness?
=250um
[Chan et al. 2007]
228
What is considered abnormal thickening of the macula?
>300um
229
What are the main 3 important causes of CRAO?
Cholesterol plaque/embolus
Thrombosis
Giant Cell Arteritis
230
List 5 signs of CRAO
superficial retinal whitening
cherry red spot
attenuated arterioles
retinal embolus visible
cattle tracking
231
why might CRAO present with a possible sector of normal retinal colour?
Dual blood supply from ciliomacular artery
232
Does everyone have a ciliomacular artery/dual blood supply?
No. About 25% of patients have it
233
What must we rule out when we see a patient with CRAO? What implications does this have for ophthalmic testing?
GCA. Therefore, as a rule, when patients over 50yo present with CRAO, fluorescein angiography must be performed to find out if there is any underlying PCA occlusion as well.
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7933845/]
234
What does an underlying PCA occlusion in a patient with a CRAO suggest?
It is virtually diagnostic of a CRAO due to GCA.
Such patients require immediate and aggressive corticosteroid therapy to prevent catastrophic visual loss.
235
What is the key differentiator between CRAO and an ophthalmic artery occlusion? How does the treatment differ?
Ophthalmic artery occlusion usually has no cherry red spot. Treatment is the same
236
What should you do if a patient with CRAO does not have an embolus on fundus examination? (2)
1. Immediate hospital referral with blood test for ESR + CRP
2. Start high dose systemic steroids [hospital handles this]
237
How can you attempt to treat a CRAO with embolus while in clinic? How does this technique work and what is the logic behind it?
Ocular massage: use the gonioscope to push on the eye [10 seconds on/5 seconds off].
Doing this will increase the IOP to hopefully increase artery pressure behind the embolus enough to dislodge it. Doesn't always work, but worth trying.
238
How should you refer for a patient with CRAO with an embolus and without suspicion of GCA? [2]
Refer to ophthalm: super urgent [particularly if onset <48 hours]
Refer to neurologist for stroke assessment and management
[*super urgent = same day referral]
239
After referring and treatment, how should you monitor a patient with CRAO?
Monthly monitoring to check for development of neovascularisation/NVG.
(Wills Eye Manual says 1-4 week follow up)
240
What is the prognosis like for CRAO?
Poor
241
How does the management of BRAO differ from CRAO?
It doesn't. Mx as per CRAO.
242
What is the incidence of choroidal naevus in caucasian?
6.5% [Blue Mountain Eye Study]
243
What does TFSOM-HHD stand for? [identifying choroidal melanoma]
Thickness >2mm
Subretinal Fluid
Symptoms [reduced vision, floaters]
Orange pigment
Margin <3mm from optic disc
Hollowness in ultrasound
Halo absent around lesion in fundus
244
What percentage of choroidal naevi meeting one criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?
3%
245
What percentage of choroidal naevi meeting 2 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?
38%
246
What percentage of choroidal naevi meeting 3 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?
58%
247
What percentage of choroidal naevi meeting more than 3 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?
Likely already melanoma
248
When should you refer a choroidal naevus to the ophthalmologist? (2)
Any new symptoms
Change in size
249
How long does it take choroidal naevi to acquire pigmentation?
After it's been there for about 6-10 years
250
What dietary choice promotes progression of AMD? [1]
Saturated fats
251
What dietary choice has a protective effect towards AMD? [2]
Omega-3
AREDS 2 supplements [Macuvision]
252
Is smoking a risk factor for AMD?
Yes
253
When should you refer AMD to the retinal specialist? [3]
Foveal thickness >300 microns
Central retinal thickness >350 microns
Wet AMD [for aVegF]
254
What size drusen is considered normal ageing?
small [druplets] <63 microns [<1/4 BV]
255
What size drusen is considered early amd?
Intermdiate drusen 63-125 microns [<1/2 BV]
256
What size drusen is considered intermediate amd?
large drusen >125 microns [size of vein @ disc]
257
What is required for a grading of late amd? [2]
Geographic atrophy or neovascularization
258
Within what range from the fovea is pathology counted for AREDS calculation?
Pathology within 2DD away from the fovea is assessed
259
List the 5 components towards AREDS calculation for the risk of AMD progression to Late AMD in 5 years
Hyper/hypo/disrupted pigment (>1/4DD) = +1
Large drusen = +1
*Reticular drusen = +1
*Bilateral intermediate drusen = +1
*End-stage AMD in fellow eye = +1
* = modifier.
260
A good mnemonic for things to consider in AMD patients is DRUSEN. What does it stand for?
Diet
Relatives
Use of amsler
Smoking
Eye tests
Nutritional supplements
261
At what stages of AMD are nutritional AREDS 2 supplements mainly used for? (2)
Intermediate AMD
The fellow eye of one eye with late amd
262
What is the benefit of taking AREDS 2 supplements?
reduce the risk of progression of intermediate AMD to late AMD
263
Can AREDS2 supplements stop progression from early amd to intermediate?
No. They can only stop progression from intermediate to late.
[https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/age-related-macular-degeneration/nutritional-supplements-age-related-macular-degeneration]
264
What is the benefit of AREDS2 supplements compared to AREDS1?
AREDS2 does not contain beta carotene, which can increase the risk of lung cancer in people who smoke or used to smoke.
265
At what stage of AMD for either eye is home monitor with amsler grid most appropriate?
Intermediate AMD. This stage can be unpredictable, and monitoring at home can be useful for early diagnosis of CNV. [The earlier the diagnosis, the better the outcome]
266
What are 7 indications to perform amsler grid in clinic? [i.e. suspected or confirmed conditions]
Wet AMD/CNV
CSCR
ERM + other vitreoretinal interface diseases
Acute Macula Neuroretinopathy
CME
NAION
Pituitary tumour
267
How might CSCR appear on amsler?
it can cause a round or oval central scotoma, depending on the shape of the neurosensory retinal detachment
268
How might CME appear on amsler?
things may appear smaller (micropsia)
269
How might NAION appear on amsler?
it may reveal an altitudinal visual field defect.
270
How may a pituitary tumour appear on amsler
it may be used to demonstrate a bitemporal hemianopia
271
What is another name for dry amd and wet amd?
Atrophic amd
Exudative amd
272
Can late stage AMD with geographic atrophy progress to wet AMD?
They are 2 distinctly different entities, however it is possible for exudative AMD/CNV to develop in an eye that already has late stage geographic atrophy.
273
Would amsler grid home monitoring be appropriate in an eye with late stage atrophic AMD [geographic atrophy]? Or should it just be reserved for the fellow eye only?
It depends on their level of vision and the size + location of the geographic atrophy. If they still have acceptable area of central vision, you could monitor for wet amd in those regions
274
Can wet amd occur in an area with existing geographic atrophy?
No, I'd imagine not. The RPE, which generates vegF, has died at the site of geographic atrophy. So any wet amd/cnv that subsequently occurs would be outside of this area, where vegF is still being produced.
275
Briefly explain the pathogenesis of geographic atrophy
Insufficient vegF delivery from the RPE to the choriocapillaris due to thicker BLinD and accumulation of lipofuscin in RPE results in the atrophy of both.
276
What risk does an AREDS score of 0-1 represent?
Low risk [3%]
277
What risk does an AREDS score of 2 represent?
Medium risk [12%]
278
What risk does an AREDS score of 3 represent?
High risk [25%]
279
What risk does an AREDS score of 4 represent?
Very High risk [50%]
280
What might drusen regression on OCT precede?
Progression to geographic atrophy
281
How often should you review the following AREDS scores:
0-1:
2:
3:
4:
0-1: 2 years
2: 1 year
3: 6 months
4: 3 months
282
Which AREDS scores should home monitor with amsler?
2+ points.
283
Is early AMD worth monitoring at home with amsler?
Not really, unless it's the fellow eye of a late stage AMD.
284
When should you refer wet AMD?
immediately. It's urgent. Because of the rapid growth of CNVMs.
285
What is the prognosis breakdown for wet AMD patients following aVEGF
1/3rd benefit forever
2/3rds will decline in 2 years
286
How soon should fluorescein angiography be performed on a patient with CNV?
Because of the rapid growth of CNVMs, Fluorescein angiography should be performed no sooner than 72 hours prior to treatment. [i.e. the treatment should stabilize it, to allow a better idea from FA results I guess?]
[AMD Clinical Practice Guidelines 6]
287
When after aVEGF treatment should the patient be evaluated?
2 weeks post treatment. I believe the ophthalmologist may handle this.
288
When no further leakage is detected from a wet AMD/CNV patient, what should the review schedule look like?
Rev 6 weeks, then every 3 months for 1 year, then every 4-6 months thereafter
{AMD Clinical Practice Guidelines 6]
289
List 5 signs of CNV recurrence
Decrease in VA
New scotomas or dysmorphopsia
New areas of focal hypopigmentation at the edge of an area of laser treatment
Persistent subretinal or sub-RPE fluid
New specks of subretinal blood
290
What grade is the AMD in the eye of a patient with intermediate drusen and PED?
Intermediate AMD. The existence of PED makes it intermediate, instead of early.
291
What general percentage of wet AMD patients will develop PED [Pigment Epithelial Detachment]?
About 80% [Fibrovascular in particular is present in 62-80% of eyes with wet AMD]
292
Can PED occur in patients with intermediate amd?
Yes
293
What are the 3 types of PEDs associated with AMD?
Serous PED
Drusenoid PED
Fibrovascular/Haemorrhagic PED
[https://link.springer.com/article/10.1007/s40123-020-00291-5]
294
Briefly explain the pathophysiology of serous PED in AMD patients
Avascular serous PED: Increased thickness and lipid deposition in the bruch's membrane reduces it's conductivity and makes it more hydrophobic. This creates a barrier to fluid passage from the RPE to the choriocapillaris.
Vascular serous PED: neovascularisation leakage at the bruchs membrane, increasing hydrostatic pressure to cause RPE detachment. [theorised by Gass]
https://amdbook.org/content/serous-ped-0 - the gass info found from here
295
Briefly explain the pathophysiology of drusenoid PED in AMD patients
Thought to be a product of enlargement and coalescence of soft drusen
296
How does the AREDS study differentiate large drusen from drusenoid PED?
Large drusen: >125 microns
Drusenoid PED: >350 microns
297
Briefly explain the pathophysiology of fibrovascular PED in AMD patients
CNV - new vessels access the sub-RPE space through breaks in bruch's membrane. The new vessels usually proliferate laterally between the RPE and bruch's membrane.
298
How do serous PEDs appear on OCT?
Dome-shaped elevations of the RPE with sharp borders over a uniform hyporeflective space.
[NB: Serous PED can be due to either AMD or CSCR. Older people, think AMD, Younger people think CSCR. CSCR will have increased choroidal thickness whereas AMD will have a thinner choroid. Can try optos FAF to check for fluorescence to also help distinguish if need be]
299
What finding on an OCT of a serous PED can imply the presence of CNV? (2)
The presence of intraretinal (IRF) or subretinal fluid (SRF)
Hyper-reflective structures within the PED
[http://assets.markallengroup.com/article-images/image-library/147/uploads/sites/9/2014/07/772507Figure-7.jpg]
300
What is a more definitive way we can rule out CNV in a patient with serous PED with suspected CNV?
Fluorescein Angiography
301
How do drusenoid PEDs appear on OCT?
They appear as RPE elevations over homogenous mildly hyper-reflective spaces
[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig4_HTML.png?as=webp]
302
How do druesnoid PEDs appear on fundus?
Well-circumscribed yellow-white elevations of the RPE that are usually within the posterior pole. Their borders are usually scalloped and they may have an irregular surface with areas of hyperpigmentations.
[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig3_HTML.png?as=webp]
303
How do serous PEDs appear on fundus?
Dome-shaped elevations of the RPE with sharp borders
304
How do fibrovascular PEDs appear on OCT?
Irregular elevations of the RPE with an interior that is optically not empty [there are areas of both hyper and hypo-reflectivity]
[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig7_HTML.jpg?as=webp]
305
What additional test can you perform in clinic when you suspect vascularisation in your PED?
OCT-angiography. Check for presence of abnormal vascular complex.
306
What percentage of AMD patients present with a serous avascular PED?
10%
307
What percentage of serous avascular PEDs will progress to CNV?
32-39%
https://link.springer.com/article/10.1007/s40123-020-00291-5 - natural course and treatment options section
308
What percentage of serous PEDs will eventually flatten and become atrophic?
21-38%
309
What percentage of serous PEDs will remain unchanged within an average follow up period {between 6 months to 2 years]?
22%
310
Are any treatments available for serous avascular PEDs?
No
311
Do serous avascular PEDs usually constitute and immediate threat to vision?
No
312
How are serous avascular PEDs managed?
Regular follow up and monitoring
313
What percentage of AMD patients will have drusenoid PEDs at some point?
8%
314
Are there any recommended treatments for drusenoid PEDs?
Currently no.
315
How should drusenoid PEDs be managed?
Regular follow up and monitoring
316
What percentage of patients with fibrovascular PEDs will experience significant vision loss (> 3 lines) during their first year if no treatment?
50%
317
What should you do if you see a fibrovascular/haemorrhagic PED?
Refer to ophthalm. They will need aVegF.
318
What is one important complication of PEDs in wet AMD patients that we should look out for?
RPE tears
319
How do RPE tears appear on fundus?
Large areas of bare choroid adjacent to an area of hyperpigmentation
320
How do RPE tears appear on OCT?
Focal, sharp disruption of the RPE, with hyper-reflectivity of the underlying choroid at the area of absent RPE
321
Where in association with the PED does an RPE tear typically form?
At the base of the PED, near the intersection of attached and detached RPE
322
Should aVegF treatment be continued in patients with PED and an RPE tear?
Yes. There is a degree of controversy, but currently multiple studies suggest continuing aVegF improves visual outcomes, and that aVegF treatment following an RPE tear can be of benefit.
323
What is CSCR?
Central Serous Chorioretinopathy. Is when you have subretinal fluid with RPE thinning +/- choroidal thickening.
(NB: subretinal fluid is directly above the RPE, so RPE intact unlike PED)
324
Briefly describe the pathophysiology of CSCR
Damaged RPE leaks fluid towards the retina
325
which age and gender most commonly present with CSCR?
20-40 year old males
326
What are the main risk factors for CSCR? (2)
High stress or psychiatric disorder [e.g. depression]
Type A personality
327
Are corticosteroids a risk factor for CSCR?
yes
328
How does CSCR typically affect vision? (2)
Sudden unilateral painless central vision loss/disturbance [typical VA 6/9 - 6/36]
Hypermetropic shift [~+0.75]
329
How might CSCR affect visual field?
Relative central or paracentral scotoma
330
Is metamorphopsia a symptom of CSCR?
yes
331
How does CSCR appear on fundus?
Oval/round lesion about 1-4DD wide, clear SRF. Is hard to see [translucent + gentle slopes]
332
How does classic CSCR [aka local serous detachment] appear on OCT?
Usually a central + foveal elevation which occurs directly above the RPE, leaving a hyporeflective/dark space undernath
333
What proportion of CSCR cases are local serous detachment?
25%
334
How does CSCR appear on FAF?
Localised lesion with prominent bright halo
335
How does CSCR appear in late-stage of fluorescein angiography?
smoke stack
336
How do we normally manage cscr?
No treatment usually, monitor every 6 to 8 week until resolution [wills eye manual]. [CSCR lecture says 4 weekly review]
337
Should you do a dilated eye exam if you spot a cscr? Why?
yes. To rule out a choroidal tumour or rRD.
338
When is fluorescein angiography indicated in a patient with CSCR? [3]
If diagnosis is uncertain/atypical presentation
If CNV is suspected
If considering laser treatment
339
How long do local serous detachment CSCRs typically take to resolve?
75% of patients spontaneously resolve in 6-9 weeks
340
What is the typical prognosis for a local serous detachment CSCR?
Excellent
341
When is laser surgery indicated in a patient with CSCR?
Persistence of a serous detachment for several months
Recurrence in an eye that sustained a permanent visual defect from a previous episode
Occurrence in contralateral eye after a permanent visual defect from a previous episode
Patient requiring prompt restoration of vision (e.g. occupational necessity)
342
Does laser therapy for CSCR come with an increased risk of CNV development?
Yes it can, hence they use low laser intensity to help mitigate that
343
What type of non-laser treatment might chronic CSCR respond to? What can this treatment do?
Photodynamic therapy: can reduce SRF. Particularly good for if very diffuse pattern
344
How is Diffuse Retinal PIgment Epitheliopathy (DRPE) distinguished from classic serous detachment cscr? [3]
Areas of RPE atrophy [best seen on FAF with RPE dropout and long "tail"]
Choroid thicker than normal [>300 microns]
Often occurs alongside a focal PED.
345
What percentage of CSCR is DRPE?
75%
346
What type of laser surgery is used in chronic cases of cscr/drpe?
focal laser
347
How long would you typically observe CSCR for late recovery until deciding to do laser?
Up to 26 weeks at most. Would probably refer before that.
348
When may be a good time to refer patients with chronic cscr?
After 12+ weeks have passed without resolution, can refer for a fluorescein angiography to assess the state of the choroid.
349
What is the prevalence of epiretinal membrane in patients over 50 years old?
6%
350
Can epiretinal membrane occur in children?
yes but rare
351
What percentage of epiretinal membranes will be secondary to a PVD of some kind?
90%
352
Other than PVD, list 3 other posterior conditions an epiretinal membrane may be secondary to
Vascular retinopathy
Diabetic retinopathy
Blunt/penetrating trauma
353
What surgeries/treatments can potentially lead to epiretinal membrane? [4]
Cataract surgery
rgRD surgery
Laser
Retinal cryotherapy
354
What is the incidence of symptomatic epiretinal membrane following rgRD surgery?
4-8%
355
What actually is an epiretinal membrane? Briefly describe it.
abnormal fibrocellular tissue/fibrosis on the retinal surface. Usually relates to an inflammatory process (b/c fibrosis)
356
What proportion of idiopathic epiretinal membranes are bilateral?
20-30%
357
What is the main symptom of epiretinal membrane and what does this tell us?
mild blur +/- metamorphopsia (if macula region is involved]
358
According to Gass' classification of epiretinal membrane, what is Grade 0?
Translucent membrane with no retinal distortion
359
According to Gass' classification of epiretinal membrane, what is Grade 1?
Irregular wrinking of the inner retinal surface + retinal distortion
360
According to Gass' classification of epiretinal membrane, what is Grade 2?
Opaque thick membrane, macula pucker/distortion of foveal pit
361
What may present as an early sign of epiretinal membrane on OCT?
Hyper-reflective little bump on the retinal surface
362
What should you look out for on the OCT of a patient with epiretinal membrane? (2)
Traction
Macula thickening + oedema
363
What might a patient commonly report in history if suffering with an epiretinal membrane, VMT, or any condition that has elicited metamorphopsia?
closing one eye to read [the eye with distortions/metamorphopsia]
364
What percentage of ERM patients also have vitreous adherence to the macula [VMA]?
About 57%
[https://www.aaojournal.org/article/S0161-6420(15)01270-1/pdf - ERM and VMT preferred practice patterns]
365
What is the difference between Vitreo-macular adhesion (VMA) and Vitreo-macula traction (VMT)?
Vitreomacular adhesion is when the vitreous gel is adhered to the macula/fovea. VMT is when this adherence causes the fovea to be raised due to a tractional force.
So VMT is VMA, but with traction.
366
Are epiretinal membranes stable or progressive?
The majority of epiretinal membranes will remain relatively stable and do not require therapy
367
Should patients with epiretinal membranes self-monitor with amsler grid at home?
Yes
368
Explain the pathophysiology behind why most patients experience little to no symptom progression after initial diagnosis.
Membrane contraction of the epiretinal membrane usually occurs soon after its formation and then stabilises
369
What percentage of epiretinal membrane patients show decline in VA over time? How long does this take?
10-25%. Progression can vary from months to years
370
What percentage of epiretinal membranes actually regress by themselves over 5 years?
25%
371
are epiretinal membranes usually treated?
Usually not treated unless progression is found to be faster. Watch + monitor
372
Can uveitis cause an epiretinal membrane?
yes
373
How is a decision for surgical management of epiretinal membrane made?
The recommendation to simply monitor or to perform surgery is mainly based on the patients' discomfort with their vision, along with their understanding of the associated risks [e.g. cataract]
374
Is surgery urgent in patients with epiretinal membrane?
No. It's elective.
375
What is the go to surgery for epiretinal membrane and VMT?
Vitrectomy with membrane peel
376
What is the level of risk of cataract formation post vitrectomy?
pretty high. Such progression occurs at different rates, and may be age dependent. Typically it's progressive nuclear cataract
377
How does vitrectomy surgery for epiretinal membrane affect VA
Usually improves VA but complete recovery is rare.
378
List 3 intraoperative complications to vitrectomy
vitreous haemorrhage
retinal surface damage
peripheral retinal breaks
379
List 3 post operative complications to vitrectomy
recurrence
cataract
retinal detachment
380
When should epiretinal membrane patients be counselled to seek optometric/ophthalmic advice? (4)
increase in floaters
loss of visual field
metamorphopsia
decrease in VA
381
What would be your biggest concern when you see a VMT?
Worried about potential of future retinal detachment
382
Suppose you saw a VMT lifting up the fovea creating a small area of serous fluid underneath, how would you manage this patient? [1st time diagnosis]
Review in 3-4 months. Then 6 months after that.
383
When would you consider surgery/vitrectomy (pars-plana vitrectomy) in a patient with VMT?
When the VMT causes vision loss that start to interfere with a person's normal daily activities
384
When is an appropriate review period for an epiretinal membrane?
once or twice a year is fine.
Could do a 6 month review for a first time diagnosis on a more noticeable epiretinal membrane. But if it's mild on first time diagnosis just see them in a year.
385
What is our target Hba1c to have good control of a patients diabetes
Less than 7%
386
Is a Hba1c of 7.5% ok?
it's ok. Room for improvement but its fine really. Actually is a good target for those taking insulin and self monitoring glucose.
387
What is our target systolic BP in diabetics?
<130mmHg
388
What is our target LDL cholesterol in diabetics?
<2.5 mmol/L
389
What is our target triglyceride level in diabetics?
<2.0mmol/L
390
What is the recommended blood glucose level range for a diabetic?
4.4-7.2 mmol/L
[Mayo clinic - american diabetes association]
391
What our targets for good diabetic control? (5)
Hba1c < 7%
Systolic BP <130mmHg
LDL cholesterol <2.5mmol/L
Triglycerides <2.0mmol/L
BGL 4.4-7.2
392
What should you suspect when a diabetic patient presents with a hyperopic shift?
Macula Oedema.
therefore must do OCT
393
How many diabetics are undiagnosed?
1 in 5 diabetics
394
What is the incidence of diabetes in australia?
4.9% (i.e. 5%)
395
According to the beaver dam study, what was the incidence of any retinopathy (e.g. MAs, haems) in non-diabetics?
6.8%
[5.1% were MAs only, 1.2% were haems only, remainder was both]
396
If you find a dot/blot haemorrhage in a patient that has not been diagnosed with diabetes, what should you do?
Send a referral letter to the GP for a BGL/systemic workup. In the letter, classify the haemorrhage as a mild Non-proliferative diabetic retinopathy.
397
What is a good screening test for a diabetic who has either had a hyperopic shift or severe reduction in vision in one eye?
Amsler grid: check for metamorphopsia from a macula oedema
398
Is smoking a risk factor for diabetic retinopathy?
yes
399
According to wisconsin grading, define minimal NPDR
MAs only
Note, this grading system is old and we now no longer have minimal as a classification
400
define mild NPDR
New grading: MAs only
[Old grading (no longer used) MAs and >/=1 of: haem, HEx, CWS, but not meeting moderate NPDR definition]
401
define moderate NPDR
New grading: more than MAs but less than severe
[Old grading (wisconsin): MAs + haems in at least 1 quadrant + 1 or more of: CWS, VB, IRMA, but not meeting severe]
402
define severe NPDR
4:2:1 rule
MAs + Haems in all 4 quadrants
Venous beading in 2 quadrants
IRMA in 1 quadrant
403
define PDR [3]
Any of:
NVD and/or NVE
Vit/pre-ret haem
NVE <1/2 disc area without NVD
404
define high risk PDR (2)
Any of:
NVD >1/4 to 1/3 disc area or existing with vit/pre-ret haem
NVE >1/2 disc area with vit/pre-ret haem
405
define advanced PDR
High risk PDR with tractional detachment involving macular or vitreous haemorrhage obscuring ability to see/grade NVD + NVE
406
define macula oedema
retinal thickening within 2DD of macula centre
407
Define CSME
Ret thickening within 500um of foveal centre
Hard lipid exudate within 500um of foveal centre
Ret thickening of >1500u which is <1500u from centre of fovea
[NB: 1500u = 1 disc diameter]
408
What is the rate of progression % of moderate NPDR to PDR in 3 years?
30-48%
409
What is the rate of progression % of severe NPDR to PDR in 1 year?
52%
410
How often should you review a diabetic with no retinopathy?
yearly
411
How often should you review a diabetic with mild NPDR?
6 months
412
How often should you review a diabetic with severe NPDR?
3 months
413
when would you provide a prompt referral to the ophthamologist in a diabetic? (4)
Severe NPDR
PDR
Unexplained vision loss
Macula oedema
414
Within what time frame should a referral to the ophthalmologist be made for a moderate NPDR?
within 12 weeks [ranzco].
From here on, monitoring of retinopathy should be coordinated alongside and ophthalmologist.
415
Within what time frame should a referral to the ophthalmologist be made for a severe NPDR?
within 4 weeks [ranzco]
416
Within what time frame should a referral to the ophthalmologist be made for a PDR?
within 1 week [ranzco]
417
Within what time frame should a referral to the ophthalmologist be made for a sudden severe visual loss [vit haem, RD, or rubeotic gluacoma]?
same day [ranzco]
418
When should a referral to the ophthalmologist be made for diabetic retinopathy?
Moderate or worse.
419
What treatment is typically administered for PDR and CSMO?
aVegF
Also can try PRP/focal PRP
420
When may vitrectomy be considered in a diabetic retinopathy patient?
last resort if poor outcome with other interventions
421
is a retinal hole safe when it is pigmented or unpigmented?
pigmented
422
What is the prevalence of WWOP in the general population?
up to 30%
423
List 2 risk factors for WWOP
High myopia
Age
424
What is WWOP indicative of in a highly myopic retina?
indicative of an area where the retina has been stretched, and is correlated with an increased risk for future retinal detachment in these eyes.
[https://www.optometrystudents.com/clinical-guide-to-degenerative-myopia/]
425
How should you manage WWOP?
Watch annually and warn of RD
426
Aside from WWOP, what other peripheral retinal degenerations are associated with retinal detachment? (4)
lattice degeneration
snail track
cystoid degeneration
retinoschisis
[mx similar to wwop]
427
What percentage of eyes with rRD also have lattice degen?
60%
428
What does typical lattice degeneration look like?
Sharply bordered white lines +/- pigment
429
What does atypical lattice degeneration (2)
No white lines
Local accumulation of "snowflakes" [frost like appearance]
430
What is the prevalence of lattice degeneration in the general population?
8-10%
[https://www.asrs.org/content/documents/fact-sheet-33-lattice-degeneration.pdf]
431
Where does regular retinoschisis occur?
splitting along the OPL plane
432
Where does reticular retinoschisis occur?
INL or NFL
433
Which form of retinoschisis is more serious: regular or reticular?
reticular is more serious [but rarely reaches posterior pole]
434
Define PVD
separation of vitreous from the ILM
435
List the 4 stages of PVD on OCT
1. Shallow +/- foveal spot (traction)
2. PVD reaches fovea but doesn't include foveola
3. Shallow ONH attachment + foveal traction
4. Complete PVD
436
What are 2 symptoms a patient with PVD may experience?
Large central ring-shaped floater (weiss ring)
Flashes [occurring opposite in the visual field to where retinal traction is]
437
What are flashes indicative of in general?
traction
438
List 3 signs of PVD on fundus examination (3)
Weiss ring
Hyaloid face pulled forwards from retina
Small pre-ret or vit haemorrhage +/- pale ret due to traction
439
What signs of trouble should you look for in patients with PVD? (6)
Tobacco dust (pigment in ant vitreous)
ret/vit haem
cells
traction (white retina)
tears
persistent unexplained photopsia/flashes
440
How should you manage PVD if no concerning signs of trouble?
Follow up review in 2 months with DFE, then reassure + advise to return if symptoms worsen
441
How should you manage PVD if there ARE concerning signs of trouble?
refer urgently.
442
What does asteroid hyalosis look like?
yellow/white specs with clear zone [lipid/calcium deposits]
443
Is asteroid hyalosis unilateral or bilateral?
often unilateral
444
is asteroid hyalosis symptomatic or asymptomatic?
often asymptomatic
445
In what age group is asteroid hyalosis common?
older patients (7th/8th decade)
446
What does synchisis scintillans look like?
White/golden cholesterol crystals found in liquified vitreous
447
Is synchisis scintillans unilateral or bilateral?
Bilateral
448
How do you manage asteroid hyalosis and synchisis scintillans?
No management/treatment.
449
What is asteroid hyalosis associated with? (4)
DM
Hypertension
Atherosclerosis
Hyperopia
450
Is asteroid hyalosis associated with PVD?
Asteroid hyalosis is never found in eyes with PVD
451
How does synchisis scintillans relate to PVD?
Only found in eyes with/after PVD [younger patients after PVD]
452
Things that still need to be covered:
For posterior:
Retinal Detachment + Hole
Macular hole
corneal FB/trauma
For anterior, need to cover:
AAU, episcleritis/scleritis, cataract, bacterial keratitis, herpetic keratitis, conjunctivitis (bacterial, viral, allergic), ocular injury/fb
453
What is a “notch” of the optic nerve?
Focal area of NRR loss where the NRR width has decreased. No more than 4 clock hours of width reduction for it to be considered a “notch”
So an inferior notch means that ISNT rule is broken for that focal area specifically. Where inferior is thinner for those clock hours (4 or less).
454
List 4 additional tests for macula oedema
Visual fields 10-2
Amsler grid
FAF
FA
Gonioscopy (check for neovascularisation of iris)
455
If you are asked about additional tests, what's a pretty safe bet most of the time? And you should probs say it even if unsure
Automated visual fields/perimetry
456
List 6 indications for checking for iris neovascularization on gonio
CRVO
Proliferative diabetic retinopathy
Glaucoma
Macula oedema (especially DMO)
Anything with neovascularization, honestly
Chronic uveitis
Full list here: https://www.aao.org/eyenet/article/diagnosis-treatment-of-neovascular-glaucoma
457
What is another name for neovascularization of the iris?
Rubeosis Iridis
458
What are the 4 stages of iris neovascularisation?
Prerubeosis: no NVI
Rubeosis: NVI (normal IOP)
secondary open angle glaucoma: NVI, NVA, fibrosis, hyphaema
secondary closed angle glaucoma: prev stage + corneal edema and ACG symptoms
[https://www.touchophthalmology.com/glaucoma/journal-articles/reversing-the-rubeotic-rampage-current-approaches-in-the-management-of-neovascular-glaucoma/]
459
How long might it take NVI (neovasc of iris) to progress to NVG (neovascular glaucoma) in diabetic patients?
Usually takes at least 1 year
[Rodrigues GB, et al. Neovascular glaucoma: a review. International Journal of Retina and Vitreous 2016;2:26. https://doi.org/10.1186/s40942-016-0051-x]
460
How long might it take NVI to progress to NVG in patients with CRVO?
NVG can develop within 1 to 6 months
[Rodrigues GB, et al. Neovascular glaucoma: a review. International Journal of Retina and Vitreous 2016;2:26. https://doi.org/10.1186/s40942-016-0051-x]
461
How dangerous is neovascular glaucoma?
Very, it rapidly progresses to permanent and devastating visual loss if left untreated
462
What is the gold standard treatment for neovascularization of the iris?
Pan-retinal photocoagulation (PRP) and aVegF to reduce neovasc. PRP can also be used if patients progress to NVG.
463
List 4 surgical treatments that can predispose to neovascularization of the iris (NVI)
Nd: YAG capsulotomy
Cataract extraction
Pars Plana Vitrectomy
Radiation treatment
[https://www.aao.org/eyenet/article/diagnosis-treatment-of-neovascular-glaucoma]
So could justify doing a gonio if these were recent to up your test numbers. However, incidence is low and realistically you'd do it if you saw elevated IOP or glaucomatous changes.
464
Things to cover next
contusion injuries and wall/floor fractures
