1555hrs Session 4 Panel Discussion, Kevin Wade, MD moderator


What about those who have an EMR.

- may be opportunity in future

Do I just go out and buy some scanners now?

- contact PITO now and get the forms you need

Is this similar to eRx in the states?

- e prescribing not likely til 2012

Any option for Mac based systems?

- not a requirement but some can

Any cost to physician from PITO for review

- no

If almost there with current vendor, what happens to transition to new system

What to do with old records

- most physicians scan old records and tag the sheets as to what they are

With large databases for ophthy needs, will PITO get us T1 lines since PITO does not allow servers in offices

How do you respond to feeling by some specialists that government feels specialist make enough money that no need to find a solution for ophthalmology that would be PITO subsidized

- not true at all, except that there is a cap at 70% of $10,000 for each physician

What do we tell our patients; need explicit consent from patient

Since info stored off site in 3rd party, does that mean others will have access to the data.

- vendors not allowed to disclose the data

- we only need consent to send data elsewhere

Have other specialists come together as a COP?

- rheumatology strongest collaboration

Given amount of data, do you see possibility, will we be charged differently for amount of storage and say something about PITO privacy committee

- vendor not allowed to charge more for more data

- for privacy, there is a committee overseeing privacy and security

Out of all approved PITO approved vendors, none are fully ophthalmology ready...where do we go now?

- do we start with an approved vendor or get another one


1545hrs Physician Information Technology: The EMR & Ophthalmology - Jeremy Smith

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Photo 15.jpg

To give PITO background and where to go with specialists

8-15% EMR adoption in BC; canada supposedly 23%

Other countries almost 100%

What is holding people back from adopting?

Barriers identified:

- set up and maintenance, not just the money but the time with 3-6 months of potential turmoil which can take 1 year to smooth out

- those who have had more than 1 year would never go back

- others concerned about data loss b/o etherial electrons

- success and failures of the past, would like to get rid of charts but then they get what is under the tip of the iceberg to help the team transition

- looked at what alberta and ontario had done re costs, planning, change management

Started with 4 principles

- learn from those ahaed of us, focus on clinical practice, prepare for future and interoperability and privacy concerns

2006-2012 Master agreement with secure private network provided and 70% reimbursement of equipment cost and software, specific vendor requirements, etc

- hope to support 4-4,500 of the 5,000 docs in BC

- currently have 2,000 enrolled

- cover one time and ongoing costs, etc, free access to private physician network

- local implementation and transition support services

1. express interest

2. intake and orientation

3. planning and analysis

4. procurement

5. implementation

6. yadda yadda

Communities of practice

- typically groups in community or specialty get together who have common goals which could benefit from an EMR

- for specialists, this COP model helps find a solution to meet their needs

150 of 2,000 docs in programs live on new PITO qualified EMR.

Has been looking at specialists in general and particular specialists

About 50% of 8,000 physicians are specialists

- about 700 - 1,000 docs in hospital setting

- about 1,000 who are in psychiatry and other specialties that don't lend well to an EMR

- some are in and out of hospital so much they really need module of hospital system

- then different ends of the spectrum of needs amongst specialists from basic scheduling, billing to full blown drawing, etc

Key for specialists

- efficient referral/consult functionality

- simple/flexible screen design

- capture data in templates during consult and have it produce consult report

- pre built diangostic and OR bookings

- billing

- remote access

Ophthalmology has surgical, primarily episodic, and primarily longitudinal/chronic care

Ophthalmology is the one specialty with specific requirements

Recognize need to meet with each specialty group to go forward

Specialist physician champions

New program for template development; 95% same needs for all docs but this last 5% needs the work to get the right templates for ophthalmology. Therefore, by getting groups of all those specialists together, makes it worth the vendors' time/money.

Interfacing of data between systems exists for meds but not yet for referral notes but that is being worked on now

Working with different health authorities a barrier; eg breakdown barriers like firewalls to hospital data on patients

Ophthalmology specifically:

Core EMR requirements same as for other docs

Same list of templates, consult generation, drawing tools, device integration needs seen in other specialists but really key to ophthalmology

Adoption by ophthalmology very slow in the province

No one EMR identified in the province as the clear winner

Not just the complete solution; some just want the basic functionality

Opportunities and next steps

- in depth requirements for ophthalmology

- form Ophthalmology COP

- breakout session following this talk to help shape the direction


1505hrs Session 3 Panel Discussion, Briar Sexton, MD moderator

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Does anyone do Tensilon testing for MG?

- Dr Cockerham opts for Ice test first

- Dr Arnold reports that survey of neuro-ophthalmologists almost never use it

Dr Kazim: does Raider's syndrome exist or were they small dissections that were being missed?

- Dr Arnold: original cases a small mass

Dr Macintosh: Horners associated with subclavian line in ICU, recoverable?

- Dr Arnold, variable

- Dr Cockerham finds chiropractic manipulation, high velocity roller coaster as things to check in your history for Horners

What is your management of atypical optic neuritis if everything normal on work up; do you use steroids?

- Dr Arnold agrees to trial of steroids. Warns that some patients have Sarcoid that could show some response to steroid. Most recent aypical optic neuritis for him was a patient with an adult glioma; thought it was sarcoid, did workup, gave steroid trial, optic nerve got bigger and more enhancing and turned out to be optic nerve glioma.

- Dr Cockerham, seeing some lymphoma and Tb for optic neuritis.


1445hrs Horner's syndrome: when to worry and why - Anthony Arnold, MD

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Painful Horner syndrome: pharmacologic testing, imaging, when to worry and why

- ptosis, miosis plus or minus anyhdrosis

Classic w/u:

- make sure Horners

- localize lesion

- determine cause

Don't really need cocaine testing but useful in small sub-population

- topical cocaine block re-uptake norepinephrine to increase its concentration so pupil should dilate if it is normal

- what do you consider abnormal vs normal?

- partial symp denervation may produce lesser response

- most people would like to see at least a 1mm change

- not that easy to get the cocaine commercially; get from hospital pharmacy, non-preserved, and degrades strength over time

Apraclonidine test taking over from cocaine

- if you have denervation super-sensitivity, the pupil will dilate from apraclonidine

- so positive test is a reversing of the dilated pupil

Photo 14.jpg

Localize lesion cos central, preganglionic, is usually BAD and post ganglionic is usually GOOD

- Hydroxyamphetamine helps localize, as if neuron injured, no release, therefore no mydriasis

- again look for change in the anisocoria

- postganglionic lesion not necessarily very good as carotid dissection is post ganglionic as are skull based lesions

- people who say that localizing is important claim that it will focus where you will look for a lesion - but would you not image everyone anyway?

Where is the pain?

If Horner's these could be dissecting aorta Sx:

- any facial pain, hemicranial or neck pain?

- dysgeusia (metallic taste)

- tinnitus

Chest tumors which tend to be malignant in Horners'

- tend to be slowly progressive development of symptoms

Anhydrosisis a BAD sign, usually pre-ganglionic

Intracranial mass

- horners with numbness of face or other CN

Headache syndromes

- usually produce postganglionic

Confirm it, decide if need to localize, determine etiology, don't order imaging when can't think of reason not to.


1425hrs Clinical approach to diplopia - Kimberley Cockerham, MD

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Different types:

CN palsy

CNIII with dilated pupil

Isolated CN palsy that progresses

Isolated CN palsy that doesn't resolve

Any new CN palsy in cancer presume cancer related

Take home messages:
- slow saccades = brain

- positive forced ductions = orbit


Step 1 assoc'd signs

- VA, pupils, typical exam

- can right off drifting out eye but not a drifting in eye

- CNIII can be confusing, check size pupil light and dark and check for RAPD

- evidence of other disease? inflammation, infection, neoplasis

- brain process, papilledema

- check head position, eyelids, periorbital changes, orbital findings, etc

- look for thyroid findings

Step 2 brain vs orbit

- slowed saccades in brain with normal forced ductions

- exact opposite of above if orbit

- use tonopen for kinder gentler forced duction

Step 3 identify pattern of motility

- does it fit a CN pattern?

- no CN pattern could be orbital or myasthenia

- maddox rod can help for smaller deviations

- CN IV, know if head tilted left it is probably right palsy but some TED patients and myasthenics can appear same way

Step 4: systemic disease

- MG, Graves, Giant Cell Arteririts, Increased ICP, MS

- don't forget typical GCA symptoms and the less common stomach pain from mesenteric ischemia

- the MG package: ptosis, XT, difficulty sustained upgaze, weak orbicularis, try the Ice test using a cold pack on the ptotic eye. If the eye pops up after ice, positive test for MG

Discuss patient 48 you female with left head turn and diplopia

- refractive errors, corneal opacities, lens, iris, macula, neurological, non- pathological

- if monocular, see if improves with pinhole

- if binocluar, no point in doing pinhole test

- thyroid patients more likely diplopic in the morning and MG as they fatigue

- paraneoplastic

- migraine

- Flake!

Back to our patient, diplopia constant except in extreme right gaze

- so esotropia and limited abduction

- has orbital pain, tearing, eyes bulgy, a bit of puffiness to eye

- remote hx of thyroid disease

- no surgical or other traumatic event

- also patient weight gain, fatigue, hair loss

- assoc'd findings: normal vision and pupils, injected conj, inc IOP on upgaze, increase resistance retropulsion

- slow eye movements in this patient, ie slow saccades therefore brain

- so now down to CNVI and related to her diabetes

- normal forced ductions in a patient with CNVI and TED findings

This patient has TED and acute onset of constant diplopia with constant velocity abnormality making this brain ie CNVI


1405hrs Current management of optic neuritis - Anthony Arnold, MD

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Optic neuritis, the final (latest) word

25 yo woman 7 day hx central visual loss, swollen disc: is this typical or atypical?

Will discuss what is typical

- relatively young, female, central unilateral evolving over days, RAPD, 2/3 show normal disc at first

- if do an MRI scan, will it enhance? - turns out yes in 95%

- typically gets better over weeks whether or not tx'd

- only 8% had central defect in ONTT study, though termed typical

- most common pattern was generalized depression (48%) but it is really a central scotoma over a bigger area, more dense centrally

- natural hx is pain to resolve over days-weeks

- visual recovery within 2-3 wks and complete at months

VA outcome generally quite good

Now, the atypical (don't go on to MS):

- systemic illness viral or vasculitis

- atypical demographic

- immune compromised or other immune disease

- no pain

- slow progression of vision loss

- non resolution of pain

- bilateral simultaneous

- macular star (neuroretinitis) ie exudates and hemorrhages

- infectious and non-infectious inflammations

Back to Typical optic neuritis:

Chance of recurrence same or other nerve 36% at 15 years and multiple recurrences more likely to lead to permanent visual loss.

If have optic neuritis, what is the change of getting MS?

- all these are based on ONTT

- overall 30% at 5 years but ranges from 15-51% based on lesions on MRI, eg 51% if more than 2 lesions

- 10 year data overall 38% but 22% with normal scan and 56% with any lesion%

- 15 year overall 50% with 25% if 0 lesions and 72% if at least one lesion!

- corroborated by other international studies

Things that might further increase risk include:

- periphlebiitis

Decreases the risk:

- preceding viral illness, bilat and simultaneous, neuroretinitis, etc

- ie if atypical presentation

Value of MRI?

- best single test of MS risk

- confirm diagnosis if otherwise not sure

- assess end visual prognosis based on location and extent of the demyelinating plaque (if intracanalicular or over a long portion of the nerve)

- this last point variably confirmed over the years

- rule out compressive lesion eg large pituitary adenoma


- oral pred at dose in ONTT, should not be used as no visual benefit and increased the recurrence rate (but perhaps if gave equivalent dose to the IV dosing, it would have helped)

- IV methylprednisolone showed to speed recovery rate but no long-term benefit

- once followed patients beyond 2 years, no longer saw any benefit in avoiding progression to MS with the IV treatment ie reduced 2 year risk progression to MS but same risk beyond 2 years

- ONTT concluded everyone should get MRI to decide whether to treat with IV steroid but MS attacks axons to cause damage so perhaps everyone should just be treated with pulse steroids for every attack

CHAMPS study looking at use of other immune modulating agent

- interferon beta-1a (avonex) treatment vs no treatment

- helped

Other immunomodulation agents being investigated at this time eg copaxone

Problem is treating alot of patients with little risk of progressing anyway.


Be sure ON is typical

Consider IV methylpred or high dose oral

Don't use low dose

Do MRI in all to assess risk

Based on risk, consider immunomodulation


1220hrs Session 2 Panel Discussion, Duncan Anderson, MD moderator

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Dr G Haye: What Tx would you take yourself

- Dr Arnold responds ASA and maybe avastin has some hope for future

- Dr Cockerham responded she would go for Hayreh approach with steroids even though little support

- Dr D Anderson opts for ASA

Dr D Anderson: 2nd eye in younger patients, is this 'disc at risk' patient

- Dr Arnold does believe in disc at risk idea and every one of the younger patients had this so called disc at risk; none of prothrombotic or homocystein factors

- Dr Cockerham adds: FDA advised makers of Viagra to do study to look for causative association of it and NAION. Notes ALL patients who took drug and got NAION had disk at risk, took pill and had sex at night. Therefore, consider sex in AM if disk at risk

Dr V asks: myositis not a listed topic but how would one treat this? Can you have optic nerve glioma with enophthalmos?

Dr Kazim responds: configuration of the orbit can allow for a relative enophthalmic appearance with the glioma just not producing enough volume to produce proptosis. The myositis question is much bigger. In children, some respond to high dose NSAID but others need adjunctive treatment like TGNalpha blockers. In adults with myositis, most respond to steroid and those that recur should be biopsied. Also, in adults, methotrexate can help for those who fail to respond.

Dr Cockerham, says Tx anagous to uveitis eg if recur, more likely to treat, etc.

Dr McFadden: Any CSR related to Viagra seen?

Dr Arnold not aware of any.


1200hrs Current and future management of nonarteritic anterior ischemic optic neuropathy - Anthony Arnold, MD

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Photo 13.jpg

What you should do with a case and with the proposed schemes for dealing with NAION.

Case example

- blurred inf VF while watching TV, no pain, inf arcuate on VF test

- dense hypertension and hyperlipidemia but cos takes meds for both; doesn't smoke except when drinks, etc

- what do you do for tests and Tx?

First, be sure it is NAION

Next, make sure not AION

Evaluate for risk Fx

Provide with prognostic info and balanced counsel

Consider prophylactic measures fellow eye


- BP, DM, Hyperlipid, smoking, and other implicated

- nocturnal hypotension

- do not look for prothrombotic factors

- no association shown routinely for carotid disease

- does Viagra and other PDE5 inhibitors have an association with NAION?: all patients on this drug have other associated risk factors but some studies did show reproducible association

Prognosis in fellow eye:

- Beck et al study, 1997

- 12-19% risk at 5 yrs

- corroborated with other study

- Fellow eye involvement seems to be very high in patients less than 50 yo

Tx attempts

- lots of unproven tx from steroids, BP raising, lowering, electrical stim, apheresis, etc

- will elaborate on failed attempts

- transvitreal radial neurotomy: very problematic data in studies

- maybe vitreous adhesions from a partial post vit detachment was the problem; so tried detaching the vitreous in a group of patients; again something that didn't make any sense

- how about intravitreal triamcinolone as it has worked for different papillopathies? again, conflicting reports on this

- how could reducing surface edema get at the compartment syndrome?

- this leads to anti-VEGF to reduce edema; one study in literature to date - not enough numbers yet

Lastly, what about oral corticosteroids

- Hayreh in Graefe's 2008, at 6 mo VA improved in 69% vs 40% controls

- VF data also improved

- disc edema resolved faster

- problems with this study: control group and treatment group based on patients' choice and medical status as to whether could tolerate; not well masked by investigator

- despite the flaws, maybe some benefit? but most ophthalmologists don't believe this

ASA prophylaxis?

- these patients likely at risk for other vascular complications such as CV disease so ASA may help prevent death from MI or stroke in these patients?


1140hrs Update on the treatment of optic nerve tumors - Michael Kazim, MD

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25% CT/MRI done in wrong place or mis-read

Helps to know what you're looking for

Optic Nerve Glioma

optic nerve, chiasm or diffuse

benign pilocytic astrocytoma, frequently Neurofibromatosis, esp if absent sphenoid wing

70% in first decade; 90% by second

At what point image child with known NF for ON glioma

CT was first improvement over plain films and showed fusiform lesion with no reactive bone changes

MRI also shows fusiform enlargement ON, with mucinous material around the ON

Conservative mgmt

- observe annually

Indications for intervention

- blind proptotic eye, progressive growth,

Surgical approach discussed with issues of how it fuses with many structures

Can MRI identify the tumor free margin?

- this was studied 25 years ago with plain films and CT so wanted to compare

- vision typically bad on presentation except in one patient

- reviewed surgical details based on location within the optic nerve

- findings: MRI not anymore reliable in localizing but could be related to reactive gliosis interpreted as involvement/recurrence

Optic Meningioma

- vision loss slow and progressive

- can be confused with optic neuritis esp in young women

- transient obscuration

- rare nerve swelling

- confounding inflammatory, infiltration, infectious diseases

MRI the gold standard with preservation of optic nerve within the tumor

Conservative management

- slow growth therefore monitor q6/12 with MRI annually

- biopsy very rare - for atypical cases

- transorbital excision?

- transcranial resection no longer has a role unless NLP and proptosis; resection is NOT simple as infiltrative

- RadioTx was considered; as no other medical therapy and surgery more harm than good

- fractionated external beam radiation; no role for gamma knife

- Surgery only vs radiation only groups compared to observed only

- vision better preserved with radiation than with surgery which resulted in lost vision abruptly...even worse if surgery plus radiation


1120hrs Compression optic neuropathy: when "glaucoma isn't glaucoma" - Kimberley Cockerham, MD

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for POAG,

- fam Hx, elevated symm IOP, slow progression but can snuff out near end, classic optic nerve cupping

Cupping of optic nerve NOT synonymous with glaucoma

- wegeners can do it too for example

Need to think of glaucoma as just one of those optic neuropathies

Compressive Optic Neuropathy

- typically no fam Hx glaucoma but still can have

- elevated ASYMMETRIC IOP, but of course if pituitary, can cup OU

Just because lots of red Xs on HRT, does not mean glaucoma

Classic teaching its optic nerve and not brain:

- originates blind spot

- not respect vertical meridian but does respect horizontal

- all these things not exclusive to glaucomatous optic neuropathy

Central scotoma:

- although classic for compressive, she found lots of tumor patients without central defect

Look for warning signs:

Could this be altered outflow?

Listen, look, palpate

- listen for complaints, look with room lights on, palpate eg thyroid, meningioma, CC fistula - can have resistance to retropulsion

Warning signs not glaucoma

- decreased vision


- colour desaturation

- nerve more pale than cupped

- atypical VF defect

Intracranial problems

- pituitary, meningiomas, other parasellar mass/infiltrate

Orbital problems

- TED, Optic nerve sheathe tumour,/infilration

- orbital tumor (eg cavernous hemangioma)

Gives patient example

- more damaged when first seen 2 years ago than expected for glaucoma

- ordered an MRI at that time which showed a massive pituitary adenoma that was interpreted as normal

Another patient:

- slowly progressive VF defect

- intermittent eyelid puffiness: episcleral outflow to orbit altered

- longstanding ocular migraines - when looked laterally, vision blacked out! this is not ocular migraine

- increased resistance to retropulsion one eye

- MRI showed large ON meningioma; responded to radioTx seven years out now

Another patient with sphenoid wing meningioma shown next

- suspect with pain, numbness, eye movement issues, ache or fullness feeling, loss of vision earlier than would expect for just glaucoma

- 75% such patients have ocular hypertension even in primary gaze

- optic nerve can be normal, have a cavitation, and not have swelling, or other compression signs

Warning signs of altered venous outflow eg CCF:

- retropulsion res, proptosis, temp fulness, eyelid edema, injected vessels

- listen Hx of high BP, valsalva, listen for fistula, look for blood in schlemm's canal

- kind of allergic looking eyes in low flow as opposed to corkscrew vessels

ON can be normal or cupped, can have venous dilation, dot/blot heme, etc

- can see enlarged superior ophthalmic vein on US, CT, MRI

Indications for intervention:

- decreased function, pain, inc IOP, disfigurement


- embolization techniques (coils, glue, particulate matter)


- note rounding of eyelids may be only finding around eye

- can have raised IOP even in primary position, but remember check IOP in restricted fields of gaze

- optic disc typically normal but cavitation can happen over time

- VF testing, like other compression ON, central scotoma is classic but often other findings....arcuate, step, etc

- ancillary tests: TSI or TSH receptor here, or Thyroid index (at VA hosp)

- indications for decompression:

--> inc IOP, VF loss, etc

So, how to distinguish: check for the warning signs

- could this be compressive optic neuropathy or altered EV flow

- look, listen, palpate

- look at the scan yourself or have someone you trust look at it.


1005hrs Session 1 Panel Discussion, Peter Dolman, MD moderator

Discussion begins 1040hrs


2/3 Rule

- clinical signs, radiographic signs, lab findings

- Dr Kazim stepwise tests

Dr Cockerham

- opts for all tests at once as some false negative anyway

- eg if hair loss, patient is hypothyroid even if T4 normal now

Dr Dolman

- here we have TSH antibody

Role of OCT

- useful tool in TED

- VF, OCT, HRT, external photos, quality of life survey

Question by Dr SH Lee on how to deal with patient with unilateral TED; if patient very demanding with one eye protruding

- time invested on first visit very important per Dr Kazim

- don't fuss with them surgically in acute phase as discussed

- however, if STABLE unilateral disease, will the other eye become involved?

--> 50% will have 2nd eye involved in first year; the others...quite variable

- Dr C totally agrees, unilateral proptosis more disfiguring. Also, although no solid proof of this, impression that decompression in one eye can trigger disease in other eye

Dr Dolman: TED is self-limiting disorder with inflammatory disorder and while the fire is burning, you don't start your reconstruction. Also, remember the house will have damage from the fire and may never be the same even after reconstruction.

Dr C like to get psychologists involved too if needed

Dr Proctor Q: Is there a role for other immunosuppressive agents in treating TED aside from corticosteroids?

- vast majority of patients will do well if you do nothing so sometimes hesitant to try other agents on these patients; in the future, we will probably have other agents to use but await results of therapeutic trial

Dr D Anderson Q: points out that area of single binocular vision on a VF good tool to show patients their stability

Photo 12.jpg


If Diamox works, when to stop?

- wait til discs no longer swollen

Dr D Anderson: agrees that most patients who come in bad, end up bad. What evidence do you have that steroids help in acute phase?

- Dr C: admits this is anecdotal but no other options; basically to prime them for impending O.R.

No proof of steroids being part of standard of care but no one should go blind in neuro-ophthy without a trial of steroids

Diamox sequels not readily available anymore.

Consider spinal cord tumors in patients and Tb as well if proteins is CSF.

How do you treat patient if has venous thrombosis?

- these patients need surgery; debate whether evacuate or Tx clot

- Tony Arnold puts patients on anticoagulants but not aggressive with TPA or other invasive surgery; do of course Tx the pressure.

- if going down the tube visually and have thrombosis, do have to go on to surgery.


0945hrs Correction of strabismus in thyroid eye disease: lessons learned - Michael Kazim, MD

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Gets show of hand for how many do strabismus Sx for TED

- nobody?

Greatest knowledge in this field from orthoptist colleagues

Take home message:

- most important part to doing this right is a good orthoptist to work with

Active disease phase: 1 yr non-smoker, 2-3 yrs for smokers

Shows histopath TED muscle with lymphocyte infiltration BETWEEN the muscle fibers

Active phase Tx:

- steroids, immunosuppressors, orbital therapy

- orthoptics: Fresnel prisms on non-dominant eye

Operate late, later if possible

- 100 post-op diplopia if operate too early

- also, scleral melt if too early

Decompression will compound motility problems

- transantral results in worsening in 50% with torsional components to so best to avoid this approach of possible

What is stable

- no change signs/sympotoms > 3months

- if strabismus, orthoptics measurements needed to show stability

- monitoring patients' diplopia complaints can be very misleading; may be better re diplopia b/o now both eyes equally bad

- thyroid normal TFTs

- pre-op CT scan NOT helpful in defining eye muscle involvement

- MRI may demonstrate active disease but expensive and controversial

Orthoptics at near and distance

- don't miss SR component that can be missed

Surgical pre-op planning:

- bilateral IR recess for chin up position, elevated IOP, make sure no SR disease, careful to avoid A-pattern

- if horiz and vertical deviation, and small, can operate on both at same time BUT if both are bigger, operate on horizontal component first then vertical as tx horizontal can alter vertical component

- confounding disease: myasthenia (co-exists in 5% of TED patients), variable findings inter and INTRA exam; XT or ptosis suspect MG too

- if prior strabismus surgery, need to get to pre TED alignment

- torsional diplopia extremely rare

INTRA-op planning

- duction testing to see stiffness of muscles

- all muscles involved disease

- no value in resection in this disease

Which muscles and how much?

- length-tension relationship different from standard muscles therefore no good schematics

- therefore, do small, medium or large

- restoration of symmetrical ductions or relaxed muscle positioning both suggested

- avoiding A- pattern has to do with separating H and V surgeries if big

FUSION is your friend.

Adjustable surgery?

- final result for TED post op is 6-8 weeks so can't do usual next day adjustment; so, only for big mistake corrections

IR Recession

- can produce lower lid retraction therefore divide LL retractors from IR, or advance LL retractors, or later date for interpositional graft

SR recession

- max out at SO even with hangback

- may produce upper lid retraction

Mgmt large angle ET

- tendon lengthening

- max recess 8-10mm

Managing conj/tenons

- perilimbal incision, tenons' lysis

Post-op mgmt

- aim to overcorrect ET, under-correct HT

- pulse corticsteroids if inflammation

- force fusion with prisms

Role of orhtoptists throughout

TALK completed 1039hrs


0925hrs Clinical approach to idiopathic intracranial hypertension - Kimberley Cockerham, MD

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A pressure dependent optic neuropathy

Range of pressures just like glaucoma, from 10-20

Crucial point: these patients can go blind. Just like glaucoma as well.

Defined: awake, alert patient

- normal neuro exam, occ. double vision, no other cause (ie Flu, Tb, etc)

- content of CSF therefore important to r/o cause

- not all classic woman of child bearing age who is overweight

- always confusing when patient thin

Specifically ask about drugs including supplements. eg. natural estrogens can be in these

Classic assocn: Vit A, steroid withdrawal, tetracylcine, naladixic acid (cipro etc)

Headache follows whole glaucoma thing, ie worse in AM just like glaucoma's IOP

Nausea, dizzines without syncope, transient visual obscurations (very brief!), intracranial noises/buzzing (like listening to sea shell), double vision horiz persistent at distance

Atypical: other neuro findings

Afferent fcn

- VA, color, VF


- ductions, versions, saccades, cross-cover

Disc Appearance

- NFL, spontaneous venous pulsations (very important tool)


- axoplasmic stasis, disc edema, compression of vessels, ischemia

- these things take time

Why 6th nerve injured: its the non-specific nerve, related to relationship to petrous temporal ridge

Pursuits not enough; patient could be asymptomatic; need cross cover in primary and side gazes

If disc drusen and raised ICP, won't detect disc swelling

B-scan, FA can help identify drusen if not obvious

Other fundus findings: CRVO, choroidal folds, subret neovasc, ION

Beware of cotton wool spots: could be malignant hypertension; also beware of vasculitis or severe abrupt elevated ICP

The work-up

- r/o ext causes

- image: CT or MRI/MRV

- lumbar puncture

- image before tapping so don't herniate the brain if big tumor; looking for massive and venous thrombosis

- structural associations: small ventricles, Chiari malformation, sinus thrombosis

Looking for cause:

- remember to get opening pressure when doing LP, get cells, protein, and save sample too eg if need to culture

- time of day matters for opening pressure too, patient position, too stressed out doing valsalva, if ICP >200mm doesn't make sense

Corbett looked at opening pressure in patients with different body weights and showed no correlation between weight and opening pressure.

Opening pressure not enough:

- infection, inflammation, neoplasia to be considered

Diag confirmed, now what?

- don't be the one to manage the headache; get neurologist or pain specialist

- our job prevent visual loss

Poor prognostic factors discussed (see talk once posted)

VF are key to management, again just like glaucoma

- if normal, observe

- nasal step: diamox 500mg BID,

Management also includes encouraging weight loss, diamox, finding cause, surgery (if diamox not working or not compliant, or VF loss at presentation)

Diamox decreases CSF production; can't be just glaucoma like doses; must be big

Annoying side effects but probably OK if sulfa allergies

Emergent mgmt:

- post-trauma, inflammation, post-infection, etc

- may need steroids

If severe visual loss: nerve sheath fenestration or shunt

Gastric bypass if obese

Admit to hospital if emergent

- consult neurology and neurosurgery

Disk at risk: very ischemic with advanced VF loss

Bad things that can happen with fenestration

- failure to correct neuropathy, conj scarring, diplopia, etc


- meningitis, peritonitis, subdural hematoma, shunt failure, visual loss, death


- glaucoma of the brain

- ICP dependent optic neuropathy

- VF key to mgmt

TALK OVER 1019hrs


0905hrs Controversies in thyroid eye disease - Michael Kazim, MD

Download mp3

Listen (no-flash)

  Photo 10.jpg

Does radioactive iodine have influence on eye disease

role of orbital readiotheraphy and orbital decompression.

I125 RAI a leading mode of therapy in the world.

Trend to completely ablate gland instead of achieving euthyroid state.

Takes up to 3 months

1997 study,does RAI cause orbitopathy

Can steroids prevent progression orbitopathy?

- if don't treat most would get worse anyway, so no control group

Does RAI promote orbitopathy?

- prospective study 443 patients with mild TED (thyroid orbitopathy)

RAI Tx in smokers increases risk of progressive disease - VERY IMPORTANT - by 6 -23%

Smoking also makes medical Tx much less successful.

Avoid RAI in high risk groups (smokers and 4 other criteria...see on-line talk once posted)

If must Tx high risk patient - completely ablate and predose with steroid

RAI studies

- 1991 Donaldson, unclassified disease stage 95% arrested progression, 76% eliminated steroids

- gave data of speakers' own study next

-other studies over the years

- orbital radiotherapy in big Mayo study used stable patients to reach conclusion that RAI no benefit

RAI works for compressive optic neuropathy in acute phase - IMPORTANT

Not effective in others.

Next discusses surgical decompression procedures...

- fatty decompression, if remove enough volume, get effect

- speaker presented own results in 88 orbits

- big proptosis patients get more effect; less effective if much is muscle expansion as the cause

- motility shown to improve

Talks ends 0950hrs.


Welcome to BCSEPS Clinical Day Blog 1May2009

Welcome to the blog from the May 1, 2009 British Columbia Society of Eye Physicians & Surgeons (BCSEPS) Clinical Day on Neuro-ophthalmology and Electronic Medical Records. Each entry has a flash-player for the audio of that talk, a link to download the audio file, and an option to listen if you do not have a flash-enabled device (certain pda/phones.) The slides will be added soon.

Comment on any of the talks

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Just beneath each blog entry for a given talk, there is the option to post a comment. These comments will be reviewed by me for approval after you submit them.


Please post comments on these talks so that we can keep the learning experience going past the conference itself.