Double trouble: Diplopia, pupils, how to prescribe prism, and what to do when things go wrong!


– [Zara] Good evening everyone. Welcome to the Deakin University optometry
alumni webinar, “Double Trouble,” where we will be bringing you insights to those
scenarios in clinical practice where you may have to think twice,
with the help of our presenters, Natalie Dowling, Geoff Sampson,
and James Armitage. I’m Zara Danehsvar, your co-alumni
president of the optometry alumni chapter, and today we are broadcasting live from
the Waurn Ponds Estate at Deakin University,
with the alumni committee members, Amanda Edgar, who’s our co-president as
well, and committee members Ash Chan and Lucy Ainge. Feel free to follow the link emailed to
you for your Intedashboard to fill out your questions during the presentation
tonight. If you have done the CPD with us before,
you would not have received this email so you can use the same logins that you did
last time, nothing would have changed. I’ll pass it over to Amanda,
who’ll be taking over now. – [Amanda] So, today’s webinar will be
recorded and posted online, on the Deakin Alumni website,
just like last time, and a webinar in resources. Please allow three to four weeks before
this occurs following tonight’s presentation. So, thanks for tuning in, everybody. After the presentation today,
like Zara said, you can claim your CPD points by filling in our online quiz. You’ve all been enrolled in this program
before, it’s Intedashboard that we use here at Deakin University for our TBRs,
and you should have received an email if you’re new to this program. If you have any questions after tonight’s
presentation, please feel free to contact one of the alumni committee. So, tonight’s presentation will run for
about 60 minutes. Each speaker will have a Q&A session
following their presentation. You can ask questions by typing into this
question box that you just used through the presentation,
and we’ll filter them to the presenters at the end of their talk. So, welcome to the second optometry alumni
webinar, “Double Trouble.” Our first speaker today is Natalie
Dowling. Natalie graduated from Deakin University
in 2017 and worked for 18 months at a rural independent practice in northeast
Victoria. During this time, and due to her
proximity, she co-managed to glaucoma with ophthalmologists and treated a vast
range of challenging therapeutic cases. Natalie is continuing to further her
experience, living the life of a locum optometrist through Queensland in New
South Wales, part of which involves working as a clinical optometrist in a
visiting clinic, alongside ophthalmologists. Natalie has also completed the ACOs
advanced certificate in children’s vision. We are lucky to have her here tonight,
and her contagious passion for rural health and therapeutics. Thank you so much for joining us today,
Natalie. And now I’ll pass it over to you to begin
your exciting presentation. – [Natalie] Hello, everyone,
I hope you can hear me. Thanks for the introduction there, Amanda. As Amanda said, my name is Natalie,
and tonight I’m just going to be having a little bit of a chat to you about dealing
with topical drug shortages. Which I thought was something of interest
at the moment just because over the last 12 months, we’ve had quite a few
shortages, beginning with Zovirax getting discontinued last October,
and then more recently, having shortages of [inaudible]
and then more extensively, of Flarex this year. So, I just wanted to have a quick chat
with you tonight about what I’ve done in situations where I’ve found myself
either feeling like I wanted a drug that I didn’t have, or worried that I was going
to lose a drug that I really wanted. So we’ll jump right in. Just a little bit more background on where
I’ve been working, when I graduated, as Amanda said, I was working in my
hometown of Yarrawonga, which is that little red dot there. It’s a small town of about 7,000 people,
and we were the only optometrists in the town. So in terms of ophthalmological support,
just a little bit to the right and down, we have one opthal in Wangaratta,
and then over all the way to Wodonga, which is just further over to the right,
another border town, there was a group practise of about five
to six opthal’s there. So, if you look at that red circle there,
you can see we had about seven opthal’s kind of servicing this area,
which is quite highly populated, about 200,000 people. So you can imagine that those opthal’s are
pretty under pressure, pretty full up. So, that was a great learning experience
for me because they were quite happy to kind of manage most things,
especially more complicated therapeutics cases. Really happy to get on the phone which
really helped for us, but also gave them a lot of help in terms
of relieving a bit of that stress for them. So tonight, I’m going to be going through
two cases. The first one I saw in Yarrawonga. So, we’ll jump in. And just before I start talking,
my photos here aren’t of, actually, my patients, they are just ones from the
interweb because I wasn’t able to get a hold of my old, anterior photos. So just excuse me, I think this is a left
eye, and we’re talking about a right. So, just to give you a bit of an idea
there. So case one, about 18 months ago as I
said, I had a 92-year-old female present to me, who was complaining of some blurry
vision and a sore right eye. Not particularly painful there,
but other kind of interesting history was she was on a multitude of medications,
which given her age is unsurprising. But about two weeks prior to her
presentation she’d begun on a new sleeping medication which she really felt was
knocking her around, and then she was becoming quite drowsy
throughout the whole day and sleeping exceptionally heavily. Other ocular history that we found
recorded, just she had some bilateral IOLs and a bit of dry macular there,
so eye vision wasn’t going to be 6/6. Unclinical presentation,
right eye was was quite down, it had 6/60 in the right eye,
no improvement on [inaudible] and 6/9 which was normal for her in the left. And when we scanned her up,
we found this huge epithelial defect taking up most of the cornea. It was only epithelial, but it was large. And then there was quite a lot of corneal
edema, which was accounting for a lot of that reduced vision there. Pressures were normal. What we could see if you interior chamber
through that hazy cornea looked okay, but it was mainly this big epithelial
defect that we were interested in. In regards to differentials at the time,
we were thinking something probably traumatic just because of the sudden
onset, and that appearance of the cornea. So we’re looking at probably an acute
corneal abrasion, or even considering it had something more [inaudible]
corneal abrasion. But that would be very,
very large for that, but it could be. So, I diagnosed, initially,
an acute corneal abrasion, and treated quite conservatively, I think,
just with a bit of Chlorsig ointment three times a day as a bit of prophylaxis,
and also keeping that eye nice and moist. And then also some preservative-free
lubricants hourly, and set their review for one day just
because of that vision being so poor. So, following up one day later,
things are going pretty good in terms of how our patient was feeling. And her vision had picked up there a bit,
you can see there, at 6/30. So, much better than 6/60, but not ideal. But what did concern me was there was this
central area of a line staining which appeared epithelial, kind of like…well,
now we can kind of see what I’m looking at there. So, it’s a raised area centrally,
with these bold type endings. So, pressures were good,
the anterior chamber was fine. So, I have to reconsider our diagnosis
here. So first of all, it could be the corneal
abrasion just healing over. Because quite often when you’ve got such a
large abrasion, the cells can kind of clump up where they’re trying to
re-adhere and build up. But we had to introduce a new differential
of a secondary traumatic herpes simplex keratitis. Which, given her age and potentially her
immune system, given her age and medications, it could be quite obtuse. So, that was our other differential. When I go treat this,
I had a chat to my mentor at the time, my boss, and I also had a little word on
the phone with the opthal who was 40 minutes away. And we all decided the best possible thing
to do here was was to treat as though we’re treating for the worst possible
outcome. So, if we overtreat it with some aciclovir
at the time, we weren’t going cause, hopefully, any long-lasting effects. But if we were to leave this and just
treat it as though it was an abrasion healing,
you’re more likely to have…more risk of having reduced vision in the future if
that all goes untreated. So that’s what we did. We treated it with Zovirax five times a
day, and we just started to review that following day. On the following day, when she came in,
there was next to no corneal staining, that line stain, that epithelial defect
had kind of healed over, and her vision was back to normal. So, that was pretty conclusive to us that
perhaps it wasn’t a secondary HSK. Reason being is that something… Oh, an HSK of that size generally wouldn’t
have been able to heal over overnight. That would be something that would take a
little bit longer. So ongoing, we just popped this patient on
some gels that night, and she was relegated to her GP,
and she was going to have a bit of a chat to her GP about maybe preventing this in
the future. Because we did think it probably came from
her being knocked out from those new sleeping meds, and maybe just brushed
across that eye, causing this abrasion. So you might be thinking at the moment
[inaudible] had Zovirax, you were supposed to be talking about
shortages. What’s your deal here? But when I got a notification,
I actually got it on Facebook last year, that Zovirax was going to be discontinued,
this case sprung to my mind immediately. Because immediately,
I was concerned and I just thought what would I have done if this patient had come
in and I needed to treat her and I didn’t have that available? As a 92-year-old patient in a rural
area…well, not because she’s in a rural area, but as a 92-year-old patient,
her mobility was not ideal, so trying to get her off to see a GP to
get some orals, especially when we’re not hundred percent sure that’s all it is,
is a bit of a pain. Not to mention the time that it would take
for if we were to decide to send her elsewhere, to an opthal or something. And also, the costs involved in going to
see someone else, if we didn’t have to have access to that topical ointment. So, I felt really lucky that
we had it there. And I was a bit concerned if we were going
to lose that topical aciclovir, what would we do? In my scaredness, I spoke to my mentor and
we did a little bit of a retrospective clinical review of what we’d been doing
over the past two years, as she’s been there for two years.
I’d only been there for six months. But we had a look at what we’d actually
been prescribing, and we found that over a two-year period, our practise had
prescribed Zovirax two or three times per month over that period. So, that’s about every two weeks. Given that two of those were misdiagnosis,
so the one that I’ve just mentioned…or not misdiagnosed, but a suspected and
incorrect suspicion. One there, and another one by me,
so my mentor was obviously a little bit better than I was. But anyway, so he was still prescribing it
fortnightly over that two-year period, so we were obviously concerned. So first thing we did is I had a bit of a
chat to our local pharmacists around town and just explained to them that I was
concerned that we would run out of this drug, and could they just keep
us updated on how much they had left in supply. We ended up running them dry before
AciVision got TGA approved, so we were pretty happy that AciVision got
approved when it did. The other thing that my mentor and I did
is that we came up with a treatment plan for how we’d be able to treat this if we
didn’t have the topical ointment available to us. So for us, that involved immediate
referral to a GP for orals, and so then, they could go through their current meds
and see if there was any interactions there. But yeah, so referral to a GP for orals,
and then be reviewing daily. Which daily reviewals for a HSK is not
generally what I would do, not necessarily. I might be checking a HSK every two to
three days. But because we’d be possibly treating a
different way treating with that oral, as something that I don’t do every day,
we’d be shortening those review times so we can make sure that this isn’t going
haywire and doesn’t need to see someone else. Thankfully, we didn’t have to do that
because TGA approved AciVision in a relatively short amount of time. So in regards to the TGA,
you might be thinking why did we go to all that fuss, creating a management plan and
chatting to our pharmacists when, obviously, TGA was going to approve the
AciVision was a given? It wasn’t really, in my eyes. The reason for that is that if you have a
look at the TGA website, it generally takes 12 months for a new
drug to be approved by TGA. And if it’s not approved by TGA,
the Therapeutic Goods Administration, if you’re not familiar,
if it’s not approved by TGA, it cannot be stocked or supplied in
Australia. So, that was a bit of an issue. I thought if this is going to take 12
months for a new medicine to be approved, then that’s 11 months,
that’s 20 cases of HSK that we’re going to have to be doing all this running
around, inter-referring, which is just a bit of a pain. So, the reason that TGA approved this a
bit quicker, a couple of reasons. Probably first, if you can see on the
right, it’s very, very small there, so apologies for that. I’ve got a screenshot there of the
medicine shortages information. And that there states that, in the red,
it says “critical.” So that’s just saying that the loss of,
the shortage of this drug to the Australian market was deemed a critical
impact on our patients, so TGA is going to do their best to find a
replacement quickly. And also, TGA had previously approved
AciVision temporarily back in 2016, when we had a shortage. So, that’s why TGA came through so
quickly. But what I wanted to get from this case
was that when you’re in a situation where you’re not sure, where you’re faced with
doing something that’s quite different to what you’d usually do, the best thing,
the best way, I think, to go about it is to have a plan. So, have a plan of what you’ll do if you
can’t get access to your drug. And make sure that if you’ve got more than
one practitioner in the practise, that you all kind of agree on that,
I think is important. Because then you can bounce off each other
and go from there. For the sake of time, we’ll move along. So we’re just going to move on to case
two, which is one that I saw only a couple of months ago now, in a rural practise,
southeast Queensland. So, this lady presented with a left red
eye, it had been there for about a week. She was noticing some occasional
throbbing, but generally the eye’s all right. She had no other health concerns,
and she explained that she was pretty much just there because her boyfriend had told
her that it was pretty red and it wasn’t getting better. Her boyfriend and their family
were a bit concerned. So, having a look at the eye,
visual was great, the cornea was no problems, and the anterior chamber was
nice and quiet. But just nasal on the left…nasal of the
cornea, I should say, on the left cons we had this raised,
staining lump. I’ve written there grade 2 from scale
hyperemia, that could go up to grade 3, I reckon.
It was pretty red. So just imagine in your head some really,
really, really nice red lump on the [inaudible]. So,
her differentials were inflamed pinguecula because it’s not encroaching over the
cornea, a bit of [inaudible] episcleritis,
or more seriously, can’t ignore more serious differentials of things like
conjunctival epithelial neoplasia. I was pretty confident that it was an
inflamed pinguecula, so usually I’d treat with Flarex three
times a day. But unfortunately, this one wasn’t…we
couldn’t get the Flarex at the time. So, I had to think of something else. So I discussed with my patient at the time
what she wanted to do, whether we change her to a different
steroid, a weaker FML, or a stronger Maxidex,
or we could go for even an NSAID. But the patient really didn’t seem too
fussed, so I said, oh, just go try some lubricants for a couple
of days, and it’ll calm down on its own eventually. So I said, here you go,
and just Nurofen if it gets painful. But I set a review for a couple of days
later, and in she came. Nothing had changed,
in terms of the clinical appearance, but the patient…I don’t know if she had
a party or something on the weekend, but she was noticing that the wound was
getting a bit more painful. She really wanted to get rid of it,
she wanted to try steroids, she told me. So, probably two main options here. I could have gone for FML a couple of
times a day, or a Maxidex a couple of times a day. And I just thought look,
if I’m going to hit it, I may as well hit it hard. So I just smacked her on some Maxidex
three times a day and thought I’d review her in a couple of days. I let her know that she should definitely
call me, like I tell all the therapeutic patients that I see,
if you have any problems at all, please call. I’m really hoping they don’t call because
that means I maybe mucked up. But she called, so that was very
frustrating. And when she called,
she just explained to me that when she put in the drop the first time, she,
for about a 15-minute period, she experienced a little bit of nausea and
maybe a little bit of dizziness. But that subsided quite quickly, so she,
the next morning, thought she’d have another go, and had the exact same
response, with a bit of nausea and a bit of dizziness there. So, she very well may have been having a
reaction to Maxidex. When I looked into the chances of nausea
or dizziness, it’s about 1 in 5,000, so not common, so a case of a little bit
unlucky, I reckon. But yeah, not common,
but that definitely can be a side effect, so I thought, let’s get her off this. In regards to how the eye looked,
it was starting to look…it was already improving just after two drops of Maxidex,
which was beautiful, but I wasn’t keen on keeping her on it. So instead, I swapped her down to some FML
four drops a day, just that little bit more frequently because it’s the weaker
steroid there. And I just explained to her the importance
of doing a frontal occlusion when putting those drops in to reduce the amount of
systemic side effects. And lastly, I drafted a letter to her GP
again, because it’s really important to keep them up to date if you are kind of
concerned that maybe a patient has a bit of an allergy or something to a drop or
anything, the GP should be kept in the loop for further things down the track. So the reason this one I thought I’d share
with you is because I maybe was a little bit too quick on going off to the Maxidex. Maxidex isn’t something I prescribe
frequently, and so maybe I should have thought a little bit more before I put on
the Maxidex. But bottom line was a patient came in with
a problem, the patient’s problem was fixed. It might have taken a little bit of
mucking around, but we did fix her problem with the FML, cleared it right up in a
couple of days. So my point to you there is that when
you’ve got a drug in shortage, consider your other options,
but just go easy on yourself. We’re all learning to be optometrists
here, so go easy on yourself. If you do something and it doesn’t work,
try something else. It’s okay. Probably don’t try too many things,
maybe send them to an opthal if something’s really not working. But yeah, if something’s not working do
try something else. Don’t get too sour at yourself. So, just some considerations,
why I thought this was still relevant even though we’ve got the Zovirax back now. Where I assume I’m the longest person
here, other than our tutors that have been, you know,
[inaudible] would have been less than five years, I’d say. So, six years is it? But already, we’ve had a couple of these
shortages, and we’ve had these discontinuations.
So these are not one-off situations. They’re going to happen again. So, just be prepared for them,
and be positive that you’ll be able to deal with it even if you don’t have
your drug of choice. I would really recommend using the link
just there for the TGA website. As I mentioned before,
the medicine shortage information site on TGA. So, that was where it had the one that
said “critical,” linked down in the bottom corner here. But the reason that is so good, I think,
is that you can look up any drug that you think might be in shortage,
or if you’re concerned it is in shortage. And it’ll definitely give you some dates. So obviously, for AciVision,
it was discontinued, so there’s no return date available. But for the Flarex, it said “This
multi-use drop is likely to be unavailable from this date to this date.” So if you’re not sure if you’ve got a drug
back, you can just check on the TGA website, and they should give you a
good idea of what to do there. Sorry, I’ve just had something pop up on
the side from…a question. And so the other two I’ve touched on here,
so don’t be afraid to change your management plan.
You’re qualified, you’ll be all right. And just lastly, if you are going to
change your management plan, understand that you haven’t done that a
million times maybe, so maybe you want to treat that a bit
closer. So yeah, that’s all from me. Please shove through some questions,
and I’ll do what I can to answer them. So actually, here’s some references I
used. That TGA one more, probably important
there. So I just got a question here,
“How do you decide which steroids to change to, i.e.
Pred Forte versus Maxidex?” Well, great question there.
It’s all to do with penetration. So, I’ll assume that…well, no,
obviously, you may not know that Pred Forte’s going to penetrate deeper
than the Maxidex. So personally, as I said,
I don’t use Maxidex very commonly. Just for anything like a UVI or something
[inaudible] Pred Forte. Really, to be honest with you,
the only times I’ve used Maxidex before working with the opthal is for one
of my post-ops and treating for CMO. Because generally, they’ve been on
Maxidex, generally, some opthal’s have put them on Maxidex post-cataract surgery. So if they’ve got CMO continuing,
I’ll continue with the Maxidex. But other than that,
I don’t really use it very much. Yeah. Any other questions,
chuck them in the chat, and I’ll do my best. “Is there an over the counter aciclovir
tablet in Queensland?” That is a good question.
I should know that, and I don’t. So, yeah. Cool.
I’ll stop there. Thanks, guys.
Hope it was okay. – Thank you for your insightful
presentation. It’s now time for our next presenter. Our second presenter for tonight is
Professor James Armitage. James graduated from Melbourne University
in 1996 and has completed a Master’s of Optometry and PhD in the Department of
Optometry and Vision Sciences at Melbourne University. After a postdoctoral fellowship at King’s
College London and the Baker IDI Heart and Diabetes Institute, he joined Monash
University as a group leader. He joined Deakin in 2012,
and his clinical interests include dry eye and glaucoma. Jame’s optometric research is seeking to
understand the modulators of ocular blood flow and how they affect the eye. We are so fortunate to have his expertise
with us tonight. Thank you for your insightful
presentation. So, I’ll pass it on to you now. – [Prof. Armitage] Excellent. So it’s a fantastic,
exciting day to be speaking with a couple of graduates. So, speaking with them today is super
exciting. And also, it was really exciting about a
month and a half ago to be able to speak…or be taught by Amanda and
Hayley [inaudible] It’s lovely to see…whatever it was,
about 129 of you up there, 130. So, that’s awesome. What I’ll do is talk to you a little bit
about glaucoma. I know you said lots of it,
but this is a kind of a messier case, and it’s something to think about. So, I will begin by acknowledging
out country. I guess we’re all around Australia,
and so I’d like to acknowledge the indigenous people from wherever we are. I’m, at the moment, in Eden,
on my holiday, so I’d like to acknowledge the Yuin people, as it’s their land that
I’m presenting from, and I pay my respect to their elder’s,
past, present and emerging. Okay, so let’s think back to the good old
days, when I’d throw up random pictures and you’d ignore me randomly.
So, we can repeat that all over again. Let’s have a look at this lady who came
into see me. I have permission to show these pictures. These are some images from the left eye. It’s just another disc image,
I think you’ve probably seen hundreds of these before. And when I looked at these,
I was kind of a little bit curious, and I thought that the superior rim was
just looking a little bit different. Anterior looked okay. It just didn’t quite gel with me. And the patient had some other risk
factors, had thin corneas. She’d not had glaucoma before,
she’d not had any respectives that had been measured at the practise where I’d
seen her, other than slightly large cup-to-disc ratios, which were mentioned. So I’d say this is a kind of a normal size
disc, and nothing too massive. Superior rim just a little bit thinner,
superior temporal, than I’d like to see, but otherwise, nothing dramatic,
around .5, .6 cup-to-disc ratio. I couldn’t see anything else of concern. So from this, you know, I don’t know,
are you concerned about this? Would you be concerned?
I don’t know. I can’t actually see any of your
responses, but it’d be worthwhile, you know, just typing in whether you think
you’re worried about this or not. Notwithstanding, I threw her on the OCT
because I was just a little bit unhappy about that appearance of the optic nerves. So I’m sure lots of you have got OCTs in
practise now. This is, as I said, not a massive disc,
it’s sort of medium-sized. I thought, as I said,
superior was just a little bit thin. And actually, when you look at the TSNE
plot, it’s just sitting largely in the green there, which is in the normal range. But I thought, you know,
I just got a feeling about that disc, and I wasn’t overly thrilled about it. I’m a left-hander, so strangely enough,
I start looking at…I [inaudible] with my left hand
most of the time. It’s my preferred hand,
so I tend to look at the left eye first. And you know, I just thought the anterior
rim, they looked a bit smaller on OCT than it should be as well. But nothing really massive that I was
concerned about. One thing, I think it’s important,
is that if you’re looking at OCT and you’re just looking down at the colours,
that’s a fully green OCT box pot. So, it’d be pretty easy to just say yeah,
that’s fine, nothing to worry about. But I was a little bit worried about the
superior rim. I think it’s thinner than it should be,
even though it’s within the normal range. Cup to disc is around .6, so you know,
it’s really not a huge cup. But it’s a 1.5 disc, 1.56-millimetre disc,
so, you know, not great. I’m just a little bit worried. So being a little bit worried,
I also did a ganglion cell, so a vertical scan on the machine that
I’ve got in the practise, and largely, it didn’t really come up with anything,
either. By the way, when I look
at ganglion cell… Just getting my error here
on my laser pointer. When I look at the GCC,
what I look for is that, you know, that C-shape is kind of normal,
and I’m looking for a chop out of either superior or anterior. So in this eye, I guess the superior rim
was just a little bit thinner than I wanted it to be. So, I’d been looking for a chop out of the
ganglion cell [inaudible] superior,
and I wasn’t really seeing much there. So, I don’t know, would anyone do anything
on this, other than watch? Does anyone…? So, you’ve got that sort of suspicion that
there’s something going on…would anyone want to treat on this? Again, I can’t hear or see
what you’re doing. I’m just going to wait,
at least to give me a bit of a feeling about if anyone wants to treat on this,
or if you’re going to watch this? Just type in “watching,” “checking,”
“check on the other eye.” Yeah, definitely. All right, so let’s check on the other
eye, then. So by the way, we did a field on this. This is the left eye field. It’s the first field…there’s a few
scattered losses. By the way, we know that three contiguous
spots at .05 are pretty suspicious for glaucoma, providing it’s repeatable. So when I did this field,
it didn’t make a hell of a lot of sense. I mean, the superior rim was the one that
I thought was a little bit worse. And there’s lots of points, there’s one,
two, three, four, five points in a row. that are pitch black on the pattern
standard deviation, so I’m a little bit concerned still. Does anyone want to treat on this eye yet? Or are you still happy to hang out,
and wait and see? Who wants to…why don’t you type in
“treat,” or “hang out.” So at the moment, I decided to hang out
because I wasn’t quite sure I really could do anything about this. Incidentally, we repeated the field in
this eye, and it was sort of the same but not the same. Still a couple of points,
but not…it didn’t actually look that bad second time around. So, then we went to the other side, yeah. So we repeated the field and got some
similar things, but nothing jumped out. So then we went to the other eye. And what do we think about this right eye? So, we’ve got a right eye, same person.
Is anyone worried here? So hopefully, lots of you have seen it. It’s probably easier to see in the
red-free, but yeah, look at this wedge defect down here. So this, to me, set alarm bells ringing,
and pretty much it sort of, for me, this is…will now tell me it’s not
glaucoma, from now on. So, you know, when we look for glaucoma,
we look for is the [inaudible], but we know in 30% of people who are
normal, it’s not [inaudible] so there’s kind of…you know,
it’s a good sign to look for, but in 30% of people who fail to
[inaudible] that have glaucoma. We know that hemorrhages,
straight hemorrhaging are a pretty strong bit of evidence. But we also know that whilst when you get
a Drance hemorrhage in glaucoma it’s really important, the statistic tells us
that up to 60% of Drance hemorrhages are not due to glaucoma,
they’re just idiopathic. They just happen. So Drances aren’t the sort of
cross-sectional, I’m going to jump the gun for glaucoma. Field losses, as you all pointed out,
field losses are a real mess. Our patients are, you know,
they’re not great at doing fields. But if you see a wedge defect like this,
that should be your best and happiest…that’s what you should be
happiest treating on. So, I didn’t bother repeating fields
because I had repeated fields and done a whole bunch of stuff. As soon as I saw this, that turned, to me,
into this is glaucoma. And interestingly, if we look at the TSNE
plot here…because again, if you’re in the habit of looking at the
colour codes, other than a teeny tiny little wedge down at the bottom,
this is all pretty much sitting in the green still. So again, this is a really important bit
of information, like, don’t look at the colour codes
particularly. Just because it’s red doesn’t mean they’ve
got glaucoma, and just because it’s green doesn’t mean they’ve got glaucoma. This is actually a slightly bigger disk,
it’s around 1.7 millimetres tall, and at .7 cup-to-disc ratio,
it is definitely thin, inferior. And you can also see from the RNFL it’s
thin, as well. And here is where the GCC is looking very,
very suspect as well. So he can see that C-shape has been
chopped out inferiorly, and this is a classic wedge defect. So to me, this is glaucoma. We didn’t do all the rest of it around
classifying and staging. The disc matches the field,
and again…so, this is a much better field, actually,
than the other eye. But it’s definitely glaucoma.
And this was very repeatable. So repeated this field,
and it kept on banging up here. So I guess, now, who’s treating this,
and who’s referring, and who’s going to do what? So just write “treat” or “refer”…or
perhaps “review,” if you want to review. What do you reckon? Notice it’s a pretty good…
it’s a pretty good field. So for me, this is… So, some people are saying “refer,” some
are saying…”new OCT,” “refer…” not quite sure what the
shorthand for those is. I’m just getting more questions coming
through, all your comments coming through to me. So yeah, this one, I just started
treating. I didn’t bother about, you know,
sending her off to Andrew Narita for him to tell me that it was glaucoma,
because I already knew it was glaucoma. There was really no need
to do anything else. So I decided to treat this. And the reason I decided to treat it is
that we have a wedge defect, there’s very [inaudible] we have
a field defect that matches the wedge defect. And then, by the way, her cornea was thin,
she’s diabetic as well, and you’ll see that field
had lost quite centrally. So my thought was, we’re going to have to
go for a 30% reduction. I phased…I can’t remember when I first
saw the patient, but I certainly saw her next time to repeat the field,
and repeat pressures. The highest pressures I could find were R
17, L 14. By the way, I write this on past ocular
history in Optimate. Highest pressures recorded were right in
there, that way you can always see it. You don’t have to go looking for them. So, we went for Xalatan. The reason why, prostaglandins are going
to give us our best chance of reducing, and, you know, why not? So Xalatan was what we went for. We went for a 30% target,
and eight weeks later, she still wasn’t at target. So remember, the next thing to do is go,
well, we didn’t quite get to target. By the way, this is the time that you do
need to definitely get the opthal involved because under the guidelines,
if the patient doesn’t meet target or needs intervention, further intervention,
they do need to make sure they get to an opthal. I’d already written to Andrew and told him
what I was doing, and was following. So when the patient didn’t meet target,
we switched to Lumigan. That didn’t help, it still was around that
R 14, L 12, R 13, L 12, and then we moved to Xalacom. And we went in the morning. So, does anyone want to tell me why we
might have tried in the morning? And has anyone tried in the morning? Yeah, so the Xalacom [inaudible]
So yeah, so remember that the beta-blockers work best during the day
because there’s not much of a sympathetic nervous system to block at night. The [inaudible] around the
prostaglandins, it’s a bit patchy. So most studies say that night time
prostaglandins is slightly better, but prostaglandins are taken in by the
cornea and converted in the cornea. So you can almost think
of it as a pro-drug. And so nighttime is slightly better,
because they peak around one to five hours, or three to five hours
after putting them in. But they have a really long half-life,
so you get the strongest effect within a couple of hours, say five hours of putting
the drug in, but it does last for a long time. And there’s a study that shows
that…there’s, you know, some studies suggest that perhaps Xalacom
would be better in the morning, others say there’s no difference. In this case, we just had a crack and said
why not try in the morning and see if we can get to target pressure? And then after just three weeks on
Xalacom, she’d met her target pressures. So really, I guess what I wanted to sort
of have a chat about is this whole idea around how do we make target pressure?
How do we set target pressure? What sort of…you know,
what sort of factors are you guys using now, when you’re choosing your
target pressures? And, it’s a good thing to think about
because, you know, it’s all right [inaudible] whatever else to just
pick a number, but I try for 20% in everyone. And anyone who’s central,
I go for about 30%, because I figure why not? It’s the best chance we’re
going to give them. We didn’t image this one,
or Andrew didn’t image this lady. We’ve actually treated both eyes because
that left eye, whilst the left eye was a little bit “Are we sure
[inaudible] in the end we just went, well, it’s looking
pretty suspect. So, we gave it a hit, as well. So, are there any questions that anyone’s
going to want to ask? Or anything you think you disagree,
or would have done differently here? – We’re just waiting for questions to come
through from the audience, James. So feel free to type in some questions
into your question box while we’ve got our expert here. But we do have one question for you,
James, in terms of normal-tension glaucoma and neuroprotective agents. So, there’s been a bit of talk in the
media lately about vitamin B12 being given patients with Alzheimer’s and
dementia, and there’s an ophthalmologist around who’s saying to prescribe B12 to
their young glaucoma patients as a neuroprotective agent. Are there any other neuroprotective agents
that you would consider or are aware of? – Yeah. So the B12 is thought to act as a
co-factor within the electron chain, transport chain, as well, I think,
and I think that’s why it’s thought to be neuroprotective. For a long time, there was this thought
that Alphagan and the alpha-agonists may be slightly neuroprotective. And it’s never really been sort of shown
conclusively, but I’m just starting a project with Simon Backhouse and
Heath [inaudible] who’s a glaucoma opthamologist,
because we’re kind of thinking that perhaps Alphagan might be improving blood
flow at the optic nerve head. So, and as well as reducing pressure,
it might actually be bringing [inaudible] to the nerve,
and therefore making things a little bit easier on the nerve. So yeah, in terms of neuroprotection,
I know the B12 story is gathering some momentum, but there’s not really
enough evidence. Having said that, it’s probably not going
to do too much harm. And yeah, the Alphagan story is something
that we’re hoping to specifically have a look at. – And we’ve got another question from the
audience, and it’s talking about whether you treat one eye first to check the
response from the drug, or whether you usually choose to treat
both eyes at the same time? – So, I don’t bother too much with
monocular trials. A, because there’s probably enough
evidence now to suggest that there’s enough spillover from the left eye to the
right and vice versa, anyway, so it’s a systemic circulation. So I kind of…I don’t think it really
does a great deal, anyway. And for me, I kind of look at people and
go, “Not sure if you’ve got glaucoma, come back in six months.” And then when I’m sure
they’ve got it, I treat. And so usually, I treat both eyes. I guess the only people I don’t treat are
where you’ve got the secondaries, and you know, one eye is absolutely fine
[inaudible] unique, or something. Otherwise, quite often you’ve got one eye
that you’re happy, like in this patient, you’ve got one eye where you go, yeah,
that’s glaucoma, and the other eye, you’re feeling worried enough about that
you might as well treat. And you know, I don’t
see any disadvantage. And in fact, if you’re going to use a
prostaglandin long-term because the side effects include that orbital fat atrophy,
you know, if both eyes, over a decade, are receding slightly because you’re
losing orbital fat, you probably don’t notice that much. But if one eye is and the other one is
not, or it’s three years behind, you can end up with
lopsided looking patients. And so, I think from a cosmetic point of
view, you know, you may as well, if you’re comfortable,
treat with both eyes. – And I’m going to ask a question from the
audience about phasing IOP, and do you always use this as a baseline
for your glaucoma management? – I try to. And the reason I do that is to say I look
at these people and I go, well, I’m a bit worried. And I booked them in usually for the
repeat field, or the field at the earliest appointment I’ve got. Like this lady was [inaudible]
9:08, so she was my 9:00 patient. So yeah, I just book them in for my first
patient of the day, and do the fields and the phasing. I don’t phase throughout the whole day,
as in get them to come in six times a day or anything like that. I just go for the earliest pressure I can
get in the morning, and ping that as the highest pressure. And someone was asking
about [crosstalk] – Okay, thank you so much for your time
tonight, James. It was great having your presentation. Really interesting for all our alumni to
hear you present again. We’re just going to hand over to Geoff
now, and introduce him. Okay, so last but not least,
we have Geoff Sampson, who is one of our senior lecturers at
Deakin University, so he really needs no introduction. After teaching at Deakin for the past six
years, his teaching and research interests are in pediatric vision development,
binocular vision, and visual neuropathology. He developed Deakin Optometry’s inaugural
school screening program. This venture has simultaneously provided
an important community service for children from underprivileged
backgrounds and training ground for future pediatric optometrists. Over the past 12 months,
Geoff has been part of a small team who have established a unique,
evidence-based clinical communication training program for second and third-year
optometry students at Deakin. Thank you so much for
joining us today, Geoff. I’ll leave it to you
for your presentation. – [Geoff] Thanks very much, Zara. And thanks for coming along, everybody. I’m going to talk tonight about diplopia,
which is probably the most literal expression of double trouble. I’ll start by just talking about a few
basics that help to give us an idea of what may be underlying a presentation
of diplopia, and then we’ll go into a couple of case reports that will hopefully
highlight some of the traps that can occur if we don’t look carefully enough. So diplopia, frankly,
can be quite intimidating. Even for me, when I deal with it on a
regular basis, it’s still a challenge clinically,
if someone comes through the door, telling you they’ve got a new presentation
of double vision. Why? Most of the time, diplopia is going to
have a benign cause that’s not too threatening for our patients. But we need to remain aware that sometimes
there can be pathological causes, and they may be quite threatening to our
patients. So it’s very important that we
differentiate those two scenarios. And that’s why it can be quite terrifying
because we know that there’s always that possibility that this may be something
that falls into the latter category, and therefore, we need to know how to
actually differentiate those scenarios. Even if it is something that’s functional
and benign, we’re not always entirely confident of the management. Because those are not things that we deal
with in practise on a regular basis. So, what do we learn if someone presents
to us with diplopia? So firstly, we know that it’s concerning
them enough to report it, so that’s some bit of a no-brainer,
really. But I think it’s important to understand
they’ve come to us because they need help. So in some shape or form,
whether or not we are someone who’s got an interest in binocular vision or
otherwise, we need to manage this somehow. But we also, from our own perspective,
need to appreciate that when there’s a recent report of diplopia,
that something has changed for that patient, and that needs to raise
our concern levels. So, we need to be thinking of algorithms,
or ways that we can work through the possibilities of what might be the
underlying cause. There’s not much point getting worried
about what the management is unless we recognise that the problem exists in the
first place. So the key to dealing with the diplopia
presentations is to develop a sense of the underlying cause, or the likeliest
underlying cause, and particularly, to differentiate our benign from our less
common, but urgent, more threatening causes. So we can go through our normal way of
doing this, where we are considering a lot of differential diagnoses. I’m sure you’re all excellent that by now,
as Deakin graduates. But frankly, there’s 30, 40,
50 of these things, and it’s not an efficient way of dealing with this. So for those of you with relatively normal
colour vision, you’ll see that some of those are green and
some of them are red. The red ones are mainly the things that
are potentially going to raise our concern levels more, where the green ones a little
bit more common and generally less concern for our patients. There’s a lot of red ones there,
even though they don’t show up all that often. So what we need is, instead of sitting
here and thinking of 30 or 40 things at the same time, it’s really not a
functional, practical way to practise. We need to actually look for clues that
will actually help us narrow that down to a handful of manageable
differentials. So, I’m going to take you to the Rio
Olympics for a minute. If you’re sitting there enjoying a drink
in the sunshine, and you’re watching the women’s marathon, and all of a sudden you
see this thing come down the road toward you, you’d be forgiven for thinking
that you’ve developed sudden diplopia. In fact, diplopia, for this scenario,
would actually look like that, which is a little bit more scary again. But even if we saw that,
we’d possibly be thinking, “I’ve been sitting in the sun too long,
maybe one too many gin and tonics.” But these are, in fact,
North Korean twins who finished 10th and 11th in the Rio marathon,
with identical times. And if you look at their leg position,
this is really synchronised swimming on the road, effectively. So if this was diplopia, though,
we’ve got some clues already. You know, these images are side-by-side,
so it tells us…when we have horizontal diplopia, all of a sudden,
a whole heap of our differentials have disappeared straight away. So this is really what we need to look at
when we’re assessing our patients’ reports of diplopia, to try and get it down to a
manageable number of differentials. So instead of this, we need some sort of
simpler algorithm, which helps us work through these, in manageable steps. So I like to break it all down to binary
questions, basically. So it’s either this or it’s that. And if you can do that, all of a sudden,
a whole heap of those differentials start to fall away and you’re left with a
manageable number. So we should never ignore the possibility
that this could be monocular rather than binocular diplopia.
How do you tell? So, if the patient is exhibiting this in
your consulting room, you ask them to cover an eye,
asked them if the diplopia is still there. If they say it’s gone away,
then it’s binocular. If it’s still there,
then it’s likely to be monocular. We can ask them how far
apart the images are. We can ask the patient to describe it,
they can also draw it, and we can utilise that as a way of
getting information from our patients. They can be quite good ways of finding out
the characteristics of what the patient’s experiencing.
So, what are the implications? Monocular diplopia is actually
surprisingly common. So in fact, if we don’t actually ask this
question, sometimes people are describing astigmatism, media opacities,
dry eye. Things along those lines that we don’t
need to be too worried about. We still need to manage them. However, if we confirm it’s binocular
diplopia, then we know we need a further, true binocular vision assessment. And the next binary question to ask is
whether it’s concomitant or whether it’s non-concomitant?
It’s a very useful next step. So again, if we’re going to explore that
question, how do we tell, so ocular motility, obviously,
is the key to this. I can hear you all groaning from as far
away as Darwin, so here he goes again. Yes, I’m obsessed with ocular motility,
but there’s a reason for it, because it answers this question for us
really effectively. If we have subtle problems,
then we can also use our cover test in non-primary gaze positions.
We underutilise this test as well. It will tell us changes when the person is
looking in non-primary gaze positions that we may not get simply by looking at
motility. And again, you know,
I’m stressing this a lot of times tonight, but we can ask the patient about the
diplopia characteristics, and whether these change
with their gaze direction. That gives us a lot of
information as well. If all of a sudden the images are further
apart in left gaze, or there’s a vertical element that develops when they’re looking
right gaze, we have information that we may not be able to see easily
with our motility test. What are the implications
of this binary question? So, concomitant strabismus is a lot less
intimidating, particularly if it’s horizontal in its presentation. Convergence insufficiency,
divergence excess, harmonisation esotropia,
all quite common presentations, and none of them are all that stressful,
and all of them can be managed by optometrists very easily. But if we confirm that it’s
non-concomitant, then there’s a higher risk of this being sinister,
and so our alert factor needs to go up substantially. We’re dealing with nerve palsies,
and if this has a vertical element in it, then we can upsell it to apply Parks 3
step to try and understand that. Or we’re dealing with restrictive
presentations, for example, something like a blowout fracture.
These can be confusing. But if we think about our agonist and
antagonist pairs, they become easier. If a blow out fracture traps our inferior
rectus, then the superior rectus is not going to be able to move into its normal
field of action, because the inferior rectus won’t let go. So, this will look like a superior rectus
palsy, but in fact, it’s entrapment of the inferior rectus. And a third range of these is our higher
order and our more scary diseases. These are brain diseases, such as INO,
inter-nuclear opthalmoplegia. So, the non-concomitant ones we need to be
much more careful of because they can’t constitute most of those ones that came up
in red on that earlier slide. So, our third binary question is whether
the presentation of diplopia is horizontal or vertical?
How do we tell? So, we can ask our patient in this case. And again, we can ask them to describe it,
or we can ask them to draw it. It’s a really helpful tool,
to get them to do that. It’s a very important question,
and the first case vignette I’ll give you in a moment will illustrate
why that’s the case. Because this can present quite subtly
sometimes, and it can look like something else that’s much more common. So, cover tests, obviously,
with subjective misalignment estimates as backups are important in this case. But if we want to tell whether something
has a vertical presentation, a Maddox rod is a really useful tool
because it allows us to measure vertical misalignment in a subtle way. Again, this will come into the first of
the two cases. What are the implications of this
horizontal versus vertical question? So, if we answer this,
our differentials change completely. So, we’re really dividing them into two
separate categories, and there’s not much crossover between
these things. So if you look at the list we’ve got there
on the slide of horizontal ones, and you look at the list on vertical ones,
there is no crossover. So, once we know the answer to this
question, we’ve all of a sudden eliminated a lot of possible differentials. So, let’s have a look at that graphically. So if we have a look at this clock tower
image, if someone comes in and draws or describes that, then we know we have a
horizontal presentation of diplopia, similar to the Rio marathon twins,
then we have a limited range of differentials that would explain that. If there’s a patient comes in describing
that, then we have a completely different range of differentials going to describe
it again. And if they…this is the
advantage of drawing. Because if they draw it like that,
all of a sudden, we have a torsional element to this. And again, that’s more likely to be
pointing to something like a fourth nerve palsy, where we know that there will
be torsional change in a presentation like that. So, we’ve narrowed this down to a very
small number of differentials if that’s the way the patient draws it. When we ask them to describe it,
they may not tell us about the rotation. What to be careful of is this. So, if they present it like this,
then we’ve got a very subtle vertical element, and a more prominent
horizontal element, then we will often miss that clinically. Because the vertical change there is not
going to be discernible with things like cover tests. Cover test is not subtle
enough to pick it up. So, we’re going to look like we have a
horizontal misalignment where in fact there’s a vertical element there as well. So the importance, again I want to stress,
of ocular motility in the…yes or no, I hear the groans again. But I want to stress the
importance of this. Because if you look at something like this
presentation, which represents inter-nuclear opthalmoplegia,
if you look at the patient front-on from far enough away, they will look
perfectly normal in primary gaze. Get them to look to the right,
and it’s okay. But if they have a right INO and they try
to look to the left, then we’ll find that the right eye does
not adapt, and then the left eye will just develop a stagnancy response to that. We’re not going to see that with primary
gaze assessment only. And then, in more general terms,
the importance of assessing comitancy. So, if we can confirm non-concomitant
strabismus and it’s accompanied by any or all of the following signs,
then we have an emergency on our hands and we need to get that person into high-level
care almost immediately, if that’s the case. Recent-onset diplopia, headaches,
other signs of illness, personality change, it’s usually described
by someone other than the patient themselves, or papilloedema,
these are showing us that we have a serious brain disease. In these cases, they need urgent referral
for neurology workups. Case vignette two will talk you through a
case that represents the importance of this.
So, let’s have a look at the first case. A 23-year-old female presents with recent
onset diplopia. You do a very simple assessment,
and you find an 8 prism diopter exotropia within your cover test. There’s no sign from your cover test of
any vertical misalignment, so it’s very easy in this case to make an
assumption that this is a decompensating convergence insufficiency. This is how they present, basically,
even though this is a fairly small angle one.
Why? We’ve got an apparent horizontal exotropia
at near, and we know that the prevalence of convergence insufficiency is very high. So it looks highly like
that that’s our problem. But if we leave it at that and we don’t
look further, then potentially we miss signs that we need to be able to process
and pick up. So, the patient, in fact, looks like this. Big deal?
So, what’s wrong with this? Presumably, hopefully,
people can see the pointer here… Thank you. So, if you have a look here,
we take a line through her pupils, then she’s actually got a head tilt to the
right. And if we look at the side of her nose
there, or how much we can see on the side of her eyes at either side,
if she had a hairstyle like mine we could see her ears, we’ll see that this woman’s
got both a head turn and a head tilt to the right.
Very subtle. So, people think that this sort of
presentation comes in with the person’s sort of head, you know,
at 90 degrees to the rest of their body. But in fact, that’s not how they come in. So if we look at that,
that shows the importance of looking carefully with our external exams. So, if we go a little bit further and we
use our Maddox rod, we actually find a 3 prism diopter left hyper misalignment. Now, we’re not going to see that with a
cover test because it’s too small. Four is about the minimum we’re going to
see. So, that’s our first Parks step in this
case, just to ask which eye is actually higher. So, this increases the 6 prism diopters in
right gaze, so straightaway we know we have a non-concomitant strabismus
presentation because the magnitude has changed in direction of gaze.
Depend on that. That’s what defines non-concomitantcy. So, a careful history. Following that, the patient admits to
falling from a push bike three days earlier, and develop diplopia 24
hours after that particular injury. So, a targeted history, again,
gives us further information here. And when we look carefully at motility,
we realise that there is a limitation of left eye depression in abduction,
these things don’t jump out at you. They are subtle, but they’re there if you
look for them. So, we’ve got a whole heap more
information now. So, I’m sure…well, I hope,
given that I taught most of you this, that you realise now that we’re dealing
with a left fourth nerve palsy in this particular case. They are very common,
and sometimes head injury or neck injury is an underlying factor in a lot of these
cases. Why, though, does it
look like an exotropia? Because that’s really what this would have
looked like clinically if we didn’t look a bit further. So to answer that, we have to think about
what we do when we use a Howell-Dwyer card whenever we put a 6 prism diopter base
down right in front of somebody, we are breaking their fusion. As soon as we break their fusion,
they are going to exhibit or manifest their horizontal misalignment. So if we’re breaking…this woman’s fusion
is broken by her 3 prism diopter left hyper misalignment, then she’s going to
show her exophoria as an exotropia. We’re going to see it straightaway. So, this is not an exotropia primarily,
and the management of this is completely different. We’re going to need to have a look at
things like vertical prisms to try and realign her, and she will use her own
head tilt and turn to try and manage that, as well. There’s no point giving this person
horizontal vision therapy, we’re not going to solve the underlying
problem in this case. So, case vignette two,
and I have to warn you that this one, unfortunately, this is a true case,
and probably won’t be ending on a particularly happy note. But I think it’s an important one,
and so we’ll work through it relatively quickly, as we’ve used up a
fair bit of time already. Ten-year-old male presented with two weeks
history of diplopia. His diplopia was horizontal. On questioning it was intermittent,
but it had been increasing in frequency over a period of time…over that two
weeks, I should say. They also reported a three-months history
of headaches, three to four episodes a week. It was a deep type of pain, but remember,
this was a 10-year-old male who’s highly intelligent, but is unsure of the
location, couldn’t get a pattern for that. Sometimes admitted it was on waking,
and sometimes he said it just goes away by itself. GP had investigated the headaches but
found no explanation for them, and there was no history of head trauma. But of interest, I hadn’t seen this
patient personally before, but they were a patient who had been at
the practise previously, and they had been wearing a full-time Rx
for three years of plus two, right and left. So, this child had normal vision on both
sides with their current glasses, but they had a 15 to 20 prism diopter
esotropia at near and distance in primary gaze. It was constant, distance and near,
alternates but preferred right fixation. Motility showed a full range of movement
in right and left, when we do the ductions particularly,
which is important for eso’s, otherwise, you can’t usually see the full range of
movement on one side. So, the esotropia appeared to be
concomitant, so from that alone, you know, alert levels tend to drop a little bit. Even more so when dry ret showed there was
some uncorrected plus there. And in fact, we had about three diopters
there, but in fact, it took nearly four diopters, right and left,
to get this child back to binocular single vision. So, no diplopia, gross random-dot
stereopsis, and there was small residual esophoria. Ocular health exam was unexceptional,
with optic nerve heads looking, in particular, looking healthy and
well-defined and well perfused. So, the diagnosis here is pretty obvious. We have an accommodative esotropia that
had decompensated secondary to undercorrected hyperopia management,
just gave him more plus at near. They wouldn’t take a full amount of
distance, and as a 10-year-old, they were given a pair of occupational
multi-focals, asked to come back in a month but told to call earlier if the
diplopia or headaches persist in the interim. Now, I still don’t know…this was 20
years ago that I saw this young man. I still don’t know whether it was clinical
intuition…it was probably clinical fear. But something just didn’t seem right to me
in that presentation, and I initiated a call to the family a
couple of days after the new glasses were collected, which was probably a bit
over a week after I’d first seen them. The mother told me straightaway,
she said no more double vision going on, but he’s closing one eye all the time now. Should I be worried about that? So, well, it kind of explains the lack of
diplopia when that child’s doing that. But she also admitted this child had been
having severe headaches and vomiting for all that day. So, this didn’t sound all that healthy to
me, and we brought them back in that afternoon. We had a look at them…I say “we” because
I had brought one of my colleagues in. I was a bit terrified at the time. A very different clinical picture. So, this child had a head turn to the
left, 25 to 30 prism diopter esotropia in primary gaze, with the new glasses on,
which was meant to get rid of the esotropia. Versions indicated it was now
non-concomitant, and the esotropia increased in left gaze,
ductions confirmed, there’s a limitation of left abductions. So, this was an entirely different
clinical picture than what they had exhibited a week before. Visual acuity was still okay,
and the internals also were not showing anything too dramatic there, either. This was a very clear, by now,
left sixth nerve palsy, and the child was referred for immediate
evaluation by a pediatric ophthalmologist, who referred also fairly quickly to a
neurologist. Unfortunately, this child had quite an
advanced glioma of the pons, a brain stem tumour, and despite some
aggressive treatment, we found out by the family that three
months later, the child, unfortunately, passed away, which was an awful outcome
for the family in particular. So, it’s a very hard way to learn a
lesson, but there was a lot of lessons involved clinically in that presentation. It was an atypical one at start,
the abduction deficit of the sixth nerve palsy was not evident,
and it was masked by an apparent perfectly good other explanation for a child’s
esotropia, in that they had undercorrected plus,
and they did have an accommodative element to that. There’s an absence of things that we might
think about as accompanying neurological signs, papilloedema,
end point nystagmus, and no esotropia at a greater distance
than near, which is what we often see with sixth nerve palsies. But it’s a tragic, but powerful lesson
about the importance of recent diplopia and headaches being highly suspicious,
and variability in strabismus presentation also being highly suspicious. We need to be alert for co-morbidities in
these cases, sometimes there’s more than one thing going on. And it’s also a good lesson to trust your
clinical intuition. If something doesn’t seem right,
you need to actually follow it through. Thankfully I did a week later,
but unfortunately, that still didn’t manage to save this child’s life,
which was awful. Mostly, sixth nerve palsies are not as
dramatic as that. A lot of them will recover spontaneously. In older people, it’s often diabetes and
hypertension. But we have to be aware of those possible
worst case outcomes. And I think that’s probably all for
tonight. And I’m sorry to end on such a depressing
note, but I think it’s an important lesson,
in this particular case. Thank you for listening. – Okay.
Thank you, Geoff. That was very good.
It’s now time for our discussion session. So for all our listeners,
you can take some time now to type in some questions for Geoff,
and we can ask them now. Is that it? – So, I think our first question, Geoff,
would really tie into your communication expertise that we could lean on,
And I noticed that in your presentation, you said they might have subtle
personality changes when some of these cases present. Could you give, like,
an insight to what they might be, or how we might pick up on that in
consultations? – Yeah, that’s a great question, Amanda. I think in these cases, generally,
it’s dependent on having someone else with the patient. Because patients, to my understanding…I
haven’t seen a lot of this personally, but I certainly have read a bit about it
for all these sort of cases. Often, if you are asking subtly a person
who is there with the patient concerned, whether it’s a child or whether it’s
another adult, sometimes you’ll have to do that in a subtle way outside the room. They will often tell you that the patient
doesn’t seem themselves, in a case like that. And that can be a subtle sign of,
unfortunately, brain injury that can go on, in those sort of cases. – Excellent, Geoff. So, we’ve got a question that’s about a
patient someone had recently, where they got diplopia for about 20
minutes after having an MRI, and they haven’t seen any diplopia since. Have you ever heard of people getting
diplopia post-MRI before? – No, that’s the first time for me.
So, I don’t really… If that person concerned has an easier
question, that would be much appreciated. Yes, no, unfortunately,
I don’t know what the scenario would be in that case. If a person concerned is still online and
able to type in what…do they know the characteristics of the diplopia?
Is it horizontal, vertical…? – Horizontal. – Horizontal.
Don’t know. I mean, it may just be,
perhaps…that may be a true decompensation. I’ve never been in an MRI,
this is your area, Amanda, you know this a lot better than me. But, you know, if you haven’t got
something that’s easy to focus on in a case like that, sometimes those things
will just unravel if there’s just a subtle CI. But I truly don’t know the answer to that
one. That’s a really interesting presentation. – Great. We’ve got another
question here for you, Geoff. It says, “I recently read a study that
suggests more than 90% of suspected divergence insufficiency in kids has
actually ended up being a partial sixth nerve palsy.
What do you think of these numbers?” – I think that that’s really good advice. It’s one of the things we didn’t have much
time to go into tonight. Ash and I have seen a few of these,
that we’ve been concerned about on vision screenings. But in fact, it’s very unusual to get a
divergence insufficiency pattern. The other three combinations,
they are quite common. But sixth nerve palsies do present with a
greater eso at distance than near, because the person is not able to diverge
fully when they look up, in a case like that. So whenever we see these,
we need to be really suspicious of it. So I didn’t know those numbers,
but they don’t surprise me. And if you’ve got that,
and a kid with a headache, who is unwell…that’s potentially an
emergency. Well, that is an emergency until proven
otherwise. – Excellent. We often also have students ask this when
learning clinical skills, what the best way is to measure
a distance phoria? So, what would you recommend? – Well, there’s a couple of ways. So, I think if it’s a horizontal phoria,
then you can get away with things like Maddox rod. You shouldn’t use them at near,
because they don’t control accommodation. But really, if you don’t have a distance
Howell-Dwyer card, which is probably the easiest way to do it, then I think,
really, von Graefe is the way to go about that. So, it works through a trial frame,
it works through a refractor head. It’s quite useful. – Good. – Thank you again, for your time, Geoff.
So that’s all we have time for tonight. Thank you so much to our presenters for
making such valuable contributions to our second webinar. It’s been very interesting. And thank you to our listeners for tuning
in and participating in tonight’s webinar. We hope you’ve really enjoyed it again,
and we’re looking forward to it next time. So next up for you, we’re actually going
to be bringing out an alumni magazine. So keep an eye out for that on Facebook. And as always, if you’re interested in
contributing, we would be happy to hear back from you and hear any feedback you
have for us. That would be great. Please feel free to provide any feedback
regarding this seminar, and the presentations,
and the presenters themselves through the survey on the…I believe it’s the
Qualtrics that was emailed to you. The alumni committee would love to hear
from you, so feel free to reach out to us at any time. We’ll be really interested to hear about
what topics you would like for us to focus on next. So the next step for you now is to fill
out your CPD questionnaires to earn your CPD points. As I mentioned earlier tonight at the
start of the webinar, we will be using Intedashboard. Some of you may have used this at
Deakin for CPD activities before, and so the email to log in would be the
same as the last one, the one that you would have used for
“Pediatric Insights.” So, this would have been made from the
email that you registered with for tonight’s webinar as well,
if you hadn’t come to any previous webinars. If you are new to the dashboard system,
you would have been sent an email with your password. If you have lost this email,
please contact one of our alumni committee members, so Lucy and Ash would
be more than happy to help you with that one, to help you reset it. Once you have followed this link,
you can change your password to something that you will actually remember. The quiz actually will be available for
the next week or so, so don’t panic if you don’t get it done
tonight. So, that’ll give you plenty of time to
finish it. If you attended our last webinar,
as I was mentioning before, the “Pediatric Insights,” you can use that
same email to log into the Intedashboard system. Thank you again for joining us,
and until next time, goodbye from the alumni team here at
Deakin Estate, and thank you again for your continued support.

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