March 27, 2025 • 22 mins
Giant Cell Arteritis (GCA) is one of the most dreaded diagnoses in ophthalmology; not only can it cause vision loss, but it can also be life threatening. So what is the threshold for going down the 'GCA diagnostic path'? When should one order an ESR and CRP? When is the concern high enough to warrant a temporal artery biopsy, and when should steroids be started? How is temporal artery biopsy changing our diagnostic alogirthm. Dr. Andrew Lee joins the podcast.
This episode of the podcast is sponsored by Thea Pharma Canada - https://www.theapharma.ca
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This episode of the podcast is sponsored by Thea Pharma Canada - https://www.theapharma.ca
Become a supporter of this podcast: https://www.spreaker.com/podcast/blind-spot-the-eye-doctor-s-podcast--5819306/support.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:10):
Hey everybody, I'm zaeo Mednik and welcome to another episode
of blind Spot. This episode is sponsored by THEA Pharma Canada.
THEA pharm of Canada is the Canadian subsidiary of THEA,
Europe's leading pioneering and innovative eye health brand. Founded in
nineteen ninety four by Henri Schibre. With five generations of history,
the Chubret family has been dedicated to I care for
(00:31):
more than one hundred and fifty years. Their commitment to
improving lives is born of their pioneering spirit. They continue
to lead the worldwide preservative free movement in eye care.
They've created innovative delivery systems. They've focused on making products
accessible and cost effective for patients. They live this mission
every day because everyone should have the same opportunities to
see the world through healthy eyes. So thank you THEO
(00:54):
Pharmer Canada for supporting blind Spot. Giant cell artiitis sir
temporal artiriitis is one of the most threaded diagnoses and ophalmology.
Not only can it be vision threatening to the point
of complete blindness, but it can be life threatening too,
So obviously it's something nobody wants to miss, but it's
not so simple. Diagnosing giant cellar to ritis can be
challenging both from a symptoms perspective and requires blood work
(01:17):
and often a temporal artery biopsy to get a definitive diagnosis.
So what's the threshold for going down the path of
GCA testing and eventually treatment. At what point is one
worried enough to order the giant cellar to rightis related
blood work? And at what point does one go down
the path of temporal artery biopsy? And if prednizone is initiated,
(01:38):
when should it be initiated and should it be oral
prednizone that's given or IV methyl prednislone. I'm joined today
by esteemed neuroopthalmologist, doctor Andrew Lee. Doctor Lee is a
professor of ophthalmology, neurology, and neurosurgery at Houston Methodist. He
serves on the editorial boards of over ten journals, including
the American Journal of Ophthalmology, Canadian Journal Ophthalmology, and I
(01:59):
and is the editor in chief the Journal of Academic Ophthalmology.
He's a recipient of the Honor Award, Secretariat Award, and
Senior Achievement Award from the American Academy of Ophthalmology. He
joined Houston Methodist Hospital and Research Institute in two thousand
and nine and it's currently Chair of the Blanton I
Institute Houston Methodist Hospital and Professor of Ophthalmology, Neurology and
Neurosurgery at the Wheal Cornell Medical College. Doctor Lei, you
(02:21):
welcome to the podcast. Thank you so much for joining me.
Speaker 2 (02:25):
Yeah, thanks for having me.
Speaker 1 (02:27):
So I gave a bit of a preface about GCA
and what pretty much everybody listening to this nos is
it's a bad diagnose. So it's one of the more
dreaded diagnoses and optomology because not only is it vision threatening,
but it's life threatening because it can cause coronary art
to writs, it can cause a lot of different things
that can and obviously kill the patient. So it's one
of those things that we definitely don't want to miss.
(02:48):
I thought for this episode, as opposed to kind of
going through some of the basic stuff that a lot
of us know, I wanted to focus on some of
the decision points that ophthalmologists and optometrists need to make
as we see a patient when we're concerned whether they
have GCA, whether it's the decision point do we get testing,
do we do a temporal artery biopsy, and do we
(03:10):
initiate steroid. When I think of GCA, I think of
it as sometimes we get referrals where patients come in
and there aren't really any ocular symptoms. It's just a
GP or an emerged doc says, I know that I
don't have any ocular symptoms, but maybe they have this
weird headache that could be GCA, and there's maybe some
job quloudication. And then there's another group of patients where
(03:32):
they come in with actually an ocular manifestation. Why don't
we start off with some of the ocular manifestations. There's
some that I think most of us optimologists to know
that if we see we're definitely not going to debate.
We're going to get the ESR and CRP and initiate
the pathway. So would you say AAIO n artritic, ischemic
(03:52):
optic neuropathies at the top of that list, you see
that there's no question you're going down the GCA path.
Speaker 2 (04:00):
Yes, that's the most common presentation, but it can be
any ophthalmic presentation. So in an elderly patient, it doesn't
matter whether it's anti schemic APOPI, aio N, or postterious
schemic gothneropty where the disc is normal a retro bolbar
optic neuropathy. Whether it's transient vision loss or double vision
(04:20):
or moss of vision from center around arter inclusion, it
doesn't really matter. What matters is that any elderly patient
with a new neuropthalmic finding should be considered to be
giant cell until proven otherwise. Even though antiero schemic goplerobiti
is the most common.
Speaker 1 (04:37):
That's a super important point because basically the threshold should
be low because so many different things can't present as GCA.
Even though aio N is kind of a classic one
we think of. Nerve palsies are one that is common.
We see a lot of patients with six nerve palsies,
for example, pretty easy to chalk it up to, I
don't want to say pretty easy to be catalier, but
(04:57):
a lot of older patients have vascular risk factors where
we can say, yeah, I could see why you have
a six nerve posy. Would you say you do an
ESRCRP on everybody who comes in with a six nerve polsy,
even if it seems vasculopathic or are you more selective?
Speaker 2 (05:13):
Yes, I think the risk of doing an es R
and CRP is so low. The threshold for doing the
test is extremely low. So any elderly patient with double vision,
regardless of whether it looks exactly like what you think
is a schemic six should have consideration for ESR and
CRP because it's just such a low risk test.
Speaker 1 (05:34):
And like you said, they're transient vision loss. So that
includes things like Ameros's fugas in Fujax. I'm not sure
what the correct pronunciation is despite using it often, even
if you are getting the Karate dopplers or maybe getting
an ECG. I'm guessing that's as well, something you'd need
to be on guard for, on watch for, at least
for GCA.
Speaker 2 (05:52):
Yes, both transient diplopia and transient vision loss, Ameros's fugas
should have an ESR and CRP considered.
Speaker 1 (05:59):
For patients NaIO N so non artoritic kind of your
DiscT risk that is a little bit of dematist vision
is not as bad as an aaio N. Again, I'm guessing,
based on this discussion so far, you would say YEP
could be in a typically presenting GCA. Get the blood
work low risk.
Speaker 2 (06:19):
Yes, and that's because there's no real way to differentiate
non arto ritic from artot aio N. Of course, if
they have palat edema and it's bilateral, or if they
have concomitant chroidal or retinal schemeia, those are obviously not
an ai N and are aaio N arteroritic. But running
the mill nai N you cannot tell that that's not
(06:42):
giant cell. So we ordered a test on all of them.
Speaker 1 (06:45):
So you're building a picture here obviously of order. The
e s R CRP platelets not a big deal. I
guess my question is that sounds easy enough to do, right,
they're blood tests, it's not a big deal. Sometimes my concern,
and I am and I'm not alone, is there's a
lot of things in my mind at least and you
know better, that can elevate someone's ESR CRP and platelets,
(07:08):
especially older people. And we know that GCA presents I
don't know if it's exclusively over age sixty, but certainly
over age sixty, and there's a lot of other confounding
things that could cause someone's inflammatory markers to be high.
So the reasons sometimes I might hesitate, and I guess
I shouldn't based on what you've answered so far. Is
what am I going to do with a positive result
(07:28):
sometimes of an ESRCRP if I'm a little bit skeptical
when I'm ordering it. Anyway, when I pretest probability is low,
then I get an elevated ESR CRP elevated platelets. Maybe
only one or two of them is elevated. How do
you deal with that knowing that those markers can be
elevated for a number of reasons.
Speaker 2 (07:47):
Yeah, so that's part of the reason we do all
three of them, because we want to have all three
markers pointing in the same direction. So you're less likely
to generate a false positive for an ESR if you
have all three point the right direction, either up or down.
And the said rate, as you already alluded to, is
very non specific, and so anything can cause it to
(08:09):
be elevated. However, it's uncommon for all three things to
be elevated, and especially if they are markedly elevated. But
of course, pretest probability is the best predictor of post
test probability. As with any test, you have to interpret it,
and false positive and false negative is part of that interpretation.
And so if a patient has a borderline elevated ESR
(08:30):
but a normal CRP and a normal platelet count and
the pretest probability for diseases low, we're just going to
go with the majority report on that. And so I
think it is incumbent upon physicians not to rely upon
the tests to make the diagnosis. Labs don't make the diagnosis.
Doctors make the diagnosis.
Speaker 1 (08:50):
Is CRP the most specific? Is that the one that
if it's really out of whack to say, to say
completely informally, that really raises your eyebrows.
Speaker 2 (09:00):
Yes, it's the combination of them that have higher sensitivity
and specificity. So it is the combination of sensitivity and
specificity that you have to work with.
Speaker 1 (09:09):
I want to take a step back before we talk
about temporal artery biopsy and aultrasound. I mentioned earlier that
you've obviously got those patients who have an ocular diagnosis,
and then you've got the patients who who don't have
an ocular diagnosis, who are coming in with a headache,
maybe some neck pain, some of these symptoms. Jaw clodication
is a big one. What is your threshold when somebody's
(09:30):
coming in for those symptoms to do an SR and CRP.
And granted that's a tough question because that's a pretty
umbrella question for a lot of different patient complaints.
Speaker 2 (09:39):
Yeah, as I mentioned, the thresh ordering a centerate and
therap for me is quite low. So it doesn't matter
whether it's the ocular version or the headache version or
the jaw clodication. We're going to order the test because
the steaks are so high. And as I mentioned, ordering
off three helps you reduce the false positive rate, but
be test likely to disease is the most powerful predictor.
(10:01):
So the strongest predictors, the highest specificity things are jaw
cloudication and temporal artery tenderness, but headache of any kind
people with have normal exams from an eye standpoint, we
still have got to consider the diagnosis and e libly patients.
Speaker 1 (10:17):
Let's talk about temporal artery biopsy. I don't know if
off themology residents are off themolgist they're still doing them now.
I know we did during our residency in Canada, and
I imagine in some programs they're still doing that in
the States, or they're sending them off somewhere else. But
with a temporal artery biopsy. That's the kind of mainstay
of diagnosis.
Speaker 2 (10:38):
Correct, it's still the gold standard, but we have an
intermediate choice now, which is called tempor artery ultrasound. Found
is being done as a non invasive way to look
for a halo sign and that halo represents the transluminailymphysitic
infiltration into the artery. And if so, if your pre
test likely the disease is high and you have a
(10:59):
positive are the ultrasound a lot of places you don't
have to do the temporary biopsy anymore. So we're reserving
the biopsy as a gold standard. And conversely, if the
like it is low and you do a temporary ultrasound
and it's negative, that's probably sufficient to make the diagnosis
without a biopsy. And we're reserving the biopsy for the
(11:21):
cases where we cannot adjudicate or if we don't believe
the ultrasound result.
Speaker 1 (11:25):
So you're doing it for those cases where you think,
I thought this ultrasound was going to show temporary right
as it didn't. Now, let's go to the biopsy.
Speaker 2 (11:33):
Yes, And a lot of tests are like that, where
there's a screening test and then there's the gold standard.
So if the screening test is positive in a high
probability case, it's probably good enough. And if it's negative
in a low probability case, that's good enough. But if
it's negative and you still think the person as John Cell,
we would proceed with the temporary biopsy.
Speaker 1 (11:52):
Are those ultrasounds fairly new that they're being used and
who's doing those ultrasounds? Because I recall in residency we
would use the ultrasound just to imagine it was a
different ultra sound. We were using it just to kind
of be able to identify the temporal artery as part
of the biopsy. But what is when did this come
on the scene, and who's trained to really give an
(12:13):
accurate interpretation of it.
Speaker 2 (12:16):
Yeah. So with as with all tests, ultrasound is very
operat or dependent, and so your listeners need to go
and find out who's doing the ultrasound in their area.
And in some ways it's a self fulfilling prophecy because
if you don't order it enough, then they can't get
used to doing it. So in the beginning we did
both on everybody so that our ultrasnography division can get
(12:37):
used to doing the tests and we would have gold
standard comparison, so they could improve their technique and know, hey,
we missed a biopsy proving Johns or we found one
and nothing was in that artery, and it helped them
improve their technique over time. If you look at the
pool data from the literature, it's pretty good. And so
it's just a matter of training your local people or
(12:58):
finding your local people to be able to do the test.
It's the same people that do karate doppler, So the
karate doppler people are the temporal artery by ultrasound people.
It's just a smaller artery. But it's the same concept,
same principles, everything else is the same, so there's nothing
really new about it. It's just putting the probe on
a different.
Speaker 1 (13:16):
Place when you were starting to kind of do both
at the same time, when you were just starting to
do the ultrasound to compare the results to the tempor
artery biopsy. I don't know if it was an official studies.
I don't think anybody's going to hold you to the results.
But was the concordance rate pretty pretty positive?
Speaker 2 (13:35):
Yes? So, and that's what the literature shows as well.
The concordance rate is pretty good. The issue with the
temporary ultrasound is more of sensitivity than specificity. So if
we see the halo signs, it's hard to blow that off.
I mean, it's really hard to have the halo sign
not be temporaries. But if it's negative. There are forms
(13:57):
of giant cell where the biopsy is just the super
way of finding it, especially the healed and treated artiiitis
forms where we're relying on disruption of the internal elastic lamina.
There's no transmural infiltration, there's no giant cells, and so
those types of cases can only be found on histologic
examination of the artery, and the ultrasounds is not sensitive
enough to pick it up.
Speaker 1 (14:19):
Another decision point for for the ophalmologist is is pregnozone
and when you start it. When I was in residency,
I recall some people would say, listen, if you think
that the suspicion is high enough that you're ordering an
ESR and CRP, then you should start prednizone. What is
your thought on the decision of when to start pregnanzone
And there's a couple aspects there. One is is it
(14:40):
going to confound the results of your temporal artery biopsy
if you go that route, and the other one is
just is it unnecessary to be putting somebody on prednizone
before you actually know what the results of your tests are.
Speaker 2 (14:51):
Yeah. So our traditional paradigm has been diseased, diagnosed, treat,
But in giant silatoritis, as you've already alluded to, its disease,
treat and then diagnose, So the order of things is
a little bit different than for traditional neuropthalmic conditions. We
definitely would treat if your pretest likely the disease is
sufficiently high. However, if the risks outweigh the benefits or
(15:14):
the pretest likely it is low, we would do the
temporary ultrasound on that person so that you don't have
to wait for the biopsy, just so you get an
idea of whether or not you should be treating or
not for this patient. Covering the patient with a short
course of steroids until we get the biopsy or the
ultrasound is probably not going to harm the person. So
it's way better to cover the person while you're working
(15:36):
it up than it is to have a vision loss
because you didn't start the steroids.
Speaker 1 (15:41):
And what's the current thought on whether pretnozone is going
to affect the results of the biopsy.
Speaker 2 (15:47):
It does affect the results of the biopsy because steroids
in general reduce all the forms and the all of
the stages of inflammatory disease. However, what it cannot do
is it will not reduce the disruption of the internal
elastic lamina. So for the tempor ultrasound, we definitely want
to have the ultrasound done as close to the starting
(16:09):
the steroid as possible. For the temporariti biopsy, you probably
have two weeks because the structural change caused by the
giant cell will still be present even if the lymphocytic
infiltration has been dissipated by steroid treatment. So two weeks
is probably your window there. It'd be better to do
it faster, and that is one of the advantages that
the ultrasound has over the temporary biopsy. It's hard to
(16:30):
get people, as you're already alluded to, to get the biopsy done,
and so ultrasounds just faster.
Speaker 1 (16:36):
Yeah, and I guess that's good that the one that
is more susceptible to steroids is the one that at
least is easier to get done, because it's easier to
get an ultrasound done than it is to get a
biopsy done. Having said that, you need to get the
ultrasound done quickly because if they've been on steroids for
a week, that's going to have more of an effect
on the ultrasound you're saying than it would have on
that biopsy.
Speaker 2 (16:55):
Yes, and you always have the biopsy to lean on
if your temporary ultrasound is neg but you think they
have the diagnosis, and even the temporary biopsy the gold standards.
Sometimes we have to do both sides because the concordance
rate is only ninety six percent. So really the bottom
line is, if you, as a clinician think they have
(17:15):
giant cell, you should treat them regardless of the biopsy,
regardless of.
Speaker 1 (17:20):
Another decision point oral versus ivy methyl preston is alone.
Again what I recall, and again what I recall is
if somebody's got an ocular manifestation, like specifically, if they've
gotten artoritic a schemic optic neuropathy, that's going to warrant
ivy methyl preston is alone. Whereas if somebody doesn't have
(17:40):
an actual vision threatening issue, but they've got what you
think is GCA based on the biopsy or initially just
based on the history and based on the blood work,
then it's reasonable to start on po oral steroids. What's
the general thought on that? Is that still accurate or
is that outdated? Is there a greater pushnail to just
(18:00):
be more aggressive with IV steroids.
Speaker 2 (18:03):
I think that's still the traditional teaching and the conventional
approach with vision loss, but not just vision loss, transient
diplopia or transient vision loss, the TIA version of it.
We would give intravenus methyl peniculin to those patients. So
the patients that have CNS manifestations, including the cranial nerve polsies,
(18:24):
we would give intervenus steroids to those as well. But
the oral steroid can be used for just the headache
people or even the jaw caudication people. So one to
one point five milligrams of oral prednice own is still okay.
But in general, most neuroptimogists would choose IV steroids for
vision loss, including transient vision loss.
Speaker 1 (18:43):
Okay, that's good. Again, I didn't realize that even like
a transient vision loss or I guess a sixth nerve
palsy as well, if you thought that it was related
to GCA, anything I related which you are attributing as
pathological from GCA, you'd be more on board with the
IV methyl pretnismone. And is it a three day course? Typically?
Speaker 2 (19:02):
Yes, there's no proven standard dosing or duration, but that'd
be a typical dosing. There's no data on the dose
or the duration, but three days is completely reasonable.
Speaker 1 (19:14):
Dosually, very valuable information. Some people are probably yelling at
me listening, don't you get it? When I was asking
those earlier questions, he's saying, do the es R and
CRP and everything. But I wanted to hammer that point home.
So I'm glad I asked you that, and I, for
one will not forget that, and I'm sure listeners won't too.
So you've been very clear on just order the ESR
and CRP and if you're concerned about well, there's a
(19:35):
lot of things that can elevate it. That's why we're
ordering all three so we can look at the whole
picture together. When we're talking about temporal artery biopsy, we
do have this new ultrasound which is very specific, not
necessarily as sensitive as we like, but that's a nice
alternative to the biopsy, which is more invasive. And can
be tough to organize. And with the pregnozone, start preaddi
zone if you're an all worried treat before you can
(19:57):
get the results. If you're concerned and IV predn is alone.
If there are any ocular manifestations John's earlier. Are there
any other thoughts here? There's a lot. It's a big topic,
but I think you've done a great job at addressing
some of those decision points that actually kind of were
confronted with on a day to day basis. Any other
main takeaways you want listeners to absorb from this talk
(20:18):
about giants letterritis.
Speaker 2 (20:20):
Yes, so, of course the main thing I want people
to learn is about giants celeritis. But they are really
four things they should be learning. Number one is giant celetteritis,
Number two is giant celetteritis, and number three is giants celetterritis,
and number four is giants aletter ritis. You should be
thinking about giant celetterritis in any elderly patient, regardless of
(20:41):
their neuropthomic presentation, regardless of whether it's the classic presentation
or not. And if you start treatment on the person
and order the tests and get the ultrasound, it can
be vision saving or life saving and so earlier diagnosis
and earlier treatment definitely make a difference in this disorder.
Giants aletter writer should be top of mind on any
(21:02):
elderly patient who's complaining about headache or any visual symptom
in the.
Speaker 1 (21:06):
Iclon and I think a good thing to realize as
I'm thinking about it is it can feel a little
bit daunting. Well, I'm not a neurophthalmologist. I'm going to
get the ESRCRP platelets back. I don't necessarily even know
what to make of that in some of those close calls,
but I'd rather have that information and then bring that
to the neuroofth themologist and say, hey, I did this.
What do you think help me interpret that? As opposed
(21:28):
to not doing it because you're a little bit daunted
by I'm not sure how I'm going to be able
to interpret it.
Speaker 2 (21:34):
Yeah, And I would just say, if you don't order
it and you call your neuropthalmologist, they're just going to
tell you to order it. So you're just adding an
extra step unnecessarily.
Speaker 1 (21:43):
Doctor Angeleie, thank you so much for joining me for
another episode of blind Spot. I really appreciate it. Take care,
Thanks for having me, and thank you everybody for listening
to another episode of blind Spot. Have a great day.
Hey everybody, I'm zaeo Mednik and welcome to another episode
of blind Spot. This episode is sponsored by THEA Pharma Canada.
THEA pharm of Canada is the Canadian subsidiary of THEA,
Europe's leading pioneering and innovative eye health brand. Founded in
nineteen ninety four by Henri Schibre. With five generations of history,
the Chubret family has been dedicated to I care for
(00:31):
more than one hundred and fifty years. Their commitment to
improving lives is born of their pioneering spirit. They continue
to lead the worldwide preservative free movement in eye care.
They've created innovative delivery systems. They've focused on making products
accessible and cost effective for patients. They live this mission
every day because everyone should have the same opportunities to
see the world through healthy eyes. So thank you THEO
(00:54):
Pharmer Canada for supporting blind Spot. Giant cell artiitis sir
temporal artiriitis is one of the most threaded diagnoses and ophalmology.
Not only can it be vision threatening to the point
of complete blindness, but it can be life threatening too,
So obviously it's something nobody wants to miss, but it's
not so simple. Diagnosing giant cellar to ritis can be
challenging both from a symptoms perspective and requires blood work
(01:17):
and often a temporal artery biopsy to get a definitive diagnosis.
So what's the threshold for going down the path of
GCA testing and eventually treatment. At what point is one
worried enough to order the giant cellar to rightis related
blood work? And at what point does one go down
the path of temporal artery biopsy? And if prednizone is initiated,
(01:38):
when should it be initiated and should it be oral
prednizone that's given or IV methyl prednislone. I'm joined today
by esteemed neuroopthalmologist, doctor Andrew Lee. Doctor Lee is a
professor of ophthalmology, neurology, and neurosurgery at Houston Methodist. He
serves on the editorial boards of over ten journals, including
the American Journal of Ophthalmology, Canadian Journal Ophthalmology, and I
(01:59):
and is the editor in chief the Journal of Academic Ophthalmology.
He's a recipient of the Honor Award, Secretariat Award, and
Senior Achievement Award from the American Academy of Ophthalmology. He
joined Houston Methodist Hospital and Research Institute in two thousand
and nine and it's currently Chair of the Blanton I
Institute Houston Methodist Hospital and Professor of Ophthalmology, Neurology and
Neurosurgery at the Wheal Cornell Medical College. Doctor Lei, you
(02:21):
welcome to the podcast. Thank you so much for joining me.
Speaker 2 (02:25):
Yeah, thanks for having me.
Speaker 1 (02:27):
So I gave a bit of a preface about GCA
and what pretty much everybody listening to this nos is
it's a bad diagnose. So it's one of the more
dreaded diagnoses and optomology because not only is it vision threatening,
but it's life threatening because it can cause coronary art
to writs, it can cause a lot of different things
that can and obviously kill the patient. So it's one
of those things that we definitely don't want to miss.
(02:48):
I thought for this episode, as opposed to kind of
going through some of the basic stuff that a lot
of us know, I wanted to focus on some of
the decision points that ophthalmologists and optometrists need to make
as we see a patient when we're concerned whether they
have GCA, whether it's the decision point do we get testing,
do we do a temporal artery biopsy, and do we
(03:10):
initiate steroid. When I think of GCA, I think of
it as sometimes we get referrals where patients come in
and there aren't really any ocular symptoms. It's just a
GP or an emerged doc says, I know that I
don't have any ocular symptoms, but maybe they have this
weird headache that could be GCA, and there's maybe some
job quloudication. And then there's another group of patients where
(03:32):
they come in with actually an ocular manifestation. Why don't
we start off with some of the ocular manifestations. There's
some that I think most of us optimologists to know
that if we see we're definitely not going to debate.
We're going to get the ESR and CRP and initiate
the pathway. So would you say AAIO n artritic, ischemic
(03:52):
optic neuropathies at the top of that list, you see
that there's no question you're going down the GCA path.
Speaker 2 (04:00):
Yes, that's the most common presentation, but it can be
any ophthalmic presentation. So in an elderly patient, it doesn't
matter whether it's anti schemic APOPI, aio N, or postterious
schemic gothneropty where the disc is normal a retro bolbar
optic neuropathy. Whether it's transient vision loss or double vision
(04:20):
or moss of vision from center around arter inclusion, it
doesn't really matter. What matters is that any elderly patient
with a new neuropthalmic finding should be considered to be
giant cell until proven otherwise. Even though antiero schemic goplerobiti
is the most common.
Speaker 1 (04:37):
That's a super important point because basically the threshold should
be low because so many different things can't present as GCA.
Even though aio N is kind of a classic one
we think of. Nerve palsies are one that is common.
We see a lot of patients with six nerve palsies,
for example, pretty easy to chalk it up to, I
don't want to say pretty easy to be catalier, but
(04:57):
a lot of older patients have vascular risk factors where
we can say, yeah, I could see why you have
a six nerve posy. Would you say you do an
ESRCRP on everybody who comes in with a six nerve polsy,
even if it seems vasculopathic or are you more selective?
Speaker 2 (05:13):
Yes, I think the risk of doing an es R
and CRP is so low. The threshold for doing the
test is extremely low. So any elderly patient with double vision,
regardless of whether it looks exactly like what you think
is a schemic six should have consideration for ESR and
CRP because it's just such a low risk test.
Speaker 1 (05:34):
And like you said, they're transient vision loss. So that
includes things like Ameros's fugas in Fujax. I'm not sure
what the correct pronunciation is despite using it often, even
if you are getting the Karate dopplers or maybe getting
an ECG. I'm guessing that's as well, something you'd need
to be on guard for, on watch for, at least
for GCA.
Speaker 2 (05:52):
Yes, both transient diplopia and transient vision loss, Ameros's fugas
should have an ESR and CRP considered.
Speaker 1 (05:59):
For patients NaIO N so non artoritic kind of your
DiscT risk that is a little bit of dematist vision
is not as bad as an aaio N. Again, I'm guessing,
based on this discussion so far, you would say YEP
could be in a typically presenting GCA. Get the blood
work low risk.
Speaker 2 (06:19):
Yes, and that's because there's no real way to differentiate
non arto ritic from artot aio N. Of course, if
they have palat edema and it's bilateral, or if they
have concomitant chroidal or retinal schemeia, those are obviously not
an ai N and are aaio N arteroritic. But running
the mill nai N you cannot tell that that's not
(06:42):
giant cell. So we ordered a test on all of them.
Speaker 1 (06:45):
So you're building a picture here obviously of order. The
e s R CRP platelets not a big deal. I
guess my question is that sounds easy enough to do, right,
they're blood tests, it's not a big deal. Sometimes my concern,
and I am and I'm not alone, is there's a
lot of things in my mind at least and you
know better, that can elevate someone's ESR CRP and platelets,
(07:08):
especially older people. And we know that GCA presents I
don't know if it's exclusively over age sixty, but certainly
over age sixty, and there's a lot of other confounding
things that could cause someone's inflammatory markers to be high.
So the reasons sometimes I might hesitate, and I guess
I shouldn't based on what you've answered so far. Is
what am I going to do with a positive result
(07:28):
sometimes of an ESRCRP if I'm a little bit skeptical
when I'm ordering it. Anyway, when I pretest probability is low,
then I get an elevated ESR CRP elevated platelets. Maybe
only one or two of them is elevated. How do
you deal with that knowing that those markers can be
elevated for a number of reasons.
Speaker 2 (07:47):
Yeah, so that's part of the reason we do all
three of them, because we want to have all three
markers pointing in the same direction. So you're less likely
to generate a false positive for an ESR if you
have all three point the right direction, either up or down.
And the said rate, as you already alluded to, is
very non specific, and so anything can cause it to
(08:09):
be elevated. However, it's uncommon for all three things to
be elevated, and especially if they are markedly elevated. But
of course, pretest probability is the best predictor of post
test probability. As with any test, you have to interpret it,
and false positive and false negative is part of that interpretation.
And so if a patient has a borderline elevated ESR
(08:30):
but a normal CRP and a normal platelet count and
the pretest probability for diseases low, we're just going to
go with the majority report on that. And so I
think it is incumbent upon physicians not to rely upon
the tests to make the diagnosis. Labs don't make the diagnosis.
Doctors make the diagnosis.
Speaker 1 (08:50):
Is CRP the most specific? Is that the one that
if it's really out of whack to say, to say
completely informally, that really raises your eyebrows.
Speaker 2 (09:00):
Yes, it's the combination of them that have higher sensitivity
and specificity. So it is the combination of sensitivity and
specificity that you have to work with.
Speaker 1 (09:09):
I want to take a step back before we talk
about temporal artery biopsy and aultrasound. I mentioned earlier that
you've obviously got those patients who have an ocular diagnosis,
and then you've got the patients who who don't have
an ocular diagnosis, who are coming in with a headache,
maybe some neck pain, some of these symptoms. Jaw clodication
is a big one. What is your threshold when somebody's
(09:30):
coming in for those symptoms to do an SR and CRP.
And granted that's a tough question because that's a pretty
umbrella question for a lot of different patient complaints.
Speaker 2 (09:39):
Yeah, as I mentioned, the thresh ordering a centerate and
therap for me is quite low. So it doesn't matter
whether it's the ocular version or the headache version or
the jaw clodication. We're going to order the test because
the steaks are so high. And as I mentioned, ordering
off three helps you reduce the false positive rate, but
be test likely to disease is the most powerful predictor.
(10:01):
So the strongest predictors, the highest specificity things are jaw
cloudication and temporal artery tenderness, but headache of any kind
people with have normal exams from an eye standpoint, we
still have got to consider the diagnosis and e libly patients.
Speaker 1 (10:17):
Let's talk about temporal artery biopsy. I don't know if
off themology residents are off themolgist they're still doing them now.
I know we did during our residency in Canada, and
I imagine in some programs they're still doing that in
the States, or they're sending them off somewhere else. But
with a temporal artery biopsy. That's the kind of mainstay
of diagnosis.
Speaker 2 (10:38):
Correct, it's still the gold standard, but we have an
intermediate choice now, which is called tempor artery ultrasound. Found
is being done as a non invasive way to look
for a halo sign and that halo represents the transluminailymphysitic
infiltration into the artery. And if so, if your pre
test likely the disease is high and you have a
(10:59):
positive are the ultrasound a lot of places you don't
have to do the temporary biopsy anymore. So we're reserving
the biopsy as a gold standard. And conversely, if the
like it is low and you do a temporary ultrasound
and it's negative, that's probably sufficient to make the diagnosis
without a biopsy. And we're reserving the biopsy for the
(11:21):
cases where we cannot adjudicate or if we don't believe
the ultrasound result.
Speaker 1 (11:25):
So you're doing it for those cases where you think,
I thought this ultrasound was going to show temporary right
as it didn't. Now, let's go to the biopsy.
Speaker 2 (11:33):
Yes, And a lot of tests are like that, where
there's a screening test and then there's the gold standard.
So if the screening test is positive in a high
probability case, it's probably good enough. And if it's negative
in a low probability case, that's good enough. But if
it's negative and you still think the person as John Cell,
we would proceed with the temporary biopsy.
Speaker 1 (11:52):
Are those ultrasounds fairly new that they're being used and
who's doing those ultrasounds? Because I recall in residency we
would use the ultrasound just to imagine it was a
different ultra sound. We were using it just to kind
of be able to identify the temporal artery as part
of the biopsy. But what is when did this come
on the scene, and who's trained to really give an
(12:13):
accurate interpretation of it.
Speaker 2 (12:16):
Yeah. So with as with all tests, ultrasound is very
operat or dependent, and so your listeners need to go
and find out who's doing the ultrasound in their area.
And in some ways it's a self fulfilling prophecy because
if you don't order it enough, then they can't get
used to doing it. So in the beginning we did
both on everybody so that our ultrasnography division can get
(12:37):
used to doing the tests and we would have gold
standard comparison, so they could improve their technique and know, hey,
we missed a biopsy proving Johns or we found one
and nothing was in that artery, and it helped them
improve their technique over time. If you look at the
pool data from the literature, it's pretty good. And so
it's just a matter of training your local people or
(12:58):
finding your local people to be able to do the test.
It's the same people that do karate doppler, So the
karate doppler people are the temporal artery by ultrasound people.
It's just a smaller artery. But it's the same concept,
same principles, everything else is the same, so there's nothing
really new about it. It's just putting the probe on
a different.
Speaker 1 (13:16):
Place when you were starting to kind of do both
at the same time, when you were just starting to
do the ultrasound to compare the results to the tempor
artery biopsy. I don't know if it was an official studies.
I don't think anybody's going to hold you to the results.
But was the concordance rate pretty pretty positive?
Speaker 2 (13:35):
Yes? So, and that's what the literature shows as well.
The concordance rate is pretty good. The issue with the
temporary ultrasound is more of sensitivity than specificity. So if
we see the halo signs, it's hard to blow that off.
I mean, it's really hard to have the halo sign
not be temporaries. But if it's negative. There are forms
(13:57):
of giant cell where the biopsy is just the super
way of finding it, especially the healed and treated artiiitis
forms where we're relying on disruption of the internal elastic lamina.
There's no transmural infiltration, there's no giant cells, and so
those types of cases can only be found on histologic
examination of the artery, and the ultrasounds is not sensitive
enough to pick it up.
Speaker 1 (14:19):
Another decision point for for the ophalmologist is is pregnozone
and when you start it. When I was in residency,
I recall some people would say, listen, if you think
that the suspicion is high enough that you're ordering an
ESR and CRP, then you should start prednizone. What is
your thought on the decision of when to start pregnanzone
And there's a couple aspects there. One is is it
(14:40):
going to confound the results of your temporal artery biopsy
if you go that route, and the other one is
just is it unnecessary to be putting somebody on prednizone
before you actually know what the results of your tests are.
Speaker 2 (14:51):
Yeah. So our traditional paradigm has been diseased, diagnosed, treat,
But in giant silatoritis, as you've already alluded to, its disease,
treat and then diagnose, So the order of things is
a little bit different than for traditional neuropthalmic conditions. We
definitely would treat if your pretest likely the disease is
sufficiently high. However, if the risks outweigh the benefits or
(15:14):
the pretest likely it is low, we would do the
temporary ultrasound on that person so that you don't have
to wait for the biopsy, just so you get an
idea of whether or not you should be treating or
not for this patient. Covering the patient with a short
course of steroids until we get the biopsy or the
ultrasound is probably not going to harm the person. So
it's way better to cover the person while you're working
(15:36):
it up than it is to have a vision loss
because you didn't start the steroids.
Speaker 1 (15:41):
And what's the current thought on whether pretnozone is going
to affect the results of the biopsy.
Speaker 2 (15:47):
It does affect the results of the biopsy because steroids
in general reduce all the forms and the all of
the stages of inflammatory disease. However, what it cannot do
is it will not reduce the disruption of the internal
elastic lamina. So for the tempor ultrasound, we definitely want
to have the ultrasound done as close to the starting
(16:09):
the steroid as possible. For the temporariti biopsy, you probably
have two weeks because the structural change caused by the
giant cell will still be present even if the lymphocytic
infiltration has been dissipated by steroid treatment. So two weeks
is probably your window there. It'd be better to do
it faster, and that is one of the advantages that
the ultrasound has over the temporary biopsy. It's hard to
(16:30):
get people, as you're already alluded to, to get the biopsy done,
and so ultrasounds just faster.
Speaker 1 (16:36):
Yeah, and I guess that's good that the one that
is more susceptible to steroids is the one that at
least is easier to get done, because it's easier to
get an ultrasound done than it is to get a
biopsy done. Having said that, you need to get the
ultrasound done quickly because if they've been on steroids for
a week, that's going to have more of an effect
on the ultrasound you're saying than it would have on
that biopsy.
Speaker 2 (16:55):
Yes, and you always have the biopsy to lean on
if your temporary ultrasound is neg but you think they
have the diagnosis, and even the temporary biopsy the gold standards.
Sometimes we have to do both sides because the concordance
rate is only ninety six percent. So really the bottom
line is, if you, as a clinician think they have
(17:15):
giant cell, you should treat them regardless of the biopsy,
regardless of.
Speaker 1 (17:20):
Another decision point oral versus ivy methyl preston is alone.
Again what I recall, and again what I recall is
if somebody's got an ocular manifestation, like specifically, if they've
gotten artoritic a schemic optic neuropathy, that's going to warrant
ivy methyl preston is alone. Whereas if somebody doesn't have
(17:40):
an actual vision threatening issue, but they've got what you
think is GCA based on the biopsy or initially just
based on the history and based on the blood work,
then it's reasonable to start on po oral steroids. What's
the general thought on that? Is that still accurate or
is that outdated? Is there a greater pushnail to just
(18:00):
be more aggressive with IV steroids.
Speaker 2 (18:03):
I think that's still the traditional teaching and the conventional
approach with vision loss, but not just vision loss, transient
diplopia or transient vision loss, the TIA version of it.
We would give intravenus methyl peniculin to those patients. So
the patients that have CNS manifestations, including the cranial nerve polsies,
(18:24):
we would give intervenus steroids to those as well. But
the oral steroid can be used for just the headache
people or even the jaw caudication people. So one to
one point five milligrams of oral prednice own is still okay.
But in general, most neuroptimogists would choose IV steroids for
vision loss, including transient vision loss.
Speaker 1 (18:43):
Okay, that's good. Again, I didn't realize that even like
a transient vision loss or I guess a sixth nerve
palsy as well, if you thought that it was related
to GCA, anything I related which you are attributing as
pathological from GCA, you'd be more on board with the
IV methyl pretnismone. And is it a three day course? Typically?
Speaker 2 (19:02):
Yes, there's no proven standard dosing or duration, but that'd
be a typical dosing. There's no data on the dose
or the duration, but three days is completely reasonable.
Speaker 1 (19:14):
Dosually, very valuable information. Some people are probably yelling at
me listening, don't you get it? When I was asking
those earlier questions, he's saying, do the es R and
CRP and everything. But I wanted to hammer that point home.
So I'm glad I asked you that, and I, for
one will not forget that, and I'm sure listeners won't too.
So you've been very clear on just order the ESR
and CRP and if you're concerned about well, there's a
(19:35):
lot of things that can elevate it. That's why we're
ordering all three so we can look at the whole
picture together. When we're talking about temporal artery biopsy, we
do have this new ultrasound which is very specific, not
necessarily as sensitive as we like, but that's a nice
alternative to the biopsy, which is more invasive. And can
be tough to organize. And with the pregnozone, start preaddi
zone if you're an all worried treat before you can
(19:57):
get the results. If you're concerned and IV predn is alone.
If there are any ocular manifestations John's earlier. Are there
any other thoughts here? There's a lot. It's a big topic,
but I think you've done a great job at addressing
some of those decision points that actually kind of were
confronted with on a day to day basis. Any other
main takeaways you want listeners to absorb from this talk
(20:18):
about giants letterritis.
Speaker 2 (20:20):
Yes, so, of course the main thing I want people
to learn is about giants celeritis. But they are really
four things they should be learning. Number one is giant celetteritis,
Number two is giant celetteritis, and number three is giants celetterritis,
and number four is giants aletter ritis. You should be
thinking about giant celetterritis in any elderly patient, regardless of
(20:41):
their neuropthomic presentation, regardless of whether it's the classic presentation
or not. And if you start treatment on the person
and order the tests and get the ultrasound, it can
be vision saving or life saving and so earlier diagnosis
and earlier treatment definitely make a difference in this disorder.
Giants aletter writer should be top of mind on any
(21:02):
elderly patient who's complaining about headache or any visual symptom
in the.
Speaker 1 (21:06):
Iclon and I think a good thing to realize as
I'm thinking about it is it can feel a little
bit daunting. Well, I'm not a neurophthalmologist. I'm going to
get the ESRCRP platelets back. I don't necessarily even know
what to make of that in some of those close calls,
but I'd rather have that information and then bring that
to the neuroofth themologist and say, hey, I did this.
What do you think help me interpret that? As opposed
(21:28):
to not doing it because you're a little bit daunted
by I'm not sure how I'm going to be able
to interpret it.
Speaker 2 (21:34):
Yeah, And I would just say, if you don't order
it and you call your neuropthalmologist, they're just going to
tell you to order it. So you're just adding an
extra step unnecessarily.
Speaker 1 (21:43):
Doctor Angeleie, thank you so much for joining me for
another episode of blind Spot. I really appreciate it. Take care,
Thanks for having me, and thank you everybody for listening
to another episode of blind Spot. Have a great day.
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