Acute Eye Disease in Rural Australia
Dimitri
Good evening everyone.
My name is Dimitri and I will be hosting tonight's webinar.
In tonight's session of the Rural Health Webinar series, we will focus on the diagnosis and management of acute eye conditions. The webinar will highlight the vital role of community optometry, referral pathways and telehealth in supporting rural GPS with effective patient care. We are joined this evening by our two presenters, Michael Yapp and Alex Craig. Michael Yapp is the head of clinical operations at the Centre of Eye Health, where he has worked since 2009. He also advocates for the optometry profession through his role at Optometry Australia. Michael has diverse clinical experience including private practice, locum work in Australia and the UK running an optical charity and working in ophthalmology practices. He has been involved in optometric education since this time as a staff optometrist at the University of New South Wales and continues to speak at conferences globally. Alex Craig is originally from Zambia, completed his education in Northern Ireland and the USA before moving to Melbourne for his optometry doctorate. He has been practising in Karratha, WA for ten years where he opened Karratha Eyecare in 2009. Alex has developed a strong interest in community education and referral pathways in optometry. I would like to begin tonight's webinar by acknowledging the traditional owners of the lands on which we are coming together from and the land on which this event is being broadcast.
I would like to pay our respects to the elders, past and present, and would also like to acknowledge any Aboriginal or Torres Strait Islander people who have joined us this evening. Just before we start, a few housekeeping things to cover. So you will notice that you are set on mute, and this is to ensure that the webinar is not disrupted by any background noise, but of course we do encourage you to use the Q&A to ask questions. The webinar is accredited for one hour of educational activities CPD. To be eligible, you must be present for the duration of the webinar.
We also kindly ask that you complete the short evaluation that will pop up at the end of the webinar. It should only take a few minutes to complete and will help us improve the format and content of future webinars. By the end of this webinar, you will be able to outline the differential diagnoses of acute eye disease, describe the implementation of treatment options, and briefly discuss available referral pathways, but for now, I am going to hand over to our first presenter for this evening Michael. Thanks, Michael.
Michael Yapp
Thanks Dimitri. To try and keep everything moving tonight and also to try and get your input, we are going to be running some polls and a few other things throughout the talk itself. If you have one available which most people will have at their fingertips, if you can grab your phones, scan the QR code or alternatively open up a browser and go to that website, what will happen is the polls will come up automatically on that phone, and you will be able to see the responses both on the presentation screen and on your phone as people respond. You can just skip your name. It is not going to be named in any of the responses, so you do not have to worry about your answers causing problems. Ultimately it is just to keep things moving and to get an idea of what you think to help people interact, I suppose with the webinar tonight. With that, we will actually kick off the first poll straight away. That should start coming live on your phone. Basically what we are interested in first up is in your primary practice, what sort of gear do you have that helps you in terms of in particular foreign bodies? Looks like we got some good well stocked practices out there which is great. More than I expected, but that is fantastic. It is good news. Excellent. Looks like we are talking to a very well set up group of doctors in terms of eye problems. Let us move that on to the next one.
Get an idea of how often you are dealing with eye problems in the day to day practice. Reasonable variation, but certainly plenty of eyeballs coming into your practices with problems, which is good for the sake of this talk, obviously. One final one for you. Just interested in how confident you are in removing foreign bodies, assuming it is something that comes in relatively regularly, whether it is something you are happy to do or not. Excellent. Good range. That should work very well for tonight's talk. Moving on from there, obviously our first talk then is going to centre around foreign bodies. Here is a patient scenario for you. Got a 68-year-old male using an angle grinder without safety goggles as they often do, sudden pain in their left eye comes into your office, but as with most GPS, you are fully booked. You might have a three week waiting list. You have got a lot of people sitting in your waiting room already, and the question is, I suppose is what do we do next? Or what do you do next with this patient? Obviously we do come across a lot of patients that do not have safety goggles. I have seen some interesting attempts to try and stop foreign bodies.
This is one of the best I found on the web, probably not the strongest safety goggles in the world, but at least they were thinking about it. It is a good start. I guess there is a few things to consider at this point in time, from your busy practices perspective, obviously you have got lots of options. The first one is to see them yourselves, manage them and if necessary refer on, if not confident with the outcome or if you are not sure you have got everything you need to be done for that patient. Some people may send it straight to the nearest ED so that the ED can take care of the problem as required, and that obviously depends on where you work and how accessible an ED is. There are other options, Obviously, if you have got an ophthalmologist in town or you have an optometrist in town are potential pathways that may be able to assist you. If it is not something that you are either comfortable with, confident with, or it is something that you would like a second opinion on, and we will talk a lot more about those pathways as we go through this talk in more detail. In terms of the pathway considerations, as I said, there is lots of different options.
It partly comes down to your equipment, your confidence, your time and what other options have you got. Every optometrist, particularly in rural areas, is going to be confident in removing foreign bodies to some degree. They will have the equipment, but you also have to think about the concept of what is it going to cost the patient. How long are they going to wait for? Who is going to do the follow up, and they are all considerations in terms of establishing pathways in your practice to managing these patients, the best way for you and the best way for your patients. The things to think about from my perspective is to have a clear list of who is available and then establish the networks around direct referrals.
Unfortunately, optometry and GPs in particular do not always communicate as well as we should do, and those pathways should be a lot more open in some ways. As an example, one of the pathways that is happened in a place like Rockhampton is rotating roster in the ED. So the ED has a list to say, okay, if I get an eye problem on a Monday, I am going to send it to this optometrist. If I get an eye problem on a Tuesday, I am going to send it on to this optometrist here, and it works out very, very well in Rockhampton. There are lots of options in terms of pathways to assist your rural practices as or when you feel appropriate, and with that, I will pass over to Alex to talk a little bit more about the actual process of the foreign bodies.
Alex Craig
Thanks Mike, and good evening to you all. So, the first thing that we are obviously going to be trying to figure out when we see foreign bodies or when we have foreign bodies come in and either referred in or walk through the door is going to be what effect or how much of an effect is this foreign body going to have on this patient's ability to see after the foreign body has been removed? The first question that I am often going to be asking myself is where is the location of the foreign body? So is it actually on the cornea or is on the conjunctiva? Foreign bodies that are very easily removed on the conjunctiva typically can be removed with a with a cotton swab or a cotton bud, whereas when we find that people when either when doctors or when I live in Caracas or I have a lot of medical offices on site, so it is a mining sites try to remove foreign objects with a cotton swab, we end up pushing the foreign body into the cornea even further, making the ultimate removal process quite challenging.
The location of where it is and what we are using to remove it is probably the first consideration. Ultimately, at the end of the day, the risk of permanent vision reduction is going to be our foremost thought. The other thing that we also want to consider is it penetrating. For those of you that do not have slit lamps, this is going to be extremely difficult to see as you cannot see depth, but there is one test which you can use which is called the Seidel sign, so I do not know if you guys are familiar with that, but essentially putting sodium fluorescein onto the cornea and looking at it under a cobalt blue light will ultimately tell you whether there is a perforation in the cornea. As you will see, aqueous humour flowing outwards through the cornea in a waterfall fashion. When we are talking about metallic foreign bodies the rust rings obviously the most important thing. I probably spend more time removing rust rings than I do actual foreign bodies, and very typically that is because the foreign body has either just been knocked out or it has been broken off inside of the eye and it has been left to oxidise, and ultimately at the end of the day then causing a significant amount of rust.
Obviously it is very important to to remove rust primarily because it is preventing inflammation. It minimises corneal damage and the risk of infection. It ensures that that the ultimate outcome for vision and visual clarity is improved, and it also improves patient comfort by alleviating all of the foreign body sensations. This is really a mechanism for functional preservation, and maintain vision, which is the most important thing. The tools that I use the most are the tools that give me the lowest energy into the eye, especially in terms of where or how the foreign body is located, so central 5 ml, I typically am going to be using a foreign body spider, which is what that looks like there on the right. It is a golf spider. It looks like a golf club. It has got a bevelled edge and a sharp corner to it. It allows for us to slice through the corneal epithelium very easily and to very typically remove the foreign body from underneath it, so to come around it and pull it out in one fell swoop. Sometimes that is obviously quite challenging depending on the nature of the foreign body or how long it has been in the eye, and as a result we have to use the Alger brush, which is a diamond tipped bur that rotates obviously very, very quickly and chews up the epithelial tissue. Now they say that these Alger brushes cannot go through the entirety of the cornea because the next layer down the stroma is too thick and too hard, but I would not test it. So if you are unfamiliar with using it obviously referring to ophthalmology or to optometry is preferred.
When we talk about what we do after we after we have removed it, so we spent the time trying to figure out how we are going to remove it and what is the least the lowest energy option. Very typically in all of these cases I will be prescribing a prophylactic antibiotic cover, and the next step and this is often quite controversial between when I see patients that have been seen in the ED, they typically walk in with this huge patch over their eye after a foreign body or even a small foreign body removal. Let us talk about that for a second. For us, no patching is ultimately preferred, especially in in smaller foreign body removals, it encourages normal blinking and interior production. So the tears have an complex in them that actually will allow for natural obviously antimicrobial properties, and so we want the eyes to blink normally and to produce tears normally, which ultimately can aid in healing. This is going to reduce infection risk, and ultimately but that that happens by avoiding a warm, moist environment, which is what this patch will typically create. It allows for us to monitor the symptoms obviously a lot better.
The only time that we would consider patching is when we would want to stop blinking from happening, and that typically is only in very, very large epithelial defects, and in those cases when we tend to see those cases, we tend to bandage them with a contact lens anyway. Ultimately, we are trying to maintain the homeostatic function of the eye as it heals, and so patching it or putting a big patch over the top of it is typically contraindicated. Does the nature of the foreign body matter? So this really only comes into play depending on the risk for either perforation or secondary infections, and the big one here is very typically organic materials. So organic materials like wood or plant matter obviously have a very high risk of infection.
Our big one that we are looking out for in this case is fungal keratitis which requires an aggressive antibiotic and antifungal regime and often and most of all of the time without patching. Metallic foreign bodies often leave rust rings. We have talked about that, and patching is often avoided as well unless unless there is a very, very large defect without infection. So anytime there is likely to be an infection, patching is definitely contraindicated. Inert non-metallic bodies like glass or plastic, which also have a lower infection risk may be patched depending on how else the eye is potentially damaged. Obviously the key consideration here around patching is to ultimately avoid patching if the infection risk is high, and considering bandage contact lenses or short-term patching for severe pain and ensuring regular follow ups to monitor healing and infection signs.
The next one is on steroids, so again, a bit of a controversial topic around whether we put steroids or not after we have removed foreign bodies, and so let us spend a bit of time sort of really just breaking that down. It is controversial for one reason and that the steroids obviously suppress the immune responses, and this can increase the infection risk in the compromised corneal tissue. They also delay wound healing by inhibiting collagen synthesis and epithelial proliferation. So while steroids are reducing the inflammation, they also may reduce scarring, so in significant trauma or in significant foreign body removal where it is central where it is likely to affect the patient's vision at times, we will then put a steroid on top of an open wound and this is obviously now you can see why this is relatively controversial. Very typically it is going to be with some antibiotics or it is going to be very shortly after re-epithelialisation has occurred. Prolonged uses of steroids obviously can create other issues in the eye.
The pressure can go up as well as obviously creation of steroids, and so we often will only really use them to control situations with significant stromal inflammation. If the eye has had a significant impact or a significant foreign body removal or a significant trauma where we ended up with a lot of swelling or changes in the stroma, we typically will use we will use a steroid as well. The same thing in central corneal involvement, and like I have said, it is often paired with antimicrobials to mitigate infection risks. Steroids are typically reserved for use after the epithelial healing has happened, and again, this is typically used to avoid delaying wound closure. Best practices around steroids would be that the initial management should always focus on the removal of the foreign body completely, infection prevention with antibiotics and lubricants and steroids are used only under specialist supervision, so typically we will do that in rural Western Australia alongside our ophthalmology colleagues via telehealth.
I can go to the next slide. Blunt trauma. I do not know what I have done to deserve this, but I have had four come in this week directly from the ED. The way that I am running through these ones is essentially breaking them down into two categories. We are looking at coupe or contre-coupe injuries, the mechanism of injuries, and so obviously the coupe injuries are going to have injuries that occur at the site of impact due to direct compression or deformation of the tissues, causing this localised damage. Examples of these obviously are corneal abrasions or oedema, lens dislocations or subluxation, orbital fractures and hyphaemia, which is that picture on the right there, so blood in the anterior chamber and contre-coupe injuries are obviously very different part of the eye, so now we are looking at the shock wave that is passed through the eye and bounced off the inside of the eye on the opposite side of the eye, and really, what we are looking for here is any sort of retinal or choroidal involvement . In the coupe injuries, our biggest concern is after managing the initial injury is 90-day glaucoma. In these cases, we often have enough compression of the anterior chamber to cause damage to the iris, and then secondary to that, it can cause a change in the way that the aqueous humour passes through the anterior chamber and vacates or exits via the trabecular meshwork, and as a result, you can get pressure that goes up, and typically we see this around the 90-day mark post incident.
Obviously these patients are watched quite closely and are monitored for pressure spikes over the three months post injury. Your contra-coupe injuries that the big ones are going to be your retinal detachments and so obviously dilating these patients is really important, and having a look at the retina and ensuring that the retina is intact. Your patients with higher risk are going to be your myopes or patients with short sighted predominantly. Obviously the key injuries are the front or the back of the eye and the clinical relevance here is that in my opinion, obviously a thorough examination of both the anterior and posterior segments is essential, and in the ones that I have seen this week, they all had CTs in ED as well. One of them had a trapdoor fracture, which is where the bottom rim of the orbit is broken, and it was actually very lucky that there was no tissue impingement there at all. So he did not end up with a sunken eye or a double vision or diplopia. All of these patients are also probably going to present with a traumatic uveitis or an iritis.
The problem with this is that the internal structures of the anterior chamber become very sticky, and they tend to stick together, and if the anterior lens sticks to the iris, they end up causing a malformation or a changing of the pathway again of the aqueous humour, and how it gets in and out of the eye and causing the pressure to rise really quickly. Acute management of these patients is one what type of injury are we looking at, ensuring that the contre-coupe of these injuries or the retina is actually intact and healthy because that is the one that is going to likely be most sight threatening for all of these patients, and then managing the anterior chamber inflammation with mydriatics to get the pupil out of the road as well as with steroids to quell the anterior chamber inflammation. All right. Back to Mike.
Thanks, Alex. Here is your second patient scenario. You got a 74-year-old female comes into your practice saying my left eye has gone very blurry. You measured at 624. They say, oh, I am not sure when it started, but what happened was I rubbed my other eye and then noticed that I could not see very well out of my left eye. They report no pain, no discharge, no hyperaemia and otherwise unremarkable ocular history. We tend to find this a lot, and it is surprising the number of people that come in and say, I do not actually know how long it has been there, but I saw it the other day, that comes along with a lot of people that say, well, it happened about three weeks ago, but I thought it would go away, so I have just left it for the moment, and I am sure that is not something that is unique to eyeballs. I am sure that is something you come across in your practice on a regular basis. We are going to go back to your phones and here is your patient scenario. Have a think about what your differential diagnoses could be for why this person has got asymptomatic marked loss of vision in one eye, which we assume is relatively acute.
If you type them in, you can type in multiple responses for your differential diagnoses and we will see what comes up. So temporal arteritis. Cataracts. Glaucoma. Retinopathy. Dislodged lenses. CRVOs, neuropathies. Excellent. Some good choices in there. Certainly quite a lot of things to think about in terms of acute painless loss of vision. Let us see where we go next. So once again you have got quite a lot of options in terms of how you would manage this patient in your practices. Obviously Alex is going to talk through the different conditions and how to assess them, but you need to measure vision. You are looking about motility pupils and fields. You want to look at the external eye and obviously at the back of the eye as well, and then from your practices, depending on your confidence and your equipment, you can decide on next steps. Another option obviously as per foreign bodies and trauma is ED, and then there is the concept of either your local ophthalmologist or optometrist depending on where you work, what your pathways are, how easy they are to access and so on. The other question at this point in time is how long has it been there? We are not sure according to the patient's history. In terms of timely, do we send it immediately?
Do we send it promptly and where do we go next, and I And I guess there are things to think about in terms of where you work, how you work, and how your relationship with your local practitioners is and considering how we can possibly improve that going forward. The other option here is telehealth. I am going to touch on telehealth for a moment, I am sure, particularly for those that you work in rural settings, telehealth is something you are very, very familiar with. The dictionary defines it as the provision of healthcare remotely by means of telecommunications technology. Now, ultimately one of the problems I have whenever I am talking about telehealth is the multiple different versions of telehealth that exist. There is many, many different ways that people can be thinking when you say the word telehealth.
It could be a direct consultation with a patient via video telephone call. In terms of remote diagnosis. It could be a synchronous consultation with a third party, so you are there with your patient and a third party on the other end giving advice, consultations and some input. It could be an asynchronous patient consultation, and this is something that happens quite a lot in optometry with ophthalmology where we send through some scans and some results a little bit like radiology and say what do you think is going on here? Can you give me your opinion where the patient is not necessarily in the chair at that point in time? You have then got remote patient assessments and this is something that is happening a lot more overseas, but it is starting to hit the Australian market in the eye game where you actually have a technician driving the toys with an optometrist or ophthalmologist viewing the results in situ at the time, so they are basically performing the assessment remotely.
There is remote treatment supervision, which is basically the same thing but is more of a surgical provision usually, and there is a lot of self-monitoring happening in optometry now where patients have the ability to actually take the device home, perform the monitoring on themselves and the results are being transmitted automatically back to the optometrist to assess the results, to say are things changing in between the consultations when we are actually seeing you and they are all different versions of telehealth. In terms of acute pathways for ophthalmology input, most, if not every optometrist, would have their ophthalmologist on speed dial to the point where if you have got a case in your chair, you can easily text them, contact them through WhatsApp, phones or whatever else. In particular, in the regional settings where the ophthalmologists may not be on site more than once a month or once a week or similar.
Obviously there is always the option of hospital registrars through places like Sydney Eye Hospital or Royal Victorian Eye and Ear where you can make that same phone call as well, but one of the models that I am going to pass over to Alex to talk about really brings in telehealth, and that is the Lions Outback Vision model.
Alex Craig
Thanks, Mike. We spent the probably the better part of ten years trying to get this model correct, and I am quite obviously quite proud of what we have been able to achieve. Obviously I work very closely with Dr Angus Turner and ophthalmologist and Lions Outback Vision. They are based up in Broome, and they run a hub and spoke system of care as well as on call ad hoc telehealth 9 to 5, Monday to Friday. There is two versions of this that we have ultimately settled on in prior iterations, I spent time in the outpatients department running ophthalmology clinics through VC essentially. We found that it was more challenging to try to get data to the correct locations within the confines of the hospital, and so we moved the model into private practice and we run a mixed version of private-public telehealth.
The way that these systems work is ultimately that all referrals that are referred into ophthalmology in the region come through Karratha Eyecare. Those referrals then are triaged and they are then seen appropriately or triaged into telehealth. We are then able to obviously assess the patients based on the need coming through from the referral, and those referrals are coming from GPs, they are coming from the hospital, they are coming from other optometrists in the region, remembering that we are 2000 km north of Perth and another sort of 900 km to Broome. Having ophthalmology on call uh via VC has proven to be an invaluable resource and has actually allowed me probably to practice far longer than I ever thought I would in regional Western Australia. The big thing that we are really very proud of is our ability to share images, so I can have a patient walk in the door and be assessed and have all of my images ultrasounds of the back of the eye, axial length measurements, whatever it needs to be, anterior images uploaded and sent to Broome where I can have an ophthalmologist sitting in front of a series of computer screens. as if he is looking at them live within another two minutes I can get them on VC through Skype and we are able to have a three-way conversation with the patient.
This has dramatically reduced the burden of the number of patients that have had to fly to Perth for tertiary care intervention, very typically relying on the Royal flying Doctor or on patients themselves to pay for services down in Perth often losing their vision as a result, and then also in terms of chronic disease management which we will touch on in the next webinar that we talk in around the burden to the patient of having to travel to Perth all the time for ophthalmology care, and so within this telehealth model, we have been able to then obviously develop co-management. It works and it works really, really, really well. Like I said, the Lions Outback Vision model is based on those two types of clinics.
One is referred in and one is ad hoc, and this also helps de-burden the public system, so we found that when we have a referral coming through from the emergency department, we are able to assess the patient, upload all of the images, all the necessary scans and then speak to an ophthalmologist all in the same day and create a tertiary care management plan, all within about 30 or 40 minutes. It certainly has certainly has revolutionised accessibility and really allows for good professional relationships to be built between primary care and tertiary care as well. None of our patients have to leave Karratha unless they need physical surgery or some form of intervention that obviously a surgeon can do so which is really, really good, so at least that is what we found.
Michael Yapp
Once again from your perspective as GPs in rural practices, there are multiple pathway options for patients with acute vision loss. It comes down to things like the availability, equipment, cost the patient wait times who is going to do the follow up, and as we just talked about the availability of telehealth either for yourself or through an optometrist to ophthalmology as required, and there are certainly things that ultimately require a discussion and a clear list of who is available, establishing those networks like we talked about before to make sure that those pathways are clear and open to help you manage your patients appropriately, and with that, we will pass back over to Alex to talk about what these patients might have had.
Alex Craig
The heading here, I have broken it down into three, so this is obviously acute painless vision loss, and we will talk about painful vision loss and we will talk about acute red eye, really want to talk about the differentials that you might want to go through as well as one or two clinical pearls that you might want to think about or clinical signs you might want to think about when these types of patients walk through your door. The first cause of acute painless vision loss would be central retinal artery occlusion. This is the stroke of the eye technically. Obviously the common causes are embolisms or thrombosis, sometimes happens with trauma and acute very quick intervention is necessary to have any really good outcome in these cases.
Most of you, I think I saw on the equipment list when you were suggesting what you have in your practices, you have a direct ophthalmoscope, so being able to view the retina in this case is actually very important. The clinical sign here that we would be looking for would be a bleached or a pale white retina with a cherry red macula, and that is obviously because the vascular supply to the macula comes from a different source. This is a clinical indication that this patient has a central retinal artery occlusion. Intervention is listed there if you are within that 0 to 4 to 6-hour window, managing, trying to get the pressure down to dislodge some form of embolise is encouraged, but the reality is that these patients often need ophthalmology intervention very, very quickly to save whatever sight they potentially have.
The big thing in this case obviously is the fellow eye. It is an ocular presentation, but there are systemic implications there, so really understanding and managing the cause with antiplatelet therapy etc. is going to obviously be our goal with these patients. Visual outcomes, like I have said, have very poor visual prognosis, especially if ischaemia has set in or lasts more than four hours, obviously a lot of risk of other comorbidities as a result of ischaemia in the eye, the most important one being glaucoma ischaemic crisis of the of the iris.
Moving on. Just to remind you, the clinical sign there is a unilateral pale white retina, very typically. CRVO, this is the central retinal vein occlusion. This one we call blood and thunder. If you look in the eye and you can get to the retina, you see blood is everywhere. There is just you barely see the retina for the amount of blood. This comes in comes in two types as well as the CRVO does, which is central retinal vein occlusion as well as branch retinal vein occlusion, so sometimes in these patients they will have painless vision loss because a tributary branch was a macular branch vein has actually ruptured as well, but in general, the acute vision loss is from swelling at the macula, so you end up with a lot of macular oedema. ACUTE intervention would be anti-VEGF intravitreal injections or steroids, long term. Steroids typically reserved for patients who have already had cataracts taken out or cataract surgeries. We refer to those as pseudophakic primarily because the steroids can cause cataracts long term, again, we are treating underlying conditions.
We can use things like retinal laser intervention for managing neovascularisation secondary to ischaemia. The outcomes in these patients are typically very good, quite tricky getting them off of the intravitreal injections. Typically, when we stop treating with anti-VEGF, a lot of the macular oedema returns, and so it is a treat and extend protocol that we run in our intervention clinics. We typically are trying to get patients to have larger and larger gaps between injections over the course of sometimes up to two or three years.
The next one is anterior ischaemic optic neuropathy. This can come in two different formats. One is arteritic, and this one very typically the hallmark sign here is your octogenarians or people in their seventh, eighth and ninth decades of life that end up getting GCA and this ties into the next one, which is transient ischaemic attacks. It can also obviously present as a non-arteritic and very typically in small vessel disease. This is also visible on the retina, and sometimes very typically will present with a very tight optic nerve as well. Intervention for these patients is high steroids. Our referral pathway here is straight into emergency or straight to Ophthalmology, and then a temporal artery biopsy as well. In non-arteritic cases, there is no real acute treatment. We are managing any of the modifiable risk factors that we possibly can. Outcomes in both of them are relatively poor, and it is quite rare to get partial recovery.
The race again in this case is similar to the CRAO in that it is to ensure that the fellow eye is preserved as well. The hallmark sign here as well, and we did not have visual field machines because it is typically not something we would expect to see in a GP practice, but most optometry practices will have a visual field machine. The clinical sign here is going to be a horizontal respecting typically inferior defect, which is quite easy to test for in most optometry practices. Including that in your referrals or knowing that when you get the referral, you get the visual field back or the letter back is indicative of this type of pathology. TIA is the next one, very similar common cause via atherosclerosis or cardioembolisms, intervention is very, very similar. This is typically what we would see is amaurosis fugax or a sign that an eye on or that an AAION or that an episode of GCA is going to occur, and that is like the vision going in and out, and almost a blacking out of vision or a greying out of vision and coming back in one eye is a hallmark clinical sign that we see in these cases and often, you will see a change in the pupillary function as well.
The other thing that you can look at the vasculature. In my experience with these cases, often it is very easy to tell which side of the which side of the neck is going to have to have a Doppler to have investigation, primarily because the blood vessels are relatively distended in the one side. Having a look with your direct ophthalmoscope in the back of the eye at the retina and examining what each eye looks like in these cases is often a very good way to tell whether there is going to be a problem with even things like GCA or TIA.
Retinal tears and breaks. This one is quite common and often screened for very well. Your most common causes here or big groups of people that are going to have this one is patients who are myopic. I had one of these on Monday, walk in the door, four-day onset, curtaining of vision, could not see anything from midline down. That is flipped over in the eye and that is my biggest concern because that means the superior retina is peeling off and as it comes off, gravity pulls it forward and it can cross over the macula. The big watershed here would be macula on versus macula off in retinal detachment.
Does the patient maintain vision? Do they have a curtaining in their vision? Do they have flashing lights or photopsia or things flashing around in their vision and new floaters that they have not seen before? The two clinical pearls there are the clinical signs and then the big one obviously is determining whether the macula is on or the macula is off. Even in patients who wear glasses, if they do not have glasses, a pinhole is fantastic for ensuring that this is posterior eye versus anterior eye. Sometimes people have reduced vision because they forgot to put their glasses on. Ensuring that we know where we are actually looking in these cases is really important. Again, if you are handy with an ophthalmoscope through a dilated pupil, retinal detachments are typically very easy to see. Very typically, they will present in the form of a horseshoe tear that turns white or a whiter colour almost instantly and quite easy to pick up, especially if they are in and around the equator of the eye. Outcomes of retinal detachments, if detected very early and again, that probably is going to be our theme tonight is trying to figure out how do we work together better to ensure that intervention for any of these conditions is as early as it possibly can be.
Outcomes are very, very good if it is detected early. The macula off has less of an urgency, primarily because the outcome is already expected to be relatively poorer, not completely blind, but poorer than if we had the macula on. It is a bit of a race again to make sure the macula stays on. Your big risk factors here are going to be, again, patients with short-sightedness, patients with trauma and the location of the tear or the break. Just to finish the clinical history or the question that really needs to be asked is what is the patient experiencing? Are they experiencing a crippling in their vision, flashing lights or floaters that they have not seen before?
The next one is going to be endophthalmitis. It is in here because it is common enough and it is a very big problem, if it does happen. This is essentially global inflammation and infection of the eye. This is most commonly after some form of eye surgery. In fact, almost completely after some form of eye surgery or intervention, more commonly after intravitreal injections. I had a patient today who had endophthalmitis two years ago as a result of a complication from an injection in Midland in Perth. These things happen everywhere. The risk is very low, but they certainly do happen. It is global inflammation of the eye and requires very, very strong antibiotics and typically hospitalisation with urgent surgery vitrectomy to remove the vitreous primarily because it acts like a bit of a scaffold for the bacteria to grow, and it grows very, very, very quickly.
Outcomes in these cases are very typically very, very poor. Retinal detachment typically accompanies these, and we end up with total permanent vision loss. Your clinical sign in this case is typically a hypopyon. This is that purulent pus where you would normally see a hyphema of blood, you would see sort of a yellowy white hypopyon sitting at the inferior anterior chamber which can be seen without a slit lamp. That is what you would be looking for in these cases or global inflammation.
Next one is going to be cellulitis. The differentiation here is going to be orbital versus preseptal. Does it involve the eye past the septum. The other thing to remember here is in children under the age of 2 or 3 where they do not have a fully developed or a strong enough septum to stop the preseptal cellulitis becoming orbital cellulitis. On the next page, I have actually got a nice little table there for you to screenshot or to take with you as a way to differentiate between the two. The biggest differentiation for us is going to be because they can look quite similar, what I look for is, is there a pupil abnormality? Can I see the pupil? Is there pupil abnormality and is the eye quiet and white? If the eye is quiet and white, then there is no pupil abnormality, then I am very confident without even looking at the posterior eye. Again, if you can get into the eye looking for any sort of congestion of the optic nerve or optic nerve head involvement with a relative afferent pupillary defect with a swinging flashlight is a really, really good way to tell whether there is going to be a problem with the type of cellulitis, and very typically, if there are going to be positive clinical signs for pupillary changes as well as colour vision is another good one.
Red cap desaturation and comparison between the two eyes, if the red is washed out, then there is an indication that there is optic nerve head involvement in these cases. These are very simple things that you can have in your practices that give you an ability to differentiate very quickly as to whether this is something that you want to manage with oral antibiotics or whether this is something that you know needs to be referred on to the Ophthalmology or co-managed.
This is that table that I was talking about, and again in your own time, you can you can go through that, if you like.
This is the last one in the causes of acute vision loss. This is migraine, mostly idiopathic or trigger based headaches with or without nausea. Typically, I tend to see more nausea presentations in children rather than adults. Most of the adults are showing up with photophobia, phonophobia as well as visual aura. An interesting thing about visual aura is that even though we do a visual field test, we cannot see it, which sometimes makes the patients feel like they are losing their mind because they are like, no, I have this aura, but it is not provable necessarily. I do visual fields on anybody that presents either with a referral from a GP or without that it is a head migraine or does have uncontrollable, consistent headaches.
Just a note on the visual field machine and what it actually allows for us to do is there is this little map there to the right hand side that shows you where the defects are likely to present in the brain as a result of having this visual field test done. This is a brilliant tool in allowing for us to know how to triage these patients and often is significant in ensuring that the patients are receiving the appropriate imaging and care, either through GPs or through the hospital emergency. Doing a very simple confrontation visual field test in your practices is a really good way to figure out whether this patient has hemispherical or even quadrant loss in the brain. Often these outcomes are managed well. The visual aura and the visual field testing can rule out other forms of headaches like we have talked about or any other visual pathway concerns.
Often these patients have full and normative visual field despite patients experiencing aura. We manage a lot of different headaches. Migraine was the one we wanted to touch on. There are a lot of other ways to manage headaches. If you are unsure or want to include optometry in the management protocol of your headaches, we are quite well equipped to do that.
Moving on to pain. Painful vision loss, big one here that we probably would see the most or that most commonly gets referred from ED is acute angle closure. Very typically these patients are of a specific group of people. This is your farsighted patients, your patients that have worn glasses for most of their life. A word just on farsightedness. It often comes with shorter eyeball lengths. When we are talking about measurement, we are talking about cornea to optic nerve. As a result, there is less space inside of the eye. The lens inside of the eye for hypermetropia patients tend to be thicker. As a result, the anterior chamber tends to be shallower. There is a much higher chance of these patients developing acute angle closure as a result of just having this anatomical predisposition. Very typically, also in these cases, if they are going to attend your practice or attend an ED, it is also often triggered by pupil dilation.
Often the question that I ask is are you getting these headaches and there is nausea and there is funny feeling when you are in the dark? Often the answer to those questions where you are going to be having acute angle closure is yes. Intervention in these cases is acute IOP lowering. As fast as we possibly can, typically we are giving these patients a cocktail of eye drops, your beta-blockers and your alpha agonists and absolutely everything you can get your hands on, as well as probably oral Diamox. The eye will not last very long at a pressure of over 40, 45. The optic nerve head will ultimately accede to compression and will eventually die. Again, the common theme here is really ensuring that the fellow eye does not go through the same thing. There is one surgical intervention which is a an LPI procedure where they put a laser hole through the top of the iris to allow for the maintenance of aqueous humour to flow through the anterior chamber despite having narrow. Short term, this is an acute blurred vision, typically present with quite a bit of nausea and significant eye pain and a fixed pupil.
If you are doing a swinging flashlight and that pupil is not moving, it is quite dilated and it is fixed in comparison to the other one, then checking for pressures, if you have tonometers in your practice is a good thing here as a clinical pearl. IOP being lowered very quickly can be very well managed, if the IOP is lowered very quickly, and again that is a relatively simple intervention.
The next one is benign intracranial hypertension. Again, if you have a good handle on your ophthalmoscope, this presents with bilaterally swollen nerves which are very apparent, include the vasculature around them, and they tend to be very raised and out towards you. Looking at it with a direct ophthalmoscope will be very apparent to you that something is the matter with the optic nerve. If you are good at using your using your ophthalmoscope, I would encourage you to be looking into the eyes of the majority of these patients if you can, and by all means dilate them. Trying to look through a 2 mL pupil with an ophthalmoscope is extremely difficult for the best of us. If you do suspect papilledema, these patients are managed or confirmed via checking the ICP or doing a spinal tap intervention is oral Diamox in reducing the CSF production, analgesia for the headache and potentially, drugs like furosemide to further reduce the overall pressure inside of the head. Outcomes in these patients are typically very, very good. We do not typically tend to see any lasting visual concerns especially once their systemic symptoms have been managed.
The next one is going to be chronic disease stuff like diabetes, macular degeneration, glaucoma and other genetic diseases. Just a note, most of what we have discussed have good outcomes with good quick and intervention and co-management plan. Working together, we have found, especially in regional Western Australia that we end up finding really good outcomes as a result.
Michael Yapp
We are almost there, ladies and gents. Thanks for sticking with us. We are up to our last patient scenario. You have got a patient that comes into your practice as a 35-year-old female, a five-day history of a red, irritated left eye with a watery discharge. Otherwise, medical history is unremarkable, but they have had a recent sore throat to go along with this red eye, which comes out when you go looking for it because they did not volunteer the information in the first place. The question then is what do we do with this five-day red irritated eye, but more importantly, what is the cause so we can treat appropriately. With that, we will launch another poll for you. If your phones are still handy, let us be specific. Given that particular patient, are we thinking viral/bacterial? Are we thinking some other cause of what this red eye might be in terms of your differential diagnoses?
Viral is the first choice. Bacterial is coming in there. Uveitis, excellent. Adenovirus, nice choice. Episcleritis as well. All good options. Looks like viral is a winner so far. Excellent. Some very good differentials in there. In the interest of time, I am going to keep moving, if that is okay. Similar story, we are going to be checking their vision, the anterior eye and their lids. The big questions really come in here, which Alex will talk about in a moment. Viral versus bacterial versus allergic versus fungal versus inflammatory. Many, many causes of acute red eyes. Then the concept then comes in to what is involved, conjunctival, lid, anterior and/or posterior chambers and where do we go next. When we think about it from a management perspective, as GPs, I am sure you are very comfortable treating these initially, There is the option of sending them to an ED, but it is probably not your best choice given it is not a particularly urgent matter.
There are the urgent care centres that are popping up in some of the urban and more city areas, which may be a reasonable place for these. There is the concept of using your local ophthalmologist and/or optometrist as required. The question is whether you treat first, whether you send it across? If you think it might be adenoviral, do you want to get it out of your practice as soon as possible and let the let the optometrists have to worry about disinfecting everything in their practices? There are lots of different ways you can go about managing these, and it comes once again down to a ______ [audio break].
Alex Craig
The third that we want to talk about, so we have talked about painless vision loss, a painful vision loss and a couple of differentials there that we thought were important. The third one is going to be acute red eye. We have talked about angle closure already before. I think the only thing here to add is looking at this infographic on the right hand side, which actually shows you what happens when we have a thicker lens and we have a closed angle, we end up getting pupil blocks, so that obviously stops the flow of aqueous humour through to the anterior chamber and out of the trabecular meshwork causing the pressure in the eye to go up substantially. That is just the mechanism of action for you to understand.
Keratitis or keratitis by definition means that the cornea is actually involved. For those of you that do not have a slit lamp, this is going to be quite challenging for you to ultimately get the absolute correct diagnosis. It may be infectious, it may be bacterial, fungal, viral or even acanthamoeba or it might be non-infectious such as some form of exposure keratitis from incomplete eyelid closure or some form of autoimmune disease that affects the tear or the ability for the eyes to produce good tears. Common symptoms including are going to be red eye, acute severe pain, photophobia, tearing, blurred vision and some form of discharge. The discharge typically tells you a lot. We will touch on that as well in the conjunctivitis slide in a moment. Bacterial keratitis also presents with dense infiltrates while viral keratitis may show some form of dendritic ulcers. Depending on what the cornea looks like really guides how you treat these patients.
Sodium fluorescein is a fantastic tool in these cases and a Wood's torch or something with cobalt blue with a magnifying glass on it that can actually isolate the cornea if you do not have access to a lamp. It often in these cases is quite good. Knowing the hallmark signs of the different types of keratitis is often quite helpful. Interventions typically depend on the cause. Topical antibiotics for bacterial keratitis is the gold standard. Antivirals or antiviral ointments for herpetic keratitis related cases is important. Antifungals for fungal infections and biguanides or other types of interventions for things like acanthamoeba. Noninfectious keratitis is managed with lubricants and by addressing the underlying conditions, so indolent ulcers, etc. Early diagnosis prevents complications like corneal scarring.
If you cannot see the depth of the lesion or you cannot isolate the lesion and feel confident in treating immediately, then in these cases we have had a really good success in creating referral pathways through optometry or even into ophthalmology for targeted treatment. Swabbing the eye in these cases as well has become more commonplace in my practice to ensure targeted therapy as well.
A little table here as well to differentiate between another form of red eye, acute red eye and that is episcleritis and scleritis. Scleritis is linked with systemic conditions, typically autoimmune conditions. It causes a severe deep boring pain. The differential here is and a good question, history that differentiates between the two of these is did it wake you up at nighttime? Pain that wakes a patient at nighttime is very typically going to be more of a scleritis than an episcleritis. Scleritis is also more likely to be global whereas your episcleritis will be targeted, nodular, can come in two different forms, but very typically is only a specific area of the conjunctiva. An easy way to differentiate that from a bacterial infection is that bacteria typically are not that clever. They are not going to infect just one little portion of the eye.
That is either going to be something that is inflammatory in nature if there is a sectoral amount of inflammation. That table there will guide you a little bit in terms of how to manage them. The difference between them in terms of outcomes and prognosis is that episcleritis typically responds really, really well to oral NSAIDs whereas scleritis requires more of a systemic workup, blood workup, etc.
Next one is uveitis. Again, very challenging to see this, if you do not know how to use a slit lamp well or you do not have access to a slit lamp, if you have been in a movie theatre and you look up and you see the beam of light as it projects to the screen and the dust that floats in that beam of light, that is what it looks like in the anterior chamber when there is cells and inflammation, and so trying to get an image in that space can be quite challenging technique, and for those of you that do not have access to slit lamp often in these cases, we would we would prefer or we would encourage to try to refer off to optometry or to ophthalmology. We often in these cases refer back, so if there is one incidence we call that idiopathic. If there are multiple incidences, especially concurrent incidences then we are very interested in things like autoimmune HLA-B27 associated conditions, trauma drug induced conditions etc., and we will be referring back to GPs for that. Intervention in these cases is topical corticosteroids and typically cycloplegia, especially for anterior uveitis and outcomes if caught on time typically very good, so if no comorbidities or secondary complications occur as a result of inaction then in these cases, not only the outcome but the management condition is typically very good.
Posterior uveitis much harder obviously to see without looking into the posterior aspect of the eye. This includes obviously vasculitis and retinitis and can be quite devastating for the eye if not picked up early. Typically this stuff can be caused by viral, bacterial, fungal mostly parasitic, and very rarely are we seeing non-infectious causes like idiopathic causes or sarcoidosis. Intervention in these cases, obviously is systemic. Again, my only point being that that timely intervention co-management and early referral is often what differentiates the outcomes in these patients. Conjunctivitis, and this is one that is seemingly easy to manage, again broken down into bacterial viral allergic or toxic intervention is the way that I typically would do it is discharge dependent, so bacterial typically will present with a mucopurulent discharge typically can be unilateral or bilateral viral is often quite watery. The eye looks a bit glassy, typically starts in one eye and jumps to the other one quite quickly. Allergic is typically both eyes.
It is very rare for somebody to have an allergic conjunctivitis in one eye, very typically because we do not walk around with one eye closed, and this is a more of a mucous discharge and responds very well to mast cell stabilisers and topical antihistamines as well as the mild steroid if required and again intervention if targeted and if correct often results in very, very good outcomes, and no significant problems to long lasting vision. Viral and adenoviral is probably the only exception here which can have recurrence of subepithelial infiltrates as a result of it having an inflammatory component to it as well. The other one that we tend to see sneaking around and just a note on conjunctivitis. The majority of all of those conjunctivitis types except for adenovirus is self-limiting in seven days anyway. If a patient presents and they have had a conjunctivitis for more than seven days, more than a week, you are potentially a little bit more concerned and moving towards looking at things like chlamydia and gonorrhoea.
Chlamydia is a very easy one to pick up on the slit lamp as well, and obviously managed very easily if intervention is quick and appropriate. I think that is probably it for me. One last thing, the chloramphenicol test, so this is something that we see is quite common, coming through GP practices as well as EDs. This is a trap. Ultimately, this makes my job significantly more difficult, blanketly applying chloramphenicol to absolutely everything in terms of the anterior eye without significant cause or thought, it typically creates more of a problem for us. Like I said, most of the conjunctivitis or the types of conjunctivitis that you will see are self-limiting. The preservatives in chloramphenicol can cause more problems than especially if it is not a bacterial conjunctivitis, and really encouraging good relationships with optometry and GP through referral and co-management, and most optometrists in regional Australia are now starting to do swabs to ensure that we are doing actually targeted management, not just blanketing everything with chloramphenicol which you guys can do too. Thank you.
Michael Yapp
Fantastic. Thanks. I have run over time. I will just finish up with obviously real GPs play a critical role in triaging and managing acute eye disease. Multiple scenarios from foreign bodies to trauma to acute loss to acute red eyes. Ultimately, what we try to do is a whirlwind tour through it, but to have you think about particularly what is the best pathway for your patients that is going to help you in your practices and help your patients get what they need when they need it through those open and clear communications. With telehealth becoming an increasingly viable option, in particular in the rural settings and apologies for the dropout and for taking too long.
Dimitri
Thank you so much, Michael and Alex, that was a great webinar. We do have just a couple of questions that have come through. I know that we have gone a little bit over time, but how do you manage photophobia post foreign body removal?
Alex Craig
That is actually an interesting one. Typically,- the way that I would triage this is that typically sealing of the cornea, especially if it is central cornea is most important. We do find that by removing the foreign body and managing the eye with ocular lubricants that the anterior chamber reaction that is actually causing the photophobia tends to subside on its own anyway without steroids. However, re-epithelialisation occurs typically between 48 and 72 hours, so getting a steroid on to that if there is a significant anterior chamber reaction a day or two days later is actually good management and still maintains good outcomes.
Dimitri
Great, and just another question as well, when epithelialisation has happened, has already occurred, what is the use of applying a steroid?
Alex Craig
Good question. Obviously in terms of when the epithelialisation has occurred, that is just obviously the very top, the concern is then going to be the stromal inflammation or the stromal involvement underneath, so applying the steroid is still beneficial in that it can clear up and slow down the ultimate relationship between the epithelium and the stroma, but it can clear up that stroma quite substantially as a result of applying it to ensure that the vision is better or has better outcomes long term.
Dimitri
Very good. All right. I think that is all the time that we have. There was also Michael, if you can just maybe pull up the cellulitis table. I think that you might have. Just in the chat box everyone, I am actually going to put the registration link for the second part of this webinar, which will be on the first Thursday of April, so make sure that you register and tune in there. It is an update on common chronic causes of vision loss in rural Australia. We would love to all see you there. Next month, as you can see on the screen we have a Rural Emergencies Case Scenarios webinar which is presented by Dr Anthony Wong, so please also register for that one. It is all free for members and non-members.
We look forward to seeing you then. In terms of CPD points for this webinar, all RACGP members, this will be done automatically for you, so that should appear on your statement either tomorrow or on Monday. If we have any non-members with us this evening, please email the rural faculty and we will send out a certificate for your records as well.
I think we have done pretty well considering. Thank you again to Alex and to Michael. That was an extremely informative webinar. Thank you for sharing your insights, your experiences and your knowledge with us all. Thank you everyone for joining us. Have a good night and we will see you soon.