Lecture: Acquired Esotropia – What’s New in 2023!

During this live webinar, we will discuss the causes and pathogenesis of various types of acquired esotropia. Complete evaluation protocol and management guidelines will be discussed. We will also highlight red flag signs to watch out for in acquired esotropia. (Level: Intermediate)

Lecturer: Dr. Divya Natarajan, Ophthalmologist, L V Prasad Eye Institute, India


>> DIVYA NATARAJAN: Hello, everyone. Thank you for joining today’s webinar. Today I’ll be talking about acquired esotropia and what we know about this entity in 2023. I have no financial disclosures. In this webinar, I will be covering about pathogenesis of various types of acquired esotropia, how we clinically evaluate such a case when it comes, and what are the different management option for this particular condition. Let’s start with a question for the audience. Which of the following do you think can be a cause of acute acquired comitant esotropia? Can it be uncorrected myopia, uncorrected hypermetropia, prolonged patching, or all of the above? You can go ahead and fill in your options. All right, great. So a lot of you think that it can be all of the above. So that’s great. The answer to this particular question is all of the above. And let’s see now actually why this particular answer is correct. Before we start, let’s understand why acquired esotropia is. So acquired esotropia may be acquired comitant esotropia or acquired incomitant esotropia. Acquired comitant esotropia has been divided into various categories. What was initially known about this particular entity called acute acquired comitant esotropia was that it was mainly of three types. This was what was initially thought. One was the Swan type or type 1. The second was type 2 or idiopathic type. The third was type 3. Subsequently further entities were added to this condition of acquired comitant esotropia, the others being acute accommodative esotropia, decompensated phoria, neurological type, cyclic type, and one type which involves excessive near work, one of the recent additions to this entity. What institutes acute acquired esotropia? It has to be a condition where the onset is six months of age. Anything where the onset is below six months of age will probably come in the infant category. Anything beyond six months of age will come in the acquired type. There should not be any lateral incomitance and it should be an acute presentation. What it does not involve is refractive accommodative type or partially accommodative type. It should not be accommodative spasm. It does not involve incomitant types like acquired sixth nerve palsy or myasthenia gravis. These last three entities may simulate a comitant type unless clearly evaluated. So it is important for to us differentiate this from the comitant type. But when we look at this entity of acute acquired comitant esotropia, how frequently do we see it in our clinics? So one of the studies which studied the largest number of such conditions was the one done where they said that approximately around 4.9% of all childhood esotropias in a hospital setting would be acute acquired comitant esotropia. Out of this, 3% of children were found to be less than ten years of age. Now, if you compare this with the rest of esotropias, almost 37% of children less than ten years of age presented to the clinic would be infantile esotropia. So you can understand that it’s a very rare entity, probably only one tenth of infant esotropia would be acute acquired comitant esotropia. Other studies have shown that the incidence is slightly higher, maybe 14 to 16%. We know what maybe it does not include. Let’s look into what it does include, actually. So this is a case, 2-year-old male child, had come to the clinic. He was seen elsewhere, and there was a slight disparity in the vision that was noted. Right eye had slightly better vision than the left eye for this child. And the child was advised long hours of patching, actually. The parents were doing a random type patching, sometimes patching the right eye, sometimes the left eye. And the patch was left on for almost an entire day. So after starting of this patching, the child was brought maybe about two weeks after starting the patching to our clinic. And this was what we noted in the child. There was a large esotropia that was seen. So this constitutes the first type of acute acquired comitant esotropia, also known as Swan type. Now, this type is precipitated by monocular occlusion, an artificial disruption of fusion. The most common cause of this is prolonged patching, sometimes there can be patching that can be done for a corneal abrasion or there may be a mechanical otosis. It can be any form of artificial disruption of fusion and the child will come up with esotropia. We know not every child that undergoes patching or has to have the patch on because of a corneal abrasion actually comes up with esotropia. So what is the mechanism here? Why only some children come up with acute acquired esotropia? And the answer is, in this particular slide, where you see that there has to be a latent convergent tendency in that child. So basically there is a very slim reserve of fusional movements. There is a tendency to convergence in such a trial. When there is an artificial description of fusion because of patching, then fusional reserve is not enough for the child to get back its divergence and it falls into a constant state of convergence. That’s what happens in this particular type of esotropia. Let’s look at another case. This was a 4-year-old female child that presented with a sudden onset inward deviation since about one week. The only significant history that the child’s mother was giving was that the child had been suffering with viral illness and had been hospitalized with the same some time ago, and four days after recovery, the child started developing this kind of a condition. If you see, vision is normal. There is a very insignificant refraction in the child. This particular entity constitutes our type 2 of acute acquired comitant esotropia, known as Franceschetti type. This type presents with many minimal refractive error, it presents with nonaccommodative, mainly there is precipitation of squint without artificial disruption of fusion here. But what happens is, just naturally, because of maybe stress, because of a viral infection in the body causing stress, or there is rigorous physical activity or minor head trauma, or sometimes if the child has a lot of psychological stress, then it can be an artificial disruption of fusion. Here again, there is very poor fusional divergence. Very slim fusional reserves. The child has been trying to fuse but any condition that stresses the child and has constant disruption of fusion has destroyed the fusional reserve. Now the child cannot diverge and therefore goes into a state of constant convergence. This is known as idiopathic type, there is no clear causal factor in this child. What we see in our clinics is very commonly this particular kind of condition. It’s quite common. Let’s see another type. This was a 6-year-old female child that presented with inward deviation since one month. A significant history here was that the child was an extensive reader. She used to read books for almost about six hours a day but has never used glasses previously. If you can see, visual acute for distance was quite poor, for near it was still good. There was a very significant refractive error, she was a high myo, close to 6 in both eyes. Stereo acuity for near was maintained. The previous cases did not have any significant refractive error but the third type actually has a significant refractive error and this refractive error is high myopia. This constitutes the third type of acquired esotropia, also known as Bielschowsky type. The pathogenesis behind this type is actually very interesting. What was thought to be the triggering factor in this type was that it was an uncorrected myopia, and there was prolonged near work. So we all know that myopes are more comfortable for near. So when a child is myopic, they cannot see distance well, especially if uncorrected. They prefer near work and they start doing more prolonged near work in time. They start focused for near more. And subsequently what happens is that the near kicks in, there is convergence, myosis and compensation. Because of that persistent convergence, it is thought that it increases the tone in both eyes and therefore the child goes into a state of constant convergence. Initially for near the child will be ortho and for distance the child would have to use the divergent forces, the child will not be able to because of the persistent convergence and the increased tone. So initially, manifestation would be a small amount of deviation because of the convergence for distance. For near, the child will still be auto tropeic in most cases but subsequently when the tone continues to increase then it will result in a state reportedly seen more in older children. Definitely they also have decreased fusional divergence. This particular entity, which was noted initially in uncorrected myopia, is quite significant, the pathogenesis, because it, again, comes into the picture when we’re talking about near work, which is a very recent type of esotropia that we are seeing in the clinics, that which is involving electronic devices, more smartphones. The principle is almost the same. Let’s look at another case. Now, this is a 3-year-old female child, complained of inward deviation noted since just ten days. As presentation she had an esotropia of almost 35. Her visual acuity was slightly lesser. Cycloplegic refraction revealed a significant amount of esotropia. She was started on glasses. After three months she is still wearing her glasses but still has a significant amount of esotropia. Now, this condition is a condition known as acute accommodative type of esotropia. This is different from type 2 because here there is significant refractive error of more than plus three diopters. There is accommodative that is present. Again, this condition presents quite acutely maybe because of poor fusional divergence, maybe because of increased stress. These are the factors that have been stipulated for this. So again, there is overconvergence because the child wants to accommodate, because of the high hypermetropia and maybe there is disparity, all these factors come into the picture and the child will have an acute presentation of esotropia. Now, we all know that this particular mechanism also works in what we commonly see in the clinics known as refractive accommodative esotropia or partially accommodative esotropia. So let me just ask you how you think an accommodative, acute accommodative esotropia is different from a refractive accommodative esotropia? So which of the following is true regarding acute accommodative comitant esotropia? Is it that in acute accommodative there is a longer period of intermittent deviation? Maybe there is a larger angle of deviation. Or they present with poor binocular vision. So you can answer the question. Okay. So it looks like there’s a lot of confusion here. So maybe it’s not so clear as to how an acute accommodative esotropia is different from a refractive accommodative esotropia. All right. Let me then explain this further. It’s actually a larger angle of deviation. So let me show you the slide which compares the most common features of acute accommodative esotropia and refractive accommodative esotropia. These are clinical features which we most commonly see with each condition. But this is not the rule. It’s most often that we see an acute accommodative esotropia having a very sudden onset. That is why it is characterized as acute accommodative. Usually they present with a constant deviation with a large angle of deviation. As I said, the theory behind this is that there is poor fusional result. So once that disappears, there is a large angle, there is a constant angle. And because there is a sudden onset, they more often present with diplopia. But because it is just short period of onset, usually binocularity is preserved. So in comparison, if we see a refractive accommodative esotropia, we see that there’s a more gradual onset. And the esotropia is noted more intermittently. What happens is it is noted only when the child tries to accommodate. So when the child is trying to read or do more near activity, that’s when the deviation will kick in. It starts with a smaller angle of deviation and subsequently fills up. And what is quite significant in this particular condition is that very often, parents will say there is a variable angle. They will see sometimes the esotropia is present and sometimes the esotropia is not present, which is understandable, because it completely relies on whether the child is accommodating or not, because fusional reserve is deteriorating slightly, slowly, gradually. They present more with asthenopia symptoms. I hope it is clear what acute accommodative esotropia usually presents with and what refractive accommodative esotropia usually presents with. Let’s move into our category of a 2-year-old male child that presented to a clinic with inward deviation noted since last three weeks. What was also quite significant was that there was a small amount of mild left side weakness and there was also a mild gate abnormality which was picked up when the child walked into the clinic. Psychoplegic fraction was not very significant in such a child. Because of the mild gait abnormality, we took this particular child, the evaluation of this particular child more seriously. If you notice, there is a small angle, 20% esotropia. And because of, as I said, associated neurological symptoms, we did the imaging for this particular child. Here is what we came up with. There was a very large tumor in the posterior fossa. There was a large cerebellar astrocytoma noted in the child, therefore hydrocephalus was also seen. This was a child who presented acutely with esotropia and with a mild gait abnormality. The gait abnormality and the left sided weakness that was picked up in the clinic by the ophthalmologist was missed by the parents, because it was very mild and because there was nothing else that changed in the child’s behavior. Subsequently, as you can see, the child underwent excision of the mass lesion. Esotropia obviously was not the primary concern here, though the child had diplopia. Esotropia was not the primary condition. The child was referred to the neurosurgeon and underwent excision of the mass lesion with a shunt. After a couple of years when everything in his neurological condition stabilized, the child also underwent surgery but still had an esotropia of close to around 16 to 18%. Otherwise the child is quite stable. You see this particular entity is also known as the neurological type of acute acquired comitant esotropia. It’s not very common, but it cannot be missed. Now, this is an emergency, this is a condition that cannot — that has to be picked up in the clinics. The pathogenesis of this condition is not really known. But maybe divergence insufficiency because of a tumor or because of pathology, is thought to be the reason. We can talk more about this particular entity later on during clinical evaluation as well. Moving on, there are some other types of acute acquired comitant esotropia. One of them is a decompensated type where there is a phoria. It remains a phoria until there is another factor, maybe surgery. So here also when there is a decompensated phoria, it is a sudden presentation of such a condition. This also as an entity very commonly seen in our clinics. Now, another type is this very interesting and a very rare type. If you see, this 4-year-old child had a normal birth and a developmental history. But had complaints of intermittent inward deviation noted since the last two months. Now, the father, when he presented, when he brought the child to the clinic, actually said that there was a variable presentation, there was no pattern that the father had noted. If you can see here, vision is good, but visual acuity is poor. This was how the child was when he presented to the clinic. We saw there was a large angle esotropia with poor stereo acuity. He presented on this particular date. We had to call him back again. So when we saw him the next day, if you see, surprisingly, the child was ortho tropeic, he had good stereo acuity at this point. Even an artificial disruption of fusion and patching of the child did not disrupt fusion, he continued to remain orthotropic throughout. We asked the father, the parents, to documents this on a daily basis. And we realized that the child was having a regular periodic presentation of esotropia and orthotropia. So this pattern was maintained consistently for around six weeks for this child before he went into a constant esotropia. Now, this particular entity institutes cyclic acquired type of esotropia. It is a very rare condition, but it follows a regular clock mechanism. The most common rhythm that we see is a 48-hour cycle. Every two days the child would be orthotropic and one day it will be esotropia. But otherwise, a 24-hour cycle, a 72-hour cycle, even a 96-hour cycle has been reported. But what has been known is that the cyclic nature remains only for a certain period, and then it eventually breaks and converts to a constant esotropia. Now, it’s a very fascinating kind of a condition. But what has to be known here is that the pathogenesis is actually not very clear. It is thought that maybe there is a noncompensatory component leading to esotropia manifestation. Or maybe there is an incomplete cerebral dominancy. But the exact pathogenesis is still not known. Finally we have come to the last case, which shows the last type of acute acquired comitant esotropia. So this was a ten-year-old male child that presented with inward deviation since the last two months. And the significant history that the parents were giving was that the child was watching videos on his mobile phone for almost close to seven hours daily. He had normal vision. His stereo acuity was still good. He hardly had any refractive error. But the history here is very significant. The child presented with a large angle constant. This constitutes acute acquired comitant esotropia. This is a condition that we see quite often in our clinics nowadays. And that is because of this. We are in a digital world. Everything involves use of phone or screens. And we see that children are also beginning to use their smartphones and use their electronic devices. And this is the cause for this new entity which is a new generation smartphone type of acute acquired comitant esotropia. The principle of presentation is actually the same as that seen in unpredicted myopes, where we saw there was persistent convergence because of prolonged near work. So what happens in a case of excessive smartphone use is that the child does not have any refractive error. Vision is good for the child. But because the smartphone or the screen is used at a very close distance, it inculcates the child to start using accommodation and convergence and that leads to persistent convergence and increased tonus of medial recti. The smartphone is very colorful and there is a tendency to keep the phone closer. The working distance tends to reduce, sometimes less than 30, sometimes even less than 20. The other tendencies that patients with this kind of esotropia have is that they start using their smartphones very close, in the sense they use it when they are lying down, maybe lying down flat on their abdomen when they start going closer to their screens or even lying on their back, then holding the phone at the distance of 33 centimeters will be very difficult, so they hold it much closer. Basically the working distance reduces quite significantly. Also it becomes very addictive. It is also known to be associated with other features like increased myopia, behavioral changes. So this is a condition that we’re seeing quite often in our clinics. And I think inquiring about smartphone use, hours of use, and the distance at which the patient or the child uses the smart phone becomes very relevant in this condition. So with this we have seen the different types of acute acquired comitant esotropia, and we have understood about maybe what causes each of these conditions and therefore what questions we should ask specifically when such a case presents. Now, let’s move on to see what else we have to evaluate when such a condition presents to our clinics. So apart from the complete workup, which is usually done for all such children, we have to stress on certain important aspects. So one is, as we just mentioned now, history taking has to be appropriate. It will give us a clue as to why this particular condition has happened. It will also give us an idea about how to start management in these cases. For example, if smartphone is thought to be the cause, maybe restricting the use of near work has to be the first step of management. So appropriate history-taking is important. Moving on, complete cycloplegic refraction is important. Refractive error has to be actually diagnosed. Maybe there is a latent hypermetropia. That has to be done and that only can be done by cycloplegic refraction. We use cyclopentolate, or atropine which is much stronger. Most studies say atropine additionally maybe brings out the hypermetropia in addition to what has been brought on by cyclopentolate, noted in case where atropine has been given. So even cyclopentolate is known fob a good enough cycloplegic agent, unless for example there is a very clear lag or even after cyclopentolate there is reaction of the pupil or some such things. In most cases, cyclopentolate is still good enough. Glasses prescription has to be given. And best corrected visual acuity has to be assessed after glasses prescription. So basically, as we all know, in children the first visit when we give glasses, that does not really tell us what is the best acuity. We have to call the child back for the next visit. It is also important, as I said, to look at binocularity and the fusional vergence range. Complete examination has to be done. A prism and cover test has to be done in lateral gazes, because if there is any incomitance, it has to be brought out. Even in vertical cases, we have to see if there is a pattern, a V or an A pattern that is coming up. We also have to look very closely whether the child has any nystagmus. So that is again a condition that has to be looked at very carefully in these patients because it is known to be associated with near logical type, which is an emergency in neurological — in cases of AACE. And finally, fundus evaluation. It’s done in every child, but here we have to be very careful in picking up maybe subtle types of papilledema. So these points should definitely be done in cases of acute acquired esotropia in our clinics. Let’s move on to a very interesting question, and let’s see what the audience thinks. So should neuroimaging be done in all cases of acute acquired comitant esotropia? So you can answer the question with yes or no, and we can discuss it further. Okay. It is interesting, because it’s maybe an equal amount who says yes and no, but no seems to be higher. Let’s see. This doesn’t have a very clear answer. But maybe I can make things slightly clearer. So when we are talking about neurological findings in cases of acute acquired comitant esotropia, we already know it’s quite a rare condition, and in this particular condition also, a neurological type of acute acquired is very rare. Review of literature states that neurological findings on MRI in such cases may be seen in about 6 to 30%. Now, this includes reports that quite a small number of patients. But what has been reported is tumors of the cerebellum, brain stem, corpus callosum, sellar, hypothalamus, and other associated neurological findings like Arnold-Chiari malformations, which are one of the most common findings in cases with neurological type of acute acquired comitant esotropia. Let me discuss this particular paper by Sheth et al. Because it studied the largest number of acute comitant acquired esotropia, it studied 338 patients. And what they found was that 16% of patients actually had positive findings on MRI. Now, positive findings on MRI meant even in incidental findings like periventricular and other findings, 22% of those 16% had an ACM. What was also very interesting was that all these 16% of the patients had the neurological examination was completely normal. So there was not any clear neurological sign or symptom that could have been picked up in these patients. And this paper also concluded that because there was lack of consistent predictive risk factors, it is always better to neuroimage in such cases. As I said, maybe this paper said that one out of every six patients came up with a significant finding on MRI. The numbers overall may be very less, but again, if it is a serious condition and if it is missed, then it cannot be excused. So until we maybe know more about clear risk factors that can tell us about a condition as being neurological type, it is always better to be on the safer side. Having said that, there are certain red flag signs, clinical signs that can point out to this being a neurological condition. There are many studies that corroborate these. One of the most important ones is that neurological cases usually have an older age at onset. They usually present after five or six years of age. They have neurological signs and symptoms in many cases. Usually neurological type of acute acquired do not have an accommodative component. And again, a very significant important finding in these is that there is a larger angle of deviation for distance than near. So there is a near-distance disparity. Esotropia is more for distance, and significantly more, more than 40% is the difference that is noted. This is again a very significant, important finding. Some reports also say that there is a small pattern, usually a V pattern that is noted in such cases with an object league muscle overaction. You have to even check for up and down gaze to bring up this particular pattern. Most cases have poor fusion, poor binocularity. There is an associated nystagmus, very commonly it may be obstructing the nystagmus and may have recurrence of esotropia. If you see a recurrent esotropia coming up, then it is important that you rule out this neurological type. I hope it is clear about how we evaluate such cases when they come to the clinic. Let’s look at management of these cases. Once we diagnose this case that comes to the clinic as acute acquired comitant esotropia, how do we think about managing? So this is a rough protocol. We usually follow this pattern. So first we’ll have to do a complete cycloplegic refraction in the first sitting. We have to give glasses if it is required. We have to start amblyopia therapy. Subsequently we have to call them back for a followup, and maybe start orthoptic exercises. Usually these cases present to the clinic quite fast. So as an interim, maybe, after giving glasses, we’ll have to start them on orthoptic therapy which includes prism glasses and fusional divergence exercises which we’ll talk about subsequently. Many of these conditions have poor fusional result, therefore it is important to start orthoptic therapy quite early in most cases. Subsequently, one option is Botox injection. That is an option only because it can be done intermittently, as an intermittent form of treatment before we think of a permanent solution. It is known to be quite effective. And you can give an injection of Botox and continue with the exercises. That is an option which doesn’t have to be done in every patient but is something that has to be offered to the patient quite early on. Sometimes also it is important if the child is young, in an amblyogenic age group. That’s again one of the indications where we can give Botox injection, because orthoptic exercises may not be a feasible option in very young children. Go what has to be clearly understood is, as I said, presentation is quite early. And it may even be variable. So multiple visits to the hospital is required. And at each visit we need to take new measurements. So multiple measurements will have to be taken. It has to be taken over a period of maybe six to eight months. And it’s very important that we do a prism adaptation in all these patients, basically because it all depends on the fusional reserve. Maybe the patient will be trying to fuse and maybe the entire amount of deviation the patient actually has is not manifested in one visit. So a prism adaptation test has to be done in almost every case. Finally, after six to eight months, waiting for a minimum of six to eight months, if there is a consistent angle, then we can plan for an extraocular muscle surgery. And it’s best to operate on the largest angle that has been found. And it is usually the one that comes up after PAT. This is usually the sequence of management protocol that we follow in the clinics. Let me touch upon a few aspects here. So orthoptic exercises, when do we use it? No clear evidence shows vision therapy helps in divergence insufficiency. It’s documented that it helps nicely, but in divergent insufficiency, we’re still not very clear. So the best therapy would be to try on fresnel prism and maybe give additional vision therapy, maybe in the form of vision therapy system or Brock string exercises. This is the principle behind that. So this is an interesting case which presented with a large angle acute esotropia, acute acquired esotropia, and was given a fresnel prism. The prism was given for an angle that was actually 45 and it brings the eyes within the fusional range and then slowly — to in the subsequent visit, after three months the patient was seen to have a slightly lesser amount of esotropia without the prism glasses and after close to around six months, he had a much lesser angle, almost close to 18% esotropia. So this particular case responded very well with fresnel prism and fusional divergence exercises. But we still don’t have enough evidence to say that it works in every case, and we also do not have enough evidence to very clearly indicate as to what cases and for how long we give such treatment. This is an option that has been reported in literature as well. The other option, as I have said, was giving injection of Botox. It’s a feasible option, especially if it can be given early. Reports have suggested good metro success rates. But the only side effect or only problem that Botox injection has is that the first injection usually gives resolution in 50% of the cases and subsequent injections, maybe with it to three injections have to be given in the patient. So as you can see, this child presented with a large esotropia, was given injection of Botox but this particular photograph was taken only two days after the injections, so optimism the child had maybe an esotropia. The same child after maybe one month or six weeks may go back and do an esotropia. But the results are variable. That is the disadvantage of this. But it is definitely a feasible option. Finally we have the option of surgery. Surgery for esotropia can be either unilateral, bimedial, maybe a unilateral, all depends on the amount of deviation the child presents with. Some studies have reported a standard surgical success. Some studies have said that an augmented surgical dose is required because for surgery it has been known to have some residual esotropia but there are no consistent findings. This was just a very brief review. Looking at the first column, the maximum number of patients in the Sheth trial, they said following standard surgical goes would give good outcome in close to 71% of the patients. The rest of the studies had much less sample size. Go still, probably surgical correction would give a good and reasonable motor outcome in most cases. But there are certain predictive factors which can give better results. So it’s been noted in different papers that there is better prognosis if there is significant hypermetropia, if there is family history of strabismus, usually there is a smaller angle of deviation. The logic that have is probably because binocularity must be maintained. Binocularity is maintained, mild or no amblyopia can give good results. So to summarize, whenever we see a case of acute acquired comitant esotropia, we have to ask relevant questions in history. We have to sometimes revisit history. It can give us clues as to what this condition could be, and therefore give a direction to the management of such a case. A new entity, increasing smartphone use, cannot be neglected, has to be looked at seriously and maybe further studies have to be done as to how this actually — and come up with a protocol as to how much of smartphone use is actually — actually can be allowed in such children. Complete cycloplegic refraction is a must. Multiple measurements and PAT test is essential before we think of final treatment. And watch out for red flag signs in cases of acute acquired comitant esotropia. Definitely such cases have to be imaged. Thank you. That probably ends my presentation. And I can take questions now. All right. I’ll start with the first question that has been asked. So in Swan type, does one eye always have less vision and poor fusion and binocularity, because of that which leads to the deviation of monocular occlusion and can these patients have good vision in both eyes? Thanks for the question. Basically here there is not a rule that it has to be monocular or have binocularity. In most cases patching is started in these cases because of such an underlying condition, because it has happened that the child has been patching in one eye, there is not a rule, it has even been known in cases where the eye has been patched for maybe two or three days because of a corneal condition or maybe because of mechanical doses. So even in such cases, even with good vision in both eyes, this particular condition can result. And the pathogenesis has nothing to do with vision here. Pathogenesis is maybe the fusion and disruption of fusion that happens. There can be good vision in both eyes as well. All right. So the next question is for acute comitant neurological esotropia, why not because of sixth nerve palsy? I’m not sure I understand this question rightly, but maybe what you want to know is that maybe there is sixth nerve palsy and not comitant esotropia. That’s a very good question. Acute incomitant esotropia or a small amount of sixth nerve palsy can look at a comitant esotropia. So a very clear examination has to be done. Sometimes it can be missed. And that is why we have to maybe have a very good fundus examination. And that is why we cannot miss imaging such patients. Various reports in literature have actually reported slight amount of incomitance, close to half reduction in cases of acute acquired comitant esotropia, so they have misdiagnosed it or maybe it’s a part of this as a sixth nerve palsy. But it could very well be. But this can be brought out by very thorough clinical evaluation. Moving on to the next question. Should we perform neuroimaging in all cases of acute acquired comitant esotropia? As I said, there are — there is a lot of confusion. But what most studies state, especially 9 study which looked at the maximum cases of acute acquired esotropia, it said that one out of every six patients of acute acquired esotropia actually had a significant intracranial pathology. And if that is the case, then I think it is better that we neuroimage, at least at our knowledge at this level. If subsequently we are able to very clearly find out what the predictive risk factors are for neurological type, then maybe we can come up with a better screening method. But ’til then, it’s always better to neuroimage, at least that’s what I do. So another interesting question as to what is the vulnerable age range of children for acquired esotropia due to excessive smartphone use? So that is again an interesting question. There is no right answer here. There is no study that has proven that this is a vulnerable age. We are seeing children, younger and younger children, actually coming in at a vulnerable age. The only factor here is that how well is the binocularity developed or how well the fusion has developed in such a child. And actually it develops at a quite young age. So I don’t think there is any particular age where a child is more vulnerable or there is a higher chance of esotropia manifesting. There are other factors like the hours of smartphone use and distance of smartphone use that become more relevant here. So that is what I would think is more relevant. But this is what is the knowledge as of now. So the next question says what is the recommended distance not only for smartphones. So as I said, near work has to be around 33 centimeters so it has to be beyond that. So anything close to 30, 33 centimeters, should be okay. But even that should never have a prolonged near work. It’s always advised, as you see even in myopia management, it is advised that we take a break. That’s where the 20-20-20 rule came, every 20 minutes you have to take a break. And I think that is more important. But definitely nothing less than 30 centimeters, that would be the distance that is required. All right. So moving on to the next question, do myopic presbyopes who do not wear reading glasses with acid esotropia fall into the category of Bielschowsky? That’s a very nice question. In fact the article by Bielschowsky about this particular condition when it was first published actually mentioned this category as well. So they said that because they are uncorrected and because they use an accommodation mode, they come into the category of Bielschowsky. So that is correct, they do, actually. So the next question says, we started to see acquired esotropia in myopic patients taking low dose atropine to control their myopia. Any explanation? I’m not very sure about this particular condition. I’m not sure if that is seen. But if you have seen it, I can’t think of any answer there. Maybe we’ll have to look into that. At what age does amblyopia occur and how does it effect permanent mechanism of vision? So again, there are multiple factors that are involved here. Because we all know that generally myopia can occur before the age of 7, 8, maybe 9 years. That’s also not a clear demarcation. But generally that is considered to be the level. But if you’re talking about amblyopia in connection with acute acquired comitant esotropia, since it’s acute, again, maybe presentation if it’s early enough, maybe amblyopia will not set in. Again, it depends on the amount of deviation, maybe, it depends on the amount of time between onset and presentation. And it depends on each child individually. So we cannot tell at what it occurs. If it happens in that age group, yes, it does set in. How it can affect permanent vision, well, that’s why amblyopia therapy has to be started first. Amblyopia is reversible. It is seen, if you have seen the management protocol, I have put amblyopia therapy as one of the initial steps. It has to be started as soon as possible. And it can be reversed. So it may or may not improve. And so the factors I mentioned before are important in actually understanding the depth of amblyopia. It all depends on that. And I hope the answer is clear. The next question is, which cases do you consider doing atropine refraction before planning for squint surgery? As I said, there was a comparison between atropine and cyclopentolate. In most cases there is maybe the cycloplegic refraction has not been done at the right time, the pupil is still restricting, the child is not compensating, or if you find angles in subsequent visits, then you consider using atropine. That’s what I do in the practice. But if everything else is okay, cyclopentolate is known to be good enough. Atropine brings up sometimes close to 2 diopters or greater. Yeah, definitely. As I said, we’ll have to be very thorough in our clinical examination before seeing that cyclopentolate is good enough. Having said that, in our clinics, sometimes it becomes very difficult to be refractions exactly 45 minutes after cyclopentolate. It becomes difficult for us to see that accommodation is still persisting after refraction after cyclopentolate. If done correctly, cyclopentolate is known to be good enough. So one of the questions is that one of the factors for amblyopia is deprivation. Again, I explain. So basically deprivation is definitely there. It’s actually not called deprivation. The type of amblyopia in such children, if it is because of strabismus, one of the eyes — the child prefers to see with one eye and the other eye goes into a state of deviation, input or output. The eye does not have its vision developing equally. So that is what happens in such cases of strabismus amblyopia. As I said, maybe children start focusing on one eye, they start preferring one eye and the other eye goes into amblyopia. And that eye usually manifests the deviation. This is a form of strabismus amblyopia. Okay. The next question is that, so can accommodative spasm be associated with Bielschowsky type of esotropia due to excessive near work like smartphone usage or other digital gadgets? That is a very good question, because that condition of accommodative spasm can actually be confused with Bielschowsky type, where refraction will come up with myopic finding. But the difference here is that most cycloplegia, that will not be seen in a case of Bielschowsky. Apart from that, there will be maybe sometimes a myosis will be seen with accommodative spasm. That’s why it’s important to understand these types, understand the pathogenesis, so we can differentiate one from the other. But it is not the same as Bielschowsky type. All right. So the next question is about Botox injection. And for how long do we give Botox injection as its effect lasts only three to four months. As regards this question, yes, Botox, the effect is known to be variable, results are known to be variable. But in strabismus, Botox has — you can go through literature, it says that Botox actually can cause even permanent recovery. It has got something to do with change that happens in the anatomy of the muscle because of Botox injection. So it is even known to cause permanent improvement. But again, it is variable. As you say, it can give good results. If the question is about how long we keep giving, so literature reports maybe around two or three injections are known to give an equal result as one surgery. So those are the statistics. I think it depends on the individual practitioner. Okay. So one question is right eye or left eye for prism. That depends, mostly, it all depends, it depends on the vision, it depends on the patient comfort. I think that that would basically be clear only after an orthoptic evaluation. So the next question is, what do you do if the cyclo gives a higher power like minus 6? As I said, that will probably come under the category of Bielschowsky type. We have to give them the refractive error. Usually patients do not have a problem accepting myopic correction. So it’s not like in hypermetropia where they will have to get used to it. It might not be a very difficult thing for the patient to adapt. So we right ahead and give that minus 6 diopters. So then, one of you shared about your experience, and says that surgery works very well and not the Botox. But stereopsis does not recover as well as the deviation. So a lot depends on the point I had discussed about predictive outcomes. So better results were found if the time between the onset of esotropia and presentation to the hospital was lesser. So basically it was a shorter duration that the patient actually had esotropia. And if we start our management, start our treatment early, it is known to actually resolve binocularity. This was the very significant predictive factor that was described. There was another paper which told about the factors of Botox and said if it’s a smaller angle and there is good binocularity already in the patient, that also gives good results. So it actually depends on the profile of the patient that presents to you. And as shown in the paper, they have studied the maximum number of patients, it resulted in 71% of good motor outcome. Basically that meant there was this 30% which did not have good binocular vision or even good motor outcome, and that was because of the slightly late presentation, amblyopia setting in or poor binocularity or loss of fusion. So it all depends on when the patient comes to you. I’ll probably leave this question about how do we do PAT for maybe some other time, because it involves a lot of orthoptics, the patient is asked to bear them for a continued period of time. There are different papers as to what time is actually suitable, some say 20 minutes, some say close to one or two days, sometimes weeks. So it’s a completely different topic. So, but yeah, it’s got a lot in it, and it’s very important to do a thorough PAT in such cases. So the next question would be that do you think some sudden onset esotropia will converge to the blind spot? So I’m not sure what is the point that you exactly want to ask me. Maybe it is that one angle where we start focusing, if it falls in the blind spot. Is it maybe something like 15 degrees? If it actually comes there, then obviously the brain and eye coordination will see to it that the eye focuses at a slightly different time. I think if that’s your question, then there will be a slight difference, because the brain is constantly working, and it tries to fuse to as reasonable an angle as possible. So one question says how many types would you consider of acute acquired accommodative esotropia. I showed you close to seven types. These types have been evolving with time. As I said, originally three types where described in literature and now we have seven or eight types including smartphone type. Things are happening with acquired esotropia and we have to look at all these types because each has a different pathogenesis. Probably just one or two questions more. But how can we — why exactly is Botox given in acute acquired esotropia. So the indications there will be — this is not discussed completely in the talk and therefore I would like to discuss it now. As I said, if it’s a younger child where there is no significant refractive error, the child has a significant esotropia, may go into amblyopia, you want to reduce that quickly. You can’t wait for six to eight months until you decide on surgery. That’s probably one of the reasons, one of the cases where you give a Botox injection. It can also be given, for example, in a very large angle esotropia, say a 75 or 80, to bring down the angle of esotropia and then start the patient on orthoptic exercises. It’s difficult to start the patient on orthoptic exercises if the patient has close to 70% angle. These are some of the specific indications. Apart from the other indications of Botox in these cases. And this question about how — what is the personal of surgery that is successful and if that is the only option. So as I show on the table, the paper with the largest number of patients showed a surgical success rate of 71%. Other reports also have been telling about surgical success rate of around 65 to 75%. But yeah, so it’s a good rate of success, if surgery is the only option. All right, then. I think maybe we can end today’s webinar. I thank everyone for joining, and participating in today’s discussion. Thank you very much. I hope this has given an insight into acquired esotropia to all of you. Thank you very much.

Last Updated: November 21, 2023

8 thoughts on “Lecture: Acquired Esotropia – What’s New in 2023!”

  1. Thank you very much for this very fruitful presentation. As a neuroophthalmologist, I have been alerted by my pediatric ophthalmologist colleague about the “smartphone” type after I started sending him these type of patients. Divya explained the condition thoroughly while also differentiating from other types.

  2. Excellent and very insightful presentation. The variations of esotropia was completely new to me, especially the case with the intermittent esotropia. Also very insightful was the impact of technology use on the child’s development of acute acquired commitant esotropia.


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