This Live Lecture provides a brief overview of the types of comitant, childhood strabismus seen in Cape Town, South Africa. The management of early onset esotropia with botulinum toxin is also discussed in more detail.

Lecturer: Dr. Christopher Tinley

The Use of Botulinum Toxin in Early Onset Esotropia from Cybersight on Vimeo.


(To translate please select your language to the right of this page)

DR TINLEY: So this afternoon, I’m going to talk to you a bit about our experience with the use of botulinum toxin for the treatment of early-onset esotropia. And I’m currently working at Red Cross War Memorial Children’s Hospital in Cape Town. It’s a large tertiary and quaternary center that services most of the Western half of the country. And we have a very busy eye clinic in the hospital, and see approximately 6,000 children in the outpatient department per year. And this is a typical patient that we see in a mixed race family, with a large angle left esotropia.

>> Can you just share your screen for everyone?

DR TINLEY: Sorry. Sorry. Should we start again? Okay. If you… Heard the audio before, that’s absolutely fine. I will start the PowerPoint presentation now. So as I said, I work in a large tertiary institution in South Africa, in Cape Town, called the Red Cross War Memorial Children’s Hospital. And this is a typical patient that we see in the eye clinic. Mixed race family, and a child with a large angle esotropia. So during the talk, we’ll cover a few topics. Firstly, what exactly is early onset esotropia? What is the point of Botox? And what are the outcomes that we’re getting in Cape Town with the use of Botox in this context? So let’s just start off with a poll question, asking the audience: What is your level of interest in strabismus currently? A, ophthalmic nurse, trainee ophthalmologist, general ophthalmologist, or pediatric ophthalmologist? Okay. So we’ve got about half and half general and pediatric ophthalmologists. Well, that’s great. That’s awesome. Okay. So about a few years ago, we did a retrospective study of the types of strabismus we saw in Cape Town, South Africa, over a 10-year period. And by and large, the most common form of strabismus we see is esotropia, almost 70%. Paralytic and strabismus syndromes, such as Brown syndrome and Duane syndrome, are relatively uncommon here. And we’ll be looking in more detail into esotropias. The majority of children we see with esotropias here are early onset esotropias, and we’ll go into the definition of this in a minute. The next biggest proportions of esotropias are the accommodative esotropias, followed by quiet and secondary to other disorders. So in the States, they classify early onset esotropia as an esotropia that presents within six months of age. It’s usually large angle, usually alternating ET, no significant refractive error, non-accommodative, no ocular pathology, usually no brain pathology, and there are other associated features. There is some controversy as to the nomenclature of this disorder. There are many names, including congenital, infantile, and early onset esotropia. And many people define it differently. Mostly you’ve got infantile and congenital esotropias — with onset in the first 12 months of age. Mainly the definition is within 6 months of age. But they all fit into the same broad category. So the second poll question is: On average, how many children do you see with early onset esotropia in your clinics per month? This is very interesting. Because I trained in the UK, and there is a trend in the Western world for decreasing numbers of children presenting with early onset esotropia. And we’re not quite sure what the reason behind this is. But current thinking is that it may be due to increased nutritional input and nutritional quality, in the First World climate. However, in South Africa, and I know in other parts of Africa, early onset esotropia is particularly rife, and in fact forms the majority of the esotropias that we see here in South Africa. So the fact that most of you see less than 5 per month, for me, is not that surprising. You guys probably see more accommodative esotropias, either fully or partially accommodative. In Cape Town, the main reasons for sensory esotropias were cataract, optic atrophy, toxoplasma scars, coloboma, and aniso amblyopia. And main CNS reasons are cerebral palsy, developmental delay, meningitis, hydrocephalus, and Down syndrome. Poll question three is what is the main racial profile of your patients with esotropia? Okay. So mostly Asian and White children. That’s interesting. Because — well, we’ll get to that later. But by far and large, the types of esotropia they get are accommodative esotropias. In Cape Town, the minority of children are White, and they’re usually more affluent and have access to private health insurance, whereas the hospital I work in is a state hospital, and so it caters mostly for the indigent population, which consists of mixed race and Black children. So this is a photograph from inside the eye clinic, and you can see children fighting over toys at a table. The majority are mixed race children, like the one with her glasses on. 81%. And 22% of the children are Black origin. Having said that, proportionately, more Black children have esotropias than mixed race children, in our population. And studies have shown that relatively small numbers of Black children develop isolated strabismus when compared to other race groups. And this cannot be explained on the basis of referral bias, as there is equal access to health care in South Africa. The risk of isolated strabismus has also been shown to be reduced in children of Black maternal ethnicity. The nature and causes of this protective effect is unknown. But may partly be attributed to a lower associated risk of hypermetropia. However, when Black children do squint, most of them develop esotropias. And, in fact, our population group has demonstrated the highest eso to exo ratio reported to date. So second to the South African Black children in Cape Town were the Egyptian Arabian children, with a high eso to exo ratio, and communities with a low eso to exo ratio were Cameroonian Black children and Singaporean Asian children. So I think, in the East, in Asia, most children develop exotropias. Of the Black children who developed esotropias, most were early onset esotropias. As opposed to other race groups, where accommodative esotropias are more common. So, for instance, in the US, White population — only 6% had early onset esotropias, and in Singapore and Asians, only 23%. Poll question number four: At what age do you plan intervention for early onset esotropia? Okay. So it seems like most of the audience opt for early onset or early intervention for early onset esotropias, which is in line with current thinking. The treatment options include early intervention, which may take the form of botulinum toxin as soon as possible after diagnosis, or indeed strabismus surgery, as soon as possible, but earlier thinking suggested that as long as the children were aligned by age 2 years, they had a good chance of developing a long-term stability of deviation — of alignment, and even gross stereopsis. In the First World, and where I grew up and was trained, in the UK, we delayed intervention for early onset esotropia, and most of them had two-stage surgery and were aligned before school-going age, as the idea of achieving stereopsis was not widely believed and practiced, as opposed to the Americans, who opted for early intervention. Just to remind you, what is it that drives stereopsis? Well, firstly, one has to have bifoveal fixation or alignment of the eyes, which then leads on to fusion, after the merging of two slightly disparate images on the retina. And then the third phase of stereopsis is stereopsis indeed, which is depth perception. The pros of doing early intervention for early onset esotropia is that we feel there is a better prognosis for achieving binocular function, and there’s a concept of “locking on”, so if you can reestablish bifoveal fixation in these children, who have started to squint for a period of time, for a significant period of time, then there’s a theory that the binocular cortical areas may indeed well be able to lock on to this binocular image, or the bifoveal image, and this drives fusion, and then later stereopsis. And it’s felt that if this is delayed until later in life — specifically after 2 years — then the prospects of a child developing robust stereopsis after the eyes are aligned is very low. And this was borne out by studies conducted by Taylor, Wright, Ing, Birch, and Kushner, where they determined that surgical correction after 2 years of age is associated with poorer stereopsis outcomes. And in a paper in JAAPOS in 2000, Birch looked at the outcomes of children who had early surgery, some before six months of age, but others up to 24 months, and she found that those realigned within 12 months of the onset of esotropia had significantly better stereopsis. Those with stereopsis were also less likely to develop consecutive exotropias and associated vertical deviations. Ing et al. in 2002 agreed with that thinking, and suggested that alignment within one year of age or within 12 months of misalignment favorably affects the percentage of patients who develop stereopsis in the treatment of congenital esotropia. So what are the risks of early intervention? Well, for toxin, you can induce a temporary ptosis. You can induce a temporary vertical deviation. If the angle of the deviation is reduced, this can induce a fixation preference, and then lead to amblyopia. And because a sharp needle is involved, globe perforation is a potential complication. As far as surgery is concerned, often it’s very difficult to get accurate measurements in very, very young children. Specifically those that are 9 or 10 months of age. And also, surgical outcomes, we know, are not 100% predictable, and we can follow tables to guide us, but outcomes are not always predictable. And in many cases, with large angle esotropias, you may need to opt for 3 or 4-muscle surgery as a first stage procedure, or do two two-stage procedures. This may leave you with a residual or consecutive deviation in a very young child. And then surgery also carries the risks of toxin, in that it can induce a fixation preference and amblyopia, as well as globe perforation. So what is Botox? It’s a toxin formed by an anaerobic, spore-forming, Gram positive bacteria, which inhibits presynaptic release of acetylcholine. It results in paralysis of muscle, usually within 2 to 3 days, with a maximum effect after 5 days. And its duration can go on for 2 to 3 months. Poll question number 5: When do you use botulinum toxin in your clinical practice? Okay. So most of you are comfortable with its use in blepharospasm. But a few of you are using toxin in strabismus. It would be interesting to know what proportion of your strabismus patients are children and what proportion are adults. I would imagine the minority of your patients are in fact children. In ophthalmology, we only use type A and B toxin. Botox is produced in the United States. Dysport is produced in the United Kingdom. The strength differs. There’s a type B toxin called Myobloc, which is relatively weaker than the others. I don’t have any experience with the use of Myobloc, but I used Dysport in the UK and Botox in South Africa. So we can use it in strabismus in the following contexts. If you want to test if an older patient may develop postoperative diplopia, you can use it as a diagnostic test, whilst more commonly, therapeutically, you can use it in paralytic strabismus, such as a 6th nerve palsy, or indeed restrictive strabismus, like thyroid eye disease. But also in childhood. So the first reports of botulinum toxin treatment for childhood strabismus came from America in the early 1990s. Where they tried botulinum toxin injections into the extraocular muscles of 413 children, ranging from 2 months to 12 years of age. A relatively short period of follow-up of only 6 months, but the results were encouraging. 61% were aligned, with an average of 1.7 injections. Their results were based on esotropias and exotropias, as well as smaller angles and larger angles. They did get complications of ptosis in 31% of children, and induced a vertical deviation in 16%. Toxin specifically for the use of infantile — or for the treatment of infantile esotropia was looked into in more detail by deAlba, a team in Italy, and their results were published in JAAPOS in 2010. They intervened in children — 442 children — less than 3 years of age. And they compared the outcome of toxin versus surgery for children with infantile esotropia. Although the two groups weren’t entirely equal, because they operated on patients surgically at a much older age. A mean of 2.5 years, as opposed to 1.5 years with the toxin group. Nevertheless, in the children undergoing toxin therapy, 50% had one injection, while another 50% had either 2 or 3 injections. And after a reasonable follow-up of 2 years, they found that the alignment within 10 prism diopters was within 45% of children following botulinum toxin, and 66% following surgery. But with children with smaller deviations, the percentage of those aligned after toxin was equal to those that underwent surgery. So what are the advantages of Botox over surgery? Well, it’s less invasive than surgery. It’s cost effective, because you can use a vial of toxin to treat 6 or 7 or 8 children in one sitting. You don’t develop scarring of the extraocular muscles. And you know that there will be a predictable period of bifoveal fixation, when the child’s exotropia wears off, and the child becomes more aligned and there’s a period of bifoveal fixation, when it reverts back to its primary position. Toxin can be easily repeated. And it can be followed by surgery, if the effect is not achieved. So at Red Cross, we decided to — because we saw such a large proportion of children with early onset esotropia, we wanted to trial toxin for these patients. And we looked into just the first few that we did in 2014 to 2015. And we have done many, many more since then. In fact, we have a toxin clinic once a month. Every afternoon, once a month, where we inject 7 or 8 children with early onset esotropia. When we started, the mean age of injection was 16 months of age, and there were slightly more females than males. 19 Black children and 14 mixed race children. None of the patients had a significant refractive error — although we did try to inject toxin in some with higher refractive errors of 5.5 diopters. But the mean was 2.7 diopters. And those with the higher refractive errors we did give specs before they underwent toxin. And the mean preoperative angle was large. 55 prism diameters of esotropia. 4 had dissociated inferior oblique overaction, and 5 had DVD. So in adults, the procedure is much more predictable and reliable, because you have electromyogram guidance. And it’s done under local anesthetic. So the patient is connected to electrodes, and your toxin needle is connected to an electrode. And first of all, you ask — if you’re doing a medial rectus toxin, you ask the patient to abduct the eye, and then you introduce the needle vertically, around the canthal area. And then you ask the patient to adduct the eye. So it’ll activate the medial rectus muscle, and you gradually advance the needle, along the vertical medial orbital wall, until you get an EMG signal, which confirms the fact that your needle is in the medial rectus muscle. And then with your needle in this position, you inject the required dose of toxin and leave the needle inside for about 25 to 30 seconds, to minimize leakage of toxin through the needle tract, before withdrawing the needle. In children, we don’t have the luxury of being able to do toxin under local anesthesia. So we use general anesthesia. At Moorfields in London, toxin is given to children under ketamine anesthesia, because this still gives an electromyogram signal, albeit very weak. In Cape Town, we don’t have EMG equipment, and we’re quite happy to use a blind technique of injecting the toxin in our patients. So it’s performed under general anesthesia, induced by gas. And we put in a laryngeal mask for the child. We book 7 cases, approximately, per afternoon, and each case takes approximately 10 minutes. It’s very important that the toxin is diluted accurately before the procedure. So we order 1 vial of 100 units Botox for the list, and then you dilute it with 2 mils of normal saline. It’s important not to agitate the bottle too vigorously, because it’s quite unstable, and denatures quickly. So you gently dilute the toxin. So your final dilution will be 5 units in 0.1 mil. And we use 1-mil syringes. Ideally you should inject the toxin with the thinnest needle you have available, which is a 30-gauge needle. We only have access to 26-gauge needles. The Brown needles. It’s critical to allow for the dead space in the needle, so that when you’re injecting the toxin, you’re not injecting the toxin into the dead space of the needle. So the dead space of the needle needs to be filled up with toxin as well. Then the procedure, the surgical procedure, is: We have fixation forceps, to grasp the limbus, and rotate the globe temporally. With the two forceps, we then grasp the medial rectus insertion through the conjunctiva, taking note of where the ciliary vessels are located. And then you engage the toxin needle into the medial rectus muscle. We then rotate the globe into the primary position, and advance the needle vertically down the medial orbital wall. And as I said earlier, EMG guidance is not used. In deAlba’s paper, he suggested using 5 units in children with a smaller angle of deviation of less than 50 diopters, and a greater dose of 7.5 units in children with a larger angle of deviation. We found these doses to be unnecessarily high. And have subsequently reduced the doses we use at the moment to 5 units, and maybe even reduce the dose further. So far, we have not seen any intraoperative complications. At two weeks, 90% of the children injected developed an exotropia, which is the desired effect. Interestingly, we had a much higher proportion of patients than deAlba who developed ptosis. But this was reassuringly short-lived in nature, usually disappearing within one or two weeks. And it was split between — 2/3 between unilateral and bilateral. We also induced vertical deviation in one patient. So this is the typical appearance of children, when they come in for one-week or two-week postop assessment. What we’re looking for is the large angle exotropia. And preferably with no ptosis. Or vertical deviation. So this is the ideal situation that you are aiming for. Often, as I said, the children came in with a partial bilateral ptosis, which usually resolved within the following week or two. So this was not particularly concerning to us. At 3 months’ assessment, 50% of children were aligned within 10 prism diopters of orthotropia. But they ranged from 14 diopters ET to 120 diopters XT. And this is largely due to residual effects of the toxin. And fusion could be demonstrated in 20% of these children. Although it’s very difficult to demonstrate fusion with great certainty in children of this age group. After one year’s assessment, we lost quite a few patients to follow-up. Hopefully because the parents were happy with their children’s alignment. But this cannot be assumed, without having seen them back in clinic. The manifest success rate reduced to 30%. And the median angle of deviation at one year was 20 prism diopters. Whereas the mean pre-op deviation was 55 prism diopters. And we could demonstrate fusion definitely in 12%. And there were no consecutive exotropias. So after toxin was given, some children with a relatively high hypermetropia were given spectacles. some were given repeat toxin within 14 months, some underwent strabismus surgery, at a mean of 14 months, and we followed them up for a mean of 8 months. So Botox for early onset esotropia appears to be safe and effective. In our hands, ptosis is a common complication, early postoperatively. But is very temporary. Our success rate for alignment at one year was 30%. And in retrospect, it seems repeating the Botox earlier might be indicated. In most patients that weren’t aligned at a year, the angle of their deviation was significantly reduced. And this may mean that the number of muscles that need to be operated on may be reduced. If they do come to surgery. Or when they do come to surgery. Early onset esotropia, unlike in other parts of the world, is very common in our setting. And I think there is a point to Botox treatment for these children. It seems earlier intervention appears to increase the chance of achieving stereopsis. Which increases the long-term stability of alignment. And the preliminary results at Red Cross War Memorial Children’s Hospital are encouraging, and these may improve further with technique and dose refinements. Thank you. Are there any questions?

>> We have some Q and A questions, if you want to bring them up on your screen.

DR TINLEY: Okay. So… Up to what age can toxin be given? Also, can it be given to infants in essential infantile esotropia? Sorry. I… Can you still hear me?

>> We can hear you.

TINLEY: I’m going to answer that question live. We tend to give toxin up to the age of 2 years. As evidence has shown that children after the age of 2 years are very unlikely to develop stereopsis with early onset esotropia. So I don’t think there’s much benefit in giving toxin to children over the age of 2 years, and I would rather resort to surgery in the first instance. Okay. The next question is: Do you inject transconjunctivally without peritomy? We have found that injecting transconjunctivally has been safe and effective, and we don’t feel the need to perform a peritomy to identify the medial rectus muscle. The problem with performing a peritomy is you’re prone to developing much more spreading and leakage of the muscles around the globe, with secondary paralytic effects on the lids and extraocular muscles. So ideally you don’t want to open the conj, when you’re injecting the toxin. So Ahmad Ali asked: Do you keep the remainder of the toxin in the fridge? And the answer is yes. We live in a Third World country, and toxin is very expensive. And I think it is still active in the fridge, if you keep it for a day or two. And we make it available to the rest of our department, in case they need it for toxin-induced ptosis in patients with corneal ulcers. So we do keep it for a few days. But you can’t keep it for more than a day or two. And then the effect wears off. So Ahmad Ali, that answers your question as well. Paromita Sanatani had a very good question. Is patching done for amblyopia after the Botox is injected? During the time that the child is exotropic? I think it’s important to see if the child has developed a fixation preference after the toxin. If there is a definite fixation preference after the toxin, then I think it is important to occlude the preferential eye, until the eyes are approximating alignment. When there may be a period of bifoveal fixation and stimulation of the binocular cortical centers. So if the child is very fixation-preferenced in the beginning, I would definitely occlude the one eye until the eyes approach the primary position. Most of them don’t require patching, though. As far as what forceps we use to grasp the muscle… We just use normal toothed forceps that we use in our squint procedure. But there should be quite large, chunky forceps, that you get a good grasp of the muscle and the muscle insertion. Irina asks: Are there any systemic side effects? No, the toxin has an exquisitely local field of action. And only paralyzes the muscle in the vicinity — the muscles in the vicinity. So we have had no systemic side effects with the use of toxin in our cohort. Good question from Dr. Altansukh. When should I repeat the Botox injection? Well, I think you have to give it at least three or four months to gauge the effect. If the patient has gone back to being esotropic after three months, then I would definitely inject toxin as soon as possible, after that. So between 3 and 4 months after initial toxin injection, if the patient has reverted to an esotropic deviation. So the next question is: What is the criteria of (inaudible)? I would certainly offer toxin to any child who reverts to esotropia after the first injection, and as I said, I would give it 3 to 4 months before this decision can be made. I do discuss the options with the parents, however, because undergoing a trial of toxin can be quite trying for the family, because the eye is all over the show for quite a prolonged period of time, and there is a period of ptosis, and it can be quite anxiety-inducing. So I offer patients another trial of toxin, if they so wish. Otherwise, I also offer parents surgery, if the first round of toxin didn’t work. But there’s certainly no harm in trying toxin again, if it hasn’t worked the first time. So the question from Kumari Fonseka is: Can we do this for adults as well? Do you experience more complications with adults? Well… I have a lot of experience with toxin in adults, and we did thousands of adults at Moorfields Eye Hospital in London. And it’s much easier to administer toxin to adults, because it can be performed under local anesthesia. But you need a lot of vocal anesthesia as well, because it can be quite an intimidating procedure as well. So you need a lot of moral support. And the advantage of performing it in adults is EMG guidance, so you know when you’ve hit the muscles and when you haven’t. But under local anesthesia, performing this procedure in adults is really straightforward. So another attendee asks: How does Botox help develop binocular single vision, as eyes generally become exotropic after Botox? Well, the theory is that BSV only develops when the children’s exotropia reverts to a period of binocular alignment or where the fixation is approximating foveal fixation in both eyes. And as we discussed earlier, there are three steps to stereopsis. And when the children’s exodeviations return to the primary position, when the toxin starts to wear off, then they will be approximating bifoveal fixation, and the disparate images on the retina will stimulate fusion, hopefully, and then go on to develop stereopsis. So it’s during that period when the patients go back to being bifoveal that the BSV develops, and that’s the theory. That’s the theory of locking on, which we discussed earlier. Ahmed Ali asks: Is there an association between maternal smoking during pregnancy and early onset esotropia? Not to my knowledge, but I haven’t specifically looked into this question. It would be interesting to see what might be the case in your community. But I don’t have a specific answer on this question. Muhammad Ramzan has asked: Do you inject 5 units in each eye? And what postop drops do you use? Yes. We inject 5 units into each medial rectus muscle. We first wash out the conjunctival sac with povidone-iodine solution, and then postop, we just give a drop of topical anesthetic. Like amethocaine or benoxinate — we don’t give postop antibiotics or steroid drops. Ivelina Pitakova asks do we have a video film of the procedure to show us? Unfortunately not, but I think in the paper by deAlba, there is a link to the procedure. In his paper. From 2002. So have a look. And I think there is a link there, on the video, of the procedure. So another attendee has asked: Is Botox treatment one step before surgery always? And I think the answer is it depends how confident a squint surgeon you are. And how aggressive you are at trying to achieve alignment within the first year of age. I certainly would always opt for toxin as a first step for early onset esotropia, purely because there are minimal risks involved, and it can avoid the potential complications that you may achieve with early surgery. So in my context, in my patients, I always offer toxin in children with early onset esotropia up to the age of about 2 years. After which time I’ll always elect for surgery as a first procedure. So if the child is still younger than 2 years of age, I’ll try toxin for the first instance. But if they’re older than 2, then I will opt for surgery as a primary procedure. So Muhammad Ramzan has asked: How many maximum injections have you given in one child? I think the maximum I’ve given is 2 or 3. Before I go on to surgery. So yeah. I don’t think you can continue indefinitely. Bearing in mind that each trial of toxin takes 3 or 4 months to gauge the effect. So if you do 3 toxin injections, almost a year has gone by, in which time you could be losing the opportunity to try and get the alignment achieved surgically. Another attendee has asked: What age is the youngest patient we’ve injected? And I think it’s around 8 or 9 months, is the youngest patient we’ve injected. But I try and get them injected as close as possible before one year of age. In our setting, it’s sometimes difficult to get all the preliminary tests performed before the child gets the toxin. So, for instance, the atropine refraction and fluoroscopy in children with esotropia. So what I’ll do is list them for the next toxin list, which is every month, and then I’ll do an atropine refraction on the table. And fluoroscopy on the table. So you’re not losing time in children with very apparent congenital or early onset esotropias. If there’s some doubt as to what the diagnosis is, and whether or not the child may have an accommodative element, I won’t toxin them early, but if it’s a barn door case of early onset esotropia, it’s important to toxin them as soon as possible, and you can correct the residual hypermetropia if it’s significant afterwards. A lot of people are asking if I have a video of this procedure. Unfortunately not. But I think there is a link to the procedure in deAlba’s paper. Or you can have a look on YouTube. I haven’t looked myself. So there’s a question: What is the cause of the bilateral ptosis after toxin? Well, ptosis and vertical deviations are common complications of toxin to the extraocular muscles because of leakage of the substance around the globe, after the injection. So if the toxin leaks to the levator muscle, then the patients will develop ptosis of the eyes. And obviously if it leaks to the inferior and superior rectus muscles, you’ll get a vertical deviation as a complication of that. How deep do I inject the needle? Well, we use a 26-gauge Brown needle, and once you’ve engaged the muscle with the needle and you rotate it back to primary position, I advance it down the medial orbital wall, right up to the hilt, actually. To the hilt of the needle, all the way down. So the needle point is in the belly of the muscle, in the fattest part of the muscle, in the belly. So I advance it quite far down the orbital wall before I inject. And then remember you must hold it there for 28 or 30 seconds before retracting it. Okay. Paromita Santani asks what percentage of the early onset esotropias are expected to be stabilized by toxin alone, thus eliminating the need for surgery? Well, in our series, only a third of the patients were stable at one year. And I expect that if they’re aligned at one year, then their alignment will be stable, because they have developed some degree of stereopsis and fusion to keep them aligned. So we’re getting results of at least 30% of children that we inject with toxin. But I think this percentage can be increased if you select your patients carefully. And inject toxin sooner rather than later. Which gives them the best chance of developing some form of stereopsis. Ahmad Ali has asked: By experience do you find a relation of degree of angle of deviation and the number of Botox injections? And although deAlba’s series did find that they needed to give more injections for greater angles, I find as long as you paralyze the medial rectus muscle with toxin, then you don’t actually need 5 units to paralyze the medial rectus muscle. We know that from the dose we use in adults, which is 2.5 units. But because of the fact that we’re injecting blind, we use a greater dose in children. But once the medial rectus muscle is paralyzed, you should get an exodeviation. And that’s all you’re really looking for, is an exodeviation after the injection. And so that’s not really dependent on the degree of pre-op deviation. Because hopefully the toxin will paralyze the medial rectus muscle completely and induce an exodeviation, despite the pre-op angle. The last question is: Are there any guidelines for the use of toxin? And where can I get it? I’m not aware of any… Guidelines for the use of toxin in children, apart from deAlba’s paper, which we used as a guideline. So definitely refer to that, if you want to start trying it. Right. Paromita Sanatani has another question. Do you inject uniocularly or in both eyes at the same time? In all patients with early onset esotropia, we inject both medial rectus muscles at the same time. You want to paralyze both medial rectus muscles, in order to achieve the exotropia that is desired. I’m not aware of anyone who would only inject one medial rectus muscle. I think that’s it. Are there any more questions? Any more questions? A lot of people have asked about the film, which I unfortunately can’t show you. Any other questions?

>> Looks like that’s all the questions for now. So thank you for your time. And we’re right at an hour mark, so I think we can wrap up now.

DR TINLEY: Thanks so much, guys. Take care.

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May 4, 2017


  1. Hello Dr. Christopher Tinley,
    Thank you very much for great webinar.
    I can’t to attend because of my work schedule.
    I also have question. Can we use botulotoxine for exotropia? For example I have patient 25 years old and now she gas exotropia after esotropia surgery in childhood?

    Dr. Olesia Ziiatdinova


    1. Hi Dr. Olesia Ziiatdinova,

      We reached out to Dr. Tinley with your question and he answered it below!

      Please note that you can sign up for Cybersight Consult to ask questions like this to expert ophthalmologists. We can even set you up directly with Dr. Tinley.

      To sign up, please click on ‘Join the Community’ on the homepage. If you have any questions on how to sign up, please email us at and we will assist you.

      Dr. Tinley’s Response:

      Yes, you can use botox to treat exotropias.

      The technique for injecting toxin into the lateral rectus muscle is slightly different, but Dan or I could explain this in more detail should they wish to proceed.

      If this particular patient has developed an exotropia after having had esotropia surgery in childhood, I do not think toxin would be a curative treatment however.

      Further surgery is likely to be necessary.

      It all depends of course on the angle of the patient’s deviation and the number and types of prior surgery the patient has undergone.


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