In this blog, I shall discuss two different topics:
1. Astigmatism arising due to IOL tilt
2. The role of lasers in the era of anti-VEGF Intravitreal injections
We shall discuss the first one in the form of an actual case.
The second topic will be discussed in general.
This type of discussion brings out the current trends and standards by the practicing ophthalmologists.
Question or Case 1:
A recent patient operated for LE cataract on 21st June, uneventful phaco surgery, was implanted with indian, hydrophillic IOL, came back 10 days later with astigmatism of -4.0 x 80. Her preop and even postop K were almost same( she has no corneal astigmatism-pre & postop). She has an abnormal IOL tilt, nasal side more anterior. IOL is in the bag, there is no zonular weakness of any sort.The IOL had completely unfolded( no haptic capture ). IOL tilts and decentrations are nothing new. But I havent seen a tilt in a in-the-bag IOL of this magnitude. What could be the underlying mechanism?
Few possibilities for tilt are
1. Inadequate unfolding of the haptic s which you have ruled out hopefully with adequate dilatation
2. Zonular weakness either preexisting pseudo exfoliation or peroperative zonular weakness again ruled out hopefully after dilatation
Have causes 1 and 2 been ruled out after complete dilatation?
Is both the haptic s in the bag?
3. Inadvertent cortical material or viscoelatics in the bag. Not many surgeons remove OVD from behind the IOL pushing a part of the optic or completely forward
4. If your rhexis is small , one could still place a hydrophilic IOL into the bag without a tilt
5. An intumescent cataract gives an unduely boggy bag after its removal and IOL may tilt within it
6. Your wound clear corneal or scleral and its apposition should also be considered . The wound needless to say may be less predictable in healing in a myope .
These are the possibilities that I could enumerate. Hope this helps.
Thanks for the query. Infact this was one of the issues I had raised with toric IOLs.
According to my UBM, USG investigations into patients like these referred to me, I have now classified Pantoscopic IOL tilts into
1) Early tilts (few days to a month) where I have been lucky enough to demonstrate
A) Viscoelastic remaining in the bag especially inferiorly. A UBM is a useful tool to demonstrate this if you do it in various axis asking the patient to look in extreme gazes I would subclassify the according to the effects in different OVDs (Ocular Visco-elastic Devices)
B) Zonular laxity or dehiscence especially in cases with exfoliation or other causes (I have seen this in one patient of homocysteinuria and one marfans)
C) Localised Choroidal Detachment( CD) superiorly I have only seen one patient with a bad astigmatism ( non corneal ) whose astigmatism reduced as the CD reduced
2) Late tilts where
A) Differential capsular opacification is almost always the cause in my experience as immediately before YAG capsulotomy many patients have large non corneal astigmatism which is immediately relieved after YAG capsulotomy
B) While in one patient on chronic pilocarpine treatment we discovered an iris and cilary body cyst on UBM
C) One patient had a differential ciliary body pull due to a cyclitic membrane superiorly under the incision and the astigmatism reduced after a sub tenons injection of steroid
D) Zonular dehiscence. one case with silicon oil causing zonular dehiscence demonstrated by serial zonular photographs over one year Of course that all is anecdotal data from patients referred to me but in such rare situations case report is our only guide and I would send you an evidence based summary if you need it (Considering the risk of persecution for reporting our own findings and getting accused of plagiarism if clinical findings of similar conditions happen to be worded similarly ,I feel safer writing at places like this forum and can pass on the pictures of the UBMs if needed)
I would love to know others experiences because the vast experience of AIOS members will definitely be extremely useful in such a less discussed clinical scenario
Thanks for bringing this up
– Large bag with low power thin IOL may have tilt in the bag causing astigmatism.
– High molecular visco-elastic in one portion of bag trapped behind IOL also can cause tilt, which will of course resolve with time.
Corneal topography will tell you the induced astigmatism due to the tilt and UBM with a Large silicone cup water bath will assist in viewing the ciliary area better to rule out localized pathology of tilt, if any. Also, most of us have suspected residual OVD and UBM can help gauge distance between posterior surface of IOL and posterior capsule and rule out any kind of collection in this area .
If you are going in to tap the lens in place it may be worth while to put a CTR also to regularize the capsular equator. I would also consider a dilated fundus exam to rule out any ciliary body or pars plana mass lesion.
I have seen such high IOL induced CYL only when the loop is stuck to itself or to the optic. If both the loops are in the bag, and opened fully, the possibilities are very few. There could be a silent dehiscence in the capsule at the equator, and the loop might have got slipped partly into it. In this case just rotation of the IOL to another meridian will help, after withdrawing the loops away from its fixation. The other possibility is a torn loop end which could tilt the optic. Careful dilated examination should give some clues as the tilt will then be asymetrical between the loops. How is the IOP? Could you post some photos?
In the era of anti-VEGFs with so many studies,whats the role of laser in management of diabetic macular edema and BRVO?
Do we really need it?
If yes then when?
Invite opinions from everyone.
Macular laser with metabolic control of DM risk factors remains the sheet anchor of DME Rx with antiVEGF/steroids/surgery as adjuvants to be used judiciously .
For BRVO macular edema , antiVEGFs/steroids will remain the mainstay because laser cannot be done in a grossly edematous macula .But sectoral laser will remain the mainstay for neovascularisation sequelae.
For me, this question got answered the day I saw an outbreak of post avastin endophthalmitis. If outcomes are comparable, I will choose the non invasive treatment each and every time once the edema is reduced to a manageable level where laser can be done.
you may argue that the incidence is close to one in few thousand, but think of the number of diabetics, AMD patients and venous occlusion patients that get treated every day with avastin and you quickly reach that critical number where we all WILL see post avastin endoph no matter how paranoid we are about asepsis.
thats my opinion, it may represent a real world take on the highly controlled RCT data that we see being published, but our patient profiles and environmental state are a little different from other countries. so, the need to integrate that into any extrapolation .
will be glad to hear other opinions.
you will be surprise that in era of ati VEGF, i have not used anti VEGF in diabetic retinopathy since last four years.
still all my patients are doing fine. it is not that i have not used, but i was not getting better suatainable result than laser, steroid and good systemic disease controll
Its good to see you in Retnet. Are you using OCT to monitor your patients with anti VGEF and Laser. Because what you say would be interesting if substantiated with OCT.
Laser does fit into the final and most sustainable decrease in macular edema, due to BRVO or DME, but anti VGEFs helps in getting there with much ease.
In BRVO CME and in DME when the edema is high. Say > 300-350 microns, and if involving fovea as we see on OCT, then i dont prefer laser. AntiVEGF or even steroid in some cases is better. But after couple of injections when edema subsides then i supplement grid laser for a longer lasting effect since injections are shortlived and can cause rebound edema. Combination of laser and antiVEGF works well in most cases.
Avastin acts acutely and IVTA prolonged effect combination of good anti-VEGF and anti-inflammatory effect is the logic. Downside is the cost and risk of glaucoma and also SCORE has shown TA not to be better than laser in BVO.
i have seen avastin injected CRVO patients developing NVG as well as BRVO cases developing NVE and vitreous haem .They may present slightly later. Avastin can be used but it may not guarantee prevention of neovascular complications .The recommendations of CRVO study group for workup, followup and PRP initiation in CRVO need to be followed even in avastin injected cases.Undilated slit lamp examinations for rubeosis and gonio to detect angle neovascularisation are often forgotten by VR surgeons who see many patients directly in dilated state after preliminary workup by a optometrist .
Sub-Topic of Topic 2
Would request opinions on when should one prefer IVTA over avastin & vice versa in diabetic edema prior to doing laser. (Lens status, OCT findings, age?)
I personally feel IVTA works better, but always give a trial of Avastin first to avoid IOP issues.
Avastin shifts the VEGF related complications temporally.
This has been seen in ROP babies receiving Avastintreatable ROP occurring months after Avastin treatment was ceased. The role of Laser for neovascular complications and the protocol established by CVOS remains the gold standard for the care of CRVO patients. The only thing that has changed is the treatment of macular edemasteroids, anti VEGFs and maybe peripheral PRP may be considered in cases without gross macular ischemia.
I have been following the discussions on Laser, Avastin, IVTA and Systemic control in DME and vein occlusions.
Like to share my experiences and thoughts:
If there is CME, whether ischemic or non-ischemic, I prefer to inject Avastin and at the first instance only, I caution the patient that regular follow up is a must and there may be requirement for further injections and laser. Usual requirement is around 3-4 injections per year and if edema recurs earlier than one month or if there is resistant edema, I consider steroid and peripheral PRP. I consider steroid early (as second or third injection) in pseudophakics. Prefer to avoid steroid injection in phakics almost always. NVE can be prevented with repeated injections of avastin. Even early NVI without or with early NVG responds very well to Avastin. IOP reduces without lowering agents!! But these cases do good (good meaning control of IOP) in long term only with aggressive PRP. In all cases that develop NV, I do laser PRP.
I dont agree with comparison of ROP here. There are many reports and I myself saw normal full retinal vascularization happening after Avastin in ROP. Yes, the babies require close follow up till full vascularization is noted. Cases where there is no progression towards normal vascularization or where there is worsening after initial improvement do require laser to avascular retina as a complete treatment.
Almost similar protocol as that of CRVO. But only thing is that I always do laser after 2-3 injections irrespective of NV and once edema settles and retinal hemorrhages clear, I prefer doing angiography guided laser to entire CNP area (modified grid laser + aggressive sectoral PRP). Doing only macular grid doesnt serve the purpose of preventing recurrent edema. (Attached a picture of laser done for BRVO- CME)
Most irritating retinal problem to deal with nowadays because there are multiple factors involved: systemic control, compliance with diet , exercise, DM treatment and follow up, metabolic control, nephropathy, lipd profile among others.
The case that I feel, responds very well, doesnt reduce by even 10 microns with any treatment and the one that I feel will not respond with any treatment shows normal foveal dip from > 800 microns within 2 weeks just with subtenon steroid and topical nepafenac in a phakic eye!!! The differentiation of edema into cystoid and spongifom thickening helps in few cases, cystoid form being favorable but this is not universal again. Presence of hard exudates near fovea is one more distressing factor.
I feel chronicity of edema is the single most important factor that determines response to treatment, more chronic being less favorable.
After explaing the importance of systemic control and after checking HbA1C(have to persuade the patients to get this done almost always as most physicians havent adapted yet), I start with avastin in almost all cases, do follow it up with focal/grid or modified grid laser after 2-3 weeks and review after 2 months. Along with first avastin, I prefer addition of subtenon steroid in pseudophakics and cases with hard exudate plaques near fovea. Cases with CSME and NV, always start with avastin and add up PRP laser 3 sittings with additional focal/grid laser in one of the sittings. I consider exclusive steroid (intravitreal) only in pseudophakics with resistant or early recurrent edema. Again, I caution the patient regarding need for repeated treatment sessions at the first visit only.
Regarding control of blood sugar at the time of intravitreal injection, I feel anything below 300 if the patient is under regular physician follow up and treatment, should not be a problem in terms of infection. Application of povidone-iodine for sufficient time is the single most important factor in preventing injection related infection. Anything more than 300 in any case or >200 in a patient without any treatment or follow up needs referral to physican first mainly to impress upon the patient the importance of DM control rather than preventing injection related infection.
For those who try to find fault: In all above instances of macular edema, treatment considered only if there is percieved diminution of vision by patient either before or after clinical evaluation!!!
Thanks and Regards
Wow! Thank you! That was a wonderful explanation. I follow nearly the same exact methodology. I have a few queries though:
There were some concerns raised at RetNet regarding role of PRP (I myself do it) in ischemic CRVO as to whether it would worsen the visual fields & hence better to only inject Avastin. Is that an option?
Those who use Avastin as a first line of treatment, (i always do laser) how soon do you see a favorable response? Do you need to re inject? If yes, how soon can you do it? When do you consider laser?
If its a non ischemic BRVO would you still consider a modified grid+sectoral laser?
Does sub tenon steroid carry a significantly lesser risk of IOP rise?
After NV appears, PRP is a must I think. Patients tend to leave the treating clinician when there is no improvement in vision with repeated injections even if counselled enough about purpose of treatment: prevention of painful blind eye. Once lost for follow up, I saw the eventual painful blind eye happening within 6 months only!!
I dont use Avastin as first line treatment. I had to give in 2 babies as first line as there was Zone 1 stage 3 ROP when they were not yet stable in NICU(one dependent on CPAP and other one-low platelet count and repeated apneic episodes). I saw them progressing to normal vascularization at 2 weeks follow up and full vascularization happened in 6 weeks. There was a baby who had aggressive Zone 1 disease with poor dilatation of pupils and NVI across pupil for whom I gave Avastin as first line. I had to do laser after 1 month as the normal vascularization was not progressing. I havent preferred reinjection any case till now. I think Dr. Alay Banker or Dr. Rohan should comment on this
I dont think there is a differentiation of ischemic or non-ischemic BRVO. All cases do show CNP in the involved segment. Only thing is whether there is NV or not. I prefer to do grid+ sectoral laser for recurrent CME (in absence of NV also) once retinal hemorrhages clear. 2 weeks prior to laser, I give Avastin again to reduce CME.
Subtenon steroid doesnt reduce the risk of IOP rise in a susceptible patient. Only advantage is that, there wont be any ACUTE HIGH (>40mmofHg) elevation which we do see with IVTA in steroid responders. We get time to monitor and manage IOP elevation with subtenon steroid. Also, if there has to be response to IVTA or ozurdex, the case responds as well to subtenon steroid.
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