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Walk in Glaucoma Patient in Your OPD : Beyond IOP – Dr. Maneesh Singh

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Walk in #Glaucoma Patient in Your OPD :

You can go ahead thank you so much i like to thank ais office especially dr namrata madam and daughter rajya sinha sir and moderator dr chandma for this honor and opportunity to be part of this program am i audible yes clear thank you so much so my topic is glaucoma beyond intraocular pressure we’ll start with the case report which is related to this topic this is

A 38 year old gentleman who came for us for opinion this patient was already on brimonidine the intraocular pressure was 12 millimeter mercury in both the eyes we went into the record the patient had a baseline pressure of 22 millimeter mercury recorded with a non-contact terminator angles were open on gonoscopy cct was high so with this cct you can see actually

22 was a normal intraocular pressure even as a baseline but the patient has very very advanced field loss both in the right eye and the left eye even though oct was showing changes in the rnfl thickness you see the disc the right at disc is around point seven with some amount of power if you see the left eye it looks to be an advanced coupling but definitely

There is some power in the left eye also what is also important that is this glaucoma a very important point in glaucoma is the disk and the field correlation if you see the disc in this right eye compared to the field when you see a normal transition glaucoma or even a primary opening a glaucoma with the 0.7 or 0.8 cupping you don’t expect such an advanced field

Loss so this is a there is a mismatch in the disk and the field finding also what is important is the presence of parallel so when you have this mismatch whenever you have power you should think of other possible causes for example when we took a history in this patient patient had a history of consumption of country looker and the patient was actually a case of a

Methyl alcohol poisoning so these patients with methanol coil poisoning after few years often present with secondary coping and can mimic glaucoma the reason i shared this case because nowadays because of use of sanitizers and because of the corona pandemic a lot of us are getting cases related to methanol toxicity so in over a period of time we may get cases like

These mimicking as glaucoma also very interesting thing about dr tulissa was also highlighting that we cannot blindly rely on the investigation we see this ocd oct is showing a thinning of the rnfl thinning of the rnfl can occur in traumatic coptic neuropathy it can occur in aiun it can occur in even methanol poisoning just presence of iron fl thinning is not an

Indication of glaucoma a correlation of all the findings is extremely important for glaucoma point of view whenever you see parallel more than cupping or early involvement of vision nomination glaucoma in a young patient or field which are obeying the vertical meridian you should always think beyond glaucoma try to look for other possible causes now coming back to

The glockma beyond interocular pressure this is the patient who i’ve been following up for years this is a 72 year old one-eyed gentleman known hypertensive he lost his left eye due to crvo right there had a six 9 and 6 vision at the time of presentation the patient had advanced normal tension glaucoma you can see the disc finding extremely advanced cupping left

Eye was hazy because of old victim the maximum pressure which was ever recorded for this patient was 12 to 16 millimeter mercury the cct was normal angles were open on gonioscopy but if you see the fields extremely advanced field loss which also matching with the advanced cupping which you are having and the patient i’ve been following for almost five years you

Can see from 2014 till 2018 the patient is on prostaglandin analog this is the patient with nomination glochma where the drug of choice is always a prostaglandin and this patient over the last five years have maintained a very good intraocular pressure at times the pressure is in single digit pressure has never gone beyond 10 or 11 millimeter mercury we have even

Done a 24 hour diurnal and then also we couldn’t find any iop spike but the disease continues to progress you can see the tendency also the patient is continuing progressing over last five years so whenever you have these patients where there is a progression even on well-controlled iop you should think that maybe there are certain non-ipv factors which might be

Coming into action in these patients this type of patient there are few investigations which are required first we should take a proper history of steroids a lot of time these patients are using oral steroids for certain systemic problems sometimes they’re using even steroid ointment occupation is important maybe the patient is a trumpet player or he plays chunk

Or does a certain exercise related to well salva maneuver gonoscopy again is very important especially in fakie guys you should recheck the gonoscopy whether you have missed any uh subtle angle closure also if all these things are fine you should go for a detailed systemic evaluation because we know ischemic factor is an important factor in glaucoma so clarity

Devaluation a cardiac evaluation a blood lipid profile blood sugar even if require you can do a neuroimaging to make sure you are not missing any other neurological problem which might be causing this progressive optic neuropathy 24-hour blood pressure measurement to look for any nocturnal dip of blood pressure is also important also look for sleep apnea you can

Take an opinion of a palmologist try to look for sleep apnea sleep apnea can lead to raise while salva and can lead to progression of glaucoma so detailed workup is extremely crucial for these patients because a lot of time we see over time these patients keep continuing to progress but what is the next option sometime in spite of all the investigation you may

Not be able to pinpoint any particular cause sometimes we believe maybe it’s just the age rate of change but you need to treat these patients so in these patients in the patient is already on prostaglandin if you want to add a adjunct the common options we have is either the beta blockers or carbonic analysis inhibitors or the brimonity trabecular tommy i will

Not keep as an option in this case because the patient is already on one medication and the pressures are again well controlled with one medication and we have other options to be added beta blocker will not be a very good option because beta blocker we all know has an effect on the optic nerve perfusion and since the pressure control is not important here so beta

Blocker may not be very good adjunct for these cases carbonic inade is inhibited for its supposed role in ocular blood flow and brimonidine for its hypothetical role in neuro protection may be a better option in this case compared to a beta blocker this brings us to the important topic of discussion today is that glockman management beyond iop we all know that

It takes 40 to 50 percent of the retinal ganglion cells to die before we can see any visible changes on the perimetry and intraocular pressure is the most important or rather the only way to control progression in our clockwork patient but even the landmark tyres like the ocular hypertension treatment study the emgt and the cngta they have shown that in spite of

Reaching the target intraocular pressure there is a group of patient which continues to progress and all these things have been highlighted in this trial so although the patient has reached the target which we have designed but the progression has not stopped so reaching target intraocular pressure will not completely stop progression so there the concept comes

If you can have a control of intraocular pressure plus in some way we can increase the retinal ganglia cell survival maybe by enhancing or improving the retinal sensitivity through neuroprotection or by improving the retinal vascularity by affecting the blood flow we may give a better treatment to our patient compared to just controlling the intraocular pressure

Now we just quickly touch the vascular factors in glaucoma we all know about the perfusion pressure perfusion pressure or the ocular blood flow is dependent on the mean arterial blood pressure and the intraocular pressure by the rest of the resistance now vascularis is something which we cannot modify it depends on the vascularity of the patient depends on arterial

Sclerosis diabetic status hypertension so this is more dependent on the systemic factors but mean arterial blood pressure is diastolic plus one third systolic minus diastolic blood pressure so let us see how ocular perfusion is affected so suppose your blood pressure is higher sorry the blood pressure is lower and the iop is higher your ocular blood flow will

Actually go down so what happens at night and again this what happens you know we all know that at night iop tends to be higher because the patient is supine and there is rays at this venous pressure so iop tends to be higher a lot of our patients do have a nocturnal deep of blood pressure so at night the bp tends to go down so if you go by this equation your

Perfusion pressure actually goes down at night so we can say that although the patient is sleeping at night the doctor is sleeping at night the disease is not sleeping so glaucoma progression probably occurs more at night than what it occurs during daytime and this is a reason why we always highlight that you should be using anti-glock or medication which give you

A 24-hour iop control and not only a daytime atp control so drugs like prostaglandin even carbonic energy inhibitor which give you a 24-hour iop control are better options in patients with normal tension glaucoma coming to ocular blood flow just for summary the one of the problem with ocular blood flow is that till now we don’t have a proper tool to measure ocular

Blood flow and we don’t know what is the ideal way and what ideal thing to be measured whether we should be checking the central arterial flow whether we should be checking the posterior arteries or the ophthalmic artery and none of the tool which have have a good predictability so this is a high inter and inter observable variability plus even when we measure the

Ocular blood flow how much impact it will create on our clinical decision is again difficult to quantify but personally i have seen in case patients with normal tension glaucoma glock you’re seeing disc changes like there are disc hemorrhages these patients you can assume that there is an issuing factor playing and these cases using a carbonic and as inhibitor as

Adjunct to prostaglandin can be a better option coming to neuro protection again not totally established in human is also on hypothesis but coming to neural partition you know if you see the what happens in the retinal ganglion cell injury there are multiple factors which lead to retinal ganglion cell death for example the intraocular pressure the ischemia genetic

Factors traffic support failure but when we are treating we are treating only the iop because rest of the factors is not totally our under our control so in some way if we can achieve target ifp plus protect the target cell the point which i was highlighting by enhancing the sensitivity of retinal ganglion cell less we can probably give a better treatment to our

Patient there are many studies on animals but this is probably the best study on neural protection what we have in humans and this is also an indirect evidence the lodges trial that is the low pressure glochma treatment study and this is what they have done they have class divided the low pressure glock my patient or normal tension patient into two groups one

Group which received brimonity in point two percent and other group received timolol and they followed up these patients for four years and what they found that over four year period the intraocular pressure was same in both the groups as expected because both brimonidine and timinolol will give you around 20 to 25 percent of iip reduction so the iop reduction was

Similar in both the groups but the progression was more in the timolol group compared to primordine group they thought that hypothesized that maybe because of the neuroprotective effect of brimonity in the progression was less in the brimoniting group compared to stimulal group or maybe because of the detrimental effect of timolol on the optic nerve perfusion the

Progression was more intimidable compared to bemoaning group so in that way they concluded that if you have a patient with low pressure glaucoma a brimonine or alpha agonist provided the door patient develop allergy will cause less visual field progression than a patient who is on timor against the indirect evidence and there were some dropouts in the brim group

Because of the allergy to conclude cochrane everybody has done a analysis on neural protection in patients with glaucoma and adults and they found that their last studies for example the logic style but till now the data is inconclusive whether we can use the monitoring purely for its neuroprotective action we still use mainly for his eye production so neuroprotein

Bermudin is sort of like hydroxychloroquine in corona a lot of us are using but probably we don’t have enough evidence to support it and another important factor i’ll highlight before i share in my presentation related to intraocular pressure you know we always think about controlling iop but we have to understand that non-complex is a very important factor in

Our population so that factor also has to be looked into whenever we are treating your patient because drugs won’t work in patients who don’t take them so always try to give a simple regime for the patients to follow always try to educate your patient every time the patient is coming also try to involve the family members in the treatment process i just give you

One example if you have a patient who is on a beta blocker with alpha agonist and a prostaglandin and you switch to a combination with the prostaglandin instead of using six drops you can make it three drops and instead of using three bottles you can make it two bottles so definitely you will make life more easy for your patients especially use the medicine more

Frequently the cost will go down the preservative will go down and these factors are equally important than thus prescribing medicine and controlling drug depression i just like to conclude saying that iup reduction is the mainstream glochma treatment but if you have a patient who is progressing in spite of well-controlled pressure try to look into other factors

The systemic factors try to look into the compliance and when using as adjunct to prosthetic learning in a normal tester glaucoma or low tension glaucoma a carbonic analysis inhibitor or alpha agonist might be a better option than a beta blocker thank you so much thank you very much

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Walk in Glaucoma Patient in Your OPD : Beyond IOP – Dr. Maneesh Singh By AIOS HQ