Optom
Cataract is a condition of the crystalline lens that renders it opaque. Opaqueness of the crystalline lens is subjectively interpreted as loss of visual acuity or functional vision loss measurable by missing of letters on the visual acuity chart. The aim of treating cataract disease non-surgically, as I discussed in the previous part of this blog, was to reduce or remove or manage deterioration of vision in early cataract disease. When neither drugs or glasses are no longer helpful in managing vision deterioration secondary to cataract disease, cataract surgery becomes the final management option. There is almost a total (100%) recovery of visual functions in a 'normal' eye after undergoing a cataract extraction surgery. The surgical options like the Extra-capsular cataract extraction (ECCE) or Intra-capsular cataract extraction (ICCE) or the more recent small incision cataract surgery (SICs) or the Phaco-emulsification cataract surgery methods are available to the cataract surgeon.
Before the Nigerian Optometrists refer patients for surgery, its very important to pay attention to the following:
1) The patient's vision has reduced to @least 6/24 & becomes incapable of functioning normally for activities of daily living.
2) The patient is at risk of inducing diseases like glaucoma as a result of the cataract.
3) The patient has only one functional eye and @ the same time the eye is cataractous.
4) The patient has a comobid condition like a retinopathy and cataract in, say, diabetes. or
5) The patient is in 'good' health condition. (People with Diabetes, Hypertension, Cardiac arrest etc are very risky to perform the cataract surgery, unless when they are in very stable conditions as ascertained by their general physician).
6) The patient must be willing to do the surgery.
7) Who is the performing Ophthalmologist?
8) What drugs are the individual on e.g. Anticoagulants, anti-platelets, systemic alpha-1a antagonists, ophthalmic and systemic steroids etc?
9) Did you discuss the likely outcomes of the surgery with the patient?
It should be known that the knowledge of the performing surgeon by the refering Optometrists build confidence in the patient and in the refering Optometrist. Its the ethical goal of the Nigerian Optometrist to restore eye sight of its patients including making the proper refferal for ocular surgery procedures.
We are therefore calling on the Nigerian Ophthalmologists to give us informations on how to access their colleagues & let them come together with Optometric representatives to discuss bilaterally with the aim of finding a common ground in cataract surgery management & in post-surgical management of this crystalline lens disease. If such relationship is officially established cataract surgery rate will rise...so too will reduced post-cataract complications!
The role of Nigerian Optometrist in eyecare service provision is indisputable; same too can be said of the high prevalence of cataract in Nigeria & in the world. If there could be a flexible relationship between the Ophthalmologists and the Optometrist as it affects management of cataract patients. We all have a stake in this. Post surgical prognosis is partly dependent on surgical procedure, patients general health condition, how 'good' the surgery was; & partly on co-management by an Optometrist.
Note that after seven(7) days post cataract extraction surgery the chances of developing endophthalmitis reduces exponentially. A stable refraction on a post cataract eye is partly dependent on prognosis following cataract extraction & partly dependent on time, in 3 weeks to 4 weeks after surgery refraction is usually stable. Management of comorbid conditions are managed appropiately after surgery wound has healed. Children less than 5 years are very difficult to implant IOLs, even if it becomes implanted, they still need to wear bifocals since IOL do not induce accomodation. Slit Lamp is very important during post cataract surgical care. Always ensure that IOP is measured in an eye following catarct surgery. Comorbid conditions like amblyopia, maculopathies, Retinopathies, Glaucomas, Uveitis etc should be managed after cataract extraction. 80-90 % of normal cataract eyes that undergo surgery have successful prognosis.
That said, Optometrists managing post cataract surgery patients should look out for:
a) Conjunctival hyperemia, subconjunctival injection, cilliary injections around the limbus.
b) Profuse discharge exceeding 7 days after surgery.
c) Continous ocular hypotension or persistant ocular hypertension.
d) Uveitis or Keratitis or Episcleritis or scleritis.
e) Associated photophobia exceeding 3 weeks to 1 month following surgery.
f) Chronic Epiphora following surgery.
g) Itching in the eye.
h) Visual acuity improvement following surgery.
i) Bleb healing.
j) Any complaint from the patient leading to reduced functional vision.
Finally, there are about 17 million persons with cataracts and unless a very good working relationship is built amongs the eye care experts (The Ophthalmologists & the Optometrists) we might not be able to reduce or eliminate the epidemic of functional blindness this disease would cause in the coming years! Shadow boxing is a mere waste of valuable time. Every day someone somewhere becomes blind. We might lose the fight if we do nothing. We can still plant a tree now, though we would have had a tree today if we had planted it 20 years ago! We still can.
Concluded...
Dr Ezebuiroh Okwudiri Victor.
optometry is discussed here, eye diseases and disabilities are highlighted and management of such ocular conditions enumerated.
Saturday, 4 February 2012
Sunday, 29 January 2012
Can cerebrospinal fluid pressure influence optic nerve head neuropathy in glaucoma?2
Optom
In my last blog on this topic, I presented cerebrospinal fluid pressure as a factor of Normal Tension Glaucoma. This could explain the reason behind the seemingly 'low' to 'normal' IOP is this group of Open angle glaucoma types. But does it totally explain the optic nerve head neuropathy?
Optic nerve head neuropathy is a function of optic nerve fibre deaths otherwise known as optic nerve fibre apoptosis. What is responsible for optic nerve fibre apoptosis in NTG? It is true that the translaminar pressure gradient on the lamina cribosa skews it posteriorly, distorting it & oftentimes disrupting its normal physiological function. It could be theorized that @ this point the optic nerve fibres start degenerating, dying off & replaced by the neuropathy @ the disk head! Two types of gene mutations is said to be associated with glaucomatous optic nerve head neuropathy- Optoneurin mutation on gene OPTN & Myocilin/trabecular meshwork glucocorticoid inducible response mutation.
Optoneurin is a coiled protein that was first identified for its anti-apoptotic activity against a genetic strain of adenovirus protein (E3-14.7K). Tumour necrosis factor alpha (TNF-alpha) stimulates the activities of Optoneurin. Optoneurin protein plays a neuro-protective role in the eyes where it is found in the retina, the non-pigmentent cilliary epithelium, the optic nerve head, the lamina cribosa and in the trabecular meshwork. It is also known for its ability to interact with tranferrin via the transferrin receptors which influences the axiomatic flow of optic nerve fibres. Over-espression of optoneurin can induce the formation of a mutant type of optoneurin that has been shown to cause retinal ganglion cell apoptosis, the E50K.
E50K mutant is a variant of Optoneurin protein that is known to stimulate cell apoptosis using Tumour Necrosis Factor alpha (TNF-alpha) as a catalyst, just like in the normal optoneurin response. Hence instead of performing its intended anti-apoptotic function, E50K has been found to stimulate retinal ganglion cell degeneration in the retina & in the optic nerve head consistant with glaucomatous optic nerve neuropathy. Again, the secretion of TNF-alpha in the retinal area is achieved over-time by stimulated ischaemia of the optic nerve vessels & elevated hydrostatic (a.k.a. translaminar) pressure in return this causes the cellular 'insult' that will produce more mutant Optoneurin in a viscious cycle of retinal ganglion cell deaths beginning from the periphery to the optic nerve head. Also the mutant E50K often interferes with the 'normal' interaction of the Optoneurin with tranferrin which influences axiomatic flow in the optic nerve fibres. E50K "dumps" the tranferrin which consequently alters axiomatic flow & hence apoptosis of nerve cell fibres if the altered axiomatic flow is not 'repaired'. About 17% cases of Normal Tension Glaucoma (NTG) patients are reported to show increased presence of mutant Optoneurin, E50K.
Myocilin, Trabecular meshwork inducible glucocorticiod response (TIGR), is a protein which in human is encoded by the MYOC gene. The MYOC gene is known to have a signal sequence, albeit not functional, that directs proteins to the peroxisomes degradation. The actual function of Myocilin protein in the trabecular meshwork, in the retina, in the optic nerve head, in the lamina cribosa, in the cornea.. in almost all structures in of eye, is unknown. But it has been found to abound in about 36% of children suffering from Juvenile onset open angle glaucoma shows over-expression of MYOC/TIGR mutant gene. 4.6% of those with adult onset open angle glaucoma, with or without high IOP, had shown increased expression of the mutant MYOC. This mutant MYOC/TIGR is theorized to use its functional signaling sequence (in normal MYOC gene the signal sequence is not functional) to direct degradation of cell protein & hence subsequently cell degradation in the lamina cribosa & in the optic nerve fibres. Mutant MYOC/TIGR to cause neuropathy by cell protein degradation via peroxisome pathway.
Ishaemia of the optic nerve blood vessels, translaminar pressure of the eye, hereditory, prolonged use of topical dexmethasones, traumatic insults, inflamation of the optic nerve head etc are likely triggers that can cause mutations of both Optoneurin protein & the myocilin protein which are shown to be precursors to glaucomatous changes in the optic nerve head. I therefore agree that optic nerve head neuropathy in NTG is a physiological issue that manifests anatomically even in the absence of high intra-ocular pressure.
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Note: There is no financial interest in this publication. thanks.
In my last blog on this topic, I presented cerebrospinal fluid pressure as a factor of Normal Tension Glaucoma. This could explain the reason behind the seemingly 'low' to 'normal' IOP is this group of Open angle glaucoma types. But does it totally explain the optic nerve head neuropathy?
Optic nerve head neuropathy is a function of optic nerve fibre deaths otherwise known as optic nerve fibre apoptosis. What is responsible for optic nerve fibre apoptosis in NTG? It is true that the translaminar pressure gradient on the lamina cribosa skews it posteriorly, distorting it & oftentimes disrupting its normal physiological function. It could be theorized that @ this point the optic nerve fibres start degenerating, dying off & replaced by the neuropathy @ the disk head! Two types of gene mutations is said to be associated with glaucomatous optic nerve head neuropathy- Optoneurin mutation on gene OPTN & Myocilin/trabecular meshwork glucocorticoid inducible response mutation.
Optoneurin is a coiled protein that was first identified for its anti-apoptotic activity against a genetic strain of adenovirus protein (E3-14.7K). Tumour necrosis factor alpha (TNF-alpha) stimulates the activities of Optoneurin. Optoneurin protein plays a neuro-protective role in the eyes where it is found in the retina, the non-pigmentent cilliary epithelium, the optic nerve head, the lamina cribosa and in the trabecular meshwork. It is also known for its ability to interact with tranferrin via the transferrin receptors which influences the axiomatic flow of optic nerve fibres. Over-espression of optoneurin can induce the formation of a mutant type of optoneurin that has been shown to cause retinal ganglion cell apoptosis, the E50K.
E50K mutant is a variant of Optoneurin protein that is known to stimulate cell apoptosis using Tumour Necrosis Factor alpha (TNF-alpha) as a catalyst, just like in the normal optoneurin response. Hence instead of performing its intended anti-apoptotic function, E50K has been found to stimulate retinal ganglion cell degeneration in the retina & in the optic nerve head consistant with glaucomatous optic nerve neuropathy. Again, the secretion of TNF-alpha in the retinal area is achieved over-time by stimulated ischaemia of the optic nerve vessels & elevated hydrostatic (a.k.a. translaminar) pressure in return this causes the cellular 'insult' that will produce more mutant Optoneurin in a viscious cycle of retinal ganglion cell deaths beginning from the periphery to the optic nerve head. Also the mutant E50K often interferes with the 'normal' interaction of the Optoneurin with tranferrin which influences axiomatic flow in the optic nerve fibres. E50K "dumps" the tranferrin which consequently alters axiomatic flow & hence apoptosis of nerve cell fibres if the altered axiomatic flow is not 'repaired'. About 17% cases of Normal Tension Glaucoma (NTG) patients are reported to show increased presence of mutant Optoneurin, E50K.
Myocilin, Trabecular meshwork inducible glucocorticiod response (TIGR), is a protein which in human is encoded by the MYOC gene. The MYOC gene is known to have a signal sequence, albeit not functional, that directs proteins to the peroxisomes degradation. The actual function of Myocilin protein in the trabecular meshwork, in the retina, in the optic nerve head, in the lamina cribosa, in the cornea.. in almost all structures in of eye, is unknown. But it has been found to abound in about 36% of children suffering from Juvenile onset open angle glaucoma shows over-expression of MYOC/TIGR mutant gene. 4.6% of those with adult onset open angle glaucoma, with or without high IOP, had shown increased expression of the mutant MYOC. This mutant MYOC/TIGR is theorized to use its functional signaling sequence (in normal MYOC gene the signal sequence is not functional) to direct degradation of cell protein & hence subsequently cell degradation in the lamina cribosa & in the optic nerve fibres. Mutant MYOC/TIGR to cause neuropathy by cell protein degradation via peroxisome pathway.
Ishaemia of the optic nerve blood vessels, translaminar pressure of the eye, hereditory, prolonged use of topical dexmethasones, traumatic insults, inflamation of the optic nerve head etc are likely triggers that can cause mutations of both Optoneurin protein & the myocilin protein which are shown to be precursors to glaucomatous changes in the optic nerve head. I therefore agree that optic nerve head neuropathy in NTG is a physiological issue that manifests anatomically even in the absence of high intra-ocular pressure.
Thanks,
Dr Ezebuiroh Victor Okwudiri.
Note: There is no financial interest in this publication. thanks.
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