Glaucomais the second most common cause of blindness and first most common cause ofirreversible blindness. The global prevalence of glaucoma for population aged40-80 yrs is 3.54%. In 2013 the number of people(aged 40-80 yrs) with glaucomaworld wide was estimated to be 64.3 million increasing to 76 million in2020(Glaucoma and projections of glaucoma blindness through 2040, AmericanAcademy of ophthalmology). One in every eight person above the age of fortyyears is either a glaucoma suspect or patient. One in every 3000 new borns is acase of congenital glaucoma.
Glaucomais a progressive optic neuropathy which has multiple risk factors, the increasein IOP being the most common and modifiable one. Many other risk factorsinclude blood supply, postural drop , diurinal variation , ethnic background,family history and older age. In central nervous system , neurons have theircell bodies in the inner retina and axons in the optic nerve. Degeneration ofthese nerves results in cupping, a characteristic appearance of the optic discand visual loss.
Glaucomabroadly can be classified into congenital and adult glaucomas. Congenitalglaucoma is mostly due to the maldevelopment of the angle of the anteriorchamber. Adult glaucomas are broadly classified into open angle and closedangle glaucomas.
Though themajor part of glaucoma patients comprise of open angle but the severity ofvision loss seems to be more disproportionate in acute angle glaucoma.
In openangle glaucoma the drainage channels are normal or subnormal but the level ofIOP increases in the eye which causes pressure and mechanical effects on theeye ball and hence the damage.
In angleclosure glaucoma the drainage channels are affected and are closed. The path toaqueous drainage is obstructed and hence the level of IOP increases and damage starts.
The normalrange of IOP is from 12-21mmhg. Glaucoma may go symptom less for a very longperiod of time and can be detected at very advanced stages.
Various tests
-Intraocularpressure measurement
-Gonioscopy(Atest to see outflow channels of the lens)
-Opticnerve imaging
-PupillaryReflex response
-Refraction
-RetinalExamination
-Slit LampExamination
-VisualAcuity
-VisualField assessment
Treatment
Medical
-BetaBlockers
Thesereduce the aqueous humour production. Examples include levobunolol, timolol,betaxolol and metipranol
-alphaagonists
Thesereduce the production of aqueous humour and increase drainage. Examples includeapraclonidine and brimonidine.
-Prostaglandinslike compounds
Theseincrease the outflow of aqueous humour. Examples include latinoprost,bimatoprost and travoprost.
-Mioticagents
These alsoincrease the outflow of aqueous humour. Examples include pilocarpine andcarbachol.
-Epinephrinecompounds
Thesecompounds such as dipivefrine also increase the outflow of aqueous humour.
-Oralmedications like carbonic anhydrase inhibitor which decrease the production ofaqueous.
Lasers
Nd Yaglaser , selective laser trabeculoplasty(SLT) and argon laser trabeculoplastyare few non surgical less invasive techniques to control intraocular pressure.
Surgery
Trabeculectomy-Surgical procedure to create an alternative fistula for drainage.
Trabeculotomy-procedure used in congenital glaucoma to rupture the schelms canal.
Goniotomy-used in congenital glaucoma to incise the trabecular meshwork.
Drainagedevice shunt surgeries used in complicated glaucomas.
Someadjustments which patients with advancedglaucomas need to adapt are improving other senses like hearing , touch ,protection from sun and low vision aids.
As Iconclude one important thing to my fellow colleagues, half of the glaucoma isyet undiagnosed, diagnosing glaucoma at an early stage will definitely delay oreven halt the progression of the disease. The aim is none of the patientssuffering from glaucoma should go blind.
Dr RayeesAhmad is Assistant Professor , GMC Anantnag