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Glaucoma. Group of diseases characterized by increased intraocular pressure resulting in damage to the optic nerve and retinal nerve fibers.
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Glaucoma Group of diseases characterized by increased intraocular pressure resulting in damage to the optic nerve and retinal nerve fibers
It is a combination of ocular conditions that result in damage to the optic nerve head and a loss of the visual field. Most forms of glaucoma follow the classic triad of (1) increased intraocular pressure, (2) optic nerve damage, and (3) a loss of side vision.
It is a symptomatic condition of the eye in which the I.O.P. exceeds the tolerance the affected eye resulting in visual dysfunction
Rise in intraocular pressure(IOP) • Determined by: 1.An increase in formation of the aqueous 2.A decrease in the drainage of the aqueous
Decreased drainage Plays: • Improper development of the angle of A.C. • Narrow configuration of the angle of A.C. • Obstruction of the trabecular mesh work (particulate material) • Peripheral anterior synechiae • Plasmoid aqueous • Pupil block (lens/seclusio pupillae)
Classification of Glaucoma A. Primary Glaucomas B.Secondary Glaucomas
Primary Glaucomas 1.Primary congenital glaucomas • Early onset congenital glaucoma(Buphthalmos) • Late onset congenital glaucoma (Infantile) • Glaucoma associated with congenital anomalies
2.Primary open angle glaucoma(POAG) a. Primary open angle glaucoma (High pressure) b.Primary open angle glaucoma (Low pressure or Normal pressure) 3.Primary angle closure glaucoma(POAG) B.Secondary Glaucomas
Primary open glaucoma(POAG) • Previously known as Chronic simple glaucoma • Defined as Chronic progressive neuropathy resulting - (Cupping of the disc) • Visual field defects • Associated with elevated IOP
Pathophysiology • Interference of outflow • May be due to degenerative changes in: • Trabecular • Schlemm’s canal • Exit channels
Fig. 3.11: Aqueous humor (green) drains through the trabecular meshwork into Schlemm's canal. • Increase outflow resistant in trabecular meshwork or in Schlemm canal
POAG:Presentations • More common than angle closure • Age 40yrs and > Much more common • Male more affected ? • Familial tendency More • Associated with diabetes 3 time more • Preferentially in subjects of Vascular sclerosis • Increased prevalence in High myopia
B/L symptom free chronic condition • Slow progressive course • Mild pain in eye/periorbital region • Frequent change of glass • Insidious onset (unnoticed till serious field impairment) • Slow and silent killer of the vision (Known as Chronic Simple Glaucoma)
Suggestions • Eye examinations: - Before Admission at primary school - Thorough if possible twice in year - If impossible Once in a year • Detail examination advised to begin Presbyopic glass • Screening camps in school or Target Population
Intra Ocular Pressure(IOP) • Great variation in open angle glaucoma • Careful tonometry is essential • Exaggeration of the normal diurnal variation • Mean of 3.7 mm of Hg • Biphasic rise in some patients may occur. • Asymmetric C.D.R.> 0.2 • Nasal displacement of blood vessels
Cupping of the disc • Physiological cupping • Pathological cupping • Cup Disc Ratio
Visual field defect • Must be determined - Central field • Peripheral field 1.Small Central/Para central Scotomas (2 to 4 degree) • Relative / Absolute
2.Sickle extension of blind spot (above/below) - Seidel’s Sign - Bjerrum’s scotoma -Roenne’s nasal step - Tubular vision small central/Para central visual field (visual acuity may or may not be affected) Generalized constriction of the peripheral field is considered as early glaucoma Peripheral field may be generalized constriction
Primary Normal Tension/Low tension Glaucoma • Ocular Hypertension
Diagnosis of POAG • Early detection(funduscopy) • Observation/follow-up • Recording of IOP different methods • CDR evaluation • Photography of the disc • Visual field central/peripheral recording and Comparing
Normal or low tension glaucoma • Glaucoma is usually high pressure inside the eye that damages the optic nerve and can result in permanent vision loss. • Normal-tension glaucoma (also called low-tension glaucoma) is a unique condition in which optic nerve damage and vision loss have occurred despite a normal pressure inside the eye.
NTG/LTG • Normal tension glaucoma (NTG), also known as low tension or normal pressure glaucoma • is a form of glaucoma in which damage occurs to the optic nerve without eye pressure exceeding the normal range. • In general, a “normal” pressure range is between 10-20 mm Hg.
Glaucoma is generally associated with high pressure in the eyes • But many cases of glaucoma occur in the absence of high pressure readings during exams.
Ocular hypertension • Ocular hypertension is an elevation of the pressure in the eye above the range considered normal with no detectable changes in vision or damage to the structures of the eyes.
Management of POAG • Reduce IOP to the level: -Doesn’t cause damage to optic nerve/fibers of the nerve -Judged by stabilizing visual field -Unchanged appearance of optic disc Visual field defect progressing after normalization of IOP Indications: • Medical +Surgical • Combination
Management • Medical Treatment • Laser treatment • Surgical treatment
1.Medical treatment Cholinergic Drugs(Parasympathomimetics effect • Pilocarpine • Carbachol • Binding cholinesterase (Anticholinesterase action) - Resulting constriction of pupil(miosis) - Contraction of ciliary muscles - Opening Trabecular meshwork - Facilitates the aqueous outflow
Adrenergic Antagonist or Beta-Blockers • Nonselective Beta1 and Beta 2agents: -Timolol maleate: Reduces IOP lowering the rate of aqueous production May result Broncho spasm and Vascular Hypotension • Selective Beta blocker (B1Blocker)
Carbonic anhydrase inhibitor • Acetazolamide Reduces IOP by decreasing: • The carbonic anhydrase depend aqueous production • Decreases the availability of Bicarbonate 2. Laser Trabeculoplasty(LT) -Argon laser or Diode laser Trabeculoplasty to control IOP -Alternative of filtration surgery 3.Trabeculectomy 4.Trabeculotomy