GLAUCOMA
داء الزرقاءLOOK OUT
One of the leading causes of blindness Visual loss is irreversible Early diagnosis and proper management is importantNot A Single Disease
A group of disorders characterized by: A progressive optic neuropathy resulting in a characteristic appearance of the optic disc, and a specific pattern of irreversible visual field defects, that are associated frequently but not invariably with raised IOP. {NTG ; OHT}Classification
Open Angle Glaucoma: A- Primary (POAG) B- Secondary (SOAG) Angle Closure Glaucoma: A- Primary (PACG) B- Secondary (SACG) 3. Congenital & Developmental Glaucoma: A- Primary Congenital Glaucoma B- Developmental Glaucoma (with associated anomalies)Pathogenesis of Glaucomatous Ocular Damage
Retinal ganglion cell death with loss of retinal nerve fibers due to: Raised IOP (mechanical theory) Pressure independent factors (vascular insufficiency theory)Chronic glaucoma: what is happening
Either: the drain blocks here
Or poor blood supply here
Damages the optic nerve..looks ‘caved in’, called ‘cupped’
POAG Chronic Simple Glaucoma
Triad (Criteria of diagnosis) RISK FACTORS: Heredity. Age (5th-7th decade) Race (Black) Myopia. Retinal disease e.g. RP, CRVO DM Hypertension Central corneal thickness
PATHOGENESIS OF IOP RISE
Impaired aqueous flow after the level of the angle e.g. Trabecular sclerosis.CLINICAL FAETURES
SYMPTOMS : ASYMPTOMATIC UNTILL TOO LATE PERIODIC CHECK UP after middle age. Mild headache, eye ache, frequent change of reading glasses, delayed dark adaptation.SIGNS : Raised IOP: Normal value Diurnal variation NTG ,OHT Tonometry: {Digital, Indentation, Applanation, pneumatic tonometer,tonopen}
Normal central corneal thickness: 545 – 550 uAdd or subtract 2.5 mmHg for each 50 u change in central corneal thickness
Glaucoma tonometry (pressure test)
Signs (Cont.)2. Optic disc changes: Cupping ( normally up to 0.4) Large Asymmetry Progressive Vertical Notching Pallor Splinter hemorrhage Nerve fiber layer atrophy Marked cupping, nasal shift of blood vessels and CRA pulsation. Glaucomatous optic atrophy
Glaucoma damage
SIGNS (Cont.)
3. Specific Visual Field Changes:(Perimetry)Initially observed in Bjerrum area (10 – 30 degrees from the fixation point )Small paracentral scotoma.Siedel scotoma (paracentral scotoma join the blind spot to form a sickle shaped scotoma)Arcuate scotoma (Siedel S. extend either above or below the fixation point)Ring (double arcuate) scotoma.SIGNS (Cont.)
5. Roenne central nasal step. Roenne peripheral nasal step. Temporal wedge 8. Tubular vision 9. Temporal island of vision. PERIMETRY HUMPHRY VFA FREDQUENCY DOUBLING PERIMETER SHORT WAVE AUTOMATED PERIMETER (SWAP)GOLDMANN PERIMETER
SIGNS (Cont.)4-. Wide open angle on Gonioscopy. NB. Slit lamp examination to rule out causes of SOAG. Documentation of optic disc changes is very important. Recent tests e.g. Nerve fiber layer analyzer (NFLA) Optical coherence tomography (OCT)
MANAGEMENT
EVALUATION & ASSESSMENT TARGET PRESSURE TEHRAPEUTIC CHOICE MEDICAL ALT or DLT FILTRATION SURGERY MONITORING & FOLLOW UPMEDICAL THERAPY
TERATMENT IS ESSENTIALLY MEDICAL TOPICAL DROPS (ORAL IS UNSUITABLE FOR LONG TERM TREATMENT) SINGLE OR COMBINATION Aim is to lower IOP Decrease aqueous production Increase aqueous drainage.MEDICAL (Cont.)
Topical beta blockers: decrease Aq. production Timolol maleate (0.25, 0.5% BD) Betaxolol (0.25% BD) in asthma. Levobunolol (0.25, 0.5% once daily) Carteolol (1% BD) low effect on lipoprotiens . SE & Contraindications? Pilocarpine (1- -4%, QDS): increase Aq. Outflow Ocular SE ? Systemic SE ? 3) Latanoprost (PG F2alpha analogue 0.005%, once daily) Increase uveoscleral aq. Outflow Expensive
MEDICAL (Cont.)
4) Dorzolamide (2% TDS ,carbonic anhydrase inhibitor), decrease Aq. Production 5) Adrenergic drugs: Epinephrine hydrochloride & Dipivefrine hydrochloride , increase outflow. Brimonidine (0.2%, BD), decrease Aq. production.ALT
Laser shots at the ant. part of TM will lead to stretching of adjacent area of TM Indication Failure of maximal tolerated medical therapy. Non compliance to medical therapy