Primary open angle glaucoma

This presentation describes all clinical aspects about primary open angle glaucoma ......
you can watch the illustrated video presentation at the following link : https://youtu.be/eA44Pu4l8Ow

1. Primary open-angle glaucoma By Dr. Amr Mounir Lecturer of Ophthalmology Sohag University

2. Background - Glaucoma is a group of irreversible, progressive optic neuropathies that can lead to severe visual field loss and blindness . - May be primary or secondary

3. Background In primary glaucoma , the elevation of IOP is not associated with any other ocular disorder In secondary glaucoma a recognizable ocular or non-ocular disorder alters aqueous outflow which, in turn, results in elevation of IOP.

4. Definition Also referred to as chronic simple glaucoma , is a generally bilateral, but not always symmetrical disease, characterized by: 1- Adult onset. 2- An IOP > 20 mmHg. 3- An open angle of normal appearance. 4- Glaucomatous optic nerve head damage. 5- Visual Field loss .

5. Incidence - The commonest type of glaucoma. - Population: Affecting 1% of the general population > 40 years. - Sex: It affects both sexes equally. - Age: most cases > 65 years. It is unusual < 40 years. - Race: more common, develops earlier, and is more severe, in black people. - Laterality: Bilateral (usually one eye before the other).

6. Risk factors and associations: 1) Family history and inheritance: POAG is frequently inherited. 2 ) Myopia: is associated with an increased incidence of POAG. 3 ) Retinal disease: - Central retinal vein occlusion. - Retinitis pigmentosa .

7. Symptoms 1) Early : Asymptomatic 2) Late : Significant loss of visual field occurs gradually. 3) Bilaterality : Patients therefore frequently present with significant visual field loss in one eye and less advanced disease in the other.

8. Signs A) IOP: 1) Raised IOP: IOPs > 20 mmHg. 2 ) Diurnal fluctuations: Diurnal fluctuations up to 5 mmHg - In POAG: this fluctuation is exaggerated . 3) Asymmetry of the IOP between the two eyes If 5 mmHg or more, should arouse suspicion

9. Signs B) Optic disc changes: 1) Baring of the curve linear blood vessels 2) Optic disc hemorrhage (Splinter or flame shaped). 3) Nasalization of central blood vessels. 4) Enlargement of the physiological cup. 5) Asymmetry cup / disc ratio between both eyes.

10. Signs 6) Specific glaucomatous cupping: - Narrow opening. - Size: large. - Depth: very deep. - Edges: overhanging. - Increase cup/disc ratio (normal = 0.3). - In advanced cases lamina cribrosa can be seen.

11. Signs C) Visual fields ( Perimetry ): Central changes 1) Paracentral scotomata : Are isolated scotomata which later becomes connected with the blind spot to form the arcuate scotoma . 2) Baring of the blind spot: Is exclusion of the blind spot from the central field (due to localized contraction of the temporal edge of the central field)

12. Signs C) Visual fields ( Perimetry ): Central changes 3) Siedel scotoma : Is a tapering wing like elongation of the upper and/or lower pole of the blind spot. 4) Bjerrum ( arcuate ) scotoma : Upper and/or lower bundle defect around and joining the blind spot and is concentric with the fixation point . 5) Annular scotoma : By fusion of the 2 (upper and lower) Bjerrum scotomata in the nasal field .

13. Signs C) Visual fields ( Perimetry ): Peripheral changes 1) Nasal field contraction: Occurs earlier than the temporal field because the temporal retinal fibres are more dense and so suffer more. 2) Roenne's nasal step: Is a sectorial nasal field defect (upper or lower) with a sharply horizontal edge. 3) Concentric contraction. 4) Tubular vision.

14. Humphrey visual field machine

15. Signs D) Gonioscopy : Shows a normal open angle

16. Target pressure : It is an IOP level below which further damage is unlikely. Therapy should maintain the IOP at or below the target level . Monitoring is performed of the optic nerve and visual fields. In the event of further damage the target IOP is reset at a lower level. - The primary aim of treatment is to prevent functional impairment of vision within the patient's lifetime by slowing the rate of ganglion cell . - Method of achieving this goal is by lowering of IOP. Aim

17. 1 ) Medical. 2 ) Laser. 3 ) Surgical . Lines of treatment:

18. Basic principles 1) Any chosen drug should be used in its lowest concentration. 2) Initial treatment is usually with one drug. 3) Follow-up 1) Medical therapy

19. 1) B-blockers 2) Alpha-2 Agonist 3) Prostaglandin analogues 4) Topical Carbonic anhydrase inhibitors 5) Systemic Carbonic anhydrase inhibitors 6) Hyperosmotic agents Antiglaucoma Drugs

20. Laser trabeculoplasty : In this procedure discrete argon or diode laser burns are applied to the trabeculum to enhance aqueous outflow and lower IOP. - Often transient effect , lasting a few years, so that laser therapy may delay the need for filtration surgery. 2) Laser treatment

21. Trabeculectomy This involves the surgical creation of a fistula between the angle of the anterior chamber and the sub- Tenon space, which allows passage of aqueous from the anterior chamber into a 'drainage bleb' under the upper eyelid Indications: 1) Failed medical therapy and/or laser trabeculoplasty. 2) Advanced disease requiring a very low target pressure. 3) Surgical treatment:

22. The Simoom 1878  ·  · · Ludwig Hans Fischer (1848-1915 ) Austrian Thank you