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Glaucoma

Short review of glaucoma

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Glaucoma

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  1. Glaucoma Presented by Amlan Chakma B.Optometry, 5th semester Assam down town University

  2. Content • Glaucoma: an overview • Congenital/Developmental glaucoma • POAG • PACG • Secondary glaucomas

  3. Glaucoma • Definition:- Glaucoma is not a single disease but 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 • Classification • Congenital/developmental glaucomas • Primary congenital glaucoma without associated anomalies • Developmental glaucoma with associated anomalies • B. Primary adult glaucomas • Primary open angle glaucoma • Primary Angle closure Glaucoma • Primary mixed mechanism glaucoma • C. Secondary glaucomas

  4. Pathogenesis of glaucomatous ocular damage As mentioned in definition, all glaucomas are characterized by a progressive optic neuropathy. It has now been recognized that progressive optic neuropathy results from the death of retinal ganglion cells in a typical pattern which results in characteristic optic disc appearance and specific visual field defects RGCs death is initiated when some pathological event blocks the transport of growth factors ( neurotrophins ) from brain to the RGCs. The blockage oh these neurotrophins causes RGCs losing their ability to maintain normal function results undergo apoptosis and also trigger apoptosis of adjacent cells

  5. Congenital glaucoma Definition:- The congenital glaucomatous are a group of diverse disorders in which abnormal high IOP results due to developmental abnormalities of the angle of anterior chamber obstructing the drainage of aqueous humour Types • Primary developmental/congenital glaucoma • Developmental glaucoma with associated congenital ocular anomalies • Developmental glaucoma with associated systemic anomalies

  6. Primary congenital/Developmental glaucoma • It refers to abnormal high IOP which results due to developmental anomaly of the angle of the anterior chamber, not associated with any other ocular or systemic anomaly • Depending upon the age of onset the developmental glaucomas are termed as follows:- 1. Newborn glaucoma 2. Infantile glaucoma 3. Juvenile glaucoma

  7. Newborn glaucoma • It is also known as True glaucoma • It is labelled when IOP is raised during intrauterine life and child is born with ocular enlargement • It accounts for about 40% of cases • 2. Infantile glaucoma • It is labelled when the disease manifests prior to the child’s third birthday • It accounts for about 55% of cases • 3. Juvenile cataract • It is labelled when disease manifest after 3 years and before adulthood • It accounts for 5% of cases

  8. Pathogenesis • Iridotrabecular junction ( Trabeculodysgenesis) is responsible for impaired aqueous outflow resulting in raised IOP • Clinical features • Lacrimation, photophobia, blepharospasm • Enlarge eyeball • Enlarge cornea • Sclera becomes thin and appears blue due to underlying uveal tissue • AC becomes deep • Lens becomes flat due to stretching of zonules • Raised IOP • Axial myopia

  9. Examination • Measurement of IOP • Measurement of corneal diameter • Slit lamp examination • Ophthalmoscopy • Gonioscopy examination reveals trabeculodysgenesis with either flat or • concave iris insertion • Treatment • Medical treatment • 2. Goniotomy • 3. Trabeculotomy • 4. Trabeculectomy

  10. Primary open angle glaucoma • POAG is a commonly bilateral disease of adult onset. • It is characterized by: :- IOP>21 mmHg at some stages :- Glaucomatous optic nerve damage :- Characteristic visual field loss as damage progress :- An open anterior chamber angle :- Absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic neuropathy

  11. Risk factors • IOP • Age • Race • Family history of POAG • DM • Myopia • Optic disc area • CCT • Corticosteroid responsiveness

  12. Pathogenesis of rise of IOP • Recently it has been proposed that reduced aqueous outflow facility occurs due to failure of aqueous outflow pump mechanism owing to trabecular meshwork stiffening and apposition of schlemm’s canal wall. Such changes are caused by :- Thickening and sclerosis of TM with faulty collagen tissue :- Narrowing of intertrabecular spaces

  13. Pathogenesis of optic neuropathy • It has now been recognized that progressive optic neuropathy results from the death of RCGs in a typical pattern which results in characteristic optic disc appearance and special visual field defects. • RCGs death is initiated when some pathologic event blocks the transport of growth factors(neutrophins ) from brain to RGCs. The blockage of these neutrophins cause the RGCs lose their ability to maintain their normal function undergo apoptosis and also trigger apoptosis of adjacent cells.

  14. Symptoms • Asymptomatic • Headache and eye ache • Scotoma may be noticed occasionally by some observant patients • Difficulty in reading and close work • Delayed dark adaptation • Significant loss of vision and blindness is the end result of untreated cases of POAG

  15. Signs • IOP :- A variation in IOP of over 5 mmHg (Schiotz) is suspicious and over 8 mmHg is diagnostic of glaucoma • Optic disc changes :- Glaucomatous changes in the optic disc can be described as early changes, advanced changes, glaucomatous optic atrophy

  16. a) Early glaucomatous changes should be suspected to exit if fundus examination reveals one or more of the following signs: • Vertically oval cup • Asymmetry of the cups. A difference of more than 0.2 between two eye is significant • Large cup i.e 0.6 or more • Pallor areas on the disc

  17. b) Advanced glaucomatous changes in the optic disc include:- • Marked cupping • Thinning of neuroretinal rim c) Glaucomatous optic atrophy include: • As the damage progresses, all the neural tissue of the disc is destroyed and the optic nerve head appears white

  18. Nomenclature of glaucomatous field defects • Isopter contraction • Baring of blind spot • Small wing shaped paracentral scotoma • Seidel’s scotoma • Arcuate or Bjerrum’s scotoma • Ring or double arcuate scotoma • Roenn’s central nasal step • Advanced glaucomatous field defect

  19. Investigations • Tonometry • CCT • DVT • Gonioscopy • Documentation of optic disc changes • Perimeter

  20. Management • Medical therapy :- The initial therapy of POAG is still medical, with surgery as the last resort • Laser trabeculoplasty • Surgical therapy :- Trabeculectomy

  21. Ocular hypertension Definition:- It is labelled when a patient has an IOP constantly more than 21 mmHg but no optic disc and visual field changes

  22. Glaucoma suspect • Anyone of the following sings in at least one eye: :- Elevated IOP, consistently more than 21mmHg by AT :- Suspicious disc changes in the form of asymmetry C/D ratio(difference>0.2), narrowing of neuroretinal rim :- Visual field consistent with glaucomatous damage

  23. Risk factors • IOP> consistently more than 30mmHg • CCT<550 um • Vertical cup disc ratio more than 0.7 • Increased age • Fellow eye of the unilateral POAG

  24. Treatment • Patients with high risk factors should be treated on the lines of POAG. The aim should be to reduce IOP by 20% • Patients with no high risk factors should be annually followed by examination of optic disc, perimetry and record of IOP

  25. Normal tension glaucoma • NTG , also referred to s low tension or normal pressure glaucoma, is usually regarded as a variant of POAG. It is characterized by: • IOP consistently equal or less than 21mmHg • Signs of optic nerve damage in a characteristic glaucomatous pattern • An open anterior chamber • Visual field loss as damage progresses • No features of secondary glaucoma or a non glaucomatous cause for the neuropathy

  26. Pathogenesis • Any etiological factors distinct from those in POAG have not been conclusively determined • Clinical features • IOP is consistently lower than 21mmHg, but is usually on the higher side of the normal range • Optic disc changes are similar to POAG • Visual field defects are essentially similar to POAG, but tend to be more deeper, steeper, more localized and closure to fixation point

  27. Treatment • Medical treatment to lower the IOP • Trabeculectomy may be considered when progressive field loss occurs despite IOP in lower teens

  28. Primary angle closure glaucoma • The term ‘angle closure’ refers to occlusion of TM by peripheral iris(ITC) obstructing aqueous outflow. Angle closure can be primary, when it occurs in an anatomically predisposed eye, or secondary to another ocular or systemic factor.

  29. Anatomical and ocular risk factors • Hypermetropic eyes • Eyes in which iris-lens diaphragm is plated anteriorly • Eyes with narrow angle of anterior chamber • Plateau iris • Heredity

  30. Pathomechanism of rise in IOP • Pupillary bock mechanism • Plateau iris configuration and syndrome • Phacomorphic mechanism

  31. ISGEO classification 1.Primary angle closure suspect a) Diagnostic criteria: • Gonioscopy should reveal ITC in greater than 270 degree angle and no PAS • IOP should be normal • Optic disc should show now glaucomatous change • Visual field should be normal • Impression:- The angle is at risk

  32. b) Investigation • Estimation of anterior chamber by oblique illumination • Slit lamp examination • Van Herick slit lamp grading of the angle c) Treatment • Prophylactic laser iridotomy • Periodic follow eye

  33. 2. Primary angle closure a) Diagnostic criteria:- • ITC noted on gonioscopy in greater than 270 degree angle • IOP elevated and /or PAS present • Optic disc and visual fields are normal • Impression:- Angle is abnormal either in function (elevated IOP) and / structure(PAS positive)

  34. b) Investigation • Estimation of anterior chamber depth by oblique illumination • Slit lamp examination • Van Herick grading • Emsley-Finchman stenopaeic slit test c) Treatment • Medical therapy to lower IOP • Lasr peripheral iridotomy • Filtration surgery

  35. 3. Primary angle closure glaucoma a) Diagnostic criteria:- • ITC is noted on gonioscopy in greater than 270 degree angle • PAS are present • IOP is elevated • Optic disc show glaucomatous damage • Visual fields show typical glaucomatous defects • Impression:- Angle is abnormal in function and structure with optic neuropathy

  36. b) pathogenesis:- PACG results from synechial closure of the angle of anterior chamber. Untreated patients with PAC may over the period convert to PACG with or without history of sub acute or acute attack of PAC Treatment:- • Laser iridotomy • Trabeculectomy

  37. Secondary glaucoma • Lens induced glaucomas • Pseudoexfolitive glaucoma • Glaucoma due to uveitis • Pigmentary glaucoma • Glaucoma associated with intraocular tumours • Neovascular glaucoma • Glaucoma in aphakia/ pseudophakia • Steroid induced glaucoma • Traumatic glaucoma

  38. Reference Comprehensive ophthalmology- A.K.Khurana Kanski’s clinical ophthalmology Net

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