the raised IOP is associated with a primary ocular or systemic disease.

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2 Ù Glaucoma - Group of disorders characterized by a progressive op6c neuropathy resul6ng in characteris6c appearance of op6c disc and a specific pa:ern of irreversible visual field defects associated with raised intraocular pressure. Ù Secondary Glaucoma Group of disorders in which the raised IOP is associated with a primary ocular or systemic disease.

3 Ù Depending on the mechanism of rise in IOP v Secondary open angle glaucoma v Secondary angle closure glaucoma Ù Depending on the causa6ve primary disease v Lens - induced glaucoma v Inflammatory glaucoma v Pigmentary glaucoma v Neovascular glaucoma

4 v Glaucomas associated with irido corneal endothelial syndromes v Pseudoexfolia6ve glaucoma v Glaucomas associated with intraocular haemorrhage v Steroid-induced glaucoma v Trauma6c glaucoma v Glaucoma-in-aphakia v Glaucoma associated with intraocular tumours v Ciliary block glaucoma

5 Raised IOP secondary to a disorder of crystalline lens Lens induced glaucoma Lens induced secondary angle closure glaucoma Lens induced secondary open angle glaucoma Phacomorphic glaucoma Phacotopic glaucoma Phacoly6c glaucoma Lens par6cle glaucoma Phacoanaphylac6c glaucoma

6 Ù Causes - v Intumescent lens v Anterior subluxa6on or disloca6on of the lens and spherophakia Ù Pathogenesis Swollen lens pushes iris forwards, oblitera6ng the angle Ù Presenta8on Acute conges6ve glaucoma and shows features of acute primary angle closure glaucoma

7 Ù Treatment v Medical treatment Control of IOP by iv mannitol, systemic acetazolamide and topical beta blockers v Laser iridotomy v Cataract extrac6on with implanta6on of PCIOL

8 Ù Trabecular meshwork is clogged by the lens proteins, macrophages which phagocytose the lens protein and inflammatory debris Ù Deep anterior chamber and aqueous may contain fine white protein par6cles, which se:le down as pseudohypopyon Ù Treatment includes medical therapy to lower IOP followed by extrac6on of hypermature cataractous lens with PCIOL implanta6on

9 Ù Trabecular meshwork is blocked by the lens par6cles floa6ng in aqueous humour. Ù Symptoms of acute rise in IOP associated with lens par6cles in the anterior chamber Ù Medical therapy to lower IOP and irriga6on aspira6on of the lens par6cles from the anterior chamber

10 Ù Fulmina6ng acute inflammatory reac6on due to an6gen an6body reac6on Ù Granulomatous inflamma6on in the involved eye Ù Preceding disrup6on of lens capsule by extracapsular cataract extrac6on, penetra6ng injury of leak of proteins from the capsule Ù IOP is raised due to inflammatory reac6on of the uveal 6ssue excited by the lens ma:er.

11 Ù Management includes medical therapy to lower IOP, treatment of iridocycli6s with steroids and cycloplegics and irriga6on aspira6on of lens ma:er from anterior chamber ( if required).

12 Non specific inflammatory glaucoma Specific hypertensive uvei8s syndrome Open angle inflammatory glaucoma Angle closure inflammatory glaucoma Fuchs uvei6s syndrome Glaucomatocycli6c crisis

13 Mechanism of rise in IOP Clinical features Management Acute open angle inflammatory glaucoma Trabecular clogging, trabecular oedema and prostaglandin induced rise in IOP Features of acute iridocycli6s associated with raised IOP with open-angle of anterior chamber Treatment of iridocycli6s and medical therapy to lower IOP by use of hyperosmo6c agents, acetazolamide and beta blockers eye drops Chronic open angle inflammatory glaucoma Chronic trabeculi6s and trabecular scarring Raised IOP, open angle, no ac6ve inflamma6on but signs of previous episode of uvei6s present Medical therapy Trabeculectomy Cyclodestruc6ve procedures

14 Ù Mechanism of rise in IOP v Secondary angle closure with pupil block v Secondary angle closure without pupil block Ù Clinical features Raised IOP, seclusio papillae, shallow anterior chamber Ù Management v Prophylaxis Local steroids and atropine to prevent forma6on of synechiae v Cura6ve treatment Medical therapy, surgical or laser iridotomy and filtra6on surgery

15 Ù Clogging up of trabecular meshwork by the pigment par6cles Ù Pa6ents with Pigment Dispersion Syndrome Ù Pigment release caused by mechanical rubbing of the posterior pigment layer of iris with zonular fibrils Ù Clinical features v Young myopic males v Glaucomatous features similar to POAG v Deposi6on of pigment granules in the anterior segment

16 v Gonioscopy pigment accumula6on along the Schwalbe s line especially inferiorly (Sampaolesi s line) v Iris transillumina6on radial slit like transillumina6on defects in the periphery Ù Treatment is exactly on the lines of POAG

17 Ù Intractable glaucoma results due to forma6on of neovascular membrane involving the angle of anterior chamber Ù E8ology Neovasculariza6on of iris following re6nal ischaemia, feature of v Prolifera6ve diabe6c re6nopathy v Central re6nal vein occlusion v Sickle cell re6nopathy v Rare causes (intraocular tumours and long standing re6nal detachment)

18 Ù Clinical profile v Pre glaucomatous stage v Open angle glaucoma stage v Secondary angle closure glaucoma Ù Treatment v Panre6nal photocoagula6on v Medical therapy not effec6ve v Ar6ficial filtra6on shunt (Seton opera6on)

19 Ù 3 en66es v Progressive iris atrophy v Chandler s syndrome v Cogan Reese syndrome Ù Presence of abnormal corneal endothelial cells which proliferate to form an endothelial membrane in the angle of anterior chamber

20 Ù Clinical features Affects middle aged women v Progressive iris atrophy iris features predominates with corectopia, atrophy and hole forma6on v Chandler s syndrome Mild iris changes and corneal oedema predominates v Cogan Reese syndrome nodular and diffuse pigmented lesions of iris, may or may not be associated with corneal changes Ù Treatment v Medical treatment v Trabeculectomy v Ar6ficial filtra6on

21 Ù Deposi6on of an amorphous grey dandruff like material on the pupillary border, posterior surface of iris and ciliary processes Ù Associated with secondary open angle glaucoma Ù Trabecular blockage by the exfolia6ve material Ù Managed on the same lines as POAG

22 Ù Hyphaema and vitreous haemorrhage Ù Red cell glaucoma Associated with fresh trauma6c hyphaema; caused by blockage of trabeculae by RBCs in pa6ents with massive hyphaema; associated with pupil block Ù Haemoly8c glaucoma Clogging of trabecular meshwork by macrophages laden with lysed RBC debris Ù Ghost cell glaucoma Aphakic or pseudophakic eyes with vitreous haemorrhage Ù Hemosidero8c glaucoma Sclero6c changes in trabecular meshwork caused by iron from phagocytosed hemoglobin

23 Ù Type of secondary open angle glaucoma which develops following topical or systemic steroid therapy Ù E8opathogenesis v Glycosaminoglycans (GAG) theory v Endothelial cell theory v Prostaglandin theory Ù Symptoms similar to POAG Ù Prevented by judicious use of steroids and regular monitoring of IOP Ù Treatment v Discon6nua6on of steroids v Medical therapy by 0.5% 6molol maleate v Filtra6on surgery

24 Ù Mechanisms v Inflammatory glaucoma due to iridocycli6s v Glaucoma due to intraocular haemorrhage v Lens induced glaucoma due to swollen lens v Angle closure glaucoma due to anterior synechiae v Epithelial or fibrous growth v Angle recession (cleavage) glaucoma Ù Management Medical therapy with topical 0.5% 6molol and oral acetazolamide and surgical interven6on according to situa6on

25 Ù Raised IOP with deep anterior chamber in early postopera6ve period Ù Secondary angle closure glaucoma due to flat anterior chamber Ù Secondary angle closure glaucoma due to pupil block Ù Undiagnosed pre exis6ng primary open angle glaucoma Ù Steroid induced glaucoma Ù Epithelial ingrowth Ù Malignant glaucoma

26 Ù Malignant melanoma, re6noblastoma Ù Mechanisms v Trabecular block due to blockage by tumour cells v Neovasculariza6on of the angle v Venous stasis v Angle closure due to forward displacement of iris lens diaphragm Ù Treatment Enuclea6on of the eyeball

27 Ù Rare condi6on occurring as complica6on of any intraocular opera6on Ù Pa6ents with primary angle closure glaucoma operated for peripheral iridectomy or trabeculectomy Ù Markedly raised IOP associated with shallow or absent anterior chamber Ù Clinical features includes severe pain and blurring of vision following any intraocular opera6on

28 Ù On examina8on, v Persistent flat anterior chamber v Markedly raised IOP v Unresponsiveness or even aggrava6on by mio6cs v Phakic, aphakic or pseudophakic Ù Treatment v Medical therapy 1% atropine drops, acetazolamide, 0.5% 6molol maleate eye drops and iv mannitol v YAG laser hyaloidotomy v Surgical therapy

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