Downloaded 41 times
Uploaded byDr. Gaurav Shukla
Neovascular glaucoma (NVG)
This document discusses three types of secondary glaucoma: neovascular glaucoma, aqueous misdirection syndrome, and uveitic glaucoma. Neovascular glaucoma is caused by fibrovascular proliferation in the anterior chamber angle due to underlying conditions like proliferative diabetic retinopathy. Aqueous misdirection syndrome involves aqueous flowing into the vitreous cavity rather than the anterior chamber. Uveitic glaucoma can develop in 10% of patients with uveitis and results from trabeculitis, steroid use, or neovascularization among other causes.
HealthcareâŚ
More Related Content
Similar to Neovascular glaucoma (NVG)
Neovascular glaucoma (NVG)
- 1. NEOVASCULAR GLAUCOMA / AQUEOUSMISDIRECTION / UVEITIC GLAUCOMA PRESENTER - DR. GAURAV SHUKLA
- 2. NEOVASCULAR GLAUCOMA ďľ Definition ďľHistory ďľ Etiology ďľ Pathophysiology ďľ Clinical course ďľ Clinical features ďľ D/DâS ďľ Investigations ďľ Treatment
- 3. ďľ DEFINITION- ďľ Severeform of secondary glaucoma characterised by fibro vascular proliferation in the anterior chamber angle ďľ ALSO KNOWN AS- ďľ 1. Thrombotic glaucoma ďľ 2. Rubeotic glaucoma ďľ 3. Congestive glaucoma ďľ 4.Hemorrhagic glaucoma
- 4. ďľ HISTORY- ďľ 1906- Coats , NVI in CRVO termed as RUBEOSIS IRIDIS ďľ 1937 - Kurtz , NVA leading to PAS formation ďľ 1963 - Weiss et al, coined the term NEOVASCULAR GLAUCOMA
- 5. ďľ ETIOLOGY- ďľ Proliferativediabetic retinopathy (M.C.C)- approx. 33% ďľ CRVO - 28% (CRVO > CRAO) ďľ Ocular ischemic disease d/t carotid artery obstruction-13% ďľ Others-
- 7. PATHOPHYSIOLOGY- ďľ CHRONIC RETINALISCHAEMIA ďľ ANGIOGENIC FACTORS RELEASED & DIFFUSED ďľ NEOVASCULARISATION OF IRIS AND ANGLE, ďľ NEOVASCULAR GLAUCOMA
- 8. ďľ Lens andvitreous act as mechanical barriers and also releases vaso-inhibitory factors ďľ So any complicated cataract surgery with PCR, aphakia more predisposition ďľ VEGF conc 50-100 times more in aqueous humor in NVG
- 9. ďľ STAGES- ďľ PRERUBEOSIS STAGE ďľ PRE GLAUCOMA (RUBEOSIS IRIDIS ) ďľ OPEN ANGLE GLAUCOMA ďľ ANGLE CLOSURE GLAUCOMA
- 10. ďľ PRE RUBEOSISSTAGE- ďľ In patients with predisposing risk factors such as PDR, CRVO, etc ďľ It is important to understand the risk of developing rubeosis irides and the chances for progression to NVG ďľ 2. Look carefully for NVI and NVA under high magnification
- 11. ďľ PRE GLAUCOMASTAGE : RUBEOSIS IRIDIS ďľ a. NVI +/- NVA ďľ b. IOP normal ďľ d. dilated tufts of preexisting capillaries and fine, randomly oriented vessels on the surface of the iris
- 12. A: Angle neovascularizationin a patient with a central retinal vein occlusion. Note vessels are superficial and found on the ciliary body band and trabecular meshwork. B: Neovascular glaucoma has progressed to angle closure in this patient. C: A patient with open-angle neovascular glaucoma, with heavy neovascularization of the open angle.
- 13. ďľ OPEN ANGLEGLAUCOMA ďľ 1. Elevated IOP ďľ 2. NVA and NVI increased ďľ 3. AC inflammatory reaction ďľ 4. Hyphema may be present ďľ 5. No PAS ďľ 6. Angles open ďľ Fibro-vascular fibrovascular membrane covering the angle and anterior surface of the iris and may even extend onto the posterior iris (HALLMARK)
- 14. ďľ Angle closureglaucoma- ďľ Most patients are detected in this stage ďľ Iris is dilated and pulled anteriorly from the lens ďľ PAS formation ďľ Fibro vascular membrane contracts leads to flat iris ďľ Ectropion uvea present ďľ IOP very high
- 15. CLINICAL FEATURES ďľ SYMPTOMS ďľSevere pain ďľ Headache ,vomiting ďľ Redness ďľ Watering ďľ Defective vision ďľ Photophobia ďľ SIGNS ďľ Reduced vision ďľ Ciliary injection ďľ Corneal edema ďľ AC with flare ďľ Hyphema ďľ Fixed dilated pupil ďľ NVI, NVA ďľ Raised IOP
- 17. ďľ DIFFERENTIAL DIAGONOSIS ďľ1. PACG - no NVI and NVA ďľ 2. UVEITIC GLAUCOMA - KPâS + ,Complicated cataract, band shaped keratopathy ďľ 3. Fuch Heterochromic Iritis - stellate KPâS, NVA+ ,NVI and NVG are rare ďľ 4. ICE syndrome - corneal decompensation, iris atrophy ďľ 5. Old trauma - angle recession, iris pigment clumps, no NVI ďľ 6. Lens induced glaucoma
- 18. ďľ INVESTIGATIONS ďľ OCULAR:- ďľ Fundus examination- ďľ Fundus Fluorescein Angiogram- to assess retinal ischemia ďľ Iris angiography- in cases of doubtful NVI, to confirm the diagnosis ďľ B scan ultrasound- if retina is not visible ďľ Electroretinogram â to assess for retinal ischemia ďľ SYSTEMIC :- ďľ - BP, FBS PPBS, Carotid Doppler, lipid profile, renal profile
- 19. ďľ TREATMENT- ďľ A.Identifying the underlying etiology and start adequate treatment to prevent the development and progression of NVG ďľ B. Once NVG develops and IOP is high, the major point of management is control of high IOP to prevent optic nerve damage
- 20. ďľ Management- ďľ Intravitrealbevacizumab- injecting 1.25-mg bevacizumab in the vitreous cavity or 1.0- to 1.25-mg bevacizumab in the anterior chamber before or concomitant with pan retinal photocoagulation PRP ďľ Pan retinal photocoagulation (PRP)- Ist line treatment ďľ DM - In established cases of PDR, PRP +/- IVB done to prevent NVG ďľ CRVO -PRP indicated only after 2 clock hours of NVA/NVI (CVOS) ďľ Ocular Ischemic Syndrome -PRP indicated for cases with retinal ischemia on FFA & refer for neurological and cardiology assessment
- 21. ďľ Pan retinalphotocoagulation- ďľ Make ischemic retina anoxic by reducing O2 demand ďľ Decreased angiogenic factor ďľ Decreased new vessels ďľ Reduces neo vascularization
- 22. ďľ Transscleral Pan-retinalcryotherapy+ cyclo-cryotherapy ďľ Gonio-photocoagulation- ďľ a. Adjunct to PRP ďľ b. LASER therapy aimed at directly treating the NVA before development of NVG ďľ c. No role once glaucoma is established ďľ d. Low-energy argon laser shots (0.2 seconds, 50-100 um, 100 - 200 mW) are applied to the neovascular tufts
- 23. ďľ Medical management- ďľAqueous suppressants- beta blockers, carbonic anhydrase inhibitors, alpha2 agonists ďľ Topical prostaglandin analogues can be tried though they may increase ocular inflammation ďľ Miotics are c/I- as they can increase inflammation and discomfort
- 24. ďľ Surgical management- ďľTrabeculectomy ďľ Tube shunts ďľ Cycloablation
- 25. ďľ Surgical management:- ďľ 1. Medical management of glaucoma with intravitreal anti-VEGF along with retinal ablation ďľ It may be sufficient to control the IOP in the open angle stage of NVG ďľ 2. Advanced stage with synechial angle closure surgical intervention for IOP lowering is often required.
- 26. ďľ Trabeculectomy :- ďľa. Intraoperative use of anti-fibrotic agents -to reduce the risk of bleb failure due to subconjunctival scarring ďľ b. The success rate of trabeculectomy with MMC in NVG at 1 year has been reported to be around 62.6% and reduced to 51.7% at 5 years * ďľ c. With the use of preoperative Bevacizumab, success rate may improve up to 95%** ďľ * Takihara Y, Inatani M, Fukushima M, Iwao K, Iwao M, Tanihara H. Trabeculectomy with mitomycin C for neovascular glaucoma: prognostic factors for surgical failure.Am J Ophthalmol 2009; 147:912â8. ďľ ** Saito Y, Higashide T, Takeda H, Ohkubo S, Sugiyama K.Beneficial effects of preoperative intravitreal bevacizumab on trabeculectomy outcomes in neovascular glaucoma. Acta Ophthalmol 2010; 88:96â102.
- 27. ďľ Tube shunts- ďľI. Glaucoma drainage devices - considered as a primary surgical procedure especially NVG, high risk for failure of conventional filtering surgery ďľ II. Scarred conjunctiva, active inflammation, vigorous new vessel growth and prior failure of trabeculectomy - indications to consider tube shunt surgery in NVG
- 28. ďľ Cycloablation :- ďľFor refractive NVG, no PL eye to relieve pain- ďľ Cyclocryotherapy ďľ TSCPC, other contact and non contact trans scleral cyclo destructive procedures ďľ Cyclo photocoagulation- 12-24 burn spots ,posterior to limbus over 360 degrees , 1500-2000 MW, 1.5-2 secs
- 30. AQUEOUS â MISDIRECTION/ MALIGNANT GLAUCOMA
- 32. ďľ Malignant Glaucoma/ Aqueous Misdirection Syndrome ďľ Definition- ďľ Von Graefe 1869 ďľ A shallow or flat anterior chamber with an inappropriately high intraocular pressure despite a patent iridectomy ďľ European Glaucoma Society; II edition ďľ Secondary angle closure glaucoma with ââposteriorââ pushing mechanism, without pupillary block, caused by the ciliary body and iris rotating forward
- 33. ďľ Malignant Glaucomaâ Etiology ďľ Surgery for angle-closure glaucoma ďľ Cessation of topical cycloplegic therapy ďľ Initiation of topical miotic therapy ďľ Laser iridotomy ďľ Laser capsulotomy ďľ Laser cyclophotocoagulation ďľ Cataract extraction ďľ Central retinal vein occlusion ďľ Argon laser suture lysis ďľ Hyperopia ďľ Short axial lengths, or nanophthalmos ďľ Spontaneously
- 34. ďľ Pathogenesis- ďľ Posteriormisdirection of aqueous flow ďľ Through hyaloid membrane into or behind the vitreous body ďľ Increase in vitreous volume ďľ Anterior rotation of the ciliary body, forward movement of the lens-iris diaphragm ďľ Shallower anterior chamber ďľ Increase in intraocular pressure
- 35.
- 36.
- 37. ďľ Clinical Presentation- ďľShallow or flat anterior chamber both centrally and peripherally ďľ No iris bombe ďľ IOP is elevated ďľ Great posterior resistance may be noted, during reformation of anterior chamber postoperatively through the paracentesis site with viscoelastic substance ďľ Anterior chamber may not deepen ďľ IOP may rise substantially ďľ Patent pi may be there ďľ Lens iris diaphragm ant placed
- 38. ďľ Trigger factors- ďľSmall, crowded anterior segment ďľ Angle closure ďľ Swelling and inflammation of the ciliary processes ďľ Anterior rotation of the ciliary body ďľ Forward movement of the lens-iris diaphragm
- 39.
- 41. Pupillary block v/sMalignant Glaucoma
- 42. ďľ Investigations- ďľ Ultrasoundbiomicroscoscopy (UBM) ďľ Ultrasound B scan: exclude other pathologies
- 43. ďľ Ultrasound biomicroscopy- ďľConfirm the diagnosis by the visualization of the anterior segment structures:- ďľ Irido-corneal touch ďľ Appositional angle closure ďľ Anterior rotation of the ciliary body ďľ Apposition to the iris
- 44. ďľ MANAGEMENT- ďľ Medicaltherapy ďľ Laser therapy ďľ Pars plana vitrectomy
- 45. ďľ Medical treatment- ďľFirst step (good results in 50% of cases) ďľ Cycloplegia with atropin 1%x 4-6/d ďľ Mydriasis with phenilephrin 2,5%x 4-6/d ďľ Anti glaucoma medications ďľ Steroids ďľ Mechanism of action- ďľ posterior push of the iris lens diaphragm ďľ Cilliary muscles relaxation ďľ Long time treatment with atropin required to prevent recurrence ďľ Î˛ blockers, Îą agonists ďľ Hyperosmotics agents: Glycerol (po), Manitol (2g/kg iv)
- 46. ďľ Laser Therapy ďľThe second line of treatment ďľ Neodymium : yttrium-aluminum-garnet (Nd:YAG) laser ďľ Anterior hyaloid rupture to release the trapped aqueous from the vitreous ďľ Several openings are made peripherally ďľ Placement of the iridectomies should be peripheral to enable anterior migration of the aqueous
- 47. ďľ Pars planavitrectomy ďľ Mechanism- ďľ To debulk the vitreous ďľ To disrupt the anterior hyaloid face ďľ Ac reformation ďľ +/- lensectomy / phacoemulsification ďľ Needed if- ďľ Medical or laser therapy fails ďľ Phakic eyes for which laser treatment is not possible ďľ Large pi through in phakic eye a good option
- 48. ďľ Pars planavitrectomy- ďľ Pseudophakic ďľ vitrectomy + anterior hyaloidotomy ďľ Phakic- ďľ Pars plana vitrectomy Âą lensectomy
- 49. ďľ Fellow eye- ďľNarrow angle is present The laser peripheral iridotomy is performed before ďľ Risk of aqueous misdirection may be reduced after iridotomy if the angle remains open and the IOP is normal ďľ Failure to provide prompt therapy to the fellow - bilateral blindness
- 50.
- 51. ďľ Uveitis isone of the most common of the inflammatory processes ďľ Acute cases (< 3 months duration) involves the anterior uvea (iritis or iridocyclitis) ďľ Chronic forms are seen having frequencies:- ďľ Anterior (45%), intermediate (15%), posterior (14%) and panuveitis (24%) ďľ â˘ Iridocyclitis most common form causing increased IOP ďľ â˘ 10% of pts with uveitis will develop OHT/OAG
- 52. Uveitic glaucoma ďľ Multifactorial ďľHypertensive uveitis ( trabeculitis) ďľ Open angle sec glaucoma - steroid induced , trabeculitis, chronic inflammatory glaucoma â trab scarring, neovascular glaucoma ďľ Closed angle sec glaucoma- acute pupil block , chronic angle closure , NVG ďľ Hypotony (acute with active acute inflammation or chronic due to ciliary shut down )
- 53. ďľ Pathophysiology- ďľ SecondaryOAG ďľ Obstruction of TM by inflammatory debris, RBCs, WBCs, fibrin, viscous inflammatory aqueous ďľ Direct inflammation and swelling of the TM endothelial cells (trabeculitis) ďľ Steroid responsiveness ďľ Formation of vascular or cuticular membranes overlying the TM as a result of chronic recurrent Inflammation
- 55. ďľ Pathophysiology- ďľ SecondaryACG ďľ Pupillary block secondary to posterior synechiae ďľ Extensive peripheral anterior synechiae ďľ Choroidal/ciliary effusions with anterior rotation of the ciliary body and resultant angle closure ďľ Neovascular glaucoma
- 56. ďľ General Principles ďľIt is uncommon for acute anterior uveitis of short duration (< 3 months) to cause persistent IOP elevation ďľ Main aim of treatment - suppressing inflammation ďľ Full physical, CXR, SI joint films, ACE levels, HLA-B27, RPR, FTA-ABS, ANA, RF, HIV ďľ HLA B27 positive accounts for 50% of cases in Caucasians,
- 57. ďľ Signs andsymptoms ďľ Pain, photophobia, tearing, decreased VA ďľ Ciliary flush, miosis, cells & flare, KPs, vitreous cells, ďľ Ant/post synechiae, iris atrophy, corneal edema and IOP changes.
- 58. ďľ Treatment forUveitic Glaucoma- ďľ Depending upon the degree of inflammation present ďľ Aimed to reduce the acute inflammation and controlling the IOP ďľ A long term treatment goal is to prevent any permanent structural damage such as cataract, corneal decompensation and glaucoma ďľ Specific Tx required in certain cases â eg: ABx for STD, TB, Toxoplasmosis
- 59. ďľ Treatment Principlesfor Uveitic Glaucoma ďľ Identification of the mechanism of IOP elevation and treatment of the underlying cause ďľ Cycloplegics and corticosteroids - mainstays of treatment to control inflammation and prevent synechiae ďľ Steroid potency:- ďľ Difluprednate (Durezol)>Dexamethasone>Prednisolone> ďľ Loteprednol (Lotemax)>FML Steroids must be tapered off ďľ Topical NSAIDS as adjunct in known steroid responders ďľ Systemic immunosuppresive Tx successful in 70% of patients unresponsive to other Tx
- 60. ďľ Treatment Principlesfor Uveitic Glaucoma ďľ Select target IOP based on duration of IOP elevation ďľ Elevated IOP initially treated with B blockers and CAIs, both topical and systemic ďľ Alpha agonists effective, although granulomatous anterior uveitis in patients taking brominidine 0.2% ďľ Miotics are C/I ďľ Laser trabeculoplasty generally ineffective in uveitic glaucoma and may result in IOP spikes. ďľ Laser PI is the treatment of choice although higher rate of secondary closure - only in pupillary block
- 61. ďľ Gonio-synechiolysis, bothlaser and surgical- effective in reversing PAS ( combined with cataract surgery ) ďľ Tube shunt surgery ďľ Slightly higher success rate than Trabeculectomy but often need medications ďľ Cyclo-destructive surgery an option in eyes with poor visual potential
- 62. ďľ Common UveiticEntities Associated with Glaucoma- ďľ Fuchs Heterochromic Iridocyclitis (FHI)- ďľ Chronic low grade inflammatory condition ďľ Heterochromia, KPs, vitreous opacities, cataract and glaucoma ďľ M=F ďľ U/L in 95% of cases. ďľ Pts usually present with a white, quiet eye complaining of decreased VA due to cataract ďľ Minimal flare and cell, fine stellate KPs ďľ Stromal iris atrophy d/t iris Transillumination defects.
- 63. ďľ PAS, posteriorsynechiae are unusual ďľ Light NV of the iris and AC angle ďľ Fine iris nodules occur in 20% of patients ďľ FA shows delayed filling, sector ischemia and NV of the iris ďľ Iris transillumination may be present.
- 64. ďľ Management ofFHI ďľ Cataract surgery in these patients is generally associated with good visual outcomes ďľ Higher incidence of post op CME, IOP spikes, hyphema and Post op uveitis ďľ Glaucoma Incidence is greater with longer term follow up ďľ Does not respond to aggressive steroid therapy and may develop steroid induced glaucoma if used inappropriately. ďľ Standard glaucoma medications are useful but often ineffective in the long term ďľ Avoid pilocarpine
- 65. ďľ Trabeculectomy withMMC as well as tube shunt sx = good success rates if medical treatment fail
- 66. ďľ Glaucomatocyclitic Crisis(Posner-Schlossman Syndrome) ďľ Recurrent unilateral attacks of mild anterior uveitis with marked elevations of IOP ďľ Young to middle aged adults, age 20-50 yrs. ďľ Symptoms, slight in relation to the level of IOP, such as slight ocular discomfort, blurred vision and ďľ Recurrences = monthly to yearly. ďľ Mild ciliary flush, epithelial edema, faint flare and scant KPs ďľ Angle is open, no synechiae ďľ A/W subsequent POAG. ďľ Etiology unknown
- 67. ďľ IOP range= 40-60 mmHg ďľ IOP return to normal between attacks ďľ Self limiting condition ďľ Corticosteroids = controlling the inflammatory process (Unlike FHI) ďľ CAIs, B-blockers and Alpha agonists are all effective in controlling IOP during acute attacks ďľ Prophylactic antiglaucoma meds and corticosteroids are not necessary between attacks
- 68. ďľ NSAIDS ďľ Glaucomasurgical procedures may be indicated if severe or prolonged attacks lead to progressive ON damage.
- 69. ďľ Common UveitisEntities Associated with Glaucoma ďľ Sarcoidosis- ďľ A multi system inflammatory disorder ďľ Young adults and African Americans ďľ Non caseating granulomas involving the lungs, liver, spleen, skin, eyes and CNS ďľ Glaucoma occurred in 10% of pts c Sarcoid related iridocyclitis
- 70. ďľ Ocular manifestationsoccur in 38-50% of sarcoidosis patients ďľ MC involves -anterior uveitis, chorioretinitis, retinal periphlebitis, optic neuritis and lacrimal gland involvement ďľ Diagnosis is made by Chest Xray = (hilar lymphadenopathy), ďľ ACE levels and lymph node or skin biopsy
- 71. ďľ Both anacute form and chronic relapsing form ďľ Initially u/l with an insidious onset ďľ Frequently develops into a chronic phase often becoming b/l ďľ Characterized by mutton fat KPs, iris nodules (Busacca and Koeppe), nodules in the AC angle and synechiae.
- 72. ďľ Glaucoma ismc associated with chronic relapsing form of sarcoid anterior uveitis ďľ Corticosteroids are usefull in the treatment of systemic and ocular sarcoidosis ďľ May require prolonged course and taper of corticosteroids ďľ Cycloplegics ďľ CAIs, B-Blockers and Alpha agonists effective ďľ As always avoid miotics ďľ Trabeculectomy c MMC, tube surgery.
- 73.