Surgery for proliferative diabetic retinopathy


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Surgery for proliferative diabetic retinopathy

  1. 1. Surgery for Proliferative Diabetic Retinopathy Dr Mamta Manik
  2. 2. Introduction • Diabetic retinopathy is now one of leading causes of potentially irreversible blindness in working age population. • Large number of eyes, however, progress toward complications requiring surgical management despite aggressive and valuable interventions. • PPV was first introduced by Machemer et al. in 1970 • There have been vast improvement both in surgical technique and outcomes
  3. 3. ETDRS Classification of Diabetic Retinopathy
  4. 4. Epidemiology • Cumulative incidence of PDR after 20 yr duration is about 14%. • Wisconsin epidemiologic studies, the prevalence of proliferative retinopathy was 60% after 25 years of diabetes in younger diabetic patients, but in older diabetics it varied from 20 to 30%. • Prevalence of blindness (VA <3/60 better eye) approximately 5% (range 3-7%) and may be as high as 8%
  5. 5. Pathophysiology • Initial insult is retinal ischaemia leading to the production of angiogenic factors • Interaction between several angiogenic factors with vascular endothelial growth factor (VEGF) being prominent. • New vessels proliferate in the vitreoretinal interface, with varying degrees of fibrous tissue proliferation • Development of posterior vitreous detachment and/or contraction of these fibrovascular membrane • Vitreous haemorrhage, tractional retinal detachment, and combined tractional–rhegmatogenous retinal detachment
  6. 6. Pan Retinal Photocoagulation mainstay of tt of PDR Avoids the need of vitrectomy
  7. 7. Indications of Vitrectomy • Media opacity – Severe Nonclearing Haemorrhage • Vitreous • Subhyaloid • Premacular – Anterior Segment Neovascularization with Vitreous Haemorrhage • Tractional defects – TRD involving or threatening Fovea – Combined tractional and rhegmatogenous detachment – Progressive fibrovascular proliferation despite adequate laser – Epiretinal membrane or opacified vitreous face causing visual loss • Complication of previous vitrectomy surgery • Ghost cell/ Hemolytic glaucoma • Anterior hyaloid fibrovascular proliferation despite adequate laser
  8. 8. Vitreous haemorrhage • Grading scale – Grade 0 No vitreous haemorrhage entire retina seen – Grade I • Some hemorrhage present, which obscures between a total of 1 to 5 clock hours of retina. • Laser photocoagulation (PRP) can be successfully performed – Grade II • Hemorrhage obscures between a total of 5 to 10 clock hours of central and/or peripheral retina, or • large hemorrhage is located posterior to the equator, with varying clock hours of anterior retina visible. • Laser is feasible, but a full panretinal photocoagulation (PRP) can not be placed – Grade III • red reflex is present, • no retinal detail seen posterior to the equator, • precluding any photocoagulation – Grade IV Dense VH with no red reflex present
  9. 9. Vitreous Haemorrhage • Early vitrectomy, within 1–4 months from onset, results in earlier recovery of vision and better functional outcome after 2 and 4 years • Benefit is greater in patients with type 1 diabetes mellitus, compared to type 2. – Macular edema is more common in type II – PVD more common in type II • Dense premacular (subhyaloidal) hemorrhage
  10. 10. Timing of vitrectomy • Duration of hemorrhage, • Type of diabetes (I or II) • Severity of retinopathy • Status of the fellow eye ( Blind or rapidly progressive visual loss) • Premacular or intragel Hg • Prior laser treatment (early if no laser done)
  11. 11. Favorable factors • Preoperative visual acuity of 5/200 or better. • Absence of NVI OR NVG. • Minimal cataract. • PRP of at least one fourth of the fundus
  12. 12. Tractional Retinal Detachment
  13. 13. Indications • Tractional macular Detachment • Peripheral tractional detachment threatening macula • Vitreopapillary traction • Traction involving Papillomacular bundle Visual improvement has been reported in 59 to 80% of cases, but vision equal to or greater than 20/200 is achieved in only 21 to 58%
  14. 14. MACULAR TRACTION RETINAL DETACHMENT • Charles and Flinn studied the natural history of diabetic extramacular traction retinal detachment. • They found a progression to macular detachment in only 13.8% of eyes at 1-year follow-up.
  15. 15. Favorable factors • Age <50 years, • Preoperative panretinal photocoagulation • Visual acuity >5/200; • No or few iris neovascularizations or retinal proliferations; • Macular detachments <30 days, and • No iatrogenic breaks.6,25
  16. 16. COMBINED TRACTION-RHEGMATOGENOUS RETINAL DETACHMENT • Extramacular rhegmatogenous detachments frequently progress to involve the macula, leading to rapid and severe visual loss. • Thus, surgical repair is indicated in combined detachments, whether or not the macula is involved.
  17. 17. Severe fibrovascular proliferation • Major threat to profound loss of vision • Early vitrectomy – Severe fibrovascular proliferation & moderately severe Neovascularization despite extensive PRP – Severe fibrovascular Proliferation • Stable or improved vision in 78% cases
  18. 18. Macular Edema and Traction • May occur after extensive PRP or premacular haemorrhage • Vitreopapillary traction • Diabetic epiretinal membranes
  19. 19. Neovascular Glaucoma • Extensive PRP or cryotherapy. • Intravitreal anti- VEGF, may be helpful as short- term adjunct to PRP or when PRP fails to cause regression of rubeosis • Opaque optical media, as vitreous hemorrhage or cataract, controlled PRP can only be performed after vitrectomy and/or cataract extraction • Silicone oil tamponade prevents recurrent vitreous hemorrhage and may induce regression of rubeosis
  20. 20. Preoperative evaluation • Optimal blood glucose management may be protective against perioperative infection. • Patients should be well informed about adjustments of medications, especially those for blood glucose and blood pressure control. • Anticoagulants as well as antiplatelet medications must be stopped or substituted at the surgeon’s suggestion. • Patients on dialysis, surgery has to be arranged between dialysis sessions.
  21. 21. Preoperative Evaluation • Correlate the history of visual decrease with possible anatomic changes • B Scan – Opacified media preventing fundus visualization, as cataract, intracameral or intravitreal hemorrhage – Most relevant information, as the presence or absence of vitreoretinal adhesions, vitreoschisis, retinal detachment, or other subretinal opacities
  22. 22. Pre-Operative Anti-Vegf • Preoperative antiangiogenic drug decrease the risk of recurrent intravitreal hemorrhage or neovascular glaucoma with rubeosis iridis. • Preoperative injections 7 days prior to surgery – Improve the outcome and – Facilitate surgical manipulations in diabetic tractional detachment.
  23. 23. Pre-Operative Anti VEGF • Potential adverse effect because fibrovascular membrane contraction can lead to rapid development or progression of tractional retinal detachment. • Timing of vitrectomy surgery may therefore be critical to avoid this complication..
  24. 24. Cataract • Cataract extraction alone or with primary lens implantation, followed by vitrectomy • Combined operation in single procedure • Advantage is much better intraoperative access to the vitreous base • Procedure of choice is phacoemulsification • All three sclerotomies are performed and trocars inserted before cataract surgery to avoid pressure changes
  25. 25. Instruments 1. 3-4 Port trocar 2. 120D lens , for peeling: 60D front lens 3. Vitreous cutter 4. Fluid needle 5. Eckardt forceps 6. horizontal scissors or vertical scissors 7. Membrane pic or knob spatula 8. Endodiathermy 9. Laser therapy 10. Scleral depressor Dye Triamcinolone or Trypan blue or BBG Tamponade air, 12–14% C3F8 or silicone oil
  26. 26. Surgical Steps Vitreous Haemorrhage 1. 3-Port system 2. Core vitrectomy 3. Posterior vitreous detachment and peripheral vitrectomy 4. Endodiathermy 5. Panretinal photocoagulation 6. Tamponade 7. Removal of the trocar cannulas Tractional Detachment 1. 4-Port system 2. Core vitrectomy 3. Peripheral vitreous rhexis 4. Bimanual dissection of tractional membranes 5. Apply PRP 6. Tamponade 7. Removal of the trocars
  27. 27. In combined procedure • Infusion is turned on only when the cutter is in the eye and vitreous removal can be started simultaneously. • Otherwise, the infusion pressure will move the lens implant anteriorly and iris incarceration into the wound can occur
  28. 28. Posterior hyaloid status • Eyes with complete PVD • Eyes with incomplete posterior hyaloid separation • Eyes with subtotal vitreous adhesion
  29. 29. Triamcinolone Acetonide • Facilitate identification of the vitreous cortex, • Due to its anti-inflammatory potential it may also help to prevent fibrin exudation in proliferative diabetic retinopathy. • Intravitreal doses of 2–4 mg of triamcinolone acetonide will offer sufficient staining with no retinal toxicity.
  30. 30. PVD Present • Opening made in posterior hyaloid • Blood might be pooled at the posterior pole, usually unclotted, and can be aspirated now with a soft- tipped fluid needle or Cutter
  31. 31. PVD & Peripheral vitrectomy • If tractional membranes are present at the posterior pole, do not induce PVD because it may cause breaks in the central retina • Try to remove all peripheral vitreous with remaining blood in it (this may wash out postoperatively and be an additional source of postoperative vitreous haemorrhage)
  32. 32. Incomplete post hyaloid Separation • Tractional membranes are present on the posterior pole. • PVD should not be induced with the usual method of suction over the posterior pole and pulling on the vitreous face • In most cases of PDR, a partial vitreous detachment is present (i.e vitreous is still attached at the disc but partially detached in the mid-periphery) or • Create peripheral Vitreous detachment
  33. 33. • Create an opening of the posterior hyaloid and remove the vitreous along the posterior vitreous face on a constant level in a circular fashion (peripheral vitreous rhexis). • Do not vitrectomize the area where the vitreous is attached. • Carefully vitrectomize further from the periphery toward the beginning of the tractional membranes • Address the membranes
  34. 34. Membrane Dissection Commonly used: (1) segmentation, (2) delamination, (3) “en bloc” dissection, (4) combined.
  35. 35. Membrane Dissection • Segmentation – Membrane is segmented by cutting bridging tissue between foci of fibrovascular adhesion • Delamination – Connections between the posterior hyaloid and fibrovascular tissue and the internal limiting membrane are cut
  36. 36. Segmentation
  37. 37. Delamination
  38. 38. Membrane Dissection • “En bloc” technique removal of the vitreous and associated vitreoretinal membranes as a single unit • Combination technique
  39. 39. Fibrovascular tissue that is firmly attached to the disc is reduced with the vitreous cutter
  40. 40. Bimanual Membrane Surgery
  41. 41. Subtotal posterior vitreous adhesion • Access to the subhyaloidal space is difficult. • Gentle suction to find lesser adherent areas vitreous (subhyaloidal hemorrhage) • Vitrector, sharp blade or subretinal pick is used to create an opening into the subhyaloidal space. • Safest areas for such manoeuvres are around the optic disc • Dissection is performed centripetally
  42. 42. Combined tractional and rhegmatogenous detachment • Dissection of tissue is started usually in an area distant from the detached retina • Preparation of tissue from the centre to the periphery is advisable. • Perfluorocarbon can be used to stabilize the posterior retina. • Peripheral retinectomies are needed in eyes where reoperations become necessary and severe anterior hyaloid fibrovascular proliferation has developed
  43. 43. Endodiathermy • Cauterize retinal bleeding sites with endodiathermy. • Start with relatively low energy, as too vigorous endodiathermy may create breaks in ischemic retinal tissue. • Avoid diathermy on the disc; this may cause destruction of nerve fibre bundles • In Bimanual system aspirate the blood with one hand and cauterize the bleeding source with endodiathermy
  44. 44. Pan Retinal Photocoagulation • Complete PRP intraoperatively • Use the scleral depressor and apply a dense PRP up to the ora serrata
  45. 45. Tamponades • Prolonged tamponade in cases of retinal breaks with traction, retinal detachments or diffuse hemorrhage • Gases as SF6, C2F6, or C3F8 • Silicone oil is of choice in reoperations or severe cases, if a longer tamponade is required,
  46. 46. Diabetic Vitrectomy Results
  47. 47. Complications • Intraoperative – Corneal edema – Lens touch – Pupillary constriction – Intraocular haemorrhage – Retinal break or detachment – Subretinal PFCl or Silicone oil • Postoperative – NVI and NVG – Cataract – Fibrinoid Syndrome – Postoperative Vitreous cavity haemorrhafe – Anterior Hyaloidal fibrovascular proliferation
  48. 48. Post vitrectomy Vitreous Hg • Recent study suggest decrease from 75% in 1980 to 30% today • Early POVH in 1st 4 weeks postoperatively • Late POVH > 4 weeks
  49. 49. Early vitreous cavity haemorrhage • Common complication after diabetic vitrectomy (30–75%) • Source – Dissected fibrovascular tissue and – Dispersion of erythrocytes from residual peripheral vitreous gel. • Preventive strategies – Careful dissection of fibrovascular membranes with complete haemostasis (by diathermy or direct pressure) – Intraocular tamponade with C3F8 – Air and SF6 no role although variable findings have been reported.1,2,3 – Intravitreal anti-VEGF therapy with bevacizumab administered 1 week .6,7,8 • Clear spontaneously within 2–6 weeks. • If persists > 6wks resurgery
  50. 50. Delayed Vitreous cavity Haemorrhage • If POVH persists > 6 weeks or occurs after 4 week PO following initial period of clear vitreous cavity • Causes – Residual fibrovascular membranes, – Reproliferative retinal neovascularisation, – Sclerotomy entry site neovascularisation (fibrovascular ingrowth).8,9 • Preventive strategy – Laser photocoagulation if existing panretinal photocoagulation is inadequate.10 – Cryotherapy to the peripheral retina and – Cryotherapy to sclerotomy entry sites.9 • Fail to clear spontaneously – Vitreous cavity washout, – Dissection of residual or reproliferative fibrovascular membranes, – Silicone oil tamponade.
  51. 51. Postoperative vitreous cavity haemorrhage • More in phakics as lens acts as a barrier between vitreous cavity and treabecular meshwork • Spontaneous clearing of haemorrhage (moderate to severe) in 3.8 weeks in apakics compared to 11.6 wks in phakics
  52. 52. Fibrinoid syndrome • Breakdown of the blood–retina barrier with in intraocular fibrin deposition. • Massive fibrin formation in the vitreous cavity (the fibrinoid syndrome) – Tractional retinal detachment, – Pupillary block, – Ciliary body detachment, – Hypotony – Rubeosis iridis with neovascular glaucoma
  53. 53. • Risk Factors – Young Age – Lensectomy, – Extensive dissection, – Intensive panretinal photocoagulation or – Scleral buckle surgery • Treatment – topical corticosteroids – tPA injection in AC – PST – Substantial fibrin deposition repeated vitrectomy, fibrin removal and silicone oil injection.
  54. 54. Anterior Hyaloidal Fibrovascular Proliferation • Most severe complication • 13% of cases • Growth of neovascular tissue onto the vitreous base, the anterior retina, ciliary body, lens capsule and iris. • Patients may present with rubeosis iridis, vitreous hemorrhage, peripheral tractional retinal detachment or hypotony
  55. 55. • Risk factors – Male gender, – Type I diabetes, – Phakic patients, – Insufficient panretinal photocoagulation, – Severe ischemia with recurrent neovascularizations, – Previous surgery with placement of a scleral buckle. • Treatment cataract extraction, lensectomy, extensive laser or cryopexy, and anterior dissection with eventual retinectomy • Endoscopic Vitrectomy • Preoperative Anti vegf helpful
  56. 56. Recent Advances
  57. 57. Important Studies
  58. 58. DRVS Group I (VH) • Severe vitreous hemorrhage (visual acuity 5/200 or less) , • 616 patients recruited • Early vitrectomy (1 to 6 months after the onset of hemorrhage) • Conventional management – vitrectomy was carried out 1 year later if hemorrhage persisted; – vitrectomy was carried out sooner if retinal detachment -involving the center of the macula occurred.
  59. 59. Results • Final visual acuity of 20/40 or better in 25% of cases (at 2-year follow-up), compared with 15% • • Advantage for early vitrectomy remained after 4 years of follow-up
  60. 60. DRVS group II (FVP) • Severe fibrovascular proliferations with VA 10/200 or better • 381 patients recruited • Eligible eyes were assigned either to early vitrectomy or to conventional management. • Conventional management – Photocoagulation when indicated, – Vitrectomy if a severe vitreous hemorrhage occurred and failed to clear spontaneously during a 6-month waiting period or – Retinal detachment involving the center of the macula
  61. 61. Result • Rate of final vision equal to or greater than 20/40 was 44% for the early vitrectomy group as compared to 28% in the conventional group with 4 years follow up
  62. 62. Conclusion • Most patients will regain or retain useful vision after diabetic vitrectomy, although the visual outcome remains unpredictable. • Diabetic vitrectomy has been demonstrated to significantly improve vision-related quality of life. • Early vitrectomy for diabetic vitreous haemorrhage has also been shown to be a highly cost-effective intervention. • Surgical outcome after diabetic vitrectomy has continued to steadily improve with advances in vitreoretinal surgical instrumentation and technique. • Development of adjunctive pharmacotherapy should enable further improvements in the future
  63. 63. References 1. Joondeph BC, Blankenship GW. Hemostatic effects of air versus fluid in diabetic vitrectomy. Ophthalmology1989; 96: 1701–1706. | PubMed | ChemPort | 2. Koutsandrea CN, Apostolopoulos MN, Chatzoulis DZ, Parikakis EA, Theodossiadis GP. Hemostatic effects of SF6 after diabetic vitrectomy for vitreous hemorrhage. Acta Ophthalmol Scand 2001; 79: 34–38. | Article | PubMed | ChemPort | 3. Yang CM, Yeh PT, Yang CH. Intravitreal long-acting gas in the prevention of early postoperative vitreous hemorrhage in diabetic vitrectomy. Ophthalmology 2007; 114: 710– 715. | Article | PubMed 4. Laatikainen L, Summanen P, Immonen I. Effect of tranexamic acid on postvitrectomy haemorrhage in diabetic patients. Int Ophthalmol 1987; 10: 153– 155. | Article | PubMed | ChemPort | 5. Ramezani AR, Ahmadieh H, Ghaseminejad AK, Yazdani S, Golestan B. Effect of tranexamic acid on early postvitrectomy diabetic haemorrhage; a randomised clinical trial. Br J Ophthalmol 2005; 89: 1041–1044. | Article | PubMed | ChemPort | 6. Yang CM, Yeh PT, Yang CH, Chen MS. Bevacizumab pretreatment and long-acting gas infusion on vitreous clear-up after diabetic vitrectomy. Am J Ophthalmol 2008; 146: 211– 217. | Article | PubMed | ChemPort | 7. Rizzo S, Genovesi-Ebert F, Di Bartolo E, Vento A, Miniaci S, Williams G. Injection of intravitreal bevacizumab (Avastin) as a preoperative adjunct before vitrectomy surgery in the treatment of severe proliferative diabetic retinopathy (PDR). Graefes Arch Clin Exp Ophthalmol 2008; 246: 837–842. | Article | PubMed | ChemPort |
  64. 64. 8.West JF, Gregor ZJ. Fibrovascular ingrowth and recurrent haemorrhage following diabetic vitrectomy. Br J Ophthalmol 2000; 84: 822–825. | Article | PubMed | ChemPort | 9.Yeh PT, Yang CM, Yang CH, Huang JS. Cryotherapy of the anterior retina and sclerotomy sites in diabetic vitrectomy to prevent recurrent vitreous hemorrhage: an ultrasound biomicroscopy study. Ophthalmology2005; 112: 2095– 2102. | Article | PubMed 10.Itakura H, Kishi S, Kotajima N, Murakami M. Persistent secretion of vascular endothelial growth factor into the vitreous cavity in proliferative diabetic retinopathy after vitrectomy. Ophthalmology 2004; 111: 1880–1884. | Article | PubMed