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Similar to Focus Co Management 2016 Dr Dolin
Focus Co Management 2016 Dr Dolin
- 1. 6/17/2016 1 Retinal considerations for refractivesurgery Michael Dollin, MD, FRCSC Assistant Professor University of Ottawa Eye Institute Ottawa, Ontario, Canada June 2, 2016 Outline • Vitreoretinal alterations during refractive surgery • Disorders of the macula • Disorders of the peripheral retina
- 2. 6/17/2016 2 Outline • Vitreoretinal alterationsduring refractive surgery • Disorders of the macula – Epiretinal membrane – Vitreomacular traction – Myopic foveoschisis – Myopic macular hole – Cystoid macular edema • Disorders of the peripheral retina – Lesions predisposing to retinal detachment – Retinal detachment – Retinoschisis Homer Simpson “Eye crusts” after laser eye surgery
- 3. 6/17/2016 3 Serious retinal complicationsafter refractive surgery are rare
- 4. 6/17/2016 4 Vitreoretinal alterations during refractivesurgery • Corneal refractive surgery (CRS) – Suction ring changes in eye shape power vectors relayed to the macula and/or vitreous base – Effect of the excimer laser shock wave appears negligible
- 5. 6/17/2016 5 Vitreoretinal alterations during refractivesurgery • Refractive lens exchange (RLE) – VR alterations similar to those induced during cataract surgery (PC trampolining, PC rupture) Thorough pre-operative dilated fundus examination is key
- 6. 6/17/2016 6 Examination techniques • Macula –Slit lamp and 90D or 78D lens – OCT? • Peripheral retina – Indirect ophthalmoscopy +/- scleral depression – Goldmann 3-mirror or wide field contact lens – Optos? Disorders of the macula • Epiretinal membrane • Vitreomacular traction • Myopic foveoschisis • Myopic macular hole • Cystoid macular edema • Diabetic macular edema MACULA
- 7. 6/17/2016 7 MACULA Epiretinal membrane (ERM) •Glial cells and laminocytes that attach to a scaffold of vitreous cortex on the inner retinal surface, typically after PVD • ERM contracture causes macular traction distorting the underlying foveal structure thickening +/- CME
- 8. 6/17/2016 8 Epiretinal membrane (ERM) •Incidence increases with age – Seen in 7% of patients ≥50 years old – 31% bilateral • May occur during any stage of vitreous separation (vitreoschisis) – In younger patients, often present in absence of PVD • Refer for Retina opinion Case • 36 year old male • Referred for macular evaluation prior to CRS • C/O mild blur OD, no distortion • High myope (-9 OU) • BCVA 20/25 OD, 20/20 OS
- 9. 6/17/2016 9 OD OS Subtle flatteningof foveal contour due to ERM Normal foveal contour Important for pre-op counseling
- 10. 6/17/2016 10 Vitreomacular adhesion (VMA) •Perifoveal vitreous separation with remaining vitreomacular attachment • Unperturbed foveal morphologic features • May or may not lead to pathologic conditions Vitreomacular traction (VMT) • Anomalous PVD accompanied by anatomic distortion of the fovea – Pseudocysts, macular schisis, cystoid macular edema, and subretinal fluid • Focal (≤ 1500μ) vs. broad (> 1500μ) • Concurrent = associated with other macular disease (e.g. ERM) • Variably symptomatic – Decreased vision, metamorphopsia, central scotoma
- 11. 6/17/2016 11 OCT essential inthe diagnosis Distinguish from vitreomacular adhesion (VMA) • Unperturbed foveal morphologic features
- 12. 6/17/2016 12 VMT • Management – Observation •1/3 will release spontaneously – Ocriplasmin (Jetrea) – Vitrectomy • 5% will require surgery due to bothersome symptoms or progression to full thickness macular hole • Refer for Retina opinion Myopic foveoschisis • Increasingly recognized entity with advent of OCT – Prevalence 9-33% of myopic eyes with staphyloma • Mechanism is mixture of tractional forces – Abnormal vitreomacular interface pulling inward – Abnormal scleral alterations pulling outward
- 13. 6/17/2016 13 • Despite oftenimpressive anatomic findings, most patients may be relatively asymptomatic – Visual loss often eventually attributed to foveal detachment and/or macular holes • Choroidal thinning often an associated feature – May reduce vision independent of schisis • Refer for Retina opinion Case • 32 yo female • Interested in CRS • Myope (-6 OU) • BCVA 20/20 OD, CF OS
- 14. 6/17/2016 14 20/20 CF Macular hole •Foveal lesion with interruption of all retinal layers from ILM to RPE • Primary (due to VMT) or secondary (e.g. traumatic) • Small ≤ 250 μ • Medium > 250 μ – 400 μ • Large > 400 μ • Status of vitreous: – With VMT – Without VMT
- 15. 6/17/2016 15 Macular hole inhigh myopes • Can be extremely subtle, if not impossible, to detect clinically – Particularly in the setting of posterior staphyloma • Obtain an OCT • Refer for Retina opinion Case • 48 year old female • Referred for retina check prior to RLE • High myope (-12 OU) • BCVA 20/30-2 OD, 20/25 OS
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- 17. 6/17/2016 17 Cystoid macular edema •Various etiologies – Vein occlusion, diabetes, radiation, uveitis, CNV, etc • Presumed inflammatory etiology post RLE Cystoid macular edema • Presumed inflammatory etiology post RLE – Stepwise approach to treatment beginning with topical therapy: – Prednisolone (e.g. Pred forte QID) – NSAID (e.g. Acular QID, Nevanac TID) – Taper slowly once CME has resolved • Refer to Retina – If not improving after 4-6 weeks of topical therapy – May require sub-Tenon’s or intravitreal steroid
- 18. 6/17/2016 18 A note aboutdiabetic macular edema • Refer to Retina if DME is detected on pre-op exam • In patients receiving anti-VEGF for DME and wishing to undergo RLE, ideal to time surgery 1 week after an injection Disorders of the peripheral retina • Lesions not predisposing to retinal detachment • Lesions predisposing to retinal detachment • Posterior vitreous detachment • Retinal detachment • Retinoschisis
- 19. 6/17/2016 19 Lesions NOT predisposingto RD • Pavingstone (cobblestone) degeneration • RPE hyperplasia and hypertrophy • Peripheral cystoid degeneration • White without pressure
- 20. 6/17/2016 20 Pavingstone (cobblestone) degeneration •Small, discrete areas of ischemic atrophy of outer retina • 22% of patients over 20 years of age, 38% bilateral • May be single or multiple and confluent • Most commonly inferior (5-7 o’clock) and anterior to the equator
- 21. 6/17/2016 21 Peripheral RPE abnormalities •Hyperplasia/Hypertrophy – Acquired secondary to mild vitreous traction, previous inflammation or trauma – Congenital (CHRPE)
- 22. 6/17/2016 22 Peripheral cystoid degeneration •Zones of microcysts with bubbly appearance posterior to the ora • Present in virtually all adults over 20 years old • Holes may form but rarely lead to RD • Coalescence and extension of cavities can progress to retinoschisis
- 23. 6/17/2016 23 White without pressure •White appearance of the equator and/or peripheral retina seen without scleral indentation • Margins often sharply demarcated from normal retina
- 24. 6/17/2016 24 Lesions predisposing toRD • Lattice degeneration • Vitreoretinal tufts • Meridional folds • Retinoschisis
- 25. 6/17/2016 25 Lattice degeneration • Crisscrossinglattice work of white lines (hyalinized blood vessels) – Typically parallels the ora seratta • 6-10% of general population – Bilateral in 33% • More common in myopes • Familial predilection • Atrophic holes within lattice present in 31% Lattice degeneration • Histopathology – ILM discontinuity – Inner retinal layer atrophy – Liquefaction of overlying vitreous – Condensation and adherence of vitreous at margin
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- 27. 6/17/2016 27 Lattice degeneration andRD • Cause of 20-30% of RRDs (present in 41%) • Due to tractional tear at lateral or posterior margin (55-70%) – 90% under 50 yo and 43% myopic – Progress rapidly and demarcation lines less likely • Due to atrophic hole within lattice (30-45%) – 70% under 40 yo and 70% myopic – Progress slowly and see demarcation lines, due to tear
- 28. 6/17/2016 28 Lattice degeneration andRD • Lifetime risk (11-year study) of RD in all patients with lattice is 1% – Increases to 2% if atrophic holes present in lattice • Presence of lattice, with or without atrophic holes on routine exam, does not require prophylactic treatment Lattice with atrophic holes
- 29. 6/17/2016 29 • 2% riskof RD • Lesion should not be treated prophylactically Atrophic hole not associated with lattice
- 30. 6/17/2016 30 Lattice with tractionalretinal tear
- 31. 6/17/2016 31 Vitreoretinal tufts • Small,peripheral retinal elevations caused by focal areas of vitreous or zonular traction – +/- surrounding RPE hyperplasia • 3 types of tufts: – Non-cystic (do not predispose to RD) – Cystic and Zonular traction (predispose to RD)
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- 33. 6/17/2016 33 • Risk ofa retinal detachment from cystic retinal tuft is quite low and estimated to be only 0.28% – Prophylactic treatment not necessary if detected on routine exam – Treat if recent flashes and floaters and break is suspected Meridional folds • Folds of redundant retina • Usually superonasal • Meridional folds can be associated with retinal breaks at the tip
- 34. 6/17/2016 34 • Prophylactic treatmentof meridional folds not necessary if detected on routine exam • Treat if recent flashes and floaters and break is suspected
- 35. 6/17/2016 35 Posterior vitreous detachment •May develop in 2-24% of eyes following CRS – Increasing incidence with increasing myopia • Patients with new onset flashes and floaters following CRS should be evaluated with DFE – Rule out retinal break • 10-15% will have a retinal tear – With hemorrhage 70% – Without hemorrhage 2-4% Weiss ring
- 36. 6/17/2016 36 Case • 26 yearold female • Sudden onset floaters post-CRS High risk for tears Refer to Retina
- 37. 6/17/2016 37 Rhegmatogenous retinal detachment •Risk of RRD after CRS is very low – Particuarly with adequate pre-operative screening for high risk peripheral retinal lesions • Characteristics of RRD are similar in patients having undergone CRS compared to patients who have not – Myopia likely contributes more to the risk of RRD than the refractive surgery itself
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- 40. 6/17/2016 40 Retinoschisis • Intraretinal degenerativeprocess with splitting of retina in periphery, accumulation of intraretinal fluid, and loss of visual function – Split of sensory retina into outer and inner layer • Found in 5% of population over 20 years • 70% are hypermetropes • Generally nonprogressive – Posterior extension 3.2% – Lateral extension 6.4% – New areas 10%
- 41. 6/17/2016 41 Retinoschisis-retinal detachment • Responsiblefor 3.2% of full-thickness RD • Expected incidence of progressive RD in patients with retinoschisis 0.05% • 2 types of RD: – Hole in outer wall only: usually do not progress or do so slowly (demarcation and RPE atrophy often present) – Hole in outer and inner walls: may result in rapidly progressive RD
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- 43. 6/17/2016 43 Differentiating retinoschisis from retinaldetachment CLINICAL FEATURE RD RS High risk group Symptoms Location Surface Hgb or pigment (Shafer’s) Scotoma Reaction to photocoagulation Shifting fluid Myopia F/F, VF loss Superotemporal Corrugated Present Relative Absent Variable Hyperopia (70%) Typically asymptomatic Inferotemporal (70%) Smooth, dome-shaped Usually absent Absolute Present Absent
- 44. 6/17/2016 44 • Chronic RRD –Retina may appear smooth, thin and transparent – May also show underlying RPE atrophy, demarcation lines, and macrocysts -- not present in retinoschisis
- 45. 6/17/2016 45 Summary • Retinal complicationsafter LASIK are rare • Complications of the myopic eye will persist – Important to inform patients that refractive surgery only corrects the refractive aspect of myopia • Pre-op dilated fundus examination of the macula and peripheral retina is very important to identify any high risk lesions – Also important post-op when vision is not as good as expected • If high risk peripheral lesions or new macular lesions are detected refer to Retina
- 46. 6/17/2016 46 Acknowledgements • Novartis • JohnD. Pitcher, III • Rahul Sharma • Parnian Arjmand Thank you
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