Surgical Therapy of CME Non-responsive to Medical Therapy Henry J Kaplan, MD Evans Professor of Ophthalmology Chair, Ophthalmology & Visual Sciences Director,

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Presentation transcript:

Surgical Therapy of CME Non-responsive to Medical Therapy Henry J Kaplan, MD Evans Professor of Ophthalmology Chair, Ophthalmology & Visual Sciences Director, Kentucky Lions Eye Center University of Louisville 25 th Iran Congress of Ophthalmology 2015

Major Principle CME associated with uveitis initially develops because of inflammatory mediators released with intraocular inflammation Therefore, the first line of treatment in uveitic CME is suppression of inflammation If inflammation is suppressed, with corticosteroids/IMT (immune suppression or biologics), and uveitic CME persists then tractional forces on the macular must be considered as a cause of persistent CME and surgical relief considered

Options for Initial Medical Therapy Three Routes of Corticosteroid Administration –Periocular Kenalog (Triamcinolone acetonide) –Intravitreal Kenalog Ozurdex (Dexamethasone) Iluvein (Flucinolone acetonide) –Oral Prednisone

i C ORTICOSTEROID R ESPONSIVE CME ii. Intravitreal Injection  Indications:  Chronic CME non- responsive to topical, periocular or systemic CS  Adjunctive therapy with Avastin, Methotrexate, …  Dose: 2-4 mg Kenalog/ ml  Side effects  Associated CS side effects (OHT, PSCC)  Veil over vision  Clean Technique –  Gloves  Topical anes with Alcaine and Tetracaine  Sterilization with topical Betadine  Topical anes with Tetravisc  Sterile lid speculum  3.5 to 4.0 mm limbus in ST or IT quadrant  ul, 27 gauge needle, 1 cc syringe

Systemic Corticosteroids Initial dose: –p.o mg/kg/d for 2 weeks –(i.v. pulse therapy - e.g. 1g/d for 3 days, continue p.o.) Slow dose tapering –≥ 40mg/d, 20 mg/bid-qid/day, for 2 weeks then –Slow taper weekly – 40, 30, 20,15, 10, 7.5, 5, D/C –Maintenance dose: ≤ 7.5 mg/d Persistent CME with resolution of inflammation after corticosteroid and IMT treatment defines medically non- responsive treatment

Approach to Medically Non-responsive CME Cause: macular distortion Objective: relief of tractional forces before permanent anatomical damage to NSR Three causes of persistent uveitic CME 2 tractional forces –Vitreomacular traction sysndrome (A-P) –Adherent posterior hyaloid (T) –Gliosis of ILM (T)

Vitreous Tractional Forces

EXAMINATION OF THE VITREOUS FOR TRACTION DYNAMIC ULTRASOUND

E XAMINATION OF THE V ITREOUS FOR PVD DYNAMIC ULTRASOUND

(1) Vitreomacular Traction Syndrome VMT - distortion of the macular contour 1 due to anteroposterior (A-P) or tangential (T) tractional forces applied by the vitreous to the parafoveal region. CME results from distorted macular architecture.

SD-OCT Helps to Better Understand Vitreo-Macular Interface

(2) Adherent Posterior Hyaloid No VMT pre-operatively on clinical examination or by SD-OCT Requires IVT injection at the time of surgery to identify existence “Figure of 8” appearance

Fig 8 Adherent Post Hyaloid

Single, as well as multiple layers of myofibroblasts, fibroblasts and astrocytes use the vitreal surface of the ILM as a scaffold (arrows) Newly formed collagen (arrow heads) present (3) Gliosis of ILM

Distortion of ILM causes tangential traction around the fovea and results in CME and inner lamellar macular holes. Clinical sign: glean to surface of macula Gliosis of ILM

Peel of Fragile ILM Gliosis

To remove and relieve foveal traction from the retinal surface. Three steps Relieve A-P traction by PPV if present (VMT) Relieve an adherent posterior hyaloid (Figure 8) – clinically invisible residual posterior hyaloid Removal of ILM (gliosis of ILM) Surgical Objective in Persistent CME

Thank You