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Targeted photocoagulation of peripheral ischemia to treat rebound edema.

Singer MA, Tan CS, Surapaneni KR, Sadda SR - Clin Ophthalmol (2015)

Bottom Line: To target the treatment to peripheral ischemia areas, a Navilas Panretinal Laser was used.A 64-year-old male with a central retinal vein occlusion and a visual acuity 20/300, and central macular thickness 318 μm presented with rubeosis.Angiography revealed extensive peripheral nonperfusion.

View Article: PubMed Central - PubMed

Affiliation: Medical Center Ophthalmology Associates, San Antonio, TX, USA.

ABSTRACT

Introduction: Peripheral retinal ischemia not detectable by conventional fluorescein angiography has been proposed to be a driving force for rebound edema in retinal vein occlusions. In this report, we examine the treatment of peripheral retinal ischemia with targeted retinal photocoagulation (TRP) to manage a patient's rebound edema.

Methods: To assess the extent of peripheral nonperfusion, an Optos 200Tx device was used. To target the treatment to peripheral ischemia areas, a Navilas Panretinal Laser was used.

Results: A 64-year-old male with a central retinal vein occlusion and a visual acuity 20/300, and central macular thickness 318 μm presented with rubeosis. Angiography revealed extensive peripheral nonperfusion. Despite TRP to areas of irreversible ischemia, after 2 months, he continued show rubeosis and rebound edema. Additional TRP laser was repeatedly added more posteriorly to areas of reversible nonperfusion, resulting in eventual resolution of rubeosis and edema.

Conclusion: In this study, we demonstrate the use of widefield imaging with targeted photo-coagulation of peripheral ischemia to treat rebound edema, while preserving most peripheral vision. In order to treat rebound edema, extensive TRP, across reversible and nonreversible areas of ischemia, had to be performed - not just in areas of nonreversible peripheral ischemia. These areas need to be mapped during episodes of rebound edema, when ischemia is at its maximum. In this way, by doing the most TRP possible, the cycle of rebound edema can be broken.

No MeSH data available.


Related in: MedlinePlus

Variation of OCT thickness with the extent of ischemia.Abbreviation: OCT, optical coherence tomography.
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f5-opth-9-337: Variation of OCT thickness with the extent of ischemia.Abbreviation: OCT, optical coherence tomography.

Mentions: Rebound edema was first described by Matsumoto et al after an observation that patients who were treated for RVO with anti-VEGF injections developed increased edema on OCT after anti-VEGF therapy was discontinued. The authors postulated that rebound edema was due to untreated peripheral ischemia, which caused VEGF production, leading to ischemia.5 It is known that TRP therapy reduces VEGF production in the retina by reducing tissue oxygen demand, thereby reducing the ischemic drive.16 It has been theorized that this effect could potentially break the cycle of rebound edema. However studies have not demonstrated this to be the case.12 We have previously shown15 that the use of anti-VEGF agents actually causes a decrease in the amount of ischemia seen on Optos widefield angiography. In a prospective cohort study, mean ischemic index was reduced from 14.8% on initial presentation to 10.3% following treatment with anti-VEGF agents.15 In the present study, we also showed that the level of nonperfusion correlates with the severity of macular edema (Figure 5).


Targeted photocoagulation of peripheral ischemia to treat rebound edema.

Singer MA, Tan CS, Surapaneni KR, Sadda SR - Clin Ophthalmol (2015)

Variation of OCT thickness with the extent of ischemia.Abbreviation: OCT, optical coherence tomography.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4335623&req=5

f5-opth-9-337: Variation of OCT thickness with the extent of ischemia.Abbreviation: OCT, optical coherence tomography.
Mentions: Rebound edema was first described by Matsumoto et al after an observation that patients who were treated for RVO with anti-VEGF injections developed increased edema on OCT after anti-VEGF therapy was discontinued. The authors postulated that rebound edema was due to untreated peripheral ischemia, which caused VEGF production, leading to ischemia.5 It is known that TRP therapy reduces VEGF production in the retina by reducing tissue oxygen demand, thereby reducing the ischemic drive.16 It has been theorized that this effect could potentially break the cycle of rebound edema. However studies have not demonstrated this to be the case.12 We have previously shown15 that the use of anti-VEGF agents actually causes a decrease in the amount of ischemia seen on Optos widefield angiography. In a prospective cohort study, mean ischemic index was reduced from 14.8% on initial presentation to 10.3% following treatment with anti-VEGF agents.15 In the present study, we also showed that the level of nonperfusion correlates with the severity of macular edema (Figure 5).

Bottom Line: To target the treatment to peripheral ischemia areas, a Navilas Panretinal Laser was used.A 64-year-old male with a central retinal vein occlusion and a visual acuity 20/300, and central macular thickness 318 μm presented with rubeosis.Angiography revealed extensive peripheral nonperfusion.

View Article: PubMed Central - PubMed

Affiliation: Medical Center Ophthalmology Associates, San Antonio, TX, USA.

ABSTRACT

Introduction: Peripheral retinal ischemia not detectable by conventional fluorescein angiography has been proposed to be a driving force for rebound edema in retinal vein occlusions. In this report, we examine the treatment of peripheral retinal ischemia with targeted retinal photocoagulation (TRP) to manage a patient's rebound edema.

Methods: To assess the extent of peripheral nonperfusion, an Optos 200Tx device was used. To target the treatment to peripheral ischemia areas, a Navilas Panretinal Laser was used.

Results: A 64-year-old male with a central retinal vein occlusion and a visual acuity 20/300, and central macular thickness 318 μm presented with rubeosis. Angiography revealed extensive peripheral nonperfusion. Despite TRP to areas of irreversible ischemia, after 2 months, he continued show rubeosis and rebound edema. Additional TRP laser was repeatedly added more posteriorly to areas of reversible nonperfusion, resulting in eventual resolution of rubeosis and edema.

Conclusion: In this study, we demonstrate the use of widefield imaging with targeted photo-coagulation of peripheral ischemia to treat rebound edema, while preserving most peripheral vision. In order to treat rebound edema, extensive TRP, across reversible and nonreversible areas of ischemia, had to be performed - not just in areas of nonreversible peripheral ischemia. These areas need to be mapped during episodes of rebound edema, when ischemia is at its maximum. In this way, by doing the most TRP possible, the cycle of rebound edema can be broken.

No MeSH data available.


Related in: MedlinePlus