COORDINATED BY ABDHISH R. BHAVSAR, MD
Welcome to Face Off, a column that explores controversial topics in the diagnosis and management of retinal diseases. Several topics are covered in each issue, with one specialist writing in favor of the treatment or surgery and another writing in opposition, regardless of whether they personally believe in that position.
In this issue, we address central retinal vein cannulation and tissue plasminogen activator (tPA) for central retinal
|Abdhish R. Bhavsar, MD, is an attending retina surgeon at the Phillips Eye Institute, Director of Clinical Research at the Retina Center, P.A., in Minneapolis, MN., and adjunct assistant professor at the University of Minnesota. He also serves as state chair of the Minnesota Diabetes Eye Exam Initiative. E-mail him about Face Off at email@example.com.|
Central retinal vein cannulation and tPA injection for CRVO
IN FAVOR OF
Leon A. Bynoe, MD: CRVO can be devastating to the eye, often producing severe and permanent loss of vision. Vitrectomy with central venous injection of tPA is about as technically challenging as an epiretinal membrane peel, is relatively safe and seems to promote visual recovery at much higher rates and magnitudes than what occurs without treatment. Furthermore, it can be combined with other treatment modalities, such as intravitreal steroid injection, to optimize outcomes. If it is reasonable to perform vitrectomy surgery to peel an epiretinal membrane, it is certainly reasonable to perform comparable surgery to treat a far more severe disease like CRVO.
Maurice B. Landers, III, MD: You can get fluids into the retinal veins with the cannula that Weiss has developed. However, there is zero level 1 evidence that this does any good, even more than 3 years after the first report of success with the procedure. Also, to my knowledge, there is not even any "word on the street" that it works, in spite of the Rx equipment having been available for several years, and there being an obvious need for any Rx that is of any major benefit to this devasting problem. It is illogical that tPA injected a long time after a clot developed in a CRVO case would dissolve the clot. On the other hand, most CRVO cases still have some blood flow (retina is not infarcted), so perhaps just mechanically pushing the "clot" downstream might be a real help. Nevertheless, no one has ever shown convincing, scientific proof, in an accepted fashion that this condition is better than the natural course of the disease. I don't accept the historical controls vs. the reported controlled cases. In summary, "Where's the beef?"
RON for CRVO
IN FAVOR OF
E. Mitchel Opremcak, MD: RON is a new vitreoretinal surgical technique that addresses CRVO as a compartment syndrome. In 180 consecutive patients (unpublished) with severe CRVO, clinical resolution occurred in 94% of patients following RON. Visual acuity (VA) improved in 70% of patients by an average of 3 lines. Anterior segment neovascularization developed in 6% of patients following RON, and postoperative complications were minor and infrequent. The anatomic and visual outcomes of RON compare favorably to the poor prognosis for patients with CRVO noted in natural history studies.
Sohan Singh Hayreh, MD, MS, PhD, DSc, FRCS, FRCOphth: There is no scientific rationale whatsoever for the whole idea of RON to decompress the central retinal vein (CRV) in CRVO.1 It is based on the lack of basic understanding of the anatomy of the optic nerve head and central retinal vein and their circulation, the site of thrombosis in CRV, and the fact that a vein which is invariably completely closed by an organized thrombus cannot be opened by "decompression." Moreover, the procedure can be a harmful. Several complications have been reported following RON, including visual field defect, choroidovitreal neovascularization and serous retinal detachment at the RON site, central retinal artery occlusion and in 43%, cataract formation.
1. Hayreh SS. Radial optic neurotomy for central retinal vein occlusion. Retina 2002;22:374-377, 827.
Arteriovenous sheathotomy for BRVO
IN FAVOR OF
Jose Garcia-Arumi, MD: Since Osterloh and Charles described the dissection of the adventitial sheath (sheathotomy) at the arteriovenous crossing, 14 authors have published their experience with this technique in the management of macular edema secondary to BRVO. The results have been controversial, as some authors have obtained a marked improvement in VA (60%-70% of the patients improving 3 or more lines) and reduction of macular edema, while others have found no differences between adventitious sheathotomy and vitrectomy alone. It is not possible to extract conclusions from these publications. Our experience during 5 years and more than 100 sheathotomies performed is that in selected cases the technique is safe and effective. Our inclusion criteria are: 1) short time of evolution (as fresh is the BRVO, as easy is to reperfuse the vein), with a limit of 6 months of evolution; 2) first class crossing. We do not operate crossing of second order. The reperfusion is easier in crossings near the optic disc, as the calibre of the vein is bigger; 3) VA 20/60 or worse. Patients with better VA usually recover spontaneously; 4) foveal thickness over 400 �m. We always perform intraoperative fluorescein angiography in order to know if we have obtained the reperfusion and decompression of the vein. Following these criteria, 75% of patients gain 3 or more lines of final BCVA.
Steve T. Charles, MD: Although I developed and first reported the concept of branch vein decompression, I abandoned the procedure after 20 cases because there is no solid evidence that it results in significant revascularization or visual improvement better than the natural history. I do not refer to these procedures as �sheathotomy� because Seitz and, later, W. Richard Green pointed out that there is no sheath. Focal laser and/or intravitreal triamcinolone are effective in many BRVO cases with persistent macular edema. It is likely that vitrectomy without vein decompression results in visual improvement in some cases and I postulated in 2000 that this is because of reduced VEGF in the macula due to decompartmentalization. Many anti-VEGF agents are in development and Macugen has been approved. It is likely that 1 or more of these agents will prove to be effective for treating macular edema secondary to BRVO although this would be offlabel.