Choriovitreal ingrowth of a large choroidal vessel after scatter retinal photocoagulation.

Choriovitreal ingrowth of a large choroidal vessel is a known complication of intense focal retinal laser photocoagulation. With a standard grey-white burn in panretinal photocoagulation where the power density used is low, such an invasion is rarely reported. We came across the complication in a clinical scenario where a patient with proliferative diabetic retinopathy and associated ocular ischemic syndrome developed the neovascular ingrowth after scatter retinal photocoagulation.

Introduction

A grey-white retinal photocoagulation burn results in a faint chorioretinal scar. Rarely does it complicate with chorioretinal and choriovitreal neovascularization if the burn is intense or confluent.[1] Rise in vascular endothelial growth factor secondary to retinal ischemia and a concomitant discontinuity in Bruch's membrane is implicated in its pathogenesis.[12] The occurrence of such complication in the form of a large choroidal vessel after a low density burn, as in scatter photocoagulation, is rarely reported. We present a clinical scenario where retinal scatter photocoagulation for proliferative diabetic retinopathy led to ingrowth of a large choroidal new vessel into epiretinal space.

Case Report

A 56-year-old lady with diabetes of 6 years reported to us with poor vision OD of 3 months duration. Diabetes was under control; anterior segment findings were normal, with a vision of light perception OD due to vitreous hemorrhage and 6/9 OS due to clinically significant macular edema. Additionally, localized areas of flat retinal neovascularization were seen along the temporal arcades OS. Since she was unwilling for the offered pars plana vitrectomy OD due to financial constrains, we went ahead treating the left eye with scatter laser photocoagulation for nasal half of retina and macular focal photocoagulation with 532 nm Nd-YAG laser (model 1149-675 Carl Zeiss Meditec AG, Jena, Germany). The laser was delivered through Mainster wide field contact lens with a spot size of 200 microns. Power and duration were adjusted to achieve a grey–white burn (200 mW and 200 mS, respectively). The pan retinal photocoagulation remained incomplete in temporal half of retina because of her failure to report back to us.

After 8 months of lost follow up the vision in the lasered eye had dropped to 6/60. Anterior segment findings were within normal limits. There was no evidence of iris or angle neovascularization. On fundus examination apart from the narrowed arterioles and white appearing venules, the macula was found obscured with a large neovascular frond and pre-retinal hemorrhage which appeared to be fed by a solitary and tortuous new vessel, apparently originating from one of the photocoagulation scars nearly 3DD nasal to the optic disc margin [Figure 1]. It traversed the optic disc and finally dissolved into the neovascular frond. In order to detect the origin and nature of the vessel, a rapid sequence fluorescein angiography was performed. The new vessel filled early in the choroidal phase of the angiogram, before the dye appeared in the retinal arteries indicative of its choroidal origin [Figure 2]. A gross delay of arterio-venous transit (3 min) prompted us to look for other systemic associations. Duplex Doppler study revealed total occlusion of left distal common carotid artery and left internal carotid artery by echogenic thrombus deposited on calcified plaques.

Figure 1

Fundus view of left eye showing white appearing venules at disc and narrowed arterioles secondary to ocular ischemic syndrome. A tortuous vessel traversing the optic disc apparently originates from a laser photocoagulation scar (arrow)

Figure 2

(a and b) Sequential early phase angiograms of left eye showing the appearance of fluorescein dye in the new vessel prior to filling the arterioles at disc, (c) Subsequent frame of angiogram in arterial phase reveals the origin of the vessel from a photocoagulation scar confirming a choriovitreal neovascularization secondary to laser photocoagulation

Discussion

Whether it is a laser-induced chorioretinal venous anastomosis in vein occlusions, or a confluent laser photocoagulation leading to choriovitreal neovascularization, the power density used in such procedures is much more than a standard scatter laser photocoagulation. Bruch's membrane is the key barrier which is breached with such intense burns.[1] A concomitant retinal ischemia favors the choroidal vessels to invade retina or vitreous through these breaks in Bruch's membrane.[2] Studies on experimental animals suggest that the optimal laser power to disrupt Bruch's membrane and establish a communication between choroid and retina is nearly fivefold (1 W)[3] than that of the energy required to achieve grey–white scatter laser burn. We believe that the treatment intensity used for our patient (200 mW) was too mild to cause that extensive a disruption of the Bruch's membrane which would allow a large choroidal vessel ingrowth through it. Reports of such large vessel ingrowth attribute it to severe clinical burns, particularly with focal retreatment.[1]

The ischemic and untreated temporal retina might have contributed the required levels of vascular endothelial growth factor for the ingrowth. The path of the new choroidal vessel from the ablated nasal retina toward the temporal unablated retina may justify it. The association of ocular ischemic syndrome in our case, and reports of classic choroidal neovascular membranes in ocular ischemic syndrome[4] may suggest that a global ischemia could possibly compromise the Bruch's membrane integrity and give rise to such complications with injuries as trivial as a standard scatter laser photocoagulation.