The montage image reveals some old inferior vitreous hemorrhage and choroidal ruptures in the posterior pole. Choroidal ruptures result from traumatic deformation of the globe causing breaks in Bruch’s membrane. There can be direct damage to central vision if the rupture involves the central macula or if there is an associated subretinal hemorrhage. Choroidal neovascularization is a frequent late complication as blood vessels grow through the opening in Bruch’s membrane. Interestingly, our patient has preretinal fibrosis associated with the inferior choroidal rupture. Evidently, there was fibrosis of neovascularization that grew from the choroid, through the retina, and into the preretinal space. There is now a thin band that reaches the disc, which likely reflects fibrosis of a blood vessel that grew along the posterior hyaloid face. A similar clinical picture was seen in patients who were treated for central retinal vein occlusions with a high-energy laser blast designed to both damage a vein and rupture Bruch’s membrane, resulting in neovascular growth into the retina and anastomosis with the damaged vein. This would generate a novel path for venous outflow from the retina. While sometimes successful, this treatment never had widespread acceptance largely because of the frequent incidence of vision-damaging preretinal fibrosis.
Another remarkable finding in our patient relates to the grayish discoloration located nasal to the fovea at the superior border of the inferotemporal choroidal rupture. OCT reveals a deep reflective lesion with associated diffuse macular edema. OCTA reveals a choroidal neovascular membrane that courses along the direction of the choroidal rupture and then terminates in a round collection of blood vessels. Concerned that the CNVM might grow and damage the fovea, we initiated anti-VEGF treatment with Avastin.