The first-line treatment to avoid visual impairment for these cases is anti-vascular endothelial growth factor therapy (VEGF).
Myopic choroidal neovascularisation (CNV) and myopic tractional maculopathy are serious complications of pathologic myopia and the former has been reported in from 5% to 10% of eyes with high myopia.1,2 Without treatment, severe visual impairment can occur. In these cases, the first-line treatment is anti-vascular endothelial growth factor therapy (VEGF).
Researchers from the Department of Ophthalmology, Osaka University Medical School, Osaka, Japan, led by Kaori Sayanagi, MD, PhD, reported 3 cases of myopia foveoschisis around myopic CNV, a rare event, that followed 3 different clinical courses visualised using swept-source optical coherence tomography (SS-OCT).3
They explained that myopic foveoschisis also is one manifestation that can occur under the general term myopic tractional maculopathy.
Patient 1, a 69-year-old woman, had an axial length of 29.71 mm, myopic CNV and myopic foveoschisis in the left eye. She was treated with intravitreal ranibizumab (IVR) (Lucentis, Genentech), and 1 month later a macular retinal detachment expanded. Following vitrectomy and gas tamponade during month 2, the macular retinal detachment and myopic foveoschisis resolved gradually.
Patient 2, a 54-year-old man, had an axial length of 30.59 mm, myopic CNV and myopia foveoschisis in the right eye. After IVR, a macular retinal detachment developed and expanded gradually until month 4. The retinal detachment and myopic foveoschisis resolved spontaneously during month 8.
Patient 3, a 66-year-old woman, had an axial length of 28.63 mm, myopic CNV and MF in the left eye. A macular retinal detachment expanded 1 month after a previous vitrectomy performed to treat the myopic foveoschisis. After intravitreal aflibercept (Eylea, Regeneron), the macular retinal detachment and myopic foveoschisis resolved gradually in month 12.
The 3 cases had CNV accompanied by subretinal fluid, and 2 of the 3 cases had outer lamellar holes.
Sayanagi and colleagues pointed out the commonalities among the 3 cases: all had myopic foveoschisis around the myopic CNV and an exacerbated macular retinal detachment during follow-up. They mentioned three hypotheses regarding the mechanisms:
Increased vitreous traction caused by anti-VEGF therapy. While the retinal detachment slowly resolved after VEGF therapy, the impact of anti-VEGF therapy cannot be excluded.
An outer lamellar hole. In addition to such previously reported cases, 4 outer lamellar holes were observed in 2 of the 3 current cases.
Subretinal fluid accumulation. The fluid accumulates after splitting of the retina progresses to a macular retinal detachment and the fluid accumulation can disrupt the balance of centripetal and centrifugal traction, resulting in spontaneous progression of the myopic traction maculopathy.
Management of these cases is not yet established because of the differing courses. The investigators advised close patient follow up and consideration of emergent surgery if the macular retinal detachment is exacerbated. Attention then should be paid to the vitreoretinal relationship using SS-OCT. They believe that further investigation of this entity is warranted to determine appropriate management.