Indirect choroidal neovascularization secondary to a posteri
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Choroidal neovascularization (CNV) secondary to traumatic choroidal rupture after direct penetrating injuries has been reported to manifest between 1 month and 4 years after ocular trauma. Generally, the retina, choroid, and Bruch’s membrane are lacerated at the time of impact by a fast-shot intraocular foreign body (IOFB). Injury to Bruch’s membrane from an IOFB results in a defect where CNV is derived from the choriocapillaris and grows into the subretinal or subpigment epithelial space.

A 26-year-old male patient without a history of systemic diseases or myopia suffered from a fast-shot metallic IOFB in his right eye while working. a penetration wound with iris incarceration was located at the nasal lower cornea in his right eye. Under a slit lamp, he was found to have a diffuse, thin hyphema and some blood clots at the position of the distorted and torn pupil (Fig. 1a). His best-corrected visual acuity (BCVA) was hand motion at 30 cm in the right eye and 18/20 in the left eye. Orbital computed tomography (CT) without contrast enhancement showed a metallic IOFB with a size of 8X4 mm floating in the vitreous cavity in different views, such as the horizontal, coronary, and sagittal views.

He underwent primary corneal repair, pars plana vitrectomy, IOFB removal and prophylactic IVI of antibiotics with vancomycin (1 mg/0.1 c.c.) and ceftazidime (2 mg/0.1 c.c.) at the end of surgery. At the beginning of vitrectomy, no retinal impact was noted. However, the IOFB dropped to the nasal and upper retinal area outside the macula while performing the vitrectomy to release vitreous traction around the IOFB. Two weeks later, his intraocular pressure in the right eye elevated abruptly to 30 mmHg with cell 3+ in the deep anterior chamber and a cloudy, swollen lens. Because of the suspicion of phacolytic glaucoma, he underwent cataract surgery. The BCVA in his right eye recovered to 20/20 5 months later, with good foveal contour except for a small retinal dimple (yellow arrow) and a segment of hyporeflectivity at the inner segment and outer segment (IS/OS) junction (white arrow) of the temporal fovea.

Twelve months after the first surgery, he returned to clinic because of a sudden onset of metamorphopsia with a decline in BCVA to 6/20 in his right eye. There was a whitish lesion at the fovea with faint retinal hemorrhage and surrounding sensory elevation. Optical coherence tomography (OCT) revealed subretinal fluid with a CNV lesion. Fluorescence angiography (FA) demonstrated that the foveal CNV was hyperfluorescent and leaking at the early phase with severe dye pooling at the late phase. He received an intravitreal injection of aflibercept (4 mg/0.1 mL) in his right eye every 8 weeks for three times; over the treatment period, OCT showed a gradual reduction of the subretinal fluid and the resolution of the CNV lesion, which completely disappeared. His right-eye BCVA improved to 16/20 without visual distortion within 3 months

In conclusion, CNV may occur later in cases of obvious foveal choroidal rupture or Bruch’s membrane rupture after posterior-segment IOFB. For the rare cases of fovea-spared injury by a metallic IOFB, it is still necessary to pay close attention to the foveal microstructure at each follow-up visit to avoid possible CNV formation. Regardless of whether CNV is direct or indirect, prompt treatment with an IVI of an anti-VEGF, such as aflibercept, as early as possible could truly provide good visual outcomes.