We had a case similar to the one reported by Hwang et al.1 The patient was a 25-year-old woman who sustained an injury in the left eye from a broken glass bottle. The superior 6.0 mm paralimbal corneal scleral tear was repaired by repositioning the uveal tissue and excising a small bead of vitreous that had prolapsed at the laceration site. Six weeks after the wound repair, the patient regained a best corrected visual acuity (BCVA) of 20/20. The wound healed well.
Four years later, the patient presented with pain and decreased vision of 1-week duration in the same eye. Slitlamp examination showed red blood corpuscles dusting the corneal endothelium. Inactive fibrovascular growth was seen in the superior angle adjacent to the old injury site. There were red blood corpuscles in the anterior chamber also and a 2.0 mm hyphema. Blister-like deposits of heme were seen on and under the lens capsule in the area most proximal to the old wound. There was a total cataract. Ultrasound biomicroscopy showed a blood clot behind the iris in some areas along with zonular laxity in the area adjacent to the previous injury. Applanation tension was 14 mm Hg. Ultrasound examination of the posterior segment was normal. The patient was put on topical steroids, cycloplegic agents, and intraocular pressure control medications. She had uneventful phacoemulsification with intraocular lens implantation (haptics fixated in the sulcus and optic captured in the capsular bag) under general anesthesia. Three weeks later, she regained a BCVA of 6/6, N6 in that eye.
Fibrovascular proliferation can occur as a sequela to penetrating globe injury. This can progress slowly over time and cause late intraocular hemorrhage. This possibility should be kept in mind in all cases of unexplained hyphema. The probable sequence of events is as follows: Fibrovascular ingrowth arises from the site of the penetrating injury from the surface of the adjacent choroid. Upon reaching the lens capsule, contraction of the fibrous element produces a microbreach in the capsule. This leads to aqueous influx and rapid hydration of the lens, causing accelerated cataractogenesis. Through the same access, the fibrovascular tissue enters the lens. Swelling of the lens exerts traction on the vascular tissue, leading to hemorrhage within the lens and in the anterior chamber.
Now that the cataract has been successfully dealt with, it remains to be seen whether further capsule contraction will cause more bleeding.
Radhika Natarajan MD
Srinivas K. Rao MD
© 2003 by Lippincott Williams & Wilkins, Inc.
1. Hwang Y-S, Lai C-C, Lee J-S, et al. Posttraumatic neovascularization in a cataractous crystalline lens. J Cataract Refract Surg 2002; 28:715-716