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Case report reveals severe persistent ocular hypertension following lens removal in traumatic posterior lens dislocation, highlighting complex outflow pathway dysfunction.
Background/Objectives: Chronic traumatic posterior lens dislocation may cause ocular hypertension through overlapping lens-induced and traumatic mechanisms. We report a delayed presentation with a dislocated hypermature lens, a phacolytic phenotype, an incomplete capsule, and severe pressure elevation persisting after lens removal. Case Presentation: A 47-year-old man presented 5 years after blunt trauma with pain, redness, and blurred vision. Visual acuity was hand motion at 10 cm, and intraocular pressure (IOP) was 44.1 mmHg. Slit-lamp examination showed corneal edema, milky material in a deep anterior chamber, and the cataractous lens behind the iris. Ultrasonography localized the lens but could not assess capsular integrity or angle anatomy. Mixed lens-induced glaucoma with possible phacolytic, lens-particle, and traumatic components was diagnosed. Two days after 25-gauge pars plana vitrectomy and lensectomy, IOP remained 45.3 mmHg despite intensive therapy, prompting trabeculectomy with mitomycin C. At 6 months, IOP was 20.1 mmHg on three agents (qualified success), and vision remained hand motion at 30 cm with persistent corneal edema, aphakia, and suspected optic-nerve damage. Conclusions: Persistent IOP elevation after the removal of visible lens material suggested established trabecular or traumatic outflow dysfunction. Incomplete characterization of the capsule and angle precluded the assignment of a single mechanism.
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Huang et al. (2026) studied this question.
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