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Case report

Spontaneous resolution of a traumatic cataract caused by an intralenticular foreign body

Rofagha, Soraya MD, MPH; Day, Shelley MD; Winn, Bryan J. MD; Ou, Judy I. MD; Bhisitkul, Robert B. MD, PhD; Chiu, Cynthia S. MD

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Journal of Cataract & Refractive Surgery: June 2008 - Volume 34 - Issue 6 - p 1033-1035
doi: 10.1016/j.jcrs.2008.01.033
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Intralenticular foreign bodies can be managed conservatively by observation alone, by removal of the foreign body and lens preservation,1 or more aggressively by primary cataract extraction and intraocular lens implantation.2 Several cases in which a traumatic lens opacity remained localized and visually insignificant for decades after the initial injury have been reported.3,4 To our knowledge, we report the first case of spontaneous resolution of a cataract following capsule violation by an intralenticular foreign body.


A healthy 49-year-old fireman was cutting wood with a table saw when he felt a foreign body strike his left eye. He noticed some mild irritation but no pain or change in vision. The patient was seen by a private ophthalmologist in the community, who diagnosed a metal foreign body perforating the sclera posterior to the iris and penetrating the lens, and was referred to our institution for further management. On presentation, the uncorrected visual acuity was 20/20 in the right eye and 20/25 in the left eye. The pupils were equal, round, and reactive to light, with no evidence of an afferent pupil defect. Extraocular movements were intact, and visual fields were full to confrontation bilaterally. Intraocular pressures were 12 mm Hg and 13 mm Hg in the right eye and left eye, respectively.

Slitlamp examination was significant for a 1.0 mm × 0.2 mm × 6.0 mm boomerang-shaped metal foreign body (Figure 1) perforating the sclera 2.0 mm posterior to the inferonasal limbus in the left eye. The foreign body protruded approximately 0.5 mm from the surface of the sclera and traveled through the pars plicata and equatorial lens capsule and was embedded in the peripheral lens cortex. The remainder of the lens appeared normal, with no evidence of disruption. The anterior chamber was deep with 1+ cells, and the remainder of the slitlamp examination was unremarkable. Dilated fundus examination did not reveal vitritis, vitreous hemorrhage, retinal hemorrhage or break, or other intraocular foreign body. Computed tomography of the orbit showed a formed globe notable only for the solitary metal foreign body, as described. The patient received intravenous cefazolin, ciprofloxacin, and tetanus toxoid and was taken to the operating room for repair.

Figure 1
Figure 1:
The intraocular metallic foreign body after surgical removal. The boomerang-shaped metal sliver measured 1.0 mm × 0.2 mm × 6.0 mm and perforated the sclera approximately 2.0 mm posterior to the inferonasal limbus.

After exposure, the foreign body external to the sclera was grasped with a serrated Bonaccolto utility forceps (Medicon) and gently pulled from the eye in its entirety. A small amount of vitreous extruded from the sclera and was removed via Weck-Cel (Metronic Ophthalmics) vitrectomy. The wound was irrigated. Examination of the eye revealed no further metal fragments; however, a linear track in the lens cortex was clearly visible. The scleral wound was repaired and the conjunctiva closed. The patient received subconjunctival vancomycin, ceftriaxone, and triamcinolone at the end of the case. He was then managed with topical moxifloxacin, prednisolone, and atropine drops.

On postoperative day 2, a 1+ posterior subcapsular cataract (PSC) and a small amount of vitreous hemorrhage adjacent to the area of injury without evidence of a retinal break were noted. On day 4, in addition to the PSC, a dense cortical cataract had evolved (Figure 2), although the visual acuity remained 20/25. The cataract had a cruciate configuration with wave-like disruption of the stromal lamellae and a central apex presumably indicating the point of greatest impact.

Figure 2
Figure 2:
Photograph of the dense cortical cataract at 4 days. The lens opacity has a cruciate configuration with wave-like disruption of the stromal lamellae and a central apex presumably indicating the point of greatest impact.

Three weeks after the repair, because of the patient's active lifestyle, prophylactic retinal cryotherapy in the area of the vitreous hemorrhage was performed. A week later, 1 month after injury, the patient subjectively felt his vision had improved. The visual acuity tested 20/25, and examination of the lens revealed resolution of more than 90% of the opacity (Figure 3). Prednisolone drops were discontinued at 2 months. At 4 months, the patient continued to report improved vision, confirmed by a measured acuity of 20/20. On slitlamp examination, a small outpouching of the posterior lens capsule was noted (Figure 4) and only a faint imprint of the original cataract remained (Figure 5).

Figure 3
Figure 3:
Photograph of the cataract 1 month after initial injury. The lens opacity faintly retains its cruciate configuration but is now over 90% resolved.
Figure 4
Figure 4:
High-magnification slitlamp photograph of the posterior lens contour at 4 months. A small outpouching of the posterior lens capsule is seen, indicating that capsule repair, causing capsule redundancy, was involved in the mechanism of lens repair.
Figure 5
Figure 5:
Photograph of the cataract at 4 months. Only a faint remnant of the original cataract remains in the nasal lens periphery, along the track created by the foreign body.


It is well documented that intralenticular foreign bodies may have a self-limited natural history without progressive cataract formation.1,3,4 Conservative management with lens preservation is a valid option, especially to preserve accommodative potential in young patients unless there is intraocular inflammation, lens-related glaucoma, or sight-threatening siderosis bulbi.

When capsule rupture leads to hydration of the lens cortex, it is hypothesized that small capsule wounds can heal without progressive cataract formation.5 According to this theory, once the epithelium proliferates, it reseals the capsule and restores the ionic balance to the intralenticular space, stabilizing the lens opacity.6 Therefore, both the size of the capsule opening and the speed at which the epithelium lays down new basement membrane will influence the magnitude of cataract formation.

Less well formulated is how the lens can restore its transparency. The early ophthalmic literature described rosette cataracts from concussive or penetrating injuries that could remain stationary but also described several cases of complete resolution, first reported by Fuchs in 1888.7 It has been proposed that resorption of small superficial lens opacities in a pseudolysosomal fashion can occur. According to this theory, the new capsule segment, produced by regenerating epithelial cells, sequesters necrotic lens material before merging with the remainder of the capsule. This hypothesis is supported by the discovery of localized areas of capsule thickening in traumatic cataracts by electron microscopy.8 In young mice, lens opacities have been shown to decrease in the second month after penetrating injury. Using TUNEL staining, damaged cells within these traumatic cataracts were seen to undergo apoptosis, perhaps induced by compression from rapidly proliferating epithelium.9

In our patient, the rapid return of translucency to the lens is not easily explained by either mechanism alone. Closer analysis of the unique X-configuration of the cataract and the wave-like stromal disruption leads to another theory, one of temporary disturbance to the lens architecture without formation of a scar. We hypothesize that most of the cortical opacity was not due to direct contact but to the misalignment of lens fibers from the propagation of a shockwave stemming from the missile. To borrow from another well-known intraocular phenomenon, we believe this is a case of lens sclopeteria. Within the scope of a month, once the capsule had sealed and proper ionic balance had returned to the intralenticular space, we suspect the fibers realigned and the original architecture was restored. The small fraction of cells directly along the track of the foreign body, noted at the time of repair, likely sustained true cellular injury and has perpetuated in the form of a scar. We hypothesize that the outpouching of the lens posteriorly represents redundant capsule generated during the healing process.

In our patient, it is possible that the small area of capsule injury and the equatorial location led to rapid sealing of the capsule defect, followed by restoration of the original architecture in misaligned but otherwise uninjured lens cortex. It is unclear how much of an effect prednisolone or the patient's healthy constitution had in mitigating cellular injury. We believe this case represents a new mechanism of lens injury, one by shockwave, which has an excellent visual prognosis and justifies attempts at lens preservation after trauma.


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