|Year : 2004 | Volume
| Issue : 4 | Page : 325-7
Posterior capsular dehiscence following blunt injury causing delayed onset lens particle glaucoma.
Sunil S Jain, P Rao, P Nayak, K Kothari
Bombay City Eye Institute & Research Centre, Mumbai, India
|Date of Submission||07-May-2003|
|Date of Acceptance||27-Jul-2003|
Sunil S Jain
Bombay City Eye Institute & Research Centre, Mumbai
| Abstract|| |
A late onset lens-particle glaucoma secondary to trauma is reported. It was treated by cataract extraction and intraocular lens placement.
Keywords: Blunt ocular trauma, posterior capsule rupture, traumatic cataract, lens, particle glaucoma
|How to cite this article:|
Jain SS, Rao P, Nayak P, Kothari K. Posterior capsular dehiscence following blunt injury causing delayed onset lens particle glaucoma. Indian J Ophthalmol 2004;52:325
|How to cite this URL:|
Jain SS, Rao P, Nayak P, Kothari K. Posterior capsular dehiscence following blunt injury causing delayed onset lens particle glaucoma. Indian J Ophthalmol [serial online] 2004 [cited 2014 Mar 9];52:325. Available from: http://www.ijo.in/text.asp?2004/52/4/325/14560
Lens injury is a major complication of blunt trauma and is seen in 30% to 65% of cases. Isolated capsule rupture involving either the anterior or the posterior capsule is rarely reported in blunt non-perforating trauma.- Disruption of the lens capsule by penetrating trauma or surgery liberates lens material, which can obstruct the trabecular meshwork. The resulting glaucoma depends on the amount of liberated lens material, the inflammatory response of the eye, and the ability of the trabecular meshwork to clear the foreign matter. Generally the glaucoma has its onset a few days after the precipitating event. In rare cases the lens material can be released long after surgery or trauma.
| Case report|| |
A 24-year-old male presented with a history of sudden decrease in vision and redness in the right eye for 2 days. The patient had a past history of blunt injury with a tennis ball to the right eye one year ago.
On examination the best-corrected visual acuity in the right eye was finger counting close to face with accurate perception and projection of light and in the left eye, 6/6. The intra-ocular pressure (IOP) was 54 mmHg in the right eye and 12 mmHg in the left. Slitlamp examination of the right eye showed conjunctival congestion, clear cornea, and deep anterior chamber with presence of free-floating lens particles [Figure - 1]. The pupil was mid-dilated, sluggish to direct light with sphincter tears. The lens showed presence of an intumescent cataract. Gonioscopy showed presence of wide-open angles. There was no sign of angle recession, and no corneal or scleral perforation was found in the right eye.
Following pupillary dilation, slitlamp examination of the anterior segment showed an intact anterior capsule. On focussing over the posterior capsule of the lens, there was a pre-existing posterior capsular dehiscence, extending along the 8 to 2 o'clock meridian [Figure - 2]. This was associated with loss of posterior lenticular convexity and protrusion of posterior sub-capsular lens fibers through the dehiscence into the anterior vitreous [Figure - 3]. Phacodonesis was absent. The fundus view was hazy. The left eye was within normal limits. Ultrasound B-scan of the right eye was within normal limits. In view of these findings a diagnosis of right eye lens-particle glaucoma was made.
Medical therapy for the elevated IOP included intravenous 250 ml of 20% mannitol (1g/kg body weight) over 45 minutes in the acute phase, followed by tablet acetazolamide 250 mg four times daily, timolol maleate 0.5% eye drops twice daily for maintenance of IOP control and 0.1% betamethasone eye drops four times daily to control the intraocular inflammation. The patient was advised cataract surgery for the treatment of lens-particle glaucoma.
The patient underwent cataract extraction by phacoemulsification with IOL implantation. The posterior lens capsule dehiscence was confirmed intraoperatively [Figure - 4]. Anterior vitrectomy was performed with an automated vitrector for the vitreous prolapse and also for the removal of the cortical matter in the anterior vitreous. In view of a large posterior capsular dehiscence, a sulcus-fixated 6 mm one-piece PMMA intraocular lens was inserted.
Postoperatively the patient was prescribed topical 1% prednisolone acetate eyedrops in tapering doses. On fundus examination the retina was within normal limits. The disc in the right eye showed a cupping of 0.4:1 with a healthy neuro-retinal rim. At the 6-month postoperative follow-up, the best-corrected visual acuity was 6/6 in right eye with IOP at 14 mmHg without any medication.
| Discussion|| |
Isolated capsule rupture, involving either the anterior or the posterior capsule, is rarely reported in blunt non- perforating trauma., The anterior capsule is considered more resistant than the posterior capsule to traumatic stress induced by distortion of the crystalline lens structure. A breach in the integrity of the capsule allows aqueous humor to hydrate the cortex resulting in the release of flocculent lens material into the anterior chamber. This predisposes an individual to uveitis and glaucoma. Hydration of the cortex can occur both acutely and progressively, resulting either from a loss of capsule integrity or from an alteration in the permeability of the intact portions of the capsule. Such changes in capsule permeability following blunt trauma have previously been described. In this patient, there was no evidence of anterior capsular trauma such as pitting of the anterior lenticular surface, surface irregularity, and localised lenticular opacity denser than the surrounding cataract, even with pupillary dilation.
Posterior capsule breaks have been reported to develop thick, fibrous, opaque margins approximately 6 weeks after concussion trauma. Despite the delayed presentation of our patient, the margins of the tear were thin and transparent [Figure - 4]. It could be postulated that the concussion, suffered a year ago, could have impaired the capsular permeability. This allowed imbibition of aqueous, hydration of the cortex and increased intralenticular swelling resulting in spontaneous rupture of the thinnest part of the capsule, the posterior pole, and release of the lens particles. This rupture might have occurred within 6 weeks of presentation and hence there was no fibrosis at the margins. The fact that the patient did not develop any form of uveitis also indicates that the rupture must have been recent.
The migration of the lens particles from the posterior chamber to the anterior chamber could be through subclinical zonular damage or subclinical damage to the anterior or the equatorial capsule. There was no phacodonesis or iridodonesis. The lack of resistance to the contrecoup forces by the pliable cortical tissue and the increased elasticity of the capsule and the zonules in these young eyes could possibly have reduced the stress on the zonules, protecting them from rupture.
Medical therapy of lens-particle glaucoma is similar to that for primary open angle glaucoma. But miotics are avoided because these patients tend to form synechiae. Cycloplegics can be used to dilate the pupil. Topical corticosteroids are used to treat the inflam-mation. Their use could delay absorption of the lens material, and their administration should be titrated to reduce inflammation and prevent synechiae formation, while allowing the retained lens material to resolve. If glaucoma from retained lens cortex does not respond quickly and adequately to the medical therapy, the lens material should be surgically removed without delay. If surgery is delayed, the lens material may remain trapped within the capsule or inflammatory membranes.
Lens particle glaucoma secondary to posterior capsular dehiscence following blunt trauma has not been reported. Surgical removal of the lens material is usually sufficient to control the IOP elevation, and additional glaucoma surgery is rarely required.
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]
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