Anterior dislocation of the crystalline lens can cause complications such as corneal edema, acute glaucoma, and uveitis. Unlike a lens dislocated into the vitreous, an anteriorly dislocated crystalline lens should always be removed.1 Corneal endothelial damage, choroidal effusion, expulsive intraocular hemorrhage, and retinal detachment may occur during lens extraction, and postoperative corneal astigmatism after a large limbal incision cannot be avoided. We describe a successful case of anterior vitrectomy and intercapsular lensectomy using the closed-chamber technique in a patient with a crystalline lens that spontaneously dislocated into the anterior chamber with corneal touch and secondary glaucoma.
A 53-year-old man presented to our clinic reporting pain in the right eye and sudden visual disturbance. The right eye had an uncorrected visual acuity (UCVA) of hand motions and the left eye, 20/100. Ciliary injection and mild corneal edema were noted in the right eye, and an anteriorly dislocated crystalline lens was touching the endothelium of the whole cornea. The lens was fixated in this position by the iris and cornea (Figure 1). There were no zonules around the dislocated crystalline lens. The pupil was fixated and semidilated, and the intraocular pressure (IOP) was 60 mm Hg. The dislocated lens had moderate nuclear sclerosis. The left eye had an IOP of 12 mm Hg and no significant abnormal findings except mild anterior capsule opacification. Mannitol was given intravenously and acetazolamide orally to lower IOP in the right eye, and surgery was performed that afternoon.
The patient had had hypertension for 10 years and a large area of shunt vessels in both retinas during presentation to our clinic 1 year previously. The patient also had phacodonesis in the right eye 4 months before the visual disturbance.
The pupil diameter, measured with the patient under general anesthesia, was 5.0 mm. The IOP could not be controlled with antiglaucoma medication. To lower IOP, vitreous aspiration from the vitreous cavity was attempted at 7 o'clock and 11 o'clock with a 23-gauge needle attached to the syringe; however, this failed. To make a tract, the corneal limbus (at 9 o'clock) and crystalline lens in the anterior chamber were penetrated to the anterior vitreous with a microvitreoretinal (MVR) blade. The vitreous cutter probe reached the anterior vitreous through the tract. A transphakic pupillary dry anterior vitrectomy was performed, and decreased IOP was detected by corneal palpation (Figure 2, A and B).
Subsequently, a partial intercapsular lensectomy was performed with a cutter probe to decrease the lens volume at 9 o'clock. The anterior chamber was penetrated at 1 o'clock with a super sharp blade, and viscoelastic material (Hyal® 2000) was injected between the cornea and crystalline lens using the soft-shell technique to separate the lens from the cornea. Hyal 2000 was injected intermittently during surgery. The pupil was constricted with intracameral carbachol (Miostat®) to prevent lens fragments from falling into the vitreous cavity. The cornea was penetrated near the limbus at 3 o'clock with the MVR blade. While the crystalline lens was supported with an infusion cannula at 3 o'clock, intercapsular phacoemulsification was performed at 9 o'clock using a sleeveless phaco handpiece (Figure 3, A and B). With decreased lens nucleus volume, the remaining nucleus, cortex, and lens capsule were removed with the vitreous cutter probe; the remaining vitreous and Hyal 2000 in the anterior chamber were also removed. No leakage at the surgical wounds was observed. Gentamicin and dexamethasone were injected subconjunctivally.
The risk for expulsive intraocular hemorrhage and corneal endothelial damage during surgery was reduced by using the closed-chamber technique. The crystalline lens separated from the corneal endothelium was removed uneventfully. On the first postoperative day, a Descemet's membrane fold and moderate corneal edema were noted. The IOP was 8 mm Hg. On the second postoperative day, there was no retinal or choroidal detachment and the IOP was 9 mm Hg. At 12 days, the UCVA was 20/400, the IOP was still stable, and the corneal edema had decreased. Three weeks after surgery, the UCVA was 20/250, the best corrected visual acuity was 20/32, and the IOP was 10 mm Hg. The preoperative corneal astigmatism was –1.25 diopters (D); 7 weeks after surgery, it was –1.50 D. Three months after the procedure, scleral fixation of an intraocular lens (IOL) (Alcon AcrySof® MA60BM) was performed. Two months later, the patient had a visual acuity of 20/25 and an IOP of 9 mm Hg (Figure 4).
Etiologies for anterior dislocation of the crystalline lens include traumatic, heredity, and spontaneous dislocation. Traumatic dislocation accounts for slightly more than 50% of cases.1 Hereditary forms of lens dislocation can be associated with other systemic anomalies (eg, Marfan's syndrome, homocystinuria, Weill-Marchesani syndrome).1–3 In our case, the patient had no history of ocular trauma and no hereditary disease on clinical examination. Thus, it was thought the dislocation was spontaneous.
Anterior dislocation of the crystalline lens can cause several complications. Corneal edema can develop through contact between the dislocated lens and the corneal endothelium, and pupillary block can occur when the pupil margin is pressed down by the anterior dislocated lens, leading to acute glaucoma.1,4,5 In our case, an anteriorly dislocated crystalline lens was touching the entire corneal endothelium and the IOP was significantly elevated. Corneal edema was not as serious, possibly because little aqueous fluid was in contact with the corneal endothelium and there was no space between the dislocated lens and corneal endothelium. Elevated IOP would have resulted from increased intravitreal pressure by the obstruction of normal aqueous flow by pupillary block.
A lens dislocated into the anterior chamber should be removed.1 Jaffe and coauthors1 suggest cryoextraction with a limbal incision and cryoprobe. According to Peyman and coauthors,6 when the anteriorly dislocated lens is soft, a standard sclerotomy should be performed and the lens cut and removed with the vitreous cutter probe. When the lens is hard, a standard sclerotomy should be performed. With this technique, the lens is extracted through a large clear corneal incision or limbal incision and the vitrectomy completed.
In our case, these surgical techniques could have caused expulsive intraocular hemorrhage with suddenly decreasing IOP and diffuse corneal endothelial injury by chafing of the lens against the corneal endothelium. Moreover, large corneal or limbal incisions can cause significant postoperative corneal astigmatism and make secondary IOL insertion difficult. Behndig5 reports a case in which anterior dislocation of the spherophakia without snapping of zonules caused corneal edema and glaucoma; a successful outcome was achieved after phacoemulsification and in-the-bag IOL implantation. The zonule was attached to the lens, and the lens capsule was preserved. However, this technique could not be used in our case.
We did not think a laser iridotomy would resolve the pupillary block because the pupil could not be constricted with miotics. In addition, there was no room for an appropriate peripheral iris site for the laser iridotomy. Although laser iridotomy was possible, the crystalline lens might have obstructed aqueous outflow through the iridotomy site. We penetrated the corneal limbus and the crystalline lens in the anterior chamber to the anterior vitreous with the MVR blade and performed a transphakic, pupillary dry anterior vitrectomy through this tract, decreasing IOP slowly and safely.
Before and during the intercapsular phacoemulsification, Hyal 2000 was injected between the cornea and the crystalline lens, separating the anterior lens capsule from the corneal endothelium (viscodissection). Alió and coauthors7 report that phacoemulsification in the anterior chamber causes no serious corneal endothelial injury and corneal edema when a space is secured between the crystalline lens and corneal endothelium with viscoelastic material.
A phaco tip was inserted in the previous tract in the crystalline lens, and intercapsular phacoemulsification was performed while preserving the lens capsule. Anis8 reports that intercapsular phacoemulsification with a small anterior capsulotomy and intact capsular bag protects the corneal endothelium better than a large can-opener capsulotomy. This supports the fact that preserving the lens capsule minimizes the risk for lens fragments falling into the vitreous cavity and has a significant role in protecting the corneal endothelium from ultrasonic power.
On the first postoperative day, our patient's IOP was 8 mm Hg, which was significantly lower than the preoperative value (60 mm Hg). This could have been from the removal of the pupillary block. The postoperative value for the corneal astigmatism was similar to the preoperative value, which could because a small incision was used. Scleral fixation of the IOL was successfully performed 3 months after surgery, and the previous small-incision surgery contributed to this.
Although our case is unusual, it reinforces the value of a small incision and the closed anterior chamber technique.
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