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Scleral perforation is a rare but potentially vision-threatening complication of scleral buckle surgery. Early presentation of these cases can be unclear and, if not promptly diagnosed, can result in hypotony and place the patient at risk of endophthalmitis.
We describe the diagnosis and management of a patient with chronic hypotony of initial unclear etiology, later determined to be secondary to perforation from a silicone scleral buckle.
A 69-year-old male with myopia (phakic manifest refraction; left eye −3.75 D) was referred for a 2-month history of hypotony and decreased vision in his left eye, initially thought to be due to a cyclodialysis cleft and managed with topical steroids and atropine with no improvement. He had a history of cataract extraction with intraocular lens (IOL) implantation in both eyes in 2002 and a retinal detachment in his left eye repaired with a #42 solid silicone scleral buckle and focal laser in 2006. Four years later, the scleral buckle eroded through the conjunctiva. Primary repair of the conjunctiva temporarily closed the defect, and full closure was achieved with a buccal mucosal autograft. He experienced recurrent episodes of inflammation since erosion of his scleral buckle, which had been managed with prednisolone drops and atropine.
At the time of presentation, best-corrected visual acuity was 20/20-1 OD and counting fingers (CF) OS, decreased from a baseline of 20/60. Intraocular pressure (IOP) was 19 mm Hg in the right eye and 2 mm Hg in the left eye. External examination revealed an elevated area superotemporally from 12 to 3, corresponding to the scleral buckle, well covered by a thin mucosal graft. There was mild hyperemia and tenderness to touch. Trace cells were visible in the anterior chamber. No cyclodialysis cleft was seen on gonioscopy. No cyclodialysis cleft was seen on ultrasound biomicroscopy (UBM), although there was a localized supraciliary effusion (Fig. 1). Posterior segment examination, including fundus photography and optical coherence tomography (OCT), revealed macular folds, tortuous retinal vessels, blurred optic disc margins, and what appeared to be intrusion of the encircling band superotemporally in the left eye (Fig. 2). The retina was otherwise attached.
Surgical exploration under local anaesthesia was performed as follows (Video 1, available online). A 3 o’clock superotemporal fornix–based conjunctival peritomy was created at the limbus with ring forceps and Wescott scissors. Subconjunctival xylocaine was used to augment topical anaesthesia. The conjunctival flap was extended posteriorly to enter the peritomy to allow access to the posterior sclera. There was significant scar tissue, making the dissection difficult. The scleral buckle was isolated. On retraction of the scleral buckle superotemporally, a globe perforation was noted under a soft silicone belt loop at the distal end of the buckle. The scleral buckle was cut with Steven scissors, removed, and sent for culture. 7-0 Vicryl sutures were used in a simple, interrupted fashion to close the perforation and reattach the ciliary body. After this, a scleral patch graft was placed over the defect and attached with fibrin sealant (Evicel; Ethicon, Somerville, N.J.) and sutured using 7-0 Vicryl. Lastly, the conjunctiva was reapposed to the limbus with fibrin sealant and peripheral 7-0 Vicryl sutures.
On postoperative day 1, the patient’s IOP was 4 mm Hg. Pressure rose to 12 mm Hg at the end of the first week, with a visual acuity of 20/400 OS. Culture results of the scleral buckle were negative. Unfortunately, on postoperative month 3, the patient presented with a dislocated left IOL and CF vision. His IOP remained stable at 14 mm Hg. Five months afterward, he underwent a combined vitrectomy and lens exchange with a scleral fixated IOL. His vision 1 week after IOL exchange returned to 20/400, and his IOP, now 9 months after closure of the scleral perforation, was 17 mm Hg. His retina remained flat postoperatively.
Globe perforation must be ruled out when any patient presents with hypotony and vision loss because it can result in endophthalmitis and permanent vision loss if prolonged. Careful history and peripheral retinal examination were instrumental in revealing that scleral perforation by the patient’s scleral buckle was the cause of his chronic hypotony. A heightened index of suspicion should be maintained for a patient with prior scleral buckle surgery and high myopia, or a disorder associated with scleral thinning. However, hypotony secondary to intrusion is also possible in patients without these risk factors and has been reported to occur as early as 3 months
Acute hypotony is commonly associated with penetrating trauma and filtering procedures, but one must always rule out other etiologies such as choroidal detachment, retinal detachment, a cyclodialysis cleft, phthisis, and uveitis, none of which was present in this case.
Risk factors for perforation in this case were repeated episodes of inflammation, myopia, and previous buckle extrusion. A possible etiology for this persistent low-grade inflammation may have been infection from mycobacteria
; however, culture of the scleral buckle was negative. If scleral buckle infection is suspected, the best treatment is removal of the buckle because bacteria can develop biofilms and are difficult to eliminate with systemic or topical antibiotics.
It is important to consider all treatment options before removing a scleral buckle because removal can result in complications, including endophthalmitis, scleral abscesses, and a re-detachment of the retina.
This case was successfully managed with a 2-step approach. The scleral defect was first sutured, followed by application of fibrin sealant and a scleral patch graft, which resulted in a Seidel negative repair and normal IOP in a week’s time. The approach to the repair of scleral perforations secondary to intrusion in the literature has been mixed, with one case of successful closure using sutures alone,