Statistics from Altmetric.com
In 1979, the hydrogel explant (Miragel, Waltham, MA, USA) was introduced as a scleral buckling material in the surgical management of retinal detachment.1 It was widely used in the 1980s and early 1990s as it was initially believed to be well tolerated, less prone to infection, and easy to manipulate.2 However, long term complications related to swelling and fragmentation of the explant have been reported over recent years,3–6 resulting in discontinuation of its use in 1995.
A 36 year old healthy man presented on 2003 with symptoms of mild right ocular discomfort. Past ocular history included a right retinal detachment repair 14 years previously, using a 907 (3×5 mm) Miragel scleral buckle (Miragel, Medical Instruments Research Associates, Waltham, MA, USA), sutured to the inferior sclera. On examination, visual acuity was 20/120 right and 20/20 left. There was no diplopia or limitation of eye movements. What was thought to be a small conjunctival cyst was noted inferiorly but, otherwise, the ocular examination was unremarkable and the retina was secure.
A year later (2004), he presented with increasing marked right ocular discomfort and diplopia in all fields. His visual acuity was unchanged, but there was marked restriction of elevation and reduction in adduction of the right eye and binocular diplopia in all fields of gaze. A tense swelling of the inferior conjunctiva was noted (fig 1, top), intraocular pressure was normal, and the retina was flat with a moderate anterior buckle effect. Computed tomography (CT) (fig 1, bottom) demonstrated a right orbital circumferential soft tissue mass surrounding the lower half of the globe with a small area of calcification. The initial diagnosis was a postoperative giant conjunctival cyst and the patient underwent surgery.
Intraoperatively, exploration revealed no conjunctival cyst, but a large encapsulated scleral buckle. The explant was friable, gel-like, and translucent, but could be removed in one piece (fig 2). A 3 mm diameter area of scleral thinning associated with calcification was found underlying the buckle inferotemporally. At 1 month follow up the patient was asymptomatic with no diplopia, unrestricted extraocular movements, and the retina was flat.
Hydrogel explants are composed of a low molecular weight hydrophilic material that is water permeable. These explants have a tendency to absorb water over the years and increase dramatically in size. The resulting complications range from a non-tender subconjunctival mass to intraocular or external extrusion.3–6 The long time lapse from buckle surgery may result in a high misdiagnosis rate. Kearney et al6 reported 17 eyes of patients with complications related to hydrogel explant swelling. In nine cases the initial diagnosis was incorrect, being mainly Graves’ disease, idiopathic orbital fibrosis, and a subconjunctival inclusion cyst.
In our case, there was a profound increase in the explant volume during a 14 year period. The resulting diplopia and restriction of extraocular movement as well as the clinical evaluation mimicked a giant orbital inclusion cyst. The correct diagnosis was only made intraoperatively. Scleral thinning and necrosis as seen in our case has been reported previously,7 resulting in intraoperative vitreous leak after removal of the expanded explant.8 In our patient, there was an area of thinned sclera, but the surrounding calcification and the early removal of the explant prevented vitreous leak.
It is important to note that patients who have undergone scleral buckling with hydrogel explants before 1995 are at risk of developing this complication. Symptoms of progressive diplopia, pain, and restriction of extraocular muscle movement in these patients should also raise the possibility of explant expansion. The assistance of a retinal surgeon may sometimes be required because of the increased risk of scleral thinning and leakage of liquid vitreous intraoperatively.