Viscodelamination of Localized Retrolental Plaques During Lens-Sparing Vitrectomy in Eyes With Pediatric Tractional Vitreoretinopathy

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U nregressed embryonic hyaloid tissue in persistent fetal vasculature (PFV) syndrome or assembly of cell migration and extracellular matrix in advanced familial exudative vitreoretinopathy (FEVR) or retinopathy of prematurity (ROP) can induce retrolental proliferation that extends from the retina to the anterior hyaloid membrane (AHM) and posterior lens capsule. [1][2][3] To preserve the clarity of the crystalline lens and to release tractional vectors, methods have demonstrated the dissection of localized retrolental plaques in lens-sparing vitrectomy (LSV) for PFV, advanced ROP, and FEVR. 2,[4][5][6][7] Mechanically stripping of proliferative tissue from the posterior lens surface during LSV frequently resulted in progressive cataract. 2,4 Lens-sparing transection of retrolental plaque at its posterior aspect using a microvitreoretinal blade or microscissors can reduce injury to the overlying lens capsule. However, transection methods risk inadvertent penetration of the anteriorly inserted retina in the retrolental tissue. [6][7][8] Still, postoperative residual retrolental tissue obscures vision. The efficacy of elimination of the localized retrolental plaques from posterior lens capsule during LSV for pediatric tractional retinopathies has not been published.
The Berger's space between the AHM and the posterior lens capsule can be dissected with viscoelastic or fluid. 9-11 Accordingly, we attempted viscoelastic delamination of retrolental plaques by exploring the Berger's space between AHM and posterior lens capsule, during LSV for FEVR, ROP, or PFV. We observed that entire removal of retrolental plaques From the Department of Ophthalmology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
The authors declare that there is no conflict of interest regarding the publication of this article. The authors declare that there is no financial relationship with any company associated with the manufacture of any instrument described in this article. The study was funded by the National Natural Science Foundation Project of China (81800837 to J. Lyu, 81770964 to P. Zhao).
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Patients and Methods
The retrospective case series included consecutive patients who had tractional vitreoretinopathies and received 23-gauge LSV surgery and viscodelamination of retrolental tissues in the affected eyes, at Shanghai Jiaotong University, Medical School, Xinhua Hospital, between August 2017 and August 2018 ( Table 1). All procedures were conducted in accordance with the Declaration of Helsinki and approved by the ethics committee of Xinhua Hospital. Informed consent for all surgical procedures was obtained from the legal guardian of participants.
Surgeries were performed to clear the visual media and unravel retinal dragging. Included were eyes with localized retrolental tissues and focal tractional retinal detachment (TRD) or distortion in the posterior pole. Excluded were eyes with marked cataract, obvious deficiency of lens capsule (tear, opacity, deformation), lens luxation, elongated ciliary process, extensive anterior proliferation, and retinal detachment, ause a lensectomy/vitrectomy was indicated.
The retrolental plaque was firstly explored with illumination under an operating microscope for its location, extent, and tractional role on the adjacent tissues. Sclerotomies for a 23-gauge LSV surgery were then made where it was advantageous to access the retrolental plaque without damage to the retina. Viscodelamination was performed before introduction of infusion. One trocar cannula in the sclerotomy was transiently removed to host an angled 26-gauge cannula. A 26-gauge cannula entered the sclerotomy, gently lifted the edge of the retrolental plaque from the posterior lens capsule with its blunt tip, and continually injected cohesive viscoelastic (Aiwei, Bausch and Lomb; Shandong Furuida Co., Ltd., Shandong, China) into the Berger's space. The viscoelastic dispersed in the Berger's space and above the retrolental plaque. The plaque was separated from the posterior lens capsule by the tension of the viscoelastic and then excised by vitreous cutter. The amount of viscoelastic used was about 0.1 mL to 0.3 mL. The opposite trocar cannula was unplugged in case of hypertension due to viscoelastic tamponade. Viscodelamination adjacent to Wieger's ligament was done with caution to preserve the zonules. For firmly adhering plaques, viscodelamination was performed in combination with peeling and cutting using vitreoretinal forceps and a vitreous cutter. Tractional vitreoretinopathies were addressed in the LSV sur-gery, followed with fluid-air exchange. The patients were in a face-down position for 7 days. Topical prednisolone acetate, fluoroquinolone, and tropicamide were each administered four times daily for two weeks postoperatively. The patients were followed up weekly, then monthly, and bimonthly for at least 12 months. Lens opacity was considered significant if it hampered the view of the posterior segment by indirect ophthalmoscopy.

Results
Eleven eyes of 11 patients received viscodelamination of retrolental plaques during 23-gauge LSV surgery. There were eight central or pericentral and three peripheral retrolental plaques with a largest diameter from 1 mm to 3 mm, in five eyes with Stage 4B FEVR, one eye with Stage 4B ROP, and five eyes with anteriorposterior PFV. Two eyes with FEVR and two eyes with PFV had mild lens opacity adjacent to retrolental plaques. One eye with PFV (Patient 11) and an inferonasal plaque had a progressive TRD involving the macula during a 10month observation before surgery.
Retrolental plaques were delaminated from the posterior lens capsule without an apparent capsular tear in 10 (91%) of the 11 eyes. After a 12-month to 18month follow-up, lens clarity along the visual axis was maintained in eight eyes (73%), including 5 eyes with FEVR (Figure 1), one eye with ROP, and 2 of 5 eyes with PFV ( Figure 2). Reversal of retinal dragging was observed in all eyes (Table 1).
In the eight eyes without a visually significant cataract after surgery, intraoperative observation and atraumatic delamination in the Berger's space revealed that the retrolental plaques were on the AHM with focal attachment to the posterior lens capsule. Preexisting mild capsular opacity in two eyes with FEVR did not significantly progress after delamination. Visual acuity available in one eye with PFV (Patient 11) improved from counting fingers to 20/500 12 months postoperatively. The other three eyes with PFV had central plaques invading the posterior lens capsule. A capsular tear occurred after viscodissection in the Berger's space near the perfused hyaloid arteries in the plaque in one eye (Patient 10), leading to a concomitant lensectomy. Progression of preexisting mild capsular opacity was observed in two eyes with PFV 3 months postoperatively; one eye (Patient 8) with significant cataract received a secondary lensectomy.

Discussion
The current report explored the Berger's space as a surgical plane for viscodelamination of retrolental plaques in eyes with advanced FEVR, ROP, and PFV during LSV surgery. The efficacy of delamination of retrolental plaques depends on how retrolental tissues invade the Berger's space and affect the posterior lens capsule. 9,11 Retrolental plaques are formed secondarily in eyes with FEVR or ROP 1 as these plaques adhere to the AHM before invading the Berger's space and posterior lens capsule. Thus, it was effective to inject viscoelastic from the adjacent Berger's space into the lens-plaque adhesion for delamination and to respect the posterior lens capsule. Efficacy of viscodelamination seemed less relative to the central or noncentral location of plaques.
In eyes with PFV, viscodelamination may be unharmful when the retrolental plaques were mostly retrograde to the AHM. 12,13 Affected eyes of Patients 7 and 11 showed retrolental plaques on the AHM with pinpoint adhesion to the posterior lens capsule and consequently they developed no obvious lenticular opacification after the surgery. It is noteworthy that Patient 11 received LSV due to a progressive TRD involving the macula. Removal of the inferonasal retrolental plaque and epiretinal tractional force yielded good anatomical and visual improvement postoperatively. However, viscodelamination is invasive for treating retrolental stalks incorporated into the posterior lens capsule, as frequently observed in eyes with PFV. Unregressed fetal hyaloid tissues may impair the formation of Berger's space and compromise the integrity of lens capsule. Lenticular changes, such as fenestrations on the posterior lens capsule, thinning, or deformation of the lens capsule, may exist in proximity to the hyaloid artery  The eye showed a temporal retinal fold and fibrovascular proliferation attaching to lens. B. A 26-gauge cannula through one sclerotomy was used to gently lift the retrolental plaque from the posterior lens capsule and to inject viscoelastic into the Berger's space. C. The plaque was separated from the lens capsule by the tension of the viscoelastic injection. The plaque was found to be on the AHM with focal adhesion to the posterior lens capsule. D. The plaque was excised bimanually with vitreoretinal forceps and a vitreous cutter. E. The plaque was entirely removed and lens clarity along the visual axis was preserved. F. Fundus examination by wide-angle fundus imaging system RetCam (clarity medical systems, Pleasanton, CA), 12-month postoperatively, showed a clear media through clear lens and improved posterior structure. system in Cloquet's canal. [13][14][15] The undetected defect of the posterior lens capsule near the plaque may account for the capsular rupture during delamination in the eye of Patient 10 and progressive cataract after delamination in the eyes of Patients 8 and 9. Such complications of viscodelamination were typically with central plaques toping at the Cloquet's canal.
Clearance of the retrolental tissues enhanced surgical visualization in LSV. Removal of contractile retrolental tissues attached to the retina allowed release of the anteroposterior vector. Thus, it encouraged anatomical recovery with resolution of TRD in all the cases.
Issues pertaining to the technique require attention. The technique is meant for localized retrolental adhesion but not for extensive lesions. In the presence of strong lens-plaque adhesion or adhesion involving Wieger's ligament, any forceful viscodelamination is prohibited because it may induce a capsular tear, anterior retinal dialysis, or zonular dehiscence. One may also combine viscodelamination with partial transection on the premise that all the traction is sufficiently released and that transection does not risk penetrating the anteriorly inserted retina. In addition, because of the limited cases in the current study, all appropriate types of retrolental plaques for a delamination during LSV have not been investigated. Shortterm observation is valuable to demonstrate the earlyphase status of the lens after surgery. Long-term stability of the lens and retina should be confirmed in a prolonged study.
In conclusion, viscodelamination may be an effective surgical alternative to the dissection of retrolental plaques related to pediatric vitreoretinopathies in selected cases undergoing LSV. The adhesion plane of the retrolental plaques and underlying etiologies affect the efficacy of delamination and the postoperative status of the lens.