Retrolaminar Migration of Intraocular Silicone Oil.

BACKGROUND: Migration of intravitreal silicone to the retrolaminar optic nerve was detected pathologically in 1983, symptomatic migration to the subarachnoid space of the optic nerve was reported in 1994, and asymptomatic intraventricular silicone was first seen radiographically in 1999. Since then, little advance has been made in understanding this phenomenon despite numerous case reports. Although some authors have restricted their attention to cases of intraventricular silicone, we believe that these represent part of a clinical spectrum and that all cases with retrolaminar silicone should be considered. The pathophysiology of silicone migration may have significant implications for the management of patients after vitrectomy. EVIDENCE ACQUISITION: Two patients were evaluated by the authors. An internet-based literature review was conducted, beginning with the key search terms "intraventricular, intracranial, subarachnoid, or optic nerve silicone," and "complications of vitrectomy or intravitreal silicone." Further searches cascaded from the initial search results. An additional 24 cases of retrolaminar migration of silicone oil were found and summarized. The relevant anatomy and pathophysiology were reviewed, with attention to additional information from enucleation studies, as well as to gaps in the current understanding of this process. RESULTS: Retrolaminar migration of silicone oil may be more common than previously thought, especially in at-risk patient groups, and may be associated with visual and neurologic symptoms. Some impressions regarding the cause and significance of this syndrome seem incorrect. Although this process is likely linked to postoperative elevations of intraocular pressure, the exact mechanisms of silicone entry into the subarachnoid space remain undefined. A number of anatomic factors may influence the movement of silicone from the orbit and in the various compartments of the subarachnoid space and ventricular system, resulting in variability of clinical presentations and radiologic findings. Implications for clinical decision making and directions for further research are discussed. CONCLUSION: Greater awareness on the part of treating physicians, systematic study of at-risk populations, and advances in imaging technology will allow further insight into this phenomenon.

Resolution of bilateral cystoid macular edema and subfoveal serous retinal detachments after treatment with bortezomib in a patient with "smoldering" multiple myeloma.

PURPOSE: To describe a case of a patient with multiple myeloma without extraocular end-organ damage but with cystoid macular edema and macular detachments who was treated with bortezomib and dexamethasone. There was a complete resolution of retinal and subretinal fluid and significant improvement of vision. METHODS: The patient's ocular disease was monitored with visual acuity, dilated fundus examinations, and optical coherence tomography before, during, and after treatment. The patient in this case report was a 43-year-old African American man with a medical history of untreated, "smoldering" multiple myeloma, hypertension, hyperlipidemia who presented to our clinic with progressive painless loss of vision in both eyes over 6 weeks. RESULTS: Before treatment with bortezomib and dexamethasone, the patient had complaints of confusion, muscle stiffness, joint pain, and 20-lb unintentional weight loss; however, he did not have hypercalcemia, renal insufficiency, anemia, or bone lesions typical of active multiple myeloma. The bilateral cystoid macular edema and subfoveal neurosensory retinal detachments, noted on presentation and confirmed by optical coherence tomography, completely resolved over the course of treatment with bortezomib and dexamethasone. CONCLUSION: This case of bilateral cystoid macular edema and subfoveal neurosensory retinal detachments is remarkable for both its presentation and response to therapy. The macular edema and macular detachments along with nonspecific complaints of confusion, muscle stiffness, joint pain, and weight loss were the presenting signs and symptoms; signs typically used as guides to initiate treatment for multiple myeloma were not present. Macular edema in the context of paraproteinemia is usually associated with Waldenstrom's macroglobulinemia and has classically been reported as "silent" with respect to fluorescein angiography. Our patient has multiple myeloma and demonstrated leakage on fluorescein angiography. The case is also notable in that there was improvement in visual acuity and restoration of normal macular anatomy after receiving eight cycles of bortezomib and dexamethasone. Bortezomib, a chemotherapeutic agent used to treat refractory or rapidly advancing multiple myeloma, had been used previously to treat similar maculopathy in Waldenstrom disease along with plasmapheresis with resolution of macular edema and improvement in visual acuity. Our patient with multiple myeloma did not require plasmapheresis for significant clinical improvement. Treatment with bortezomib and dexamethasone alone was sufficient to clear the bilateral cystoid macular edema and subretinal fluid.