HEADACHES SECONDARY TO INTRAVENTRICULAR SILICONE OIL SUCCESSFULLY MANAGED WITH VENTRICULOPERITONEAL SHUNT Paul M. Hruby, MD,* Preeti R. Poley, MD,* Patricia A. Terp, MD,* William E. Thorell, MD,† Eyal Margalit, MD, PhD‡*
Purpose: To describe a case of intravitreal silicone oil (SO) migration into the cerebral ventricles with secondary chronic headaches. Methods: Retrospective case report. Chart review. Single patient. Results: A 51-year-old man with a history of proliferative diabetic retinopathy underwent surgery for traction retinal detachment using SO. Postoperatively, he developed elevated intraocular pressure, headaches, and a blind painful eye, which was enucleated. Neuroimaging revealed SO within the cerebral ventricles. Five years after the initial retinal detachment surgery, the patient developed chronic headaches. Lumbar puncture revealed an elevated opening pressure. The headaches were initially managed medically. A ventriculoperitoneal shunt was placed after the headaches persisted, which resulted in their complete resolution at 6 weeks after shunt placement. Conclusion: Ocular hypertension after intravitreal SO placement may play a role in SO intracranial migration. In the case presented, intraventricular SO was the apparent cause of elevated intracranial pressure and headaches. As all published cases of intraventricular SO migration reporting intraocular pressure to this point have described ocular hypertension, careful monitoring of intraocular pressure and aggressive control of ocular hypertension in the presence of intravitreal SO is recommended. RETINAL CASES & BRIEF REPORTS 7:288–290, 2013
From the *Departments of Ophthalmology and Visual Sciences, and †Neurosurgery, University of Nebraska Medical Center, Omaha, Nebraska; and ‡VA NebraskaWestern Iowa Health Care System, Omaha, Nebraska.
Case Report A 51-year-old man with traction retinal detachment and vitreous hemorrhage secondary to proliferative diabetic retinopathy underwent pars plana vitrectomy, membrane peel, and SO placement. Preoperative intraocular pressure (IOP) was normal. After surgery, the eye gradually lost light perception in the presence of normal IOP. Four months after surgery, the patient developed neovascular glaucoma, eye pain, and elevated IOPs as high as 52 mmHg. Ocular hypertension was treated with topical pressure-lowering agents. After treatment was instituted, IOP varied over the next 8 months from 19 mmHg to 46 mmHg, in part because of patient treatment noncompliance. The patient later underwent enucleation of the blind eye. Five years after the initial retinal detachment surgery, the patient presented with neck stiffness and occipital headaches. Routine supine brain magnetic resonance imaging was obtained and demonstrated intraventricular high-attenuation foci consistent with SO in the frontal horns of the lateral ventricles and in the optic recess of the third ventricle (Figure 1). Subsequent head computed tomography in the prone position demonstrated high-attenuation foci in the bilateral occipital horns of the lateral ventricles and in
I
ntravitreal silicone oil (SO) is commonly used for retinal tamponade in cases of complicated retinal detachment. Some of the more common complications associated with the use of SO include glaucoma, optic nerve atrophy, ocular inflammation, cataract, and keratopathy.1 The incidence of migration of SO into the cerebral ventricles is unknown. To our knowledge, only five cases2–7 without a known optic nerve pit have been reported in the literature, with none describing surgical intervention. We present a patient with SO migration to the cerebral ventricles and chronic headaches successfully treated with a ventriculoperitoneal shunting procedure. 288
SO MIGRATION INTO THE CEREBRAL VENTRICLES
Fig. 1. Axial T2-weighted FLAIR magnetic resonance imaging demonstrating SO in the frontal horns of the lateral ventricles.
the suprasellar cistern, consistent with nondependent SO. Lumbar puncture showed clear cerebrospinal fluid and an opening pressure of 27 cm H2O. Chronic headaches associated with nausea, vomiting, and dizziness ensued, but medical management was unsuccessful. After 6 months, a decision was made to proceed with a ventriculoperitoneal shunt. Postoperative head computed tomography showed successful shunt placement and persistence of the SO in the ventricles (Figure 2). At the 6 week postoperative follow-up, the headaches had resolved.
Discussion Severe glaucoma leading to cavernous degeneration of the optic nerve posterior to the lamina cribrosa is thought to be caused by hyaluronic acid from the vitreous forced into the optic nerve. A similar degeneration of the optic nerve with globules of SO infiltrating its entire length was seen in an enucleated eye of a patient with retinal detachment previously repaired by vitrectomy and SO placement.8 Although the exact mechanism is unknown, it is possible that ocular hypertension and degeneration of the optic nerve may create a pathway for SO to migrate to the subarachnoid space or cerebral ventricles. Five cases of intravitreal SO migration to the central nervous system in eyes without a known optic pit have This study was supported in part by an unrestricted grant from the Research to Prevent Blindness. None of the authors have any financial/conflicting interests to disclose. Reprint requests: Eyal Margalit, MD, PhD, Department of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, 985540 Nebraska Medical Center, Omaha, NE 68198-5540; e-mail: [email protected]
289
Fig. 2. Axial computed tomography with supine positioning demonstrating right posterior shunt with tip in the right lateral ventricle. Silicone oil can be seen within the left frontal horn.
been reported to date.2–7 Of these, 3 cases2,4,5 describe ocular hypertension after SO retinal tamponade ranging from 384 to 70 mmHg.5 The remaining two cases6,7 make no mention of the patient’s IOP history. Our patient’s maximum IOP of 52 mmHg is consistent with these previous reports. Our patient had chronic headaches recalcitrant to medical management, as well as dizziness. Whether these symptoms are a direct result of silicone within the cerebral ventricle is unknown. However, given that SO is used experimentally to create hydrocephalus in animals,9 it is reasonable to contend our patient’s elevated opening pressure on lumbar puncture was secondary to SO and may have therefore been the cause of the headaches. Kiilgaard et al10 examined 19 patients for SO migration with magnetic resonance imaging and concluded central nervous system SO migration is likely rare, although maximum intraocular tension was 34 mmHg and no patients had previous evidence of glaucoma. However, reported cases of SO intracranial migration report a higher range of IOPs. With our current limited knowledge, it seems prudent to carefully monitor IOP and aggressively treat ocular hypertension after SO placement, regardless of visual status, to guard against this complication. In addition, a high index of suspicion should be exercised for neurologic symptoms in patients who have undergone intravitreal SO placement with postoperative ocular hypertension, even if the SO or eye has subsequently been removed.
290
RETINAL CASES & BRIEF REPORTS´ 2013 VOLUME 7 NUMBER 3
Key words: central nervous system, cerebral ventricles, intravitreal, silicone oil, ventriculoperitoneal shunt, glaucoma. References 1. Gallemore RP, McCuen BW. Silicone oil in vitreoretinal surgery. In: Ryan SJ, ed. Retina Vol. III: Surgical Retina. 4th ed. St Louis, MO: CV Mosby; 2006:2211–2234. 2. Eller AW, Friberg TR, Mah F. Migration of silicone oil into the brain: a complication of intraocular silicone oil for retinal tamponade. Am J Ophthalmol 2000;129:685–688. 3. Williams RL, Beatty RL, Kanal E, Weissman JL. MR imaging of intraventricular silicone: case report. Radiology 1999;212:151–154. 4. Yu JT, Apte RS. A case of intravitreal silicone oil migration to the central nervous system. Retina 2005;25:791–793.
5. Fangtian D, Rongping D, Lin Z, Weihong Y. Migration of intraocular silicone into the cerebral ventricles. Am J Ophthalmol 2005;140:156–158. 6. Tatewaki Y, Kurihara N, Sato A, et al. Silicone oil migrating from intraocular tamponade into the ventricles: case report with magnetic resonance image findings. J Comput Assist Tomogr 2011;35:43–45. 7. Jabbour P, Hanna A, Rosenwasser R. Migration of silicone oil in the cerebral intraventricular system. Neurologist 2011;17:109–110. 8. Shields C, Eagle R. Pseudoschnabel’s cavernous degeneration of the optic nerve secondary to intraocular silicone oil. Am J Ophthalmol 1989;107:714–717. 9. Wisniewski HK, Weller RO, Terry RD. Experimental hydrocephalus produced by the subarachnoid infusion of silicone oil. J Neurosurg 1969;31:10–14. 10. Kiilgaard JF, Milea D, Logager V, la Cour M. Cerebral migration of intraocular silicone oil: an MRI study. Acta Ophthalmol 2011;89:522–525.
Purpose: To describe a case of intravitreal silicone oil (SO) migration into the cerebral ventricles with secondary chronic headaches. Methods: Retrospective case report. Chart review. Single patient. Results: A 51-year-old man with a history of proliferative diabetic retinopathy underwent surgery for traction retinal detachment using SO. Postoperatively, he developed elevated intraocular pressure, headaches, and a blind painful eye, which was enucleated. Neuroimaging revealed SO within the cerebral ventricles. Five years after the initial retinal detachment surgery, the patient developed chronic headaches. Lumbar puncture revealed an elevated opening pressure. The headaches were initially managed medically. A ventriculoperitoneal shunt was placed after the headaches persisted, which resulted in their complete resolution at 6 weeks after shunt placement. Conclusion: Ocular hypertension after intravitreal SO placement may play a role in SO intracranial migration. In the case presented, intraventricular SO was the apparent cause of elevated intracranial pressure and headaches. As all published cases of intraventricular SO migration reporting intraocular pressure to this point have described ocular hypertension, careful monitoring of intraocular pressure and aggressive control of ocular hypertension in the presence of intravitreal SO is recommended. RETINAL CASES & BRIEF REPORTS 7:288–290, 2013
From the *Departments of Ophthalmology and Visual Sciences, and †Neurosurgery, University of Nebraska Medical Center, Omaha, Nebraska; and ‡VA NebraskaWestern Iowa Health Care System, Omaha, Nebraska.
Case Report A 51-year-old man with traction retinal detachment and vitreous hemorrhage secondary to proliferative diabetic retinopathy underwent pars plana vitrectomy, membrane peel, and SO placement. Preoperative intraocular pressure (IOP) was normal. After surgery, the eye gradually lost light perception in the presence of normal IOP. Four months after surgery, the patient developed neovascular glaucoma, eye pain, and elevated IOPs as high as 52 mmHg. Ocular hypertension was treated with topical pressure-lowering agents. After treatment was instituted, IOP varied over the next 8 months from 19 mmHg to 46 mmHg, in part because of patient treatment noncompliance. The patient later underwent enucleation of the blind eye. Five years after the initial retinal detachment surgery, the patient presented with neck stiffness and occipital headaches. Routine supine brain magnetic resonance imaging was obtained and demonstrated intraventricular high-attenuation foci consistent with SO in the frontal horns of the lateral ventricles and in the optic recess of the third ventricle (Figure 1). Subsequent head computed tomography in the prone position demonstrated high-attenuation foci in the bilateral occipital horns of the lateral ventricles and in
I
ntravitreal silicone oil (SO) is commonly used for retinal tamponade in cases of complicated retinal detachment. Some of the more common complications associated with the use of SO include glaucoma, optic nerve atrophy, ocular inflammation, cataract, and keratopathy.1 The incidence of migration of SO into the cerebral ventricles is unknown. To our knowledge, only five cases2–7 without a known optic nerve pit have been reported in the literature, with none describing surgical intervention. We present a patient with SO migration to the cerebral ventricles and chronic headaches successfully treated with a ventriculoperitoneal shunting procedure. 288
SO MIGRATION INTO THE CEREBRAL VENTRICLES
Fig. 1. Axial T2-weighted FLAIR magnetic resonance imaging demonstrating SO in the frontal horns of the lateral ventricles.
the suprasellar cistern, consistent with nondependent SO. Lumbar puncture showed clear cerebrospinal fluid and an opening pressure of 27 cm H2O. Chronic headaches associated with nausea, vomiting, and dizziness ensued, but medical management was unsuccessful. After 6 months, a decision was made to proceed with a ventriculoperitoneal shunt. Postoperative head computed tomography showed successful shunt placement and persistence of the SO in the ventricles (Figure 2). At the 6 week postoperative follow-up, the headaches had resolved.
Discussion Severe glaucoma leading to cavernous degeneration of the optic nerve posterior to the lamina cribrosa is thought to be caused by hyaluronic acid from the vitreous forced into the optic nerve. A similar degeneration of the optic nerve with globules of SO infiltrating its entire length was seen in an enucleated eye of a patient with retinal detachment previously repaired by vitrectomy and SO placement.8 Although the exact mechanism is unknown, it is possible that ocular hypertension and degeneration of the optic nerve may create a pathway for SO to migrate to the subarachnoid space or cerebral ventricles. Five cases of intravitreal SO migration to the central nervous system in eyes without a known optic pit have This study was supported in part by an unrestricted grant from the Research to Prevent Blindness. None of the authors have any financial/conflicting interests to disclose. Reprint requests: Eyal Margalit, MD, PhD, Department of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, 985540 Nebraska Medical Center, Omaha, NE 68198-5540; e-mail: [email protected]
289
Fig. 2. Axial computed tomography with supine positioning demonstrating right posterior shunt with tip in the right lateral ventricle. Silicone oil can be seen within the left frontal horn.
been reported to date.2–7 Of these, 3 cases2,4,5 describe ocular hypertension after SO retinal tamponade ranging from 384 to 70 mmHg.5 The remaining two cases6,7 make no mention of the patient’s IOP history. Our patient’s maximum IOP of 52 mmHg is consistent with these previous reports. Our patient had chronic headaches recalcitrant to medical management, as well as dizziness. Whether these symptoms are a direct result of silicone within the cerebral ventricle is unknown. However, given that SO is used experimentally to create hydrocephalus in animals,9 it is reasonable to contend our patient’s elevated opening pressure on lumbar puncture was secondary to SO and may have therefore been the cause of the headaches. Kiilgaard et al10 examined 19 patients for SO migration with magnetic resonance imaging and concluded central nervous system SO migration is likely rare, although maximum intraocular tension was 34 mmHg and no patients had previous evidence of glaucoma. However, reported cases of SO intracranial migration report a higher range of IOPs. With our current limited knowledge, it seems prudent to carefully monitor IOP and aggressively treat ocular hypertension after SO placement, regardless of visual status, to guard against this complication. In addition, a high index of suspicion should be exercised for neurologic symptoms in patients who have undergone intravitreal SO placement with postoperative ocular hypertension, even if the SO or eye has subsequently been removed.
290
RETINAL CASES & BRIEF REPORTS´ 2013 VOLUME 7 NUMBER 3
Key words: central nervous system, cerebral ventricles, intravitreal, silicone oil, ventriculoperitoneal shunt, glaucoma. References 1. Gallemore RP, McCuen BW. Silicone oil in vitreoretinal surgery. In: Ryan SJ, ed. Retina Vol. III: Surgical Retina. 4th ed. St Louis, MO: CV Mosby; 2006:2211–2234. 2. Eller AW, Friberg TR, Mah F. Migration of silicone oil into the brain: a complication of intraocular silicone oil for retinal tamponade. Am J Ophthalmol 2000;129:685–688. 3. Williams RL, Beatty RL, Kanal E, Weissman JL. MR imaging of intraventricular silicone: case report. Radiology 1999;212:151–154. 4. Yu JT, Apte RS. A case of intravitreal silicone oil migration to the central nervous system. Retina 2005;25:791–793.
5. Fangtian D, Rongping D, Lin Z, Weihong Y. Migration of intraocular silicone into the cerebral ventricles. Am J Ophthalmol 2005;140:156–158. 6. Tatewaki Y, Kurihara N, Sato A, et al. Silicone oil migrating from intraocular tamponade into the ventricles: case report with magnetic resonance image findings. J Comput Assist Tomogr 2011;35:43–45. 7. Jabbour P, Hanna A, Rosenwasser R. Migration of silicone oil in the cerebral intraventricular system. Neurologist 2011;17:109–110. 8. Shields C, Eagle R. Pseudoschnabel’s cavernous degeneration of the optic nerve secondary to intraocular silicone oil. Am J Ophthalmol 1989;107:714–717. 9. Wisniewski HK, Weller RO, Terry RD. Experimental hydrocephalus produced by the subarachnoid infusion of silicone oil. J Neurosurg 1969;31:10–14. 10. Kiilgaard JF, Milea D, Logager V, la Cour M. Cerebral migration of intraocular silicone oil: an MRI study. Acta Ophthalmol 2011;89:522–525.
