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Retinal Detachment with Severe Proliferative Vitreoretinopathy in Terson Syndrome
Retinal Detachment with Severe Proliferative Vitreoretinopathy in Terson Syndrome Michaela V elikay, MD, 1 Peter Datlinger, MD, 1 Ulrike Stolba, MD, 1 Andreas Wedrich, MD, 1 Susanne Binder, MD, 1 Norbert Hausmann, MD2 Background: In several reports, early vitrectomy has been proposed for eyes with vitreous hemorrhage due to Terson syndrome as a means to hasten visual recovery. But the development of nuclear sclerosis and the neurologic problems arising from this disease encourage surgeons to wait for spontaneous resorption, especially with young patients. Although the formation of epiretinal membranes has been described, to the authors' knowledge retinal detachment with proliferative vitreoretinopathy in Terson syndrome never has been observed. Methods: The authors report five eyes from four patients with Terson syndrome due to spontaneous aneurysm rupture, in whom retinal detachment with proliferative vitreoretinopathy developed. Results: The early onset and the severe clinical course of proliferative vitreoreti nopathy in these eyes showed parallels to traumatic proliferative vitreoretinopathy. The retina in all eyes could be reattached. Conclusion: The authors point out the necessity for accurate and close follow-up and early, extensive surgical treatment in Terson syndrome, especially in patients with a reduced general state of health. Ophthalmology 1994;101:35-37
Terson syndrome is characterized by a spontaneous or traumatic rupture of cerebral vessels with a sudden in crease of intracranial pressure, which causes disturbances in the circulation in retinal vessels and finally leads to retinal, subhyloidal, and intravitreal hemorrhage in one or both eyes. Although spontaneous resorption of the blood often occurs in this disease, 1•2 early vitrectomy in patients with bilateral hemorrhages has been proposed to hasten rehabilitation. 3.4 Epiretinal membrane formation is known to be a long term sequelae in 78% of the eyes. 5 But, to our knowledge, retinal detachment with severe proliferative vitreoreti nopathy (PVR) after Terson syndrome has not been de scribed previously. From a consecutive series of 16 pa tients with this disease operated on within the last 8 years, Originally received: December I, 1992. Revision accepted: June 28, 1993. 1 1st University Eye Clinic, Vienna, Austria. 2 Feldkirch Eye Hospital, Feldkirch, Austria. Reprint requests to Michaela Velikay, MD, 1st University Eye Clinic, Spitalgasse 2, A-1090 Vienna, Austria.
we report five eyes of four patients in whom retinal de tachment with PVR developed.
Case Reports Included in this study were only patients with spontaneous aneurysm rupture; patients with traumatic subarachnoid hem orrhages were excluded to rule out the possibility of a traumatic origin ofthe PVR. Patients with previous eye disease ofany kind also were excluded. Case 1. A 42-year-old woman was admitted to the Neuro surgical Department of the University Clinic on December 27, 1991, with a subarachnoid hemorrhage due to rupture of an aneurysm of the anterior communicating artery. Aneurysm clipping was performed after 4 days. Three months later, the patient was referred to the eye clinic. Both eyes had dense in travitreal hemorrhages, which completely obscured the fundus view. One month later, when the patient regained partial con sciousness, results of an echographic examination showed a fun nel-shaped retinal detachment in the right eye (Fig I) and a central retinal detachment with massive fibrous proliferation in the left.
35
Ophthalmology
Volume 101, Number 1, January 1994
Figure 1. Case 1. Preoperative echography (right eye, temporal side, optic disc and macula area) shows an intravitreal hemorrhage and retinal de tachment.
On April27, 1992, improvement of the patient's general sta tus allowed ocular surgery. Surgery was performed on the left eye first . During vitrectomy, dense fibrotic tissue with a broad insertion over almost the entire posterior pole was found, de taching the central retina. Because there was no retinal tear, an iatrogenic hole using endodiathermy was created to drain a con siderable amount of central subretinal blood. An encircling band was placed, and silicone oil was used as a tamponade. One week later, surgery was performed on the right eye where a funnel-shaped detachment had been diagnosed. Surgery con sisted of lensectomy, placement of an encircling band, vitrec tomy, endodrainage, silicone oil tamponade, and endolaser. A retinal tear was not detected during surgery. Anatomic success was achieved in both eyes. In the right eye, however, the retina appeared less atrophic than in the left. The postoperative course was uneventful, and the silicone oil was removed from the left eye 6 months later. Due to the patient's poor general state of health, exact visual acuity could not be recorded, but at least light perception was noted in both eyes. Case 2. In October 1989, a 44-year-old woman was ad mitted to the Neurosurgical Department with sudden loss of consciousness. Cerebral angiography disclosed two aneurysms of the right internal carotid artery and massive bleeding into the subarachnoid space. Two weeks later, an aneurysm clipping was performed. The patient regained consciousness after a few days and complained of visual loss in the right eye. At the first ocular examination, an intravitreal hemorrhage completely obscured the view into the right fundus. No disorders of the left eye were found. On December 6, 1989, the retina of the right eye echo graphically remained attached. Results of follow-up examination on April 4, 1990, showed that the intravitreal hemorrhage had cleared. Results also showed a retinal detachment in the lower quadrants with PVR CP4 type 2 with a horseshoe tear at the 6-o'clock position. Visual acuity was limited to hand motions. Vitreoretinal surgery consisted of cryopexy, placement of an encircling band and a scleral buckle, vitrectomy and membrane peeling, as well as a silicone oil tam ponade and endolaser. The retina was reattached, and visual acuity improved to 20/400. Over the following months, macular pucker developed and the lens opacified. Phacoemulsification and membrane peeling were performed in December, but vision
36
remained the same. At the last follow-up in March 1992, the retina remained attached. Case 3. A 30-year-old woman was first seen on August 8, 1988, at the University Clinic's Neurosurgical Department, with an aneurysm rupture of the anterior communicating artery and basal artery. Aneurysm clipping was performed, but the post operative recovery was hampered by infections and seizures. During the first ocular examination on January 8, 1989, vision in both eyes was limited to hand motions due to dense vitreous hemorrhages. Echographically, the retinas were attached. On January 16, 1989, vitrectomy of the right eye was performed. We observed a broad trunk of proliferated tissue inserting into the optic disc and temporal arcade, which was excised com pletely. No pathologic changes were found in the peripheral ret ina. Postoperative visual acuity recovered to 20/100. Due to extensive blepharospasm, a detailed fundus examination was impossible. Because the intravitreal hemorrhage in the left eye showed no sign of resolution, vitrectomy was performed on April 4, 1989. Again, dense fibrotic tissue had to be removed from the optic disc and temporal arcades, disclosing an attached retina without tears. The peripheral retina was normal; the vitreous cavity was filled with air. The operation was performed under general anesthesia; therefore, we were able to make a careful fundus examination of the right eye. A peripheral, shallow retinal detachment due to a horseshoe tear at the 7-o'clock position was found, and a buckling procedure was performed in the same session. The ret ina reattached and visual acuity remained 20/100. Over the next 14 days, a massive inflammatory reaction de veloped with hypopyon formation in the left eye which quickly resolved under combined antibiotic and anti-inflammatory treatment. Visual acuity recovered to 20/200. On May 2, 1990, we found a giant tear from the 9- to !-o'clock positions and a total retinal detachment in the left eye. A second vitrectomy with cryopexy, an encircling procedure, and perfluoropropane gas injection was performed immediately. In the postoperative course, the retina reattached. Seven weeks later, additional laser treatment on the encircling buckle was performed in the left eye. During the following year, the lens opacified in this eye and visual acuity again reduced to hand motions. Results of the echographic examination in October 1990 showed that the giant tear had reopened and enlarged to 200° and that the retina was totally redetached. Phacoemulsification, membrane peeling, and a silicone oil tamponade were needed to reattach the retina. One month later, we operated on the eye again because of regrowth of preretinal membranes. Anatomic success was achieved, but vision re mained limited to hand motions. At the last follow-up visit in August 1992, both eyes had attached retinas; the left eye had a secondary glaucoma, which is treated with local therapy, and a partial atrophy of the optic nerve. The right eye still achieved visual acuity of 20/100. Case 4. A 41-year-old man had a subarachnoid bleeding caused by an aneurysm rupture of the anterior communicating artery on July 14, 1990. Aneurysm clipping was performed within I week. One month later, he regained consciousness and complained ofvisual loss in the right eye. On December 7, 1990, he was examined for the first time. An intravitreal hemorrhage in the right eye was seen; the retina was attached echographically. The left eye was normal. Two months later, a retinal detachment in the upper nasal quadrant was observed echographically. The vitrectomy disclosed a retinal detachment with PVR Cl type I and an epiretinal membrane covering the posterior pole. Because the retina could not be sufficiently relaxed, stellate folds had to
V elikay et al · Retinal Detachment in T erson Syndrome be excised. The eye was filled with silicone oil, the retina was reattached, and endolaser was performed. One month postop eratively, the patient achieved a visual acuity of 20/65. The sil icone oil was removed in April 1991. Four months later, massive reproliferation occurred and caused a retinal detachment with PVR C6 type 4. A lensectomy, a vitrectomy, a 360° retinotomy, and endolaser treatment were necessary to reattach the retina. Vision recovered to 20/500. At the most recent follow-up visit, the central retina remained attached, whereas preretinal mem branes have developed on the retinotomy sides. Vision remained the same.
Discussion The mechanisms of intraocular hemorrhage associated with subarachnoid bleeding have been the subject of some controversy in earlier articles. Most authors now agree that transmitted pressure through the cerebrospinal fluid again is transmitted anteriorly within the intravaginal space of the orbital portion of the optic nerve, obstructing venous drainage from the eye. 2 .4· 6 •7 The acute venous en gorgement and stasis-either alone, or in addition to the acute plethora of the ophthalmic artery-cause the fine papillary and retinal capillaries to rupture and are the reasons for intraocular hemorrhage. 4 The clinical pictures range from papilledema and ret inal bleeding to intravitreal hemorrhage, which can have a delayed occurrence. 2 Walsh and Hedges6 found the de gree ofintraocular hemorrhage corresponded directly with the onset rapidity and magnitude of intracranial bleeding and the presence or absence of cerebral edema. The post capillary venules with their thin walls and wide lumens are particularly vulnerable to a sudden increase in intra luminar pressure. 8 The intraretinal bleeding causes small breaks in the internal-limiting membrane and gives access for the blood to propagate into the vitreous cavity.5 In cases of longstanding intravitreal hemorrhages, the sep aration of the posterior hyaloid face leads to the formation of dome-shaped membranes of various extent in the pos terior pole.9 However, the clinical course of our patients clearly shows that additional events must have taken place, since the eyes developed retinal detachments with severe PVR. To understand why these findings were not reported pre viously, we first have to explore the internal and neurologic aspects of this disease. It is known that the mortality rate of patients with subarachnoid bleeding is substantially higher in individ uals with secondary retinal or vitreous hemorrhages and that patients with bilateral hemorrhages have an even higher mortality rate. 2· ' 0 But the therapeutic abilities in intensive care units and neurosurgical departments have been improved within the last 10 years, and survival rate has increased, so that patients who had very little chance in the past, now survive.'' Because of their semi-conscious
to comatose state on admission, our patients obviously did belong to this group. This could be the reason why retinal detachment with PVR was not observed before in eyes with Terson syndrome. The breakdown of the blood-retinal barrier and the retinal ischemia aggravated by general asphyxia are the suspected main reasons for the acute and severe course of PVR in our patients. From our experience, we conclude that an accurate and close follow-up in Terson syndrome is necessary, es pecially in patients with a reduced general state of health. Early and extensive surgical treatment should be consid ered in patients with severe intracranial and intravitreal bleeding as soon as epiretinal membrane formation is found echographically, so that PVR can be treated in its early stage. Because of increased survival rate of patients with severe intracranial bleeding, we expect PVR in eyes with Terson syndrome to be observed more often in the future. '\
References 1. Khan SG, Frenkel M. Intravitreal hemorrhage associated with rapid increase in intracranial pressure (Terson's syn drome). Am J Ophthalmol 1975;80:37-43. 2. Shaw HE Jr, Landers MB III. Vitreous hemorrhage after intracranial hemorrhage. Am J Ophthalmol 1975;80:207-13. 3. Clarkson JG, Flynn HW Jr, Daily MJ. Vitrectomy inTer son 's syndrome. Am J Ophthalmol 1980;90:549-52. 4. Huber A, Kloti R, Landolt E. Terson's syndrome. Neu roophthalmol 1988;8:223-33. 5. Schultz PN, Sobol WM, Weingeist TA. Long-term visual outcome in Terson syndrome. Ophthalmology 1991 ;98: 1814-19. 6. Walsh FB, Hedges TR Jr. Optic nerve sheath hemorrhage. The Jackson Memorial lecture. Am J Ophthalmol 1951 ;34: 509-27. 7. Smith DC, Keams TP, Sayre GP. Preretinal and optic nerve sheath hemorrhage: pathologic and experimental aspects in subarachnoid hemorrhage. Trans Am Acad Ophthalmol Otolaryngol 1957;61 :201-11. 8. Archer DB. Richardson Cross lecture. Traumatic retinal vasculopathy. Trans Ophthalmol Soc UK 1986;105:361 84. 9. Weingeist TA, Goldman EJ, Folk JC, eta!. Terson's syn drome: clinicopathologic correlations. Ophthalmology 1986;93: 1435-42. 10. Gutierrez Diaz A, Jimenez Carmena J, Ruano Martin F, et a!. Intraocular hemorrhage in sudden increased intracranial pressure (Terson syndrome). Ophthalmologica 1979; 179: 173-6. 11. Deruty R, Mottolese C, Pe!issou-Guyotat I, Soustiel JF. Management of the ruptured intracranial aneurysm-early surgery, late surgery, or modulated surgery? Personal ex perience based upon 468 patients admitted in two periods ( 1972-1984 and 1985-1989). Acta Neurochir 1991 ;113:1-10.
37
Terson syndrome is characterized by a spontaneous or traumatic rupture of cerebral vessels with a sudden in crease of intracranial pressure, which causes disturbances in the circulation in retinal vessels and finally leads to retinal, subhyloidal, and intravitreal hemorrhage in one or both eyes. Although spontaneous resorption of the blood often occurs in this disease, 1•2 early vitrectomy in patients with bilateral hemorrhages has been proposed to hasten rehabilitation. 3.4 Epiretinal membrane formation is known to be a long term sequelae in 78% of the eyes. 5 But, to our knowledge, retinal detachment with severe proliferative vitreoreti nopathy (PVR) after Terson syndrome has not been de scribed previously. From a consecutive series of 16 pa tients with this disease operated on within the last 8 years, Originally received: December I, 1992. Revision accepted: June 28, 1993. 1 1st University Eye Clinic, Vienna, Austria. 2 Feldkirch Eye Hospital, Feldkirch, Austria. Reprint requests to Michaela Velikay, MD, 1st University Eye Clinic, Spitalgasse 2, A-1090 Vienna, Austria.
we report five eyes of four patients in whom retinal de tachment with PVR developed.
Case Reports Included in this study were only patients with spontaneous aneurysm rupture; patients with traumatic subarachnoid hem orrhages were excluded to rule out the possibility of a traumatic origin ofthe PVR. Patients with previous eye disease ofany kind also were excluded. Case 1. A 42-year-old woman was admitted to the Neuro surgical Department of the University Clinic on December 27, 1991, with a subarachnoid hemorrhage due to rupture of an aneurysm of the anterior communicating artery. Aneurysm clipping was performed after 4 days. Three months later, the patient was referred to the eye clinic. Both eyes had dense in travitreal hemorrhages, which completely obscured the fundus view. One month later, when the patient regained partial con sciousness, results of an echographic examination showed a fun nel-shaped retinal detachment in the right eye (Fig I) and a central retinal detachment with massive fibrous proliferation in the left.
35
Ophthalmology
Volume 101, Number 1, January 1994
Figure 1. Case 1. Preoperative echography (right eye, temporal side, optic disc and macula area) shows an intravitreal hemorrhage and retinal de tachment.
On April27, 1992, improvement of the patient's general sta tus allowed ocular surgery. Surgery was performed on the left eye first . During vitrectomy, dense fibrotic tissue with a broad insertion over almost the entire posterior pole was found, de taching the central retina. Because there was no retinal tear, an iatrogenic hole using endodiathermy was created to drain a con siderable amount of central subretinal blood. An encircling band was placed, and silicone oil was used as a tamponade. One week later, surgery was performed on the right eye where a funnel-shaped detachment had been diagnosed. Surgery con sisted of lensectomy, placement of an encircling band, vitrec tomy, endodrainage, silicone oil tamponade, and endolaser. A retinal tear was not detected during surgery. Anatomic success was achieved in both eyes. In the right eye, however, the retina appeared less atrophic than in the left. The postoperative course was uneventful, and the silicone oil was removed from the left eye 6 months later. Due to the patient's poor general state of health, exact visual acuity could not be recorded, but at least light perception was noted in both eyes. Case 2. In October 1989, a 44-year-old woman was ad mitted to the Neurosurgical Department with sudden loss of consciousness. Cerebral angiography disclosed two aneurysms of the right internal carotid artery and massive bleeding into the subarachnoid space. Two weeks later, an aneurysm clipping was performed. The patient regained consciousness after a few days and complained of visual loss in the right eye. At the first ocular examination, an intravitreal hemorrhage completely obscured the view into the right fundus. No disorders of the left eye were found. On December 6, 1989, the retina of the right eye echo graphically remained attached. Results of follow-up examination on April 4, 1990, showed that the intravitreal hemorrhage had cleared. Results also showed a retinal detachment in the lower quadrants with PVR CP4 type 2 with a horseshoe tear at the 6-o'clock position. Visual acuity was limited to hand motions. Vitreoretinal surgery consisted of cryopexy, placement of an encircling band and a scleral buckle, vitrectomy and membrane peeling, as well as a silicone oil tam ponade and endolaser. The retina was reattached, and visual acuity improved to 20/400. Over the following months, macular pucker developed and the lens opacified. Phacoemulsification and membrane peeling were performed in December, but vision
36
remained the same. At the last follow-up in March 1992, the retina remained attached. Case 3. A 30-year-old woman was first seen on August 8, 1988, at the University Clinic's Neurosurgical Department, with an aneurysm rupture of the anterior communicating artery and basal artery. Aneurysm clipping was performed, but the post operative recovery was hampered by infections and seizures. During the first ocular examination on January 8, 1989, vision in both eyes was limited to hand motions due to dense vitreous hemorrhages. Echographically, the retinas were attached. On January 16, 1989, vitrectomy of the right eye was performed. We observed a broad trunk of proliferated tissue inserting into the optic disc and temporal arcade, which was excised com pletely. No pathologic changes were found in the peripheral ret ina. Postoperative visual acuity recovered to 20/100. Due to extensive blepharospasm, a detailed fundus examination was impossible. Because the intravitreal hemorrhage in the left eye showed no sign of resolution, vitrectomy was performed on April 4, 1989. Again, dense fibrotic tissue had to be removed from the optic disc and temporal arcades, disclosing an attached retina without tears. The peripheral retina was normal; the vitreous cavity was filled with air. The operation was performed under general anesthesia; therefore, we were able to make a careful fundus examination of the right eye. A peripheral, shallow retinal detachment due to a horseshoe tear at the 7-o'clock position was found, and a buckling procedure was performed in the same session. The ret ina reattached and visual acuity remained 20/100. Over the next 14 days, a massive inflammatory reaction de veloped with hypopyon formation in the left eye which quickly resolved under combined antibiotic and anti-inflammatory treatment. Visual acuity recovered to 20/200. On May 2, 1990, we found a giant tear from the 9- to !-o'clock positions and a total retinal detachment in the left eye. A second vitrectomy with cryopexy, an encircling procedure, and perfluoropropane gas injection was performed immediately. In the postoperative course, the retina reattached. Seven weeks later, additional laser treatment on the encircling buckle was performed in the left eye. During the following year, the lens opacified in this eye and visual acuity again reduced to hand motions. Results of the echographic examination in October 1990 showed that the giant tear had reopened and enlarged to 200° and that the retina was totally redetached. Phacoemulsification, membrane peeling, and a silicone oil tamponade were needed to reattach the retina. One month later, we operated on the eye again because of regrowth of preretinal membranes. Anatomic success was achieved, but vision re mained limited to hand motions. At the last follow-up visit in August 1992, both eyes had attached retinas; the left eye had a secondary glaucoma, which is treated with local therapy, and a partial atrophy of the optic nerve. The right eye still achieved visual acuity of 20/100. Case 4. A 41-year-old man had a subarachnoid bleeding caused by an aneurysm rupture of the anterior communicating artery on July 14, 1990. Aneurysm clipping was performed within I week. One month later, he regained consciousness and complained ofvisual loss in the right eye. On December 7, 1990, he was examined for the first time. An intravitreal hemorrhage in the right eye was seen; the retina was attached echographically. The left eye was normal. Two months later, a retinal detachment in the upper nasal quadrant was observed echographically. The vitrectomy disclosed a retinal detachment with PVR Cl type I and an epiretinal membrane covering the posterior pole. Because the retina could not be sufficiently relaxed, stellate folds had to
V elikay et al · Retinal Detachment in T erson Syndrome be excised. The eye was filled with silicone oil, the retina was reattached, and endolaser was performed. One month postop eratively, the patient achieved a visual acuity of 20/65. The sil icone oil was removed in April 1991. Four months later, massive reproliferation occurred and caused a retinal detachment with PVR C6 type 4. A lensectomy, a vitrectomy, a 360° retinotomy, and endolaser treatment were necessary to reattach the retina. Vision recovered to 20/500. At the most recent follow-up visit, the central retina remained attached, whereas preretinal mem branes have developed on the retinotomy sides. Vision remained the same.
Discussion The mechanisms of intraocular hemorrhage associated with subarachnoid bleeding have been the subject of some controversy in earlier articles. Most authors now agree that transmitted pressure through the cerebrospinal fluid again is transmitted anteriorly within the intravaginal space of the orbital portion of the optic nerve, obstructing venous drainage from the eye. 2 .4· 6 •7 The acute venous en gorgement and stasis-either alone, or in addition to the acute plethora of the ophthalmic artery-cause the fine papillary and retinal capillaries to rupture and are the reasons for intraocular hemorrhage. 4 The clinical pictures range from papilledema and ret inal bleeding to intravitreal hemorrhage, which can have a delayed occurrence. 2 Walsh and Hedges6 found the de gree ofintraocular hemorrhage corresponded directly with the onset rapidity and magnitude of intracranial bleeding and the presence or absence of cerebral edema. The post capillary venules with their thin walls and wide lumens are particularly vulnerable to a sudden increase in intra luminar pressure. 8 The intraretinal bleeding causes small breaks in the internal-limiting membrane and gives access for the blood to propagate into the vitreous cavity.5 In cases of longstanding intravitreal hemorrhages, the sep aration of the posterior hyaloid face leads to the formation of dome-shaped membranes of various extent in the pos terior pole.9 However, the clinical course of our patients clearly shows that additional events must have taken place, since the eyes developed retinal detachments with severe PVR. To understand why these findings were not reported pre viously, we first have to explore the internal and neurologic aspects of this disease. It is known that the mortality rate of patients with subarachnoid bleeding is substantially higher in individ uals with secondary retinal or vitreous hemorrhages and that patients with bilateral hemorrhages have an even higher mortality rate. 2· ' 0 But the therapeutic abilities in intensive care units and neurosurgical departments have been improved within the last 10 years, and survival rate has increased, so that patients who had very little chance in the past, now survive.'' Because of their semi-conscious
to comatose state on admission, our patients obviously did belong to this group. This could be the reason why retinal detachment with PVR was not observed before in eyes with Terson syndrome. The breakdown of the blood-retinal barrier and the retinal ischemia aggravated by general asphyxia are the suspected main reasons for the acute and severe course of PVR in our patients. From our experience, we conclude that an accurate and close follow-up in Terson syndrome is necessary, es pecially in patients with a reduced general state of health. Early and extensive surgical treatment should be consid ered in patients with severe intracranial and intravitreal bleeding as soon as epiretinal membrane formation is found echographically, so that PVR can be treated in its early stage. Because of increased survival rate of patients with severe intracranial bleeding, we expect PVR in eyes with Terson syndrome to be observed more often in the future. '\
References 1. Khan SG, Frenkel M. Intravitreal hemorrhage associated with rapid increase in intracranial pressure (Terson's syn drome). Am J Ophthalmol 1975;80:37-43. 2. Shaw HE Jr, Landers MB III. Vitreous hemorrhage after intracranial hemorrhage. Am J Ophthalmol 1975;80:207-13. 3. Clarkson JG, Flynn HW Jr, Daily MJ. Vitrectomy inTer son 's syndrome. Am J Ophthalmol 1980;90:549-52. 4. Huber A, Kloti R, Landolt E. Terson's syndrome. Neu roophthalmol 1988;8:223-33. 5. Schultz PN, Sobol WM, Weingeist TA. Long-term visual outcome in Terson syndrome. Ophthalmology 1991 ;98: 1814-19. 6. Walsh FB, Hedges TR Jr. Optic nerve sheath hemorrhage. The Jackson Memorial lecture. Am J Ophthalmol 1951 ;34: 509-27. 7. Smith DC, Keams TP, Sayre GP. Preretinal and optic nerve sheath hemorrhage: pathologic and experimental aspects in subarachnoid hemorrhage. Trans Am Acad Ophthalmol Otolaryngol 1957;61 :201-11. 8. Archer DB. Richardson Cross lecture. Traumatic retinal vasculopathy. Trans Ophthalmol Soc UK 1986;105:361 84. 9. Weingeist TA, Goldman EJ, Folk JC, eta!. Terson's syn drome: clinicopathologic correlations. Ophthalmology 1986;93: 1435-42. 10. Gutierrez Diaz A, Jimenez Carmena J, Ruano Martin F, et a!. Intraocular hemorrhage in sudden increased intracranial pressure (Terson syndrome). Ophthalmologica 1979; 179: 173-6. 11. Deruty R, Mottolese C, Pe!issou-Guyotat I, Soustiel JF. Management of the ruptured intracranial aneurysm-early surgery, late surgery, or modulated surgery? Personal ex perience based upon 468 patients admitted in two periods ( 1972-1984 and 1985-1989). Acta Neurochir 1991 ;113:1-10.
37