International Ophthalmology 15: 163-171, 1991. 9 1991 KluwerAcademic Publishers. Printedin the Netherlands.
Bilateral blindness in cavernous sinus thrombosis* Carine Coutteel1, Anita Leys1, Eric Fossion2 & Luc Missotten ~ 1Department of Ophthalmolog) , and-~ Departmen t of Head and Neck Surgery, University Hospital St. Rafa~l, Leuven, Belgium
Key words: anterior ischemic optic neuropathy (AION), cavernous sinus thrombosis (CST), central retinal artery occlusion (CRAO), sepsis Abstract
An unusual case of bilateral blindness secondary to a cavernous sinus thrombosis is reported. A woman who had undergone reconstructive surgery after tumor resection of the floor of the mouth, was readmitted 1 month later with bilateral proptosis and signs of sepsis. There were no complaints of blurred vision. A CT-scan of the orbits demonstrated a bilateral cavernous sinus thrombosis (CST) secondary to an infection at the skull base behind the myocataneous flap. A few days later she became blind, due to bilateral central retinal artery occlusion and anterior ischemic optic neuropathy. The general critical condition improved with intensive AB treatment. The patient recovered well without neurological defects apart from her permanent bilateral blindness. There were no signs of tumor recurrence. To our knowledge, this is the first documented case of bilateral blindness in a patient suffering from CST.
Introduction
Case report
Cavernous sinus thrombosis (CST) was first described in 1921 by Duncan [1]. Knapp in 1968 [2] described the ocular abnormalities characteristic of the condition. Prior to the antibiotic era, septic CST was a uniformly fatal complication of head and neck infection. Grove [3] collected 400 cases with a mortality of almost 100% with the introduction of antibiotics. Yarrington [4] found a fall in mortality to 12-14%. Cavernous sinus thrombosis rarely causes blindness. Few studies in the literature on cavernous sinus thrombosis include extensive ophthalmic investigations [5-7]. This report presents a patient who developed bilateral blindness after bilateral cavernous sinus thrombosis.
A woman, aged 50 years, was referred to the head and neck surgery unit in November 1987 because of a tumoral process of the right anterolateral floor of the mouth. A few months prior to admission, she had noted some pain and discomfort while eating. Afterwards she developed foetor ex ore and swallowing problems. On clinical examination the tumor was seen to be invading the mandibula and the myelohyoid- and genioglossal muscles. A pathological lymphnode was palpated in the right submandibular region. A biopsy taken on admission, confirmed the diagnosis of a well-differentiated spinocellular epithelioma of the floor of the mouth. As the systemic screening for general metastasis was negative, and the patient was staged T4N1M0. In December 1987, the tumor was irradiated with 6 Mev photons of the linear accelerator on the oral
Presented at the Combinedmeetingof the MaculaSocietyand Retina Society.Fluoresceinconference,June 21, 1989, Boston.
164
C. Coutteel et al.
Fig. 1. A. CT-scan demonstrating bilateral cavernous sinus thrombosis (arrows). B. CT-scan demonstrating bilateral ophthalmic vein thrombosis (arrows).
Bilateral blindness in cavernous sinus thrombosis
cavity and as the right cervical lymphnodes with a readout dose of 46 Gy in 41/2 weeks. At the end of January 1988, when the tumor had partially regressed, wide block resection of the right floor of the mouth with the dento-alveolar segment, and a right functional neck dissection were performed. The defect was closed by a pectoralis major osteomyocutaneous flap which includes the fifth rib. However, necrosis of the transplant secondary to a large hematoma made a replacement necessary, with free lattissimus dorsi myocutaneous flap 3 days after the first operation. Postoperatively, the patient recovered well and she was discharged ten days later. On the 14th of March, 6 weeks after the first operation, the patient was readmitted, as an emergency, with headache, swelling of the eyelids and bilateral proptosis, more marked on the right side. On examination she was febrile (38.5~ There was no neck stiffness. A CT-scan at that time showed a thrombosis of the right jugular vein extending to the superior bulb. Intensive parenteral antibiotic treatment was started immediately with amoxicilline 2 g/day, metronidazole 2 g/day and oxacilline 2 g/day. Anticoagulants or steroids were not used. The following day an ophthalmological evaluation was made: bilateral swelling of the eyelids, marked chemosis of the conjunctivae, bilateral proptosis, good visual acuity, isocoria but sluggish reaction to light and marked restriction of eye movements in all directions bilaterally. On fundus examination there was some venous enlargement. The optic discs were normal. The right trigeminal function was impaired with hyposthesia in the division of V1 and reduced corneal reflex. The clinical picture was suggestive of cavernous sinus thrombosis. This was confirmed by a second CT-scan, which showes (Fig. 1A), thrombosis of both ophthalmic veins (Fig. 1B) as well as some fibrosis or infection at the right skull base. Therefore the following day, on the 16th of March 1988, a surgical reintervention was performed under general anesthesia; the wound on the neck was reopened to find out the location of a possible infection. No collection was found. Cultures taken from the wound, however, were positive for Staphylococcus aureus, which were sensitive to the previously started antibiotic
165
treatment. The patient's condition started to improve over the following days and the proptosis regressed. The patient still seemed to have good vision, although communication was poor because of the endotracheal tube, which was left in place for 24 hours. Four days later the patient had no perception of light anymore. On examination there was only a mild proptosis left. The swelling of the eyelids and chemosis were regressed. Eye motility was still limited. The pupil diameters were changing from one moment to the other, but the reaction to light was very poor. Both optic discs were edematous and pale. There was a bilateral macular cherry red spot, dark enlarged veins, a few hemorrhages along the veins, and the arterial bloodcolumn was segmented (Fig. 2A, B). The diagnosis of bilateral central retinal artery occlusion and anterior ischemic optic neuropathy was made. There was no evidence for choroidal infarction. A fluorescein angiography could not be performed at this time as the patient's situation was too critical. Prednisone was given intravenously in shots 4 • 20 mg over the next 24 h and acetylsalicylate acid 2 g/day was started. There was no recovery of vision. A fluorescein angiography, performed 1 week later, showed almost no perfusion of the CRA (central retinal artery) and there was leakage on the optic discs. The choroidal perfusion appeared to be normal (Fig. 3A, B). The left optic disc was covered by a lump of necrotic tissue that seemed to crumble off into the vitreous over the next week; the right optic disc was edematous and pale (Fig. 4A, B). At this time the pupils were semi-dilated and non-reactive. On the 5th of May, 6 weeks after the retinal vascular accident, neovascularisation on the left optic disc developed and was complicated by a vitreous hemorrhage. On the right side, there was a pale optic disc without new vessels (Fig. 5A, B). There was no rubeosis iridis, and intraocular pressures were normal. Abduction was limited on both sides. One month later the right optic disc became atrophic, the left optic disc was covered by a vitreous hemorrhage. The patient had recovered well and her general condition was satisfactory. There
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C. Coutteel et al.
Fig. 2. Fundus photographs demonstrating bilateral CRAO and AION: Note the bilateral edematous optic discs, the macular cherry red spot, the dark enlarged veins and segmented arterial blood columns (right eye: A; left eye: B).
Bilateral blindness in cavernous sinus thrombosis
167
Fig. 3. Fluorescein angiogram 1 week after the first presentation: there is almost no perfusion of the central retinal artery and there is leakage on both optic discs (right eye: A; left eye: B).
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Fig. 4. Fundus photographs taken 2 weeks after the first presentation. A: right eye: pale edematous optic disc. B: left eye: necrotic tissue covering the lower part of the optic disc and floating in the vitreous (arrow).
Bilateral blindness in cavernous sinus thrombosis
169
Fig. 5. Fundus photographs taken 6 weeks after the vascular accident. A: right eye: pale optic disc without new vessels. B: left eye: neovascularisation on the left optic disc complicated by a vitreous hemorrhage.
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were no neurological defects apart from bilateral blindness, non-reactive pupils and limited abduction. There were no signs of tumor recurrence two years after the initial surgery.
Discussion
Septic cavernous sinus thrombosis is an uncommon disease and should be differentiated from orbital cellulitis [8]. High resolution computed tomography (CT) may be in addition to a good clinical evaluation [9, 10]. In our case, the clinical picture of CST was clear. First there was bilateral ocular involvement (proptosis, lid edema, chemosis, ophthalmoplegia and enlarged retinal veins) and right trigeminal function impairment. Secondly, the source of the septic embolism was known (wound infection in the right side of the neck and thrombosis of the right jugular vein extending to the bulb as shown on the first CT-scan). It is striking that the patient developed a sudden bilateral blindness at a time that her general condition had improved slightly. Although some authors believe that antibiotics in conjunction with anticoagulants used early in the course of CST reduce residual morbidity [11], in this case the risk of bleeding was thought to be too high because there had been bleeding problems during the initial surgery. Consequently the patient was not treated with anticoagulants once the diagnosis of bilateral CST was made. Blindness of an eye as a result of CST is uncommon. According to Walsh and Hoyt, CST in itself does not account for loss of vision [12]. Residual blindness occurs in less than 10% of patients with CST [13]. It may be the result of corneal ulcers due to poor lid closure [14], C R A O secondary to pressure at the orbital apex [7, 8], emboli [15] or internal carotid arteritis [16], ischemic optic neuropathy without C R A O [6], toxic neuritis secondary to adjacent purulent inflammation of the optic nerve [17]. In our patient, however, there was blindness of both eyes. In the literature we have found only one case of septic CST associated with blindness: Harbour et al. reported a case of CST
complicated with amaurosis. The autopsy showed bilateral infarcted optic nerves. The patient, however, had multiple neurological defects and died [18]9 In our patient we noticed a central retinal artery occlusion combined with pale swollen optic discs on both eyes at the same time. The diagnosis of CRAO was evident on fundoscopy (macular cherry red spot and retinal ischemic edema) and on fluorescein angiography (almost no filling of the central retinal artery). The diagnosis of AION was made because there was bilateral optic disc edema and necrotic tissue on the left optic disc crumbling into the vitreous. The presence of central retinal vein occlusion (CRVO) cannot be ruled out. Further retrograde thrombosis from the ophthalmic veins is possible. The retinal veins were enlarged but there were only few hemorrhages and the appearance of the papilledema was more suggestive of AION (pale, necrotic tissue present on left optic disc). The obstruction was probably situated in the ophthalmic artery before its division into the posterior ciliary artery and the central retinal artery, though there was no evidence of choroidal infarction on fluorescein angiography. Some perfusion disturbances of the choroid might have been present, but were not detectable or may have improved again as the first fluorescein angiogram could only be performed 1 week after the vascular accident. Hayreh demonstrated that after occlusion of one or more of the posterior ciliary arteries, filling of the choroid takes place via collaterals from the posterior episcleral arterial plexus [19]. Carotid angiography has not been performed. It is unlikely that the radiotherapy (46 Gy on the oral cavity and the neck) has played any role in the development of the ocular vascular complications, since the upper border of the radiation field was located in the palatum durum. The scatter dose at the cavernous sinus and the optic nerve (>3 cm out of the radiation field) has been calculated to be respectively 3,6% (= 1.6 Gy) and 0.9% (= 0.4 Gy) of the administered dose. A very similar fundus picture associated with bilateral blindness has been published very recently by Guyer et al. in a case of non-Hodgkin lympho-
Bilateral blindness in cavernous sinus thrombosis
ma [20]. Histopathologic examination revealed infiltration of the pial septa by tumor and septic thrombi in the central retinal arteries. In conclusion, the mortality rate of CST has been reduced a lot for the last few years, but severe complications still occur.
ll.
12. 13.
References
14. 15.
1. Duncan A. Contributions to morbid anatomy. Edin Med Surg J 1821; 17: 311-366. 2. Knapp H. Ueber Verstopfung des Blutgef~isse des Auges. Albrecht Von Graefes Arch Klin Exp Ophthalmo11868; 18: 207-251. 3. Grove WE. Septic and aseptic types of thrombosis of the cavernous sinus. Arch Otolaryngol 1936; 24: 29-50. 4. Yarrington CT. Cavernous sinus thrombosis revisited. Proc R Soc Med 1977; 70: 456-459. 5. Geggel HS, Isenberg SJ. Cavernous sinus thrombosis as a cause of unilateral blindness. Ann Ophthalmol 1982; 14: 569-574. 6. Friberg TR, Sogg RL. Ischemic optic neuropathy in cavernous sinus thrombosis. Arch Ophthalmo11978; 96" 453-456. 7. Boniuk M. The ocular manifestations of ophthalmic vein and aseptic cavernous sinus thrombosis. Amer Acad of Ophthal & Otolaryngol 1972; 76: 1519-1534. 8. Price CD, Hamersoff SB, Richards RD: Cavernous sinus thrombosis and Orbital Cellulitis. South Med J 1971; 64: 1243-1247. 9. Ahmadi J, Keane JR, Segall HD et al. CT observations pertinent to septic cavernous sinus thrombosis. AJNR 1985; 6: 755-758. 10. Chung W, Chang KH et al. Computed tomography of
16.
17. 18.
19.
20.
171
cavernous sinus diseases. Neuroradiology 1988; 30: 319328. Levine SR, Twyman RE, Gilman S. The role of anticoagulation in cavernous sinus thrombosis. Neurology 1988; 38: 517-522. Walsh FB, Hoyt WF. Clinical neuro-ophthalmology, ed 3. Baltimore, Williams & Wilkins Co, 1969, pp 1892-1896. Shaw RE. Cavernous sinus thrombosis: A review. Br Jr Surg 1952; 40: 40-48. Gupta MC, Ahuja OP, Kumar S. Cavernous sinus thrombosis. Indian J Med Sci 1970; 24: 748--753. Mehra KS, Somani PN. Multiple emboli in central retinal artery following cavernous sinus thrombosis. J All India Ophthal Soc 1967; 15: 71-72. Mathew NT, Abraham J, Taori GM et al. Internal carotid artery occlusion in cavernous sinus thrombosis. Arch Neurol 1971; 24: 11-16. Taylor PJ. Cavernous sinus thromboflebitis. Br J Ophthalmol 1957; 41: 228-237. Harbour RC, Trobe JD, Ballinger WE. Septic cavernous sinus thrombosis associated with gingivitis and parapharyngeal abcess. Arch Ophthalmol 1984; 102: 94-97. Hayreh SS, Baines JAB. Occlusion of the posterior ciliary artery. I. Effects on choroidal circulation. Br J Ophthalmol 1972; 56: 719-735. Guyer DR, Green R, Schachat AP et al. Bilateral ischemic optic neuropathy and retinal vascular occlusions associated with lymphoma and sepsis. Ophthalmology 1990; 97: 882888.
Address for offprints: C. Coutteel, Department of Ophthalmology, University Hospital St. Rafa61, Leuven, Capucijnenvoer 33, 3000 Leuven, Belgium
Bilateral blindness in cavernous sinus thrombosis* Carine Coutteel1, Anita Leys1, Eric Fossion2 & Luc Missotten ~ 1Department of Ophthalmolog) , and-~ Departmen t of Head and Neck Surgery, University Hospital St. Rafa~l, Leuven, Belgium
Key words: anterior ischemic optic neuropathy (AION), cavernous sinus thrombosis (CST), central retinal artery occlusion (CRAO), sepsis Abstract
An unusual case of bilateral blindness secondary to a cavernous sinus thrombosis is reported. A woman who had undergone reconstructive surgery after tumor resection of the floor of the mouth, was readmitted 1 month later with bilateral proptosis and signs of sepsis. There were no complaints of blurred vision. A CT-scan of the orbits demonstrated a bilateral cavernous sinus thrombosis (CST) secondary to an infection at the skull base behind the myocataneous flap. A few days later she became blind, due to bilateral central retinal artery occlusion and anterior ischemic optic neuropathy. The general critical condition improved with intensive AB treatment. The patient recovered well without neurological defects apart from her permanent bilateral blindness. There were no signs of tumor recurrence. To our knowledge, this is the first documented case of bilateral blindness in a patient suffering from CST.
Introduction
Case report
Cavernous sinus thrombosis (CST) was first described in 1921 by Duncan [1]. Knapp in 1968 [2] described the ocular abnormalities characteristic of the condition. Prior to the antibiotic era, septic CST was a uniformly fatal complication of head and neck infection. Grove [3] collected 400 cases with a mortality of almost 100% with the introduction of antibiotics. Yarrington [4] found a fall in mortality to 12-14%. Cavernous sinus thrombosis rarely causes blindness. Few studies in the literature on cavernous sinus thrombosis include extensive ophthalmic investigations [5-7]. This report presents a patient who developed bilateral blindness after bilateral cavernous sinus thrombosis.
A woman, aged 50 years, was referred to the head and neck surgery unit in November 1987 because of a tumoral process of the right anterolateral floor of the mouth. A few months prior to admission, she had noted some pain and discomfort while eating. Afterwards she developed foetor ex ore and swallowing problems. On clinical examination the tumor was seen to be invading the mandibula and the myelohyoid- and genioglossal muscles. A pathological lymphnode was palpated in the right submandibular region. A biopsy taken on admission, confirmed the diagnosis of a well-differentiated spinocellular epithelioma of the floor of the mouth. As the systemic screening for general metastasis was negative, and the patient was staged T4N1M0. In December 1987, the tumor was irradiated with 6 Mev photons of the linear accelerator on the oral
Presented at the Combinedmeetingof the MaculaSocietyand Retina Society.Fluoresceinconference,June 21, 1989, Boston.
164
C. Coutteel et al.
Fig. 1. A. CT-scan demonstrating bilateral cavernous sinus thrombosis (arrows). B. CT-scan demonstrating bilateral ophthalmic vein thrombosis (arrows).
Bilateral blindness in cavernous sinus thrombosis
cavity and as the right cervical lymphnodes with a readout dose of 46 Gy in 41/2 weeks. At the end of January 1988, when the tumor had partially regressed, wide block resection of the right floor of the mouth with the dento-alveolar segment, and a right functional neck dissection were performed. The defect was closed by a pectoralis major osteomyocutaneous flap which includes the fifth rib. However, necrosis of the transplant secondary to a large hematoma made a replacement necessary, with free lattissimus dorsi myocutaneous flap 3 days after the first operation. Postoperatively, the patient recovered well and she was discharged ten days later. On the 14th of March, 6 weeks after the first operation, the patient was readmitted, as an emergency, with headache, swelling of the eyelids and bilateral proptosis, more marked on the right side. On examination she was febrile (38.5~ There was no neck stiffness. A CT-scan at that time showed a thrombosis of the right jugular vein extending to the superior bulb. Intensive parenteral antibiotic treatment was started immediately with amoxicilline 2 g/day, metronidazole 2 g/day and oxacilline 2 g/day. Anticoagulants or steroids were not used. The following day an ophthalmological evaluation was made: bilateral swelling of the eyelids, marked chemosis of the conjunctivae, bilateral proptosis, good visual acuity, isocoria but sluggish reaction to light and marked restriction of eye movements in all directions bilaterally. On fundus examination there was some venous enlargement. The optic discs were normal. The right trigeminal function was impaired with hyposthesia in the division of V1 and reduced corneal reflex. The clinical picture was suggestive of cavernous sinus thrombosis. This was confirmed by a second CT-scan, which showes (Fig. 1A), thrombosis of both ophthalmic veins (Fig. 1B) as well as some fibrosis or infection at the right skull base. Therefore the following day, on the 16th of March 1988, a surgical reintervention was performed under general anesthesia; the wound on the neck was reopened to find out the location of a possible infection. No collection was found. Cultures taken from the wound, however, were positive for Staphylococcus aureus, which were sensitive to the previously started antibiotic
165
treatment. The patient's condition started to improve over the following days and the proptosis regressed. The patient still seemed to have good vision, although communication was poor because of the endotracheal tube, which was left in place for 24 hours. Four days later the patient had no perception of light anymore. On examination there was only a mild proptosis left. The swelling of the eyelids and chemosis were regressed. Eye motility was still limited. The pupil diameters were changing from one moment to the other, but the reaction to light was very poor. Both optic discs were edematous and pale. There was a bilateral macular cherry red spot, dark enlarged veins, a few hemorrhages along the veins, and the arterial bloodcolumn was segmented (Fig. 2A, B). The diagnosis of bilateral central retinal artery occlusion and anterior ischemic optic neuropathy was made. There was no evidence for choroidal infarction. A fluorescein angiography could not be performed at this time as the patient's situation was too critical. Prednisone was given intravenously in shots 4 • 20 mg over the next 24 h and acetylsalicylate acid 2 g/day was started. There was no recovery of vision. A fluorescein angiography, performed 1 week later, showed almost no perfusion of the CRA (central retinal artery) and there was leakage on the optic discs. The choroidal perfusion appeared to be normal (Fig. 3A, B). The left optic disc was covered by a lump of necrotic tissue that seemed to crumble off into the vitreous over the next week; the right optic disc was edematous and pale (Fig. 4A, B). At this time the pupils were semi-dilated and non-reactive. On the 5th of May, 6 weeks after the retinal vascular accident, neovascularisation on the left optic disc developed and was complicated by a vitreous hemorrhage. On the right side, there was a pale optic disc without new vessels (Fig. 5A, B). There was no rubeosis iridis, and intraocular pressures were normal. Abduction was limited on both sides. One month later the right optic disc became atrophic, the left optic disc was covered by a vitreous hemorrhage. The patient had recovered well and her general condition was satisfactory. There
166
C. Coutteel et al.
Fig. 2. Fundus photographs demonstrating bilateral CRAO and AION: Note the bilateral edematous optic discs, the macular cherry red spot, the dark enlarged veins and segmented arterial blood columns (right eye: A; left eye: B).
Bilateral blindness in cavernous sinus thrombosis
167
Fig. 3. Fluorescein angiogram 1 week after the first presentation: there is almost no perfusion of the central retinal artery and there is leakage on both optic discs (right eye: A; left eye: B).
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C. Coutteel et al.
Fig. 4. Fundus photographs taken 2 weeks after the first presentation. A: right eye: pale edematous optic disc. B: left eye: necrotic tissue covering the lower part of the optic disc and floating in the vitreous (arrow).
Bilateral blindness in cavernous sinus thrombosis
169
Fig. 5. Fundus photographs taken 6 weeks after the vascular accident. A: right eye: pale optic disc without new vessels. B: left eye: neovascularisation on the left optic disc complicated by a vitreous hemorrhage.
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were no neurological defects apart from bilateral blindness, non-reactive pupils and limited abduction. There were no signs of tumor recurrence two years after the initial surgery.
Discussion
Septic cavernous sinus thrombosis is an uncommon disease and should be differentiated from orbital cellulitis [8]. High resolution computed tomography (CT) may be in addition to a good clinical evaluation [9, 10]. In our case, the clinical picture of CST was clear. First there was bilateral ocular involvement (proptosis, lid edema, chemosis, ophthalmoplegia and enlarged retinal veins) and right trigeminal function impairment. Secondly, the source of the septic embolism was known (wound infection in the right side of the neck and thrombosis of the right jugular vein extending to the bulb as shown on the first CT-scan). It is striking that the patient developed a sudden bilateral blindness at a time that her general condition had improved slightly. Although some authors believe that antibiotics in conjunction with anticoagulants used early in the course of CST reduce residual morbidity [11], in this case the risk of bleeding was thought to be too high because there had been bleeding problems during the initial surgery. Consequently the patient was not treated with anticoagulants once the diagnosis of bilateral CST was made. Blindness of an eye as a result of CST is uncommon. According to Walsh and Hoyt, CST in itself does not account for loss of vision [12]. Residual blindness occurs in less than 10% of patients with CST [13]. It may be the result of corneal ulcers due to poor lid closure [14], C R A O secondary to pressure at the orbital apex [7, 8], emboli [15] or internal carotid arteritis [16], ischemic optic neuropathy without C R A O [6], toxic neuritis secondary to adjacent purulent inflammation of the optic nerve [17]. In our patient, however, there was blindness of both eyes. In the literature we have found only one case of septic CST associated with blindness: Harbour et al. reported a case of CST
complicated with amaurosis. The autopsy showed bilateral infarcted optic nerves. The patient, however, had multiple neurological defects and died [18]9 In our patient we noticed a central retinal artery occlusion combined with pale swollen optic discs on both eyes at the same time. The diagnosis of CRAO was evident on fundoscopy (macular cherry red spot and retinal ischemic edema) and on fluorescein angiography (almost no filling of the central retinal artery). The diagnosis of AION was made because there was bilateral optic disc edema and necrotic tissue on the left optic disc crumbling into the vitreous. The presence of central retinal vein occlusion (CRVO) cannot be ruled out. Further retrograde thrombosis from the ophthalmic veins is possible. The retinal veins were enlarged but there were only few hemorrhages and the appearance of the papilledema was more suggestive of AION (pale, necrotic tissue present on left optic disc). The obstruction was probably situated in the ophthalmic artery before its division into the posterior ciliary artery and the central retinal artery, though there was no evidence of choroidal infarction on fluorescein angiography. Some perfusion disturbances of the choroid might have been present, but were not detectable or may have improved again as the first fluorescein angiogram could only be performed 1 week after the vascular accident. Hayreh demonstrated that after occlusion of one or more of the posterior ciliary arteries, filling of the choroid takes place via collaterals from the posterior episcleral arterial plexus [19]. Carotid angiography has not been performed. It is unlikely that the radiotherapy (46 Gy on the oral cavity and the neck) has played any role in the development of the ocular vascular complications, since the upper border of the radiation field was located in the palatum durum. The scatter dose at the cavernous sinus and the optic nerve (>3 cm out of the radiation field) has been calculated to be respectively 3,6% (= 1.6 Gy) and 0.9% (= 0.4 Gy) of the administered dose. A very similar fundus picture associated with bilateral blindness has been published very recently by Guyer et al. in a case of non-Hodgkin lympho-
Bilateral blindness in cavernous sinus thrombosis
ma [20]. Histopathologic examination revealed infiltration of the pial septa by tumor and septic thrombi in the central retinal arteries. In conclusion, the mortality rate of CST has been reduced a lot for the last few years, but severe complications still occur.
ll.
12. 13.
References
14. 15.
1. Duncan A. Contributions to morbid anatomy. Edin Med Surg J 1821; 17: 311-366. 2. Knapp H. Ueber Verstopfung des Blutgef~isse des Auges. Albrecht Von Graefes Arch Klin Exp Ophthalmo11868; 18: 207-251. 3. Grove WE. Septic and aseptic types of thrombosis of the cavernous sinus. Arch Otolaryngol 1936; 24: 29-50. 4. Yarrington CT. Cavernous sinus thrombosis revisited. Proc R Soc Med 1977; 70: 456-459. 5. Geggel HS, Isenberg SJ. Cavernous sinus thrombosis as a cause of unilateral blindness. Ann Ophthalmol 1982; 14: 569-574. 6. Friberg TR, Sogg RL. Ischemic optic neuropathy in cavernous sinus thrombosis. Arch Ophthalmo11978; 96" 453-456. 7. Boniuk M. The ocular manifestations of ophthalmic vein and aseptic cavernous sinus thrombosis. Amer Acad of Ophthal & Otolaryngol 1972; 76: 1519-1534. 8. Price CD, Hamersoff SB, Richards RD: Cavernous sinus thrombosis and Orbital Cellulitis. South Med J 1971; 64: 1243-1247. 9. Ahmadi J, Keane JR, Segall HD et al. CT observations pertinent to septic cavernous sinus thrombosis. AJNR 1985; 6: 755-758. 10. Chung W, Chang KH et al. Computed tomography of
16.
17. 18.
19.
20.
171
cavernous sinus diseases. Neuroradiology 1988; 30: 319328. Levine SR, Twyman RE, Gilman S. The role of anticoagulation in cavernous sinus thrombosis. Neurology 1988; 38: 517-522. Walsh FB, Hoyt WF. Clinical neuro-ophthalmology, ed 3. Baltimore, Williams & Wilkins Co, 1969, pp 1892-1896. Shaw RE. Cavernous sinus thrombosis: A review. Br Jr Surg 1952; 40: 40-48. Gupta MC, Ahuja OP, Kumar S. Cavernous sinus thrombosis. Indian J Med Sci 1970; 24: 748--753. Mehra KS, Somani PN. Multiple emboli in central retinal artery following cavernous sinus thrombosis. J All India Ophthal Soc 1967; 15: 71-72. Mathew NT, Abraham J, Taori GM et al. Internal carotid artery occlusion in cavernous sinus thrombosis. Arch Neurol 1971; 24: 11-16. Taylor PJ. Cavernous sinus thromboflebitis. Br J Ophthalmol 1957; 41: 228-237. Harbour RC, Trobe JD, Ballinger WE. Septic cavernous sinus thrombosis associated with gingivitis and parapharyngeal abcess. Arch Ophthalmol 1984; 102: 94-97. Hayreh SS, Baines JAB. Occlusion of the posterior ciliary artery. I. Effects on choroidal circulation. Br J Ophthalmol 1972; 56: 719-735. Guyer DR, Green R, Schachat AP et al. Bilateral ischemic optic neuropathy and retinal vascular occlusions associated with lymphoma and sepsis. Ophthalmology 1990; 97: 882888.
Address for offprints: C. Coutteel, Department of Ophthalmology, University Hospital St. Rafa61, Leuven, Capucijnenvoer 33, 3000 Leuven, Belgium
