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Show Journal of Clinical Neuro- ophthalmology 10( 3): 193- 196, 1990. © 1990 Raven Press, Ltd., New York Anterior Ischemic Optic Neuropathy and Branch Retinal Artery Occlusion in Cavernous Sinus Thrombosis Amod Gupta M. D., Subhadra Jalali, M. D., R. K. Bansal, M. D., and S. P. S. Grewal, M. D. A 60- year- old woman developed embolic occlusion of a branch retinal artery following septic cavernous sinus thrombosis. Two days later it was followed by loss of light perception due to embolic or vasculitic ischemic optic neuropathy. Recurrent emboli from a focus of carotid arteritis in cavernous sinus thrombosis may be responsible for visual loss in such eyes. Key Words: Cavernous sinus thrombosis-- Branch retinal artery occlusion- Ischemic optic neuropathy. From the Department of Ophthalmology, Postgraduat~ Institute of Medical, Education & Research, Chandlgarh India. Address correspondence and reprint requests to Dr. Amod Gupta, Additional Professor and Head, at Departmen~ of Ophthalmology, Postgraduate Institute of Medical, Education & Research, Chandigarh 160012 India. 193 Septic cavernous sinus thrombosis, though rarely seen in the post antibiotic era, still carries considerable mortality and morbidity in the developing countries ( 1). Visual complications are reported to occur in 10- 22% of these patients ( 2,3). Most of the cases reported in the literature, however, belong to an era when modern diagnostic techniques were not available ( 3). The mechanism of visual loss in such cases was not clear and was often attributed to toxic neuritis ( 4), central retinal artery occlusion secondary to orbital cellulitis ( 5,6), or corneal ulceration resulting from failure of lid closure ( 1). Embolic retinal artery occlusion was observed in one case of cavernous sinus thrombosis ( 7). More recently, a case of ischemic optic neuropathy was reported to result from decreased flow in the posterior ciliary arteries as a result of raised intraorbital pressure ( 8). We report a patient who developed embolic branch retinal artery occlusion and anterior ischemic optic neuropathy following septic cavernous sinus thrombosis. CASE REPORT A sixty- year- old woman was seen in consultation with history of multiple boils on the lips followed by massive swelling of the left eyelids and cheek. When seen by us she had experienced high fever and altered sensorium for 8 days. There was no history of seizures or vomiting. She had multiple boils on the lips, gross swelling of the left cheek, marked edema of the left eyelids, and conjunctival chemosis. Movements of the left globe were severely restricted. A satisfactory evaluation of the anterior segment, fundus, and intraocular pressure was not possible. The right eye was nor- 194 A. GUPTA ET AL. FIG. 1. Contrast enhanced computerized axial scan shows a filling defect ( arrow) in the left cavernous sinus that may represent a total occlusion of the left internal carotid artery. mal. An enhanced computerized axial tomogram showed a filling defect in the left cavernous sinus suggestive of cavernous sinus thrombosis and/ or a thrombosis of the internal carotid artery ( Fig. 1). Repeated bacterial cultures from blood, spinal fluid, and the boils did not reveal any microorganisms. Her total leukocyte count was 11,200 cells/ mm3 with 76% polymorphonuclear leukocytes and the erythrocyte sedimentation rate was 38 mm in the first hour. She was treated with intravenous crystalline penicillin 120 million U/ day, clox~ cillin 8 glday, gentamycin 180 mg/ day, and metromdazole 2 glday. One week after instituting therapy, the ophthalmic examination revealed visual acuity of right eye 6/ 12 and left eye 6/ 36. The intraocular pressure was right eye 17 mm and left eye 14 mm. The right eye was normal. Examination of the left eye revealed moderate ptosis. The elevation of the left eye was restricted. There was no proptosis and only minimal conjunctival congestion. She had a relative left afferent pupillary defect. Ophthalmoscopy re- FIG. 2. Fundus photograph ( left eye) shows pale optic disc edema, retinal whitening more intense below the macula and a cherry- red spot. J Clin Neuro- ophtlw/ mol. Vol. 10. No. 3. 1990 FIG. 3. Fluorescein angiography on the same day as Fig. 2, arterial phase reveals perfusion of only the upper temporal arteriole with ~ ocal spasm ( arrow) and hypoperfusion of the optiC diSC. vealed pale optic disc edema with marked attenuation of upper nasal, lower nasal, and lower temporal branches of the central retinal artery. The occluded arterioles showed boxcar phenomenon. There was a cherry- red spot at the macula with ischemic clouding and whitening of the retina in the lower temporal quadrant, particularly so within the arcade ( Fig. 2). There were also multiple superficial retinal hemorrhages in the distribution of occluded arterioles. The arterial phase fluorescein angiogram demonstrated hypoperfusion of the optic disc and late phase showed intense staining of the disc ( Figs. 3 and 4). Two days later she experienced a sudden total loss of vision in the left eye, although her systemic condition was steadily improving. Examination revealed no perception of light in this eye. On fundoscopy she had pale disc edema, increased retinal opacification of the lower half of the posterior pole, and the blood column in the lower temporal arteriole was not visible ( Fig. 5). Fluorescein angiogra- FIG. 4. In recirculation phase angiogram, there is intense staining of the optic disc and boxcar formation in the lower trunk of the central retinal artery ( arrow). Retinal veins from the nasal retina are still empty ( arrow head). EMBOLIC OCCLUSION AFTER CAVERNOUS SINUS THROMBOSIS 195 FIG. 5. Fundus photograph 2 days later, when patient had no light perception, shows increased opacification in the lower half and collapse of the lower temporal arteriole ( arrow). phy 2 weeks later showed recanalization of the arterial tree, decreased capillarity of the optic disc, delayed and patchy filling of the peripapillary choroid, and a peripapillary halo ( Fig. 6). Since the patient had no other neurological deficit, carotid angiography was not contemplated. Her ECG, serum cholesterol, plain radiographs of the chest and paranasal sinuses, and a complete collagen profile did not reveal any other systemic illness. She was normotensive and nondiabetic. Four months later, the vision was unchanged. The ocular movements were normal and the patient was ambulatory. DISCUSSION Our patient developed characteristic features of septic cavernous sinus thrombosis following boils FIG. 6. Two weeks later, fluorescein angiography in arterial phase shows recanalized arterioles, nor~ alization of the spasm in the upper temporal artenole, and peripapillary halo. Note marked choroidal hypoperfusion in temporal watershed zone and patchy choroidal hypofluorescence nasal to the disc. on the lips. These included marked periorbital edema, conjunctival chemosis, ophthalmoplegia, loss of vision, high grade fever, and altered sensorium. A contrast computed tomography ( CT) scan revealed a fulling defect in the left cavernous sinus suggesting an internal carotid artery occlusion. Though CT scan has not been proven to be sensitive in demonstrating occlusion of the cavernous sinus, multiple filling defects in the normal enhancing cavernous sinus are considered to represent thrombi in the sinus ( 9). Internal carotid and ophthalmic artery occlusions due to phycomycosis are very frequent, but involvement of the cavernous sinus per se in such patients is less common ( 10). The intracavernous part of the internal carotid artery can infrequently develop inflammatory spasm, focal arteritis, thrombotic occlusion, or tissue necrosis of its walls in septic infections of the cavernous sinus ( 5,8,11). Mathew and coworkers ( 11) demonstrated by arteriography complete blockage of the internal carotid artery in two patients with unilateral blindness from cavernous sinus thrombosis. They postulated both embolic and thrombotic phenomenon to explain the arterial occlusions. Friberg and Sogg ( 8) thought that focal arteritis of the posterior ciliary arteries could be an additional factor besides raised intraocular pressure in the pathogenesis of ischemic optic neuropathy in their patient. Bickerstaff ( 12) showed that the high incidence of hemiplegia in children is a result of septic carotid arteritis in the neck with subsequent embolization. Embolic episodes are reported to occur in 40% of the cases of septic cavernous sinus thrombosis predominantly to the lungs, although any part of the body can be affected ( 13). Mehra and Somani ( 7) reported a case of occlusion of central retinal artery due to multiple emboli from septic cavernous sinus thrombosis, but they did not document this either by fundus photography or by fluorescein angiography. We believe that the loss of light perception in our patient 2 days after the initial episode of branch arterial occlusion was due to recurrent emboli into the optic nerve head. Moreover, loss of light perception does not occur in central retinal arterial occlusion. Brown et al. ( 14) concluded that loss of light perception in cases of central retinal artery occlusion occurs only if there is concomitant occlusion of the optic nerve head circulation. In our case, another unlikely view could be the extension of internal carotid arteritis on to the branches of ophthalmic artery, thereby affecting the short posterior ciliary arteries. In view of the improved orbital and general condition and the 1Clin Neuro- ophthalmol. Vol. 10. No. 3. 1990 196 A. GUPTA ET AI. sudden onset of symptoms, it is, however, likely to be an embolic phenomenon only. REFERENCES 1. Gupta Me Ahuja OP, Kumar S. Cavernous sinus thrombosis: report of a case with brief review of the literature. Ind / Med Sci 1970; 24: 74S- 73. 2. South Wick FS, Richardson EP, Swartz MN. Septic thrombOSIS of the dural venous sinuses. Medicine 1986; 65: 82- 106. 3. Shaw RE. Cavernous sinus thrombosis: a review. Br / Surg 1952; 40: 40- 8. 4. Taylor PJ. Cavernous sinus thrombophlebitis. Br / OphthaImol 1957; 41: 228- 37. 5. Price CD, Hameroff SB, Richards RD. Cavernous sinus thrombosis and orbital cellulitis. South Med / 1971; 64: 124~ 47. 6. Fox SL, West GB. Thrombosis of the cavernous sinus. / AMA 1947; 134: 1452- 56. 7. Mehra KS, Somani PN. Multiple emboli in central retinal I Clin Neuro- ophthalmol, Vol. 10, No. 3, 1990 artery following cavernous sinus thrombosi:, } All India Ophthalmol Soc 1967; 15: 71- 3. 8. Friberg TR, Sogg RL. Ischaemic optic neuropathy in cavernous sinus thrombosis. Arch OphthalmoI1978; 96: 45~. 9. Ahmadi J, Keane JR, Sgall HD, Zee CS. CT observations pertinent to septic cavernous sinus thrombosis. Am / Nuclear RadioI1985; 6: 755- 8. 10. Landav lW, Newcomer YD. Acute cerebral phycomycosis ( mucurmycosis): report of a paediatric patient successfully treated with amphoterecin Band cycloheximide and review of pertinent literature. / Pediatr 1962; 61: 363- 85. 11. Mathew NT, Abraham J, Taori GM, Iyer GV. Internal carotid artery occlusion in cavernous sinus thrombosis. Arch NeuroI1971; 24: 11- 16. 12. Bickerstaff ER. Aetiology of acute hemiplegia in children. Br Med / 1964; 2: 82- 7. 13. Parsons M. Intracranial venous thrombosis. Post Grad Med / 1967; 43: 409- 14. 14. Brown GC, Magargal LE, Sergott R. Acute obstruction of retinal and choroidal circulation. Ophthalmology 1986; 93: 1373- 82. [CLcavernoussinusthrombosis] |
