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Orbital Hemorrhage with Loss of Vision
ORBITAL HEMORRHAGE WITH LOSS OF VISION RICHARD
L.
PETRELLI, M.D., E. ANTHONY PETRELLI, WILLIAM E. ALLEN III, M.D.
M.D.,
AND
New Haven, Connecticut
Orbital hemorrhage is a condition not often encountered by the ophthalmologist. Although frequently of insidious onset, it may occasionally occur with dramatic rapidity and serious consequences to the patient's vision. For this reason, it is important to be aware of the entity and its various causes. We encountered a case of orbital hemorrhage that we believe was caused by an intraorbital vascular abnormality, possibly a hemangioma. CASE REPORT A 58-year-old woman was referred to us with the symptoms of severe right orbital pain, decreased vision, and proptosis of the right eye, nausea, vomiting, dizziness, and chills of several hours' duration. While playing golf several hours earlier she suddenly had pressure behind the right eye followed by deterioration of vision and bulging of the eye. One month previously she had had an episode of transient right orbital pain while bending over. She was otherwise in good health and denied any illnesses. She was in acute distress with severe right orbital pain and intermittent retching. Vital signs were normal, and motor and sensory systems were intact. Visual acuity was no light perception in the right eye and 6/4.5 (20/15) in the left eye. Right proptosis was noted with exophthalmos of 7 mm as compared to the left eye by Hertel measurements. The right pupil was dilated at 4 mm and did not react to direct or consensual light stimulation. The left pupil reacted briskly to direct but not consensual stimulation. A complete external ophthalmoplegia of the right eye was noted. Corneal sensation and all branches of the fifth cranial nerve were intact. No bruits were heard in either orbit and no pulsation was evident. A slight blepharoptosis of the right upper eyelid was present. No engorgement of the conjunctival vessels was noted. The applanation pressures were R.E.: 20 mm
From the Department of Ophthalmology and Visual Science (Drs. R. L. and E. A. Petrelli), and Diagnostic Radiology (Dr. Allen), Yale University School of Medicine; and the Department of Ophthalmology, Hospital of St. Raphael (Drs. R. L. and E. A. Petrelli), New Haven, Connecticut. Reprint requests to Richard L. Petrelli, M.D., 455 Orange St., New Haven, CT 06511.
Hg and L.E.: 15 mm Hg. Retinal examination showed no papilledema or striae. The patient was admitted to the hospital for further examination. Figure 1 shows her appearance soon after admission. She was examined by a neurosurgeon. A lumbar puncture showed a clear colorless cerebrospinal fluid with normal opening pressure. X-rays of the skull and orbits were normal. Bilateral carotid angiography was interpreted initially as normal. No aneurysm of the internal carotid artery or of the ophthalmic artery was shown (Fig. 2). Computed axial tomography, however, revealed a discrete circumscribed mass greatly attenuated in the right orbit between the optic nerve and the lateral rectus muscle (Fig. 3). The lesion was more attenuated than the surrounding soft tissues. The clinical history and computed tomography scan together indicated that this mass most likely represented hemorrhage compressing the optic nerve. Because of these findings, a lateral orbitotomy was performed to decompress and explore the right orbit. Retraction of the bone flap and exposure of the lateral rectus muscle and optic nerve resulted in release of serosanguineous fluid. Palpation within the muscle cone into the orbital apex failed to reveal any mass. A biopsy specimen of central conal tissue was reported as "segments of loose fibrous fatty tissue." The postoperative course was uneventful. The right eye did not recover vision. The visual field was normal in the left eye. Further evaluation of the angiograms by means of subtraction studies revealed enlarged feeding vessels to a region of hyper-
Fig. 1 (Petrelli, Petrelli, and Allen). Right eye, Clinical appearance showing proptosis, blepharoptosis, and dilated pupil. The subconjunctival hemorrhage appeared after hospital admission.
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Fig. 2 (Petrelli, Petrelli, and Allen). Right internal carotid angiogram. Left, Arterial phase. The ophthalmic artery (arrows) and its branches appear normal. Right, Venous phase showing no evidence of abnormality.
vascularity with early filling of venous sinusoids, and residual blush in the orbit (Fig. 4). Nine months after surgical exploration a second computed axial tomogram showed a much reduced mass in the right orbit (Fig. 5). The patient continued to be asymptomatic with conservative management. DISCUSSION
Krohel and Wright! recently reported the clinical findings in 17 patients with orbital hemorrhage. Although some patients had a painless, space-occupying lesion developing over a period of months, most had an acute onset of the
Fig. 3 (Petrelli, Petrelli, and Allen). Computed axial tomograph showing a large mass of high attenuation within the muscle cone of the right orbit. The optic nerve is displaced medially.
hemorrhage. The patients ranged in age from 2 to 80 years and there were twice as many females as males. Proptosis ranged from 1.5 to 16 mm, and eyelid ecchymoses were present in eight cases. Pain in 12 cases and vomiting in nine cases was noted. Nine patients had limitation of extraocular movements, four had disk edema, and two had choroidal folds. Associated factors included one case of hypertension, one of anemia, one of Willebrand's disease, and a woman in the second stage of labor. Venograms were abnormal in nine out of ten cases, showing varices in five cases, a mass lesion in three cases, and hypervascularity in one case. Blood cysts were shown pathologically in five cases. The authors stated that the visual prognosis in older patients was poor as irreversible visual loss was too rapid to allow effective treatment, whereas the prognosis in younger patients was much better, especially if immediate surgical drainage was done. Wright'' had reported earlier that of 627 cases of orbital disease observed between 1968 and 1973, vascular causes of proptosis ranked third (67 cases) after thyroid dysfunction and fractures. Of these 67 cases, congenital primary varix was most common (31 cases). Among those with varices, proptosis was first noted any time
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Fig. 4 (Petrelli, Petrelli, and Allen). A subtraction study of the right internal carotid angiogram. Left, Arterial phase showing an area of hypervascularity with enlarged feeding vessels and early venous filling (arrows). Right, Venous phase showing a residual blush of contrast material (thin arrows) which is thought to represent venous sinusoids characteristic of hemangiomas. Note the position of the choroidal crescent (thick arrow).
from birth to early childhood and was often associated with dilated veins in the eyelids, episcleral tissues, or elsewhere in the body. The proptosis increased with crying or coughing and became static in late adolescence. In one case of unsuspected varix, the patient had sudden painful proptosis with vomiting after which orbital hemorrhage was noted. On plain roentgenograms, common findings were orbital enlargement and
Fig. 5 (Petrelli, Petrelli, and Allen). Computed axial tomograph, obtained nine months after surgery, showing a small residual mass in the apex of the right orbit.
phleboliths. Orbital venography was most important diagnostically. Carotid arteriography showed displacement of the ophthalmic artery. Cavernous hemangioma (ten cases) was the next most common vascular cause of proptosis. These patients were older, ranging in age from 35 to 70 years and the proptosis developed more slowly (from two to 25 years). In all patients the pedicle of the hemangioma originated in the superior orbital fissure. Venography and carotid angiography subtraction studies delineated the tumor and helped to differentiate it from orbital varix and lymphangioma, which was sometimes difficult before the advances in contrast radiology." Lloyd" believes carotid angiography subtraction studies may be totally diagnostic of hemangioma, showing a fine network of vessels, a feeding arterial supply from a vascular pedicle originating from the superior or inferior orbital fissure, and contrast pooling. Any mass lesion may also produce flattening of the choroidal crescent. A cavernous hemangioma may hemorrhage, forming a blood cyst that may simulate a superior orbital fissure syn-
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drome." Hoods described a patient with orbital cavernous hemangioma who was originally thought to have had an orbital hemorrhage. Outside the capsule of the hemangioma were thin-walled cavernous vessels apparently in the process of being incorporated into the lesion, which may explain not only the means by which a hemangioma enlarges, but also how it may hemorrhage. Orbital lymphangiomas- may also cause proptosis, which is usually under 10 mm and slowly progressive. A frequent event is hemorrhage into the lymphangioma ("chocolate cysts") that can appear as a subconjunctival hemorrhage or proptosis. Muscle imbalances are common. Optic atrophy may occur with optic nerve compression. Although often difficult to distinguish from hemangiomas, lymphangiomas are less likely to regress and more likely to infiltrate and hemorrhage as they are not so encapsulated as hemangiomas. A rare variant of the angiomas, which should be mentioned, is the hemangiopericytoma. Aneurysm is an important cause of proptosis and orbital hemorrhage. Intracavernous aneurysms" occur more commonly in women older than age 50 years. They can arise from the cavernous branches of the internal carotid artery or the ophthalmic artery. The first signs and symptoms depend on the size and location of the aneurysm which, as it enlarges, may cause palsies of the third, fifth, and sixth cranial nerves associated with severe orbital pain. The pupil may be middilated or small and immobile depending on the degree of involvement of the parasympathetic and sympathetic fibers. If the aneurysm ruptures, a carotidcavernous fistula" may develop. Pulsating exophthalmos with orbital bruits and conjunctival venous congestion are the usual signs. Visual loss is a common, devastating consequence and may be immediate or gradual, with retinal ischemia often evident. Ruptured aneurysms, where the ophthalmic artery originates
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from the internal carotid artery, have resulted in intraorbital bleeding." Aneurysms of the intraorbital part of the ophthalmic artery occur rarely." The clinical signs may be similar to those of the other aneurysms described. Pain, proptosis, and sudden loss of vision caused by optic nerve compression may follow rupture of such an aneurysm. Any patient in whom the diagnosis of an aneurysm is possible should have cerebral arteriography, which is diagnostic. Lloyd'? distinguished primary orbital varices (congenital varix) from secondary orbital varices. The latter type may be an orbital manifestation of a carotidcavernous fistula or an arteriovenous malformation. Such malformations may be intracranial or intraorbital. The symptoms of the fistula and malformation are similar. In the malformation there is no capillary bed between the artery and vein. It may be congenital, spontaneous, or traumatic. It is rare and less of a threat to vision than the carotid-cavernous fistula. Trauma should always be considered in the differential diagnosis of orbital hemorrhage, as it can be overlooked and is, indeed, its most common cause.! In other patients one may find associated conditions such as leukemia, hemophilia, various clotting disorders, sickle cell disease, and malaria." Finally, there are certain cases of spontaneous orbital hemorrhage in which there are no associated local or systemic diseases. In our patient, the sudden onset of severe pain, proptosis, external and internal ophthalmoplegia, and rapid loss of vision was compatible with a vascular accident. No bruit or ocular pulsation as in an arteriovenous fistula was noted. No retinal striae or circulatory disturbances as might be expected in an expanding orbital mass were evident. The conjunctival hematoma appeared after hospital admission. The preliminary carotid angiogram was normal, which ruled out any aneurysm from the cavernous sinus to the orbit. The
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computed tomography scan, however, revealed a 12-mm mass in the middle and posterior aspect of the orbit between the lateral rectus muscle and optic nerve that was being displaced medially. Because it was more attenuated than the surrounding soft tissues, the mass was interpreted as hemorrhage. Further evaluation of the angiogram by means of a subtraction study revealed an area of hypervascularity with enlarged feeding vessels and early filling of venous sinusoids with a residual blush. This appearance was most consistent with a hemangioma in this area of the orbit. The preliminary angiogram did not reveal the vascular abnormality, which is often the case with these lesions usually because of the slow circulation within them." Subtraction studies are necessary to elucidate such vascular abnormalities. At surgery no mass was observed or palpated. Nine months later, a second scan showed a small residual mass in the apex of the orbit. We hypothesize that at the time of surgery the hematoma was removed and the ruptured lesion was too small to identify. The posterior location of the lesion adjacent to the optic foramen resulted in optic nerve compression with loss of vision when the lesion ruptured within the enclosed space. These findings indicated an orbital apex syndrome. Should the patient become symptomatic, a more extensive surgical procedure may be indicated.
597
SUMMARY
A 58-year-old woman had the sudden onset of unilateral painful proptosis, ophthalmoplegia, vomiting, and loss of vision. Computed axial tomography showed a mass that was greatly attenuated in the orbit. The initial reading of the internal carotid angiogram was normal, but a subtraction study showed a hypervascular lesion within the orbit with features indicating a hemangioma. Orbital decompression failed to restore the vision as intraorbital hemorrhage had irreparably damaged the optic nerve. ACKNOWLEDGMENTS
Shelby J. Galloway, M.D., provided the films of the cerebral angiograms, and Anthony Parisi, M.D., referred the patient to us. REFERENCES 1. Krohel, G. B., and Wright,]. E.: Orbital hemorrhage. Am. ]. Ophthalmol. 88:254, 1979. 2. Wright, J. E.: Orbital vascular anomalies. Trans. Am. Acad. Ophthalmol, Otolaryngol. 78:606, 1974. 3. Lloyd, G.: Radiology of the Orbit. London, W. B. Saunders Co., 1975, pp. 102; 1l0. 4. Jones, 1. S., and ]akobiec, F. A.: Diseases of the Orbit. Hagerstown, Harper and Row, 1979, pp. 279; 305; 306. 5. Hood, C. 1.: Cavernous hemangioma of the orbit. Arch. Ophthalmol. 83:49, 1970. 6. Buncic, J.: Neurophthalmic signs of vascular disease. Int. Ophthalmol. Clin. 18:123, 1978. 7. Flanagan,]. C.: Vascular problems of the orbit. Ophthalmology 86:896, 1979. 8. deRaad, R.: The ophthalmic artery. In Newton, T. H., and Potts, D. G. (eds.): Radiology of the Skull and Brain, vol. 2. St. Louis, C. V. Mosby, 1974, p. 1374.
L.
PETRELLI, M.D., E. ANTHONY PETRELLI, WILLIAM E. ALLEN III, M.D.
M.D.,
AND
New Haven, Connecticut
Orbital hemorrhage is a condition not often encountered by the ophthalmologist. Although frequently of insidious onset, it may occasionally occur with dramatic rapidity and serious consequences to the patient's vision. For this reason, it is important to be aware of the entity and its various causes. We encountered a case of orbital hemorrhage that we believe was caused by an intraorbital vascular abnormality, possibly a hemangioma. CASE REPORT A 58-year-old woman was referred to us with the symptoms of severe right orbital pain, decreased vision, and proptosis of the right eye, nausea, vomiting, dizziness, and chills of several hours' duration. While playing golf several hours earlier she suddenly had pressure behind the right eye followed by deterioration of vision and bulging of the eye. One month previously she had had an episode of transient right orbital pain while bending over. She was otherwise in good health and denied any illnesses. She was in acute distress with severe right orbital pain and intermittent retching. Vital signs were normal, and motor and sensory systems were intact. Visual acuity was no light perception in the right eye and 6/4.5 (20/15) in the left eye. Right proptosis was noted with exophthalmos of 7 mm as compared to the left eye by Hertel measurements. The right pupil was dilated at 4 mm and did not react to direct or consensual light stimulation. The left pupil reacted briskly to direct but not consensual stimulation. A complete external ophthalmoplegia of the right eye was noted. Corneal sensation and all branches of the fifth cranial nerve were intact. No bruits were heard in either orbit and no pulsation was evident. A slight blepharoptosis of the right upper eyelid was present. No engorgement of the conjunctival vessels was noted. The applanation pressures were R.E.: 20 mm
From the Department of Ophthalmology and Visual Science (Drs. R. L. and E. A. Petrelli), and Diagnostic Radiology (Dr. Allen), Yale University School of Medicine; and the Department of Ophthalmology, Hospital of St. Raphael (Drs. R. L. and E. A. Petrelli), New Haven, Connecticut. Reprint requests to Richard L. Petrelli, M.D., 455 Orange St., New Haven, CT 06511.
Hg and L.E.: 15 mm Hg. Retinal examination showed no papilledema or striae. The patient was admitted to the hospital for further examination. Figure 1 shows her appearance soon after admission. She was examined by a neurosurgeon. A lumbar puncture showed a clear colorless cerebrospinal fluid with normal opening pressure. X-rays of the skull and orbits were normal. Bilateral carotid angiography was interpreted initially as normal. No aneurysm of the internal carotid artery or of the ophthalmic artery was shown (Fig. 2). Computed axial tomography, however, revealed a discrete circumscribed mass greatly attenuated in the right orbit between the optic nerve and the lateral rectus muscle (Fig. 3). The lesion was more attenuated than the surrounding soft tissues. The clinical history and computed tomography scan together indicated that this mass most likely represented hemorrhage compressing the optic nerve. Because of these findings, a lateral orbitotomy was performed to decompress and explore the right orbit. Retraction of the bone flap and exposure of the lateral rectus muscle and optic nerve resulted in release of serosanguineous fluid. Palpation within the muscle cone into the orbital apex failed to reveal any mass. A biopsy specimen of central conal tissue was reported as "segments of loose fibrous fatty tissue." The postoperative course was uneventful. The right eye did not recover vision. The visual field was normal in the left eye. Further evaluation of the angiograms by means of subtraction studies revealed enlarged feeding vessels to a region of hyper-
Fig. 1 (Petrelli, Petrelli, and Allen). Right eye, Clinical appearance showing proptosis, blepharoptosis, and dilated pupil. The subconjunctival hemorrhage appeared after hospital admission.
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Fig. 2 (Petrelli, Petrelli, and Allen). Right internal carotid angiogram. Left, Arterial phase. The ophthalmic artery (arrows) and its branches appear normal. Right, Venous phase showing no evidence of abnormality.
vascularity with early filling of venous sinusoids, and residual blush in the orbit (Fig. 4). Nine months after surgical exploration a second computed axial tomogram showed a much reduced mass in the right orbit (Fig. 5). The patient continued to be asymptomatic with conservative management. DISCUSSION
Krohel and Wright! recently reported the clinical findings in 17 patients with orbital hemorrhage. Although some patients had a painless, space-occupying lesion developing over a period of months, most had an acute onset of the
Fig. 3 (Petrelli, Petrelli, and Allen). Computed axial tomograph showing a large mass of high attenuation within the muscle cone of the right orbit. The optic nerve is displaced medially.
hemorrhage. The patients ranged in age from 2 to 80 years and there were twice as many females as males. Proptosis ranged from 1.5 to 16 mm, and eyelid ecchymoses were present in eight cases. Pain in 12 cases and vomiting in nine cases was noted. Nine patients had limitation of extraocular movements, four had disk edema, and two had choroidal folds. Associated factors included one case of hypertension, one of anemia, one of Willebrand's disease, and a woman in the second stage of labor. Venograms were abnormal in nine out of ten cases, showing varices in five cases, a mass lesion in three cases, and hypervascularity in one case. Blood cysts were shown pathologically in five cases. The authors stated that the visual prognosis in older patients was poor as irreversible visual loss was too rapid to allow effective treatment, whereas the prognosis in younger patients was much better, especially if immediate surgical drainage was done. Wright'' had reported earlier that of 627 cases of orbital disease observed between 1968 and 1973, vascular causes of proptosis ranked third (67 cases) after thyroid dysfunction and fractures. Of these 67 cases, congenital primary varix was most common (31 cases). Among those with varices, proptosis was first noted any time
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Fig. 4 (Petrelli, Petrelli, and Allen). A subtraction study of the right internal carotid angiogram. Left, Arterial phase showing an area of hypervascularity with enlarged feeding vessels and early venous filling (arrows). Right, Venous phase showing a residual blush of contrast material (thin arrows) which is thought to represent venous sinusoids characteristic of hemangiomas. Note the position of the choroidal crescent (thick arrow).
from birth to early childhood and was often associated with dilated veins in the eyelids, episcleral tissues, or elsewhere in the body. The proptosis increased with crying or coughing and became static in late adolescence. In one case of unsuspected varix, the patient had sudden painful proptosis with vomiting after which orbital hemorrhage was noted. On plain roentgenograms, common findings were orbital enlargement and
Fig. 5 (Petrelli, Petrelli, and Allen). Computed axial tomograph, obtained nine months after surgery, showing a small residual mass in the apex of the right orbit.
phleboliths. Orbital venography was most important diagnostically. Carotid arteriography showed displacement of the ophthalmic artery. Cavernous hemangioma (ten cases) was the next most common vascular cause of proptosis. These patients were older, ranging in age from 35 to 70 years and the proptosis developed more slowly (from two to 25 years). In all patients the pedicle of the hemangioma originated in the superior orbital fissure. Venography and carotid angiography subtraction studies delineated the tumor and helped to differentiate it from orbital varix and lymphangioma, which was sometimes difficult before the advances in contrast radiology." Lloyd" believes carotid angiography subtraction studies may be totally diagnostic of hemangioma, showing a fine network of vessels, a feeding arterial supply from a vascular pedicle originating from the superior or inferior orbital fissure, and contrast pooling. Any mass lesion may also produce flattening of the choroidal crescent. A cavernous hemangioma may hemorrhage, forming a blood cyst that may simulate a superior orbital fissure syn-
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drome." Hoods described a patient with orbital cavernous hemangioma who was originally thought to have had an orbital hemorrhage. Outside the capsule of the hemangioma were thin-walled cavernous vessels apparently in the process of being incorporated into the lesion, which may explain not only the means by which a hemangioma enlarges, but also how it may hemorrhage. Orbital lymphangiomas- may also cause proptosis, which is usually under 10 mm and slowly progressive. A frequent event is hemorrhage into the lymphangioma ("chocolate cysts") that can appear as a subconjunctival hemorrhage or proptosis. Muscle imbalances are common. Optic atrophy may occur with optic nerve compression. Although often difficult to distinguish from hemangiomas, lymphangiomas are less likely to regress and more likely to infiltrate and hemorrhage as they are not so encapsulated as hemangiomas. A rare variant of the angiomas, which should be mentioned, is the hemangiopericytoma. Aneurysm is an important cause of proptosis and orbital hemorrhage. Intracavernous aneurysms" occur more commonly in women older than age 50 years. They can arise from the cavernous branches of the internal carotid artery or the ophthalmic artery. The first signs and symptoms depend on the size and location of the aneurysm which, as it enlarges, may cause palsies of the third, fifth, and sixth cranial nerves associated with severe orbital pain. The pupil may be middilated or small and immobile depending on the degree of involvement of the parasympathetic and sympathetic fibers. If the aneurysm ruptures, a carotidcavernous fistula" may develop. Pulsating exophthalmos with orbital bruits and conjunctival venous congestion are the usual signs. Visual loss is a common, devastating consequence and may be immediate or gradual, with retinal ischemia often evident. Ruptured aneurysms, where the ophthalmic artery originates
APRIL, 1980
from the internal carotid artery, have resulted in intraorbital bleeding." Aneurysms of the intraorbital part of the ophthalmic artery occur rarely." The clinical signs may be similar to those of the other aneurysms described. Pain, proptosis, and sudden loss of vision caused by optic nerve compression may follow rupture of such an aneurysm. Any patient in whom the diagnosis of an aneurysm is possible should have cerebral arteriography, which is diagnostic. Lloyd'? distinguished primary orbital varices (congenital varix) from secondary orbital varices. The latter type may be an orbital manifestation of a carotidcavernous fistula or an arteriovenous malformation. Such malformations may be intracranial or intraorbital. The symptoms of the fistula and malformation are similar. In the malformation there is no capillary bed between the artery and vein. It may be congenital, spontaneous, or traumatic. It is rare and less of a threat to vision than the carotid-cavernous fistula. Trauma should always be considered in the differential diagnosis of orbital hemorrhage, as it can be overlooked and is, indeed, its most common cause.! In other patients one may find associated conditions such as leukemia, hemophilia, various clotting disorders, sickle cell disease, and malaria." Finally, there are certain cases of spontaneous orbital hemorrhage in which there are no associated local or systemic diseases. In our patient, the sudden onset of severe pain, proptosis, external and internal ophthalmoplegia, and rapid loss of vision was compatible with a vascular accident. No bruit or ocular pulsation as in an arteriovenous fistula was noted. No retinal striae or circulatory disturbances as might be expected in an expanding orbital mass were evident. The conjunctival hematoma appeared after hospital admission. The preliminary carotid angiogram was normal, which ruled out any aneurysm from the cavernous sinus to the orbit. The
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computed tomography scan, however, revealed a 12-mm mass in the middle and posterior aspect of the orbit between the lateral rectus muscle and optic nerve that was being displaced medially. Because it was more attenuated than the surrounding soft tissues, the mass was interpreted as hemorrhage. Further evaluation of the angiogram by means of a subtraction study revealed an area of hypervascularity with enlarged feeding vessels and early filling of venous sinusoids with a residual blush. This appearance was most consistent with a hemangioma in this area of the orbit. The preliminary angiogram did not reveal the vascular abnormality, which is often the case with these lesions usually because of the slow circulation within them." Subtraction studies are necessary to elucidate such vascular abnormalities. At surgery no mass was observed or palpated. Nine months later, a second scan showed a small residual mass in the apex of the orbit. We hypothesize that at the time of surgery the hematoma was removed and the ruptured lesion was too small to identify. The posterior location of the lesion adjacent to the optic foramen resulted in optic nerve compression with loss of vision when the lesion ruptured within the enclosed space. These findings indicated an orbital apex syndrome. Should the patient become symptomatic, a more extensive surgical procedure may be indicated.
597
SUMMARY
A 58-year-old woman had the sudden onset of unilateral painful proptosis, ophthalmoplegia, vomiting, and loss of vision. Computed axial tomography showed a mass that was greatly attenuated in the orbit. The initial reading of the internal carotid angiogram was normal, but a subtraction study showed a hypervascular lesion within the orbit with features indicating a hemangioma. Orbital decompression failed to restore the vision as intraorbital hemorrhage had irreparably damaged the optic nerve. ACKNOWLEDGMENTS
Shelby J. Galloway, M.D., provided the films of the cerebral angiograms, and Anthony Parisi, M.D., referred the patient to us. REFERENCES 1. Krohel, G. B., and Wright,]. E.: Orbital hemorrhage. Am. ]. Ophthalmol. 88:254, 1979. 2. Wright, J. E.: Orbital vascular anomalies. Trans. Am. Acad. Ophthalmol, Otolaryngol. 78:606, 1974. 3. Lloyd, G.: Radiology of the Orbit. London, W. B. Saunders Co., 1975, pp. 102; 1l0. 4. Jones, 1. S., and ]akobiec, F. A.: Diseases of the Orbit. Hagerstown, Harper and Row, 1979, pp. 279; 305; 306. 5. Hood, C. 1.: Cavernous hemangioma of the orbit. Arch. Ophthalmol. 83:49, 1970. 6. Buncic, J.: Neurophthalmic signs of vascular disease. Int. Ophthalmol. Clin. 18:123, 1978. 7. Flanagan,]. C.: Vascular problems of the orbit. Ophthalmology 86:896, 1979. 8. deRaad, R.: The ophthalmic artery. In Newton, T. H., and Potts, D. G. (eds.): Radiology of the Skull and Brain, vol. 2. St. Louis, C. V. Mosby, 1974, p. 1374.