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Ischemic Orbital Compartment Syndrome as a Complication of Spinal Surgery in the Prone Position
Ischemic Orbital Compartment Syndrome as a Complication of Spinal Surgery in the Prone Position Igal Leibovitch, MD,1 Robert Casson, FRANZCO,1 Caroline Laforest, MBBS,1 Dinesh Selva, FRANZCO1,2 Objectives: To report a patient with ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Design: Interventional case report. Methods: An 80-year-old man underwent a prolonged lumbar decompression laminectomy for spinal stenosis, under general anesthesia in the prone position. Several hours later, the patient complained of left periocular pain and reduced vision. Examination revealed significant facial edema, left proptosis, and a tight orbit, as well as no light perception and elevated intraocular pressure in the left eye, with complete internal and external ophthalmoplegia. Main Outcome Measures: Clinical course, imaging findings, management, and final outcome. Results: Magnetic resonance imaging confirmed the clinical diagnosis of a compartment syndrome with elevated intraorbital tension. A lateral canthotomy and cantholysis were performed, and high-dose IV steroids were started. The proptosis and facial swelling subsided gradually, but no improvement was noted in left visual acuity or left ocular movements. Conclusion: It is important to be familiar with this rare complication after prolonged surgery in the prone position. Although the prognosis seems to be poor, it is essential to monitor these patients perioperatively and to intervene surgically and medically once the diagnosis of orbital compartment syndrome is established. Ophthalmology 2006;113:105–108 © 2006 by the American Academy of Ophthalmology.
Visual loss is a known devastating perioperative complication of prolonged surgery in the prone position.1,2 The most common etiology is ischemic optic neuropathy (ION), attributed to decreased ocular perfusion pressure, possible blood loss, anemia, or hemodilution.1,2 Other possible reasons for visual loss include central retinal artery occlusion, central retinal vein occlusion, or cortical blindness.3 In all previous reports, the visual loss was painless, and there were no significant orbital signs or symptoms.1–3 We present the first report of a painful ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position.
Originally received: April 24, 2005. Accepted: September 16, 2005. Manuscript no. 2005-348. 1 Oculoplastic and Orbital Division, Department of Ophthalmology and Visual Sciences, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia. 2 Departments of Surgery and Medicine, University of Adelaide, Adelaide, Australia. The authors state that no conflicting relationships exist, and that no financial support was obtained for the article. ⴱCorrespondence to Dr Igal Leibovitch, Oculoplastic and Orbital Division, Department of Ophthalmology and Visual Sciences, Royal Adelaide Hospital, North Terrace, Adelaide, 5000, South Australia, Australia. E-mail: [email protected]. © 2006 by the American Academy of Ophthalmology Published by Elsevier Inc.
Case Report An 80-year-old man, with no significant systemic or ocular diseases, underwent an 8-hour L3–L5 decompression laminectomy for lumbar spinal stenosis, under general anesthesia in the prone position. Intraoperatively, his head was supported on a silicone head rest (Fig 1). On extubation, some facial and periorbital swelling was noted. Several hours later, the patient complained of significant left periocular pain and reduced vision. Examination revealed facial edema with 4 mm of left proptosis and a tight orbit (Fig 2). The left visual acuity (VA) was no light perception (LP), intraocular pressure (IOP) was 45 mmHg, and there was complete internal and external ophthalmoplegia. Ocular examination showed corneal edema with a large abrasion and Descemet’s folds, a middilated and nonreactive pupil, and an advanced cataract with pigment on the anterior capsule. The fundus could not be clearly visualized due to the corneal edema and cataract, but the optic nerve seemed very pale, and retinal hemorrhages were seen in the posterior pole. Right eye examination results were normal, and VA was 20/20. Urgent magnetic resonance imaging with angiography demonstrated proptosis, extraocular muscle enlargement, and severe globe tenting (an angle of almost 90° between the scleras on both sides of the optic nerve), a cardinal sign of markedly elevated intraorbital tension (Fig 3). No orbital hemorrhage or cavernous sinus thrombosis was seen. A lateral canthotomy and cantholysis were performed, and highdose IV methylprednisolone (1 g) and acetazolamide (500 mg) were started. Immediately after the decompression, the orbit felt less tense, but no changes in vision or pupil reactivity were noted. The proptosis and facial swelling subsided over several weeks (Fig 4). ISSN 0161-6420/06/$–see front matter doi:10.1016/j.ophtha.2005.09.025
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Figure 1. The silicone headrest used for the prone-position spinal surgery. Arrow, chin rest position; arrowhead, forehead rest position.
In his last follow-up in our clinic, 4 months later, left eye VA was still no LP, and there was marked ptosis and complete left ophthalmoplegia. The corneal edema subsided, but there were Descemet’s folds and advanced cataract, and the retina could not be visualized.
Figure 3. Axial T2-weighted magnetic resonance imaging showing the facial edema and left proptosis (white arrow) and extraocular muscle enlargement. The posterior globe angle on the right side is normal (160°), whereas significant globe tenting and optic nerve stretching on the left side (black arrows) create an angle of almost 90°.
Discussion In performing spinal surgery on a patient who is placed in the prone position, the patient’s face is supported by a soft headrest device that is designed to secure the head while minimizing pressure on facial structures, especially the globes. It is estimated that the incidence of visual disturbances and blindness after anesthesia for these major surgical procedures varies between 0.05% and 1%.3 Stevens et al4 reviewed the ophthalmic complications in 3450 patients who underwent spinal surgeries and identified 7 who were diagnosed with postoperative visual loss (an incidence of 0.2%). The main reasons were posterior ION, central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), and occipital lobe infarcts. Ho et al1 reviewed
Figure 2. Severe facial edema and left proptosis (top) and conjunctival chemosis (bottom).
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Figure 4. Four months after spinal surgery. Facial swelling and proptosis resolved, but there was still ptosis and ophthalmoplegia.
Leibovitch et al 䡠 Orbital Compartment Syndrome published case reports on ION after spine surgery with the patient in the prone position. Most of the patients were diagnosed with posterior ION (17/22), and only a minority (5/22) had anterior ION. They also found that visual loss was frequently bilateral (40% of anterior ION and 47% of posterior ION cases). They suggested that prolonged surgery in the prone position, decreased ocular perfusion pressure, blood loss and anemia/hemodilution, as well as infusion of large quantities of IV fluids are some of the potential factors involved in the etiology of postoperative ION. Similar findings were reported by Myers et al5 in a study group of 37 patients who experienced visual loss after scoliosis surgery. In all previously reported cases, visual loss after prone position surgery was painless and was not associated with significant orbital signs or symptoms. We found only one recent case report of blindness and rectus muscle injury after a 7-hour spinal surgery, but there were no signs of increased orbital pressure, and only the rectus muscle was involved.6 The described patient’s vision did not recover, but the adduction defect resolved completely. To our knowledge, our patient had the first reported case of an ischemic orbital compartment syndrome after prone position surgery. Only one similar presentation has been described, in a patient trapped with his head in a dependant position for 12 hours after a car accident.7 Although several risk factors for visual loss were identified, as mentioned earlier, the exact reason was not fully elucidated. One of the possible factors in the pathogenesis is elevation in IOP during prone position. This is supported by a study reported by Cheng et al.8 They measured IOP in 20 patients without any eye pathologies who were scheduled for spine surgery in the prone position. Intraocular pressure was measured at different positions and at different stages of anesthesia. They found that the pressure was increased in prone positioning and during anesthesia, compared with the supine position and while the patient is awake. Direct pressure on the globes and periorbital structures is an additional etiologic factor. It was suggested that exophthalmos or a low nasal bridge allows the medial aspect of the globes to be in greater direct contact with the headrest device, and as the periorbital area becomes relatively more swollen and edematous than the nasal bridge, the pressure on the globes will be even more significant.9 Atwater et al10 measured the surface pressure on the face of a patient placed in the prone position with the most commonly used prone positioning devices, a non–face-contoured positioner and a new face-contoured device. They found that surface pressures on the face in a patient placed in the prone position average below 30 mmHg, but small areas of high pressure (⬎50 mmHg) exist in all patients—primarily over the chin, but also on the forehead immediately superior to the supraorbital ridge. Increased orbital venous pressure can lead to a decrease in arterial perfusion pressure and may be involved in the pathogenesis of orbital and ocular ischemia. A head-down and prone position can result in facial and orbital edema with increased venous pressure, especially after prolonged surgery and with large volumes of intraoperative fluid replacement.2 A prone position may also contribute to in-
creased orbital venous pressure from increased abdominal venous pressure, especially in obese patients. We postulate that, in our case, the progressive orbital edema secondary to the prone position, and possible unilateral direct pressure from the headrest device on periorbital structures, resulted in congestion at the orbital apex, with a subsequent compartment syndrome and ischemic orbit. The pale optic nerve and retinal hemorrhages reflect the severe ocular arterial ischemia and venous congestion. The findings of corneal edema, Descemet’s folds, a middilated and nonreactive pupil, and an advanced cataract with pigment on the anterior capsule suggest a possible acute rise in IOP that could have been an additional factor contributing to ocular ischemia. The prolonged operation was a significant factor in the irreversible ischemia and poor overall visual and functional prognosis. Our patient was not obese and did not receive large volumes of fluid replacement intraoperatively (1000 ml in 8 hours), and so these factors did not play a significant role in the pathogenesis of orbital edema. An orbital compartment syndrome constitutes an ocular emergency. Once the diagnosis is suspected, an urgent decompression of the orbit with lateral canthotomy, cantholysis, and, possibly, division of the orbital septum is required. Orbital imaging (computed tomography or magnetic resonance imaging) could be time consuming and, therefore, should be done after the urgent decompression. In the event of inadequate relief of tension with soft tissue release, bony decompression may be necessary. Any associated elevated IOP requires treatment, and high-dose IV steroids may also have a role.7,11 In our patient, the lateral canthotomy and cantholysis reduced the orbital tension significantly, but the prolonged orbital and ocular ischemia was irreversible and resulted in complete visual loss and ophthalmoplegia. Ophthalmologists, as well as neurosurgeons and anesthesiologists, should be familiar with this additional mechanism of visual loss in patients undergoing prolonged surgery in the prone position. Although the visual prognosis is poor, if an orbital compartment syndrome is identified, aggressive and prompt management may reduce the risk of a poor outcome.
References 1. Ho VT, Newman NJ, Song S, et al. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol 2005;17: 38 – 44. 2. Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: review of the literature. Surv Ophthalmol 2005;50:15–26. 3. Williams EL. Postoperative blindness. Anesthesiol Clin North America 2002;20:605–22, viii. 4. Stevens WR, Glazer PA, Kelley SD, et al. Ophthalmic complications after spinal surgery. Spine 1997;22:1319 –24. 5. Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery: a review of 37 cases. Spine 1997;22:1325–9. 6. Kumar N, Jivan S, Topping N, Morrell AJ. Blindness and rectus muscle damage following spinal surgery. Am J Ophthalmol 2004;138:889 –91.
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Ophthalmology Volume 113, Number 1, January 2006 7. Fuller R, Vote BJ. Upside down orbitopathy: unilateral orbital dependent-tissue oedema causing total visual loss. Clin Experiment Ophthalmol 2001;29:265–7. 8. Cheng MA, Todorov A, Tempelhoff R, et al. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001;95:1351–5. 9. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as
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a complication of patient positioning for spinal surgery. A case report. Spine 1992;17:600 –5. 10. Atwater BI, Wahrenbrock E, Benumof JL, Mazzei WJ. Pressure on the face while in the prone position: ProneView versus Prone Positioner. J Clin Anesth 2004;16:111– 6. 11. Linberg JV. Orbital compartment syndromes following trauma. Adv Ophthalmic Plast Reconstr Surg 1987;6:51– 62.
Visual loss is a known devastating perioperative complication of prolonged surgery in the prone position.1,2 The most common etiology is ischemic optic neuropathy (ION), attributed to decreased ocular perfusion pressure, possible blood loss, anemia, or hemodilution.1,2 Other possible reasons for visual loss include central retinal artery occlusion, central retinal vein occlusion, or cortical blindness.3 In all previous reports, the visual loss was painless, and there were no significant orbital signs or symptoms.1–3 We present the first report of a painful ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position.
Originally received: April 24, 2005. Accepted: September 16, 2005. Manuscript no. 2005-348. 1 Oculoplastic and Orbital Division, Department of Ophthalmology and Visual Sciences, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia. 2 Departments of Surgery and Medicine, University of Adelaide, Adelaide, Australia. The authors state that no conflicting relationships exist, and that no financial support was obtained for the article. ⴱCorrespondence to Dr Igal Leibovitch, Oculoplastic and Orbital Division, Department of Ophthalmology and Visual Sciences, Royal Adelaide Hospital, North Terrace, Adelaide, 5000, South Australia, Australia. E-mail: [email protected]. © 2006 by the American Academy of Ophthalmology Published by Elsevier Inc.
Case Report An 80-year-old man, with no significant systemic or ocular diseases, underwent an 8-hour L3–L5 decompression laminectomy for lumbar spinal stenosis, under general anesthesia in the prone position. Intraoperatively, his head was supported on a silicone head rest (Fig 1). On extubation, some facial and periorbital swelling was noted. Several hours later, the patient complained of significant left periocular pain and reduced vision. Examination revealed facial edema with 4 mm of left proptosis and a tight orbit (Fig 2). The left visual acuity (VA) was no light perception (LP), intraocular pressure (IOP) was 45 mmHg, and there was complete internal and external ophthalmoplegia. Ocular examination showed corneal edema with a large abrasion and Descemet’s folds, a middilated and nonreactive pupil, and an advanced cataract with pigment on the anterior capsule. The fundus could not be clearly visualized due to the corneal edema and cataract, but the optic nerve seemed very pale, and retinal hemorrhages were seen in the posterior pole. Right eye examination results were normal, and VA was 20/20. Urgent magnetic resonance imaging with angiography demonstrated proptosis, extraocular muscle enlargement, and severe globe tenting (an angle of almost 90° between the scleras on both sides of the optic nerve), a cardinal sign of markedly elevated intraorbital tension (Fig 3). No orbital hemorrhage or cavernous sinus thrombosis was seen. A lateral canthotomy and cantholysis were performed, and highdose IV methylprednisolone (1 g) and acetazolamide (500 mg) were started. Immediately after the decompression, the orbit felt less tense, but no changes in vision or pupil reactivity were noted. The proptosis and facial swelling subsided over several weeks (Fig 4). ISSN 0161-6420/06/$–see front matter doi:10.1016/j.ophtha.2005.09.025
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Ophthalmology Volume 113, Number 1, January 2006
Figure 1. The silicone headrest used for the prone-position spinal surgery. Arrow, chin rest position; arrowhead, forehead rest position.
In his last follow-up in our clinic, 4 months later, left eye VA was still no LP, and there was marked ptosis and complete left ophthalmoplegia. The corneal edema subsided, but there were Descemet’s folds and advanced cataract, and the retina could not be visualized.
Figure 3. Axial T2-weighted magnetic resonance imaging showing the facial edema and left proptosis (white arrow) and extraocular muscle enlargement. The posterior globe angle on the right side is normal (160°), whereas significant globe tenting and optic nerve stretching on the left side (black arrows) create an angle of almost 90°.
Discussion In performing spinal surgery on a patient who is placed in the prone position, the patient’s face is supported by a soft headrest device that is designed to secure the head while minimizing pressure on facial structures, especially the globes. It is estimated that the incidence of visual disturbances and blindness after anesthesia for these major surgical procedures varies between 0.05% and 1%.3 Stevens et al4 reviewed the ophthalmic complications in 3450 patients who underwent spinal surgeries and identified 7 who were diagnosed with postoperative visual loss (an incidence of 0.2%). The main reasons were posterior ION, central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), and occipital lobe infarcts. Ho et al1 reviewed
Figure 2. Severe facial edema and left proptosis (top) and conjunctival chemosis (bottom).
106
Figure 4. Four months after spinal surgery. Facial swelling and proptosis resolved, but there was still ptosis and ophthalmoplegia.
Leibovitch et al 䡠 Orbital Compartment Syndrome published case reports on ION after spine surgery with the patient in the prone position. Most of the patients were diagnosed with posterior ION (17/22), and only a minority (5/22) had anterior ION. They also found that visual loss was frequently bilateral (40% of anterior ION and 47% of posterior ION cases). They suggested that prolonged surgery in the prone position, decreased ocular perfusion pressure, blood loss and anemia/hemodilution, as well as infusion of large quantities of IV fluids are some of the potential factors involved in the etiology of postoperative ION. Similar findings were reported by Myers et al5 in a study group of 37 patients who experienced visual loss after scoliosis surgery. In all previously reported cases, visual loss after prone position surgery was painless and was not associated with significant orbital signs or symptoms. We found only one recent case report of blindness and rectus muscle injury after a 7-hour spinal surgery, but there were no signs of increased orbital pressure, and only the rectus muscle was involved.6 The described patient’s vision did not recover, but the adduction defect resolved completely. To our knowledge, our patient had the first reported case of an ischemic orbital compartment syndrome after prone position surgery. Only one similar presentation has been described, in a patient trapped with his head in a dependant position for 12 hours after a car accident.7 Although several risk factors for visual loss were identified, as mentioned earlier, the exact reason was not fully elucidated. One of the possible factors in the pathogenesis is elevation in IOP during prone position. This is supported by a study reported by Cheng et al.8 They measured IOP in 20 patients without any eye pathologies who were scheduled for spine surgery in the prone position. Intraocular pressure was measured at different positions and at different stages of anesthesia. They found that the pressure was increased in prone positioning and during anesthesia, compared with the supine position and while the patient is awake. Direct pressure on the globes and periorbital structures is an additional etiologic factor. It was suggested that exophthalmos or a low nasal bridge allows the medial aspect of the globes to be in greater direct contact with the headrest device, and as the periorbital area becomes relatively more swollen and edematous than the nasal bridge, the pressure on the globes will be even more significant.9 Atwater et al10 measured the surface pressure on the face of a patient placed in the prone position with the most commonly used prone positioning devices, a non–face-contoured positioner and a new face-contoured device. They found that surface pressures on the face in a patient placed in the prone position average below 30 mmHg, but small areas of high pressure (⬎50 mmHg) exist in all patients—primarily over the chin, but also on the forehead immediately superior to the supraorbital ridge. Increased orbital venous pressure can lead to a decrease in arterial perfusion pressure and may be involved in the pathogenesis of orbital and ocular ischemia. A head-down and prone position can result in facial and orbital edema with increased venous pressure, especially after prolonged surgery and with large volumes of intraoperative fluid replacement.2 A prone position may also contribute to in-
creased orbital venous pressure from increased abdominal venous pressure, especially in obese patients. We postulate that, in our case, the progressive orbital edema secondary to the prone position, and possible unilateral direct pressure from the headrest device on periorbital structures, resulted in congestion at the orbital apex, with a subsequent compartment syndrome and ischemic orbit. The pale optic nerve and retinal hemorrhages reflect the severe ocular arterial ischemia and venous congestion. The findings of corneal edema, Descemet’s folds, a middilated and nonreactive pupil, and an advanced cataract with pigment on the anterior capsule suggest a possible acute rise in IOP that could have been an additional factor contributing to ocular ischemia. The prolonged operation was a significant factor in the irreversible ischemia and poor overall visual and functional prognosis. Our patient was not obese and did not receive large volumes of fluid replacement intraoperatively (1000 ml in 8 hours), and so these factors did not play a significant role in the pathogenesis of orbital edema. An orbital compartment syndrome constitutes an ocular emergency. Once the diagnosis is suspected, an urgent decompression of the orbit with lateral canthotomy, cantholysis, and, possibly, division of the orbital septum is required. Orbital imaging (computed tomography or magnetic resonance imaging) could be time consuming and, therefore, should be done after the urgent decompression. In the event of inadequate relief of tension with soft tissue release, bony decompression may be necessary. Any associated elevated IOP requires treatment, and high-dose IV steroids may also have a role.7,11 In our patient, the lateral canthotomy and cantholysis reduced the orbital tension significantly, but the prolonged orbital and ocular ischemia was irreversible and resulted in complete visual loss and ophthalmoplegia. Ophthalmologists, as well as neurosurgeons and anesthesiologists, should be familiar with this additional mechanism of visual loss in patients undergoing prolonged surgery in the prone position. Although the visual prognosis is poor, if an orbital compartment syndrome is identified, aggressive and prompt management may reduce the risk of a poor outcome.
References 1. Ho VT, Newman NJ, Song S, et al. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol 2005;17: 38 – 44. 2. Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: review of the literature. Surv Ophthalmol 2005;50:15–26. 3. Williams EL. Postoperative blindness. Anesthesiol Clin North America 2002;20:605–22, viii. 4. Stevens WR, Glazer PA, Kelley SD, et al. Ophthalmic complications after spinal surgery. Spine 1997;22:1319 –24. 5. Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery: a review of 37 cases. Spine 1997;22:1325–9. 6. Kumar N, Jivan S, Topping N, Morrell AJ. Blindness and rectus muscle damage following spinal surgery. Am J Ophthalmol 2004;138:889 –91.
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Ophthalmology Volume 113, Number 1, January 2006 7. Fuller R, Vote BJ. Upside down orbitopathy: unilateral orbital dependent-tissue oedema causing total visual loss. Clin Experiment Ophthalmol 2001;29:265–7. 8. Cheng MA, Todorov A, Tempelhoff R, et al. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001;95:1351–5. 9. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as
108
a complication of patient positioning for spinal surgery. A case report. Spine 1992;17:600 –5. 10. Atwater BI, Wahrenbrock E, Benumof JL, Mazzei WJ. Pressure on the face while in the prone position: ProneView versus Prone Positioner. J Clin Anesth 2004;16:111– 6. 11. Linberg JV. Orbital compartment syndromes following trauma. Adv Ophthalmic Plast Reconstr Surg 1987;6:51– 62.