- Email: [email protected]
The Enigma of Orbital Compartment Syndrome After Lumbar Spine Surgery in the Prone Position: Case Report and Literature Review
Case Report
The Enigma of Orbital Compartment Syndrome After Lumbar Spine Surgery in the Prone Position: Case Report and Literature Review Jorge Luiz Amorim Correa1,2 and Marcus Andre´ Acioly2,3
Key words Central retinal artery occlusion - Ischemic optic neuropathy - Orbital compartment syndrome - Perioperative visual loss - Prone position - Spine surgery -
Abbreviations and Acronyms CRAO: Central retinal artery occlusion ION: Ischemic optic neuropathy OCS: Orbital compartment syndrome POVL: Perioperative visual loss From the 1Division of Neurosurgery, Galeão Air Force Hospital, Rio de Janeiro; 2Postgraduate Program in Neurology, Federal University of the State of Rio de Janeiro, Rio de Janeiro; and 3Division of Neurosurgery, Fluminense Federal University, Rio de Janeiro, Brazil To whom correspondence should be addressed: Jorge Luiz Amorim Correa, M.D., M.Sc. [E-mail: [email protected]] Citation: World Neurosurg. (2018) 110:309-314. https://doi.org/10.1016/j.wneu.2017.11.111 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.
INTRODUCTION Patients might expect some adverse effects following a spinal elective procedure, such as spinal pain or nerve injury, but awaking blind is a devastating complication for both the patient and the surgical team.1-4 The American Society of Anesthesiologists Task Force defined perioperative visual loss (POVL) as a permanent impairment or total loss of sight associated with a spinal procedure under general anesthesia from immediate preoperative assessment to discharge.5 POVL is a rare occurrence following nonocular surgeries2-4 and affects <0.2% of all spinal surgeries.6-8 The precise incidence remains obscure.2 Two major causes of POVL in the scope of nonocular surgery are known: ischemic optic neuropathy (ION) and central retinal artery occlusion (CRAO).1,3,4 In a multiinstitutional study, Lee et al.1 analyzed 93 patients affected by POVL associated with spinal surgery. ION was the most
- BACKGROUND:
Perioperative visual loss after spinal surgery is a devastating complication for the patient and the surgical team. Two known major causes are ischemic optic neuropathy and central retinal artery occlusion (CRAO). Traditional understanding of CRAO has been consistently related to occurrence of periocular trauma and signs of increased intraorbital pressure in addition to visual loss. However, such orbital signs are not a feature of any common perioperative visual loss syndrome.
- CASE
DESCRIPTION: A 55-year-old woman underwent prolonged lumbar decompression and fusion for spinal stenosis under general anesthesia in the prone position. At the end of surgery, periocular hyperemia, corneal edema, and a tense orbit on the right side were noted. Complete internal and external ophthalmoplegia was observed on examination. Orbital computed tomography confirmed the clinical diagnosis of orbital compartment syndrome. Bony decompression was performed, but the treated eye remained blind. Resolution of the complete ophthalmoplegia was observed during late follow-up.
- CONCLUSIONS:
In retrospect, patients diagnosed with often misunderstood CRAO and ischemic optic neuropathy with orbital signs after spinal surgery most likely had orbital compartment syndrome. The inclusion of orbital signs in the clinical picture of ischemic optic neuropathy and CRAO is not only incorrect but also gives the impression of therapeutic futility, thereby preventing successful orbital decompression in a timely fashion.
common etiology in 89% of the patients, especially posterior ION, whereas CRAO accounted for 11% of the collected cases.1 Central retinal vein occlusion, occipital lobe infarct, and orbital compartment syndrome (OCS) have been rarely reported in patients with POVL.8-11 Although anterior ION is most likely caused by vascular occlusion or the lack of perfusion to the anterior optic nerve head, posterior ION occurs as a result of optic nerve infarction posterior to the lamina cribrosa.3 CRAO is characterized by the lack of blood supply to the entire retina, which is analogous to an acute stroke of the eye.3,4,12 CRAO represents an endorgan ischemia, which is frequently associated with underlying atherosclerotic disease.12 Finally, OCS is an ophthalmologic emergency, which is characterized by an acute rise in intraorbital pressure, placing the optic nerve and intraorbital structures at risk.13
WORLD NEUROSURGERY 110: 309-314, FEBRUARY 2018
The traditional understanding of CRAO in the neurosurgery and anesthesiology literature has been consistently related to the occurrence of periocular trauma and signs of increased intraorbital pressure, in addition to visual loss in most cases.1 This is illustrated by the frequent reports of concomitant decreased supraorbital sensation, ophthalmoplegia, proptosis, ptosis, corneal abrasion, and even unilateral erythema in the scope of CRAO.1,14-19 Such orbital signs have also been reported in association with ION,1,20 but with an incidence much smaller than for CRAO. In retrospect, patients diagnosed with often misunderstood CRAO and ION with orbital signs after spinal surgery most likely had OCS. The recognition of OCS instead of ION and CRAO is of utmost importance, as management strategies are completely different. We describe a patient affected by OCS after posterior
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Figure 1. Preoperative imaging. (A) Plain radiography showing lumbar degenerative scoliosis. (B and C) Computed tomography images showing
lumbar spinal surgery in the prone position, emphasizing all relevant aspects to differentiate OCS from ION and CRAO through a literature review. The patient provided informed consent for the publication of this study.
CASE DESCRIPTION History and Examination A 55-year-old woman had chronic low back pain radiating to the right leg (L5 territory) for 2 years. Symptoms were typically exacerbated by walking, leading to a diagnosis of neurogenic claudication. With time, progressive paraparesis evolved, and the patient needed assistance to walk right before admission. No sphincter dysfunction was noted. Her medical history included diabetes
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
lumbar stenosis at L4-5 (B) and L5-S1 (C). (D) Sagittal T2-weighted magnetic resonance imaging showing severe stenosis and endplate changes at L4-5.
mellitus, hypertension, and thyroid dysfunction with Graves ophthalmopathy, all of which were under medical control. Imaging demonstrated lumbar spine degenerative scoliotic changes and segmental instability in the L4-5 segment on plain radiographs. Magnetic resonance imaging showed multilevel spinal stenosis from L3-4 to L5-S1, but especially in L4-5, with Modic type I plateau changes and disc herniation at this level. Computed tomography indicated calcification of the L4-5 disc (Figure 1). The symptoms were refractory to conservative management, and the patient was scheduled for surgery. The patient underwent a 7-hour procedure with 2level lumbar decompression (L4-5 and L5-S1) and scoliosis correction by posterolateral instrumentation from T12 to S1 under general anesthesia in the
Figure 2. Right proptosis, periocular hyperemia, chemosis, and mydriasis were noted right after turning the patient from prone to supine position.
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prone position. Her head was positioned over an O-shaped soft headrest with the left side of the face up. The patient received transfusion of one unit of packed erythrocytes. At the end of surgery, right after turning the patient from prone to supine position, periocular hyperemia, corneal edema, and a tense orbit on the right side were noted. Complete internal and external ophthalmoplegia was observed on examination. Funduscopy could not be performed owing to corneal edema. No abnormal findings in the left eye were apparent (Figure 2). Urgent orbital CT demonstrated right proptosis, enlargement and stretching of the optic nerve, and intraorbital muscle edema (Figure 3). Mannitol, corticosteroids, and acetazolamide were initiated. Orbital signs progressively worsened over a few hours, and the patient complained of pain in the right orbit (Figure 3). The patient underwent digital subtraction angiography, which revealed occlusion of the right ophthalmic artery (Figure 4). No aneurysms or cavernous sinus thrombosis was documented. Operation and Postoperative Course After consultation with an ophthalmologist, bony orbital decompression was performed 26 hours after spinal surgery, in which the lateral wall of the orbit was removed (Figure 5). After orbital surgery,
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CASE REPORT JORGE LUIZ AMORIM CORREA AND MARCUS ANDRÉ ACIOLY
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Figure 3. (A) Orbital computed tomography revealed extraocular muscle enlargement, periocular soft tissue edema, and blurring of orbital fat. (B) Symptoms progressed over a few hours, and the patient developed severe proptosis and chemosis.
the globe progressively softened, and proptosis slightly subsided. During the following days, improvement of swelling and proptosis was gradual, taking several months for complete resolution. The patient was followed for 5 months; at her last follow-up consultation, the treated eye remained blind, but a marked resolution of complete ophthalmoplegia was observed (Figure 6). DISCUSSION Hollenhorst et al.17 were potentially the first to call attention to the phenomenon
of POVL during posterior cervical spine surgeries in the prone position. In 1954, they described a series of 8 patients affected by different degrees of orbital and ocular signs and performed a detailed experimental study on monkeys.17 Ocular lesions could be produced by lowering the blood pressure and by applying compression to the orbital contents, showing that their patients and experimental models shared the same pathophysiologic substrate for the occurrence of the condition.17 Apart from hypotension and ocular globe compression, several preoperative
Figure 4. Digital subtraction angiography of the right internal carotid artery (lateral view) demonstrating complete occlusion of the right ophthalmic artery (arrow).
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and intraoperative factors have been implicated in the development of POVL.1-3,21 The best evidence available indicates that preoperative anemia, vascular risk factors (e.g., hypertension, diabetes, peripheral artery disease, and coronary artery disease), obesity, tobacco consumption, prolonged surgery, and substantial intraoperative blood loss may be associated with POVL.22 An American Society of Anesthesiologists Advisory considers high-risk patients as patients undergoing surgery in the prone position, in whom prolonged procedures and substantial blood loss might be expected.22 The prone position is particularly involved in the setting in which most POVL is observed.3 This occurs because of the significant increase in intraocular pressure22 in anesthetized patients, especially in the Trendelenburg position.14,23 Given that ocular perfusion pressure is regulated by the difference between mean arterial blood pressure and intraocular pressure, any significant decrease in mean arterial blood pressure or increase in intraocular pressure may lead to visual loss. If external ocular globe compression also figures in this scenario, in addition to retinal and anterior chamber ischemia, ischemia of extraocular muscles is noted.4 In that situation, visual loss may occur because of direct damage to the optic nerve or the vasa nervorum, which leads to ION, or even to the retina, when intraorbital pressure surpasses central retinal artery pressure, thereby leading to CRAO.13 When external pressure is released, reperfusion results in transudation of fluids into the tissue spaces, which causes even more intraorbital compartmental pressure and ultimately leads to proptosis, extraocular muscle damage, and chemosis.4,17 This has been a major source of diagnostic controversy since the clinical and experimental study by Hollenhorst et al.17 Five of their patients experienced not only the characteristic findings of CRAO on funduscopy but also signs of increased intraorbital pressure, such as proptosis, ophthalmoplegia, and chemosis, which are typical of OCS.17 This has led to several equivocal descriptions of CRAO after spinal surgery in the prone position, in which the orbital signs were interpreted as a part of the clinical picture.14-16,18,19 In
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Figure 5. (A and B) Intraoperative photographs of bony decompression (A), demonstrating bulging orbital fat through the lateral orbital wall at the end of the procedure (B). (C)
fact, patients can have either ION or CRAO together with OCS, depending on individual susceptibility. From the clinical standpoint, ION is typically characterized by painless visual loss noted right after awaking from surgery or within 48 hours of surgery.4 Funduscopy helps differentiate anterior from posterior ION, as anterior ION demonstrates optic disc edema, with or without peripapillary flame-shaped hemorrhage, whereas funduscopy appears normal with posterior ION.1,4 CRAO also manifests with painless, sudden visual loss with distinctive macular and/or retinal edema and cherry-red spots on funduscopy.1,4,12 Afferent pupillary reflex and pupillary light reflex are noticeably reduced or absent in both ION and CRAO.1,4,12 Imaging is not useful for diagnosis and is mainly used to rule out pituitary apoplexy or occipital lobe infarction.2
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Postoperative computed tomography with three-dimensional reconstruction demonstrates extent of bony removal.
The clinical picture in OCS is much more apparent and includes orbital symptoms in addition to vision loss.13 Patients complain of sudden onset of decreased vision, painful periorbital edema, or proptosis.13 OCS typically develops following blunt trauma to the face or recent ocular surgery13,24 and is very rare in the scope of spinal surgeries in the prone position. To the best of our knowledge, only 3 other patients affected by OCS were reported in the literature after lumbar spine surgeries (Table 1).9-11 Symptoms were mostly recognized a few hours after surgery9-11 except in the present case, in which hyperemia of the eyelids was noted before the patient awoke. Although management of ION and CRAO is generally conservative and supportive by trying to restore ocular perfusion, OCS is an ophthalmologic emergency and should be promptly decompressed with
Figure 6. At 5 months after spinal surgery, eyelid swelling and proptosis resolved and marked improvement in ophthalmoplegia was noted, but there was still ptosis.
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canthotomy and cantholysis even before further imaging to minimize visual loss.13,24 This is in line with the fact that patients who undergo decompression within 2 hours after facial trauma experience maximal visual recovery.24 After this time window, visual recovery is far from satisfactory.24 Mannitol and acetazolamide can be used before decompression as well as corticosteroids, although their role in OCS has not been assessed in a systematic fashion.13 If canthotomy and cantholysis fail to restore retinal and optic nerve perfusion, the insertion of the superior limb of the lateral canthal tendon or even the orbital septum may be released.9,13 Bony decompression is recommended as the last resort of surgical treatment.13 In such situations, emergent orbital computed tomography is indicated, as it is often immediately available, to rule out large intraorbital hematomas.13 Orbital imaging may reveal posterior globe tenting, which is illustrated by the conical shape adopted by the ocular globe, indicating a rise in intraorbital pressure.13,25 In cases with suspected vascular anomalies, magnetic resonance angiography or cerebral angiography should be performed.13 Analyzing the present report and previous descriptions,9,11 it is worth noting that patients underwent imaging investigation before definitive treatment, suggesting that OCS diagnosis is still underrecognized in the scope of POVL. Two patients underwent canthotomy and cantholysis,9,11 whereas our patient was operated on for bony decompression. Timing of decompression was generally late in the course of disease, taking >24 hours for definitive treatment.11 We decided on bony decompression as the first measure because of the time required for surgical
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CASE REPORT JORGE LUIZ AMORIM CORREA AND MARCUS ANDRÉ ACIOLY
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Table 1. Summary of Reported Cases of Orbital Compartment Syndrome After Lumbar Surgery in the Prone Position
Study
Age (years)/ Risk Sex Factors
Surgery Length (hours)
Perioperative Forehead Events Side Numbness Ophthalmoplegia Proptosis
Treatment
Outcome
Leibovitch et al., 20069
80/M
No
8
Not reported
L
Not reported
Internal and external
Yes
Canthotomy, MP, ACTZ
Blind, no ocular movements, ptosis
Tachfouti et al., 200710
45/M
No
4
Not reported
L
Not reported
Internal and external
Yes
Corticosteroid
Blind, complete recovery of ophthalmoplegia, ptosis
Yu et al., 200811
68/M
DM, HTN
4
Blood and plasma transfusion
R
Not reported
Internal and external
Yes
Mannitol, canthotomy, MP, ACTZ
Blind, no ocular movements, ptosis
Present study
55/F
DM, HTN, Graves
7
Blood transfusion
R
Yes
Internal and external
Yes
Mannitol, bony decompression, MP, ACTZ
Blind, marked recovery of ophthalmoplegia, ptosis
M, male; L, left; MP, methylprednisolone; ACTZ, acetazolamide; DM, diabetes mellitus; HTN, hypertension; R, right; F, female; Graves, Graves ophthalmopathy.
decision making. We attributed the symptoms initially to CRAO, but with time the diagnosis of OCS became clear, with the development of proptosis and chemosis. Any further delay in our patient could increase the likelihood of permanent injury to the optic nerve or extraocular muscles if we were willing to respect the above-mentioned stepwise OCS surgical management. Although visual outcome was generally dismal in all 4 reports,9-11 our patient experienced marked improvement in extraocular muscle function. This suggests that surgical management should not be ruled out, even in the case of late disease, as treatment goals should also include recovery of extraocular muscle function. Despite all efforts to treat POVL, total or partial permanent visual loss occurs in most cases. The following preventive strategies should be carefully applied in all patients who are candidates for spine surgery in the prone position: continuous monitoring of mean arterial blood pressure during the entire procedure to avoid hypotension; keeping the head in neutral position with the globe freely located and elevated above the trunk to facilitate venous return; balancing of fluid replacement with crystalloid and colloids; routinely monitoring hematocrit and hemoglobin with blood transfusion if needed; and staging the surgical procedure, even with increased rates of surgical infection.5 This last issue is relevant. In retrospect, our patient was affected by a
segmental disease in the context of degenerative scoliosis with several medical comorbidities. Thus, we might have performed a limited or staged procedure to reduce the risks of POVL.
CONCLUSIONS OCS is a rare, but underreported additional mechanism of visual loss during prolonged spinal surgery in the prone position. All spine surgeons and anesthesiologists should be aware of its occurrence, as prompt recognition and management are of utmost importance for visual and extraocular muscle function outcomes. The inclusion of orbital signs in the clinical picture of ION and CRAO is not only incorrect but also gives the impression of therapeutic futility, thereby preventing successful orbital decompression in a timely fashion. Preventive measures are a key issue and should be adopted to reduce the risks of POVL. REFERENCES 1. Lee LA, Roth S, Posner KL, Cheney FW, Caplan RA, Newman NJ. The American Society of Anesthesiologists postoperative visual loss registry. Anesthesiology. 2006;105:652-659. 2. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol. 2008;145: 604-610. 3. Nickels TJ, Manlapaz MR, Farag E. Perioperative visual loss after spine surgery. World J Orthop. 2014; 5:100-106.
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4. Roth S. Perioperative visual loss: what do we know, what can we do? Br J Anaesth. 2009; 103(suppl 1):i31-i40. 5. Apfelbaum JL, Roth S, Connis RT, Domino KB, Lee LA, Nickinovich DG, et al. Practice advisory for perioperative visual loss associated with spine surgery: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Anesthesiology. 2012;116: 274-285. 6. Patil CG, Lad EM, Lad SP, Ho C, Boakye M. Visual loss after spine surgery: a population-based study. Spine (Phila Pa 1976). 2008;33:1491-1496. 7. Shen Y, Drum M, Roth S. The prevalence of perioperative visual loss in the United States: a 10year study from 1996 to 2005 of spinal, orthopedic, cardiac, and general surgery. Anesth Analg. 2009;109:1534-1545. 8. Stevens WR, Glazer PA, Kelley SD, Lietman TM, Bradford DS. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976). 1997;22: 1319-1324. 9. Leibovitch I, Casson R, Laforest C, Selva D. Ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Ophthalmology. 2006;113:105-108. 10. Tachfouti S, Karmane A, El Moussaif H, Boutimzine N, Daoudi R. Orbital ischemia syndrome after surgical intervention of the spine. A case report [in French] Bull Soc Belge Ophtalmol. 2007;305:27-30. 11. Yu YH, Chen WJ, Chen LH, Chen WC. Ischemic orbital compartment syndrome after posterior spinal surgery. Spine (Phila Pa 1976). 2008;33: E569-E572. 12. Varma DD, Cugati S, Lee AW, Chen CS. A review of central retinal artery occlusion: clinical presentation and management. Eye (Lond). 2013;27: 688-697.
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13. Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D. Orbital compartment syndrome: the ophthalmic surgical emergency. Surv Ophthalmol. 2009;54:441-449. 14. Asok T, Aziz S, Faisal HA, Tan AK, Mallika PS. Central retinal artery occlusion and ophthalmoplegia following spinal surgery in the prone position. Med J Malaysia. 2009;64:323-324. 15. Chung MS, Son JH. Visual loss in one eye after spinal surgery. Korean J Ophthalmol. 2006;20:139-142. 16. Delattre O, Thoreux P, Liverneaux P, Merle H, Court C, Gottin M, et al. Spinal surgery and ophthalmic complications. A French survey with review of 17 cases. J Spinal Disord Tech. 2007;20: 302-307. 17. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness occurring during anesthesia for neurosurgical operations. AMA Arch Ophthalmol. 1954;52: 819-830.
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18. Stambough JL, Cheeks ML. Central retinal artery occlusion: a complication of the knee-chest position. J Spinal Disord. 1992;5:363-365. 19. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as a complication of patient positioning for spinal surgery. A case report. Spine (Phila Pa 1976). 1992;17:600-605. 20. Kumar N, Jivan S, Topping N, Morrell AJ. Blindness and rectus muscle damage following spinal surgery. Am J Ophthalmol. 2004;138:889-891. 21. Ho VT, Newman NJ, Song S, Ksiazek S, Roth S. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol. 2005;17:38-44. 22. Cheng MA, Todorov A, Tempelhoff R, McHugh T, Crowder CM, Lauryssen C. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology. 2001;95:1351-1355. 23. Ozcan MS, Praetel C, Bhatti MT, Gravenstein N, Mahla ME, Seubert CN. The effect of body inclination during prone positioning on intraocular
pressure in awake volunteers: a comparison of two operating tables. Anesth Analg. 2004;99:1152-1158. 24. Sun MT, Chan WO, Selva D. Traumatic orbital compartment syndrome: importance of the lateral canthomy and cantholysis. Emerg Med Australas. 2014;26:274-278. 25. Dalley RW, Robertson WD, Rootman J. Globe tenting: a sign of increased orbital tension. AJNR Am J Neuroradiol. 1989;10:181-186. Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 31 July 2017; accepted 20 November 2017 Citation: World Neurosurg. (2018) 110:309-314. https://doi.org/10.1016/j.wneu.2017.11.111 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.
WORLD NEUROSURGERY, https://doi.org/10.1016/j.wneu.2017.11.111
The Enigma of Orbital Compartment Syndrome After Lumbar Spine Surgery in the Prone Position: Case Report and Literature Review Jorge Luiz Amorim Correa1,2 and Marcus Andre´ Acioly2,3
Key words Central retinal artery occlusion - Ischemic optic neuropathy - Orbital compartment syndrome - Perioperative visual loss - Prone position - Spine surgery -
Abbreviations and Acronyms CRAO: Central retinal artery occlusion ION: Ischemic optic neuropathy OCS: Orbital compartment syndrome POVL: Perioperative visual loss From the 1Division of Neurosurgery, Galeão Air Force Hospital, Rio de Janeiro; 2Postgraduate Program in Neurology, Federal University of the State of Rio de Janeiro, Rio de Janeiro; and 3Division of Neurosurgery, Fluminense Federal University, Rio de Janeiro, Brazil To whom correspondence should be addressed: Jorge Luiz Amorim Correa, M.D., M.Sc. [E-mail: [email protected]] Citation: World Neurosurg. (2018) 110:309-314. https://doi.org/10.1016/j.wneu.2017.11.111 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.
INTRODUCTION Patients might expect some adverse effects following a spinal elective procedure, such as spinal pain or nerve injury, but awaking blind is a devastating complication for both the patient and the surgical team.1-4 The American Society of Anesthesiologists Task Force defined perioperative visual loss (POVL) as a permanent impairment or total loss of sight associated with a spinal procedure under general anesthesia from immediate preoperative assessment to discharge.5 POVL is a rare occurrence following nonocular surgeries2-4 and affects <0.2% of all spinal surgeries.6-8 The precise incidence remains obscure.2 Two major causes of POVL in the scope of nonocular surgery are known: ischemic optic neuropathy (ION) and central retinal artery occlusion (CRAO).1,3,4 In a multiinstitutional study, Lee et al.1 analyzed 93 patients affected by POVL associated with spinal surgery. ION was the most
- BACKGROUND:
Perioperative visual loss after spinal surgery is a devastating complication for the patient and the surgical team. Two known major causes are ischemic optic neuropathy and central retinal artery occlusion (CRAO). Traditional understanding of CRAO has been consistently related to occurrence of periocular trauma and signs of increased intraorbital pressure in addition to visual loss. However, such orbital signs are not a feature of any common perioperative visual loss syndrome.
- CASE
DESCRIPTION: A 55-year-old woman underwent prolonged lumbar decompression and fusion for spinal stenosis under general anesthesia in the prone position. At the end of surgery, periocular hyperemia, corneal edema, and a tense orbit on the right side were noted. Complete internal and external ophthalmoplegia was observed on examination. Orbital computed tomography confirmed the clinical diagnosis of orbital compartment syndrome. Bony decompression was performed, but the treated eye remained blind. Resolution of the complete ophthalmoplegia was observed during late follow-up.
- CONCLUSIONS:
In retrospect, patients diagnosed with often misunderstood CRAO and ischemic optic neuropathy with orbital signs after spinal surgery most likely had orbital compartment syndrome. The inclusion of orbital signs in the clinical picture of ischemic optic neuropathy and CRAO is not only incorrect but also gives the impression of therapeutic futility, thereby preventing successful orbital decompression in a timely fashion.
common etiology in 89% of the patients, especially posterior ION, whereas CRAO accounted for 11% of the collected cases.1 Central retinal vein occlusion, occipital lobe infarct, and orbital compartment syndrome (OCS) have been rarely reported in patients with POVL.8-11 Although anterior ION is most likely caused by vascular occlusion or the lack of perfusion to the anterior optic nerve head, posterior ION occurs as a result of optic nerve infarction posterior to the lamina cribrosa.3 CRAO is characterized by the lack of blood supply to the entire retina, which is analogous to an acute stroke of the eye.3,4,12 CRAO represents an endorgan ischemia, which is frequently associated with underlying atherosclerotic disease.12 Finally, OCS is an ophthalmologic emergency, which is characterized by an acute rise in intraorbital pressure, placing the optic nerve and intraorbital structures at risk.13
WORLD NEUROSURGERY 110: 309-314, FEBRUARY 2018
The traditional understanding of CRAO in the neurosurgery and anesthesiology literature has been consistently related to the occurrence of periocular trauma and signs of increased intraorbital pressure, in addition to visual loss in most cases.1 This is illustrated by the frequent reports of concomitant decreased supraorbital sensation, ophthalmoplegia, proptosis, ptosis, corneal abrasion, and even unilateral erythema in the scope of CRAO.1,14-19 Such orbital signs have also been reported in association with ION,1,20 but with an incidence much smaller than for CRAO. In retrospect, patients diagnosed with often misunderstood CRAO and ION with orbital signs after spinal surgery most likely had OCS. The recognition of OCS instead of ION and CRAO is of utmost importance, as management strategies are completely different. We describe a patient affected by OCS after posterior
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CASE REPORT JORGE LUIZ AMORIM CORREA AND MARCUS ANDRÉ ACIOLY
Figure 1. Preoperative imaging. (A) Plain radiography showing lumbar degenerative scoliosis. (B and C) Computed tomography images showing
lumbar spinal surgery in the prone position, emphasizing all relevant aspects to differentiate OCS from ION and CRAO through a literature review. The patient provided informed consent for the publication of this study.
CASE DESCRIPTION History and Examination A 55-year-old woman had chronic low back pain radiating to the right leg (L5 territory) for 2 years. Symptoms were typically exacerbated by walking, leading to a diagnosis of neurogenic claudication. With time, progressive paraparesis evolved, and the patient needed assistance to walk right before admission. No sphincter dysfunction was noted. Her medical history included diabetes
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
lumbar stenosis at L4-5 (B) and L5-S1 (C). (D) Sagittal T2-weighted magnetic resonance imaging showing severe stenosis and endplate changes at L4-5.
mellitus, hypertension, and thyroid dysfunction with Graves ophthalmopathy, all of which were under medical control. Imaging demonstrated lumbar spine degenerative scoliotic changes and segmental instability in the L4-5 segment on plain radiographs. Magnetic resonance imaging showed multilevel spinal stenosis from L3-4 to L5-S1, but especially in L4-5, with Modic type I plateau changes and disc herniation at this level. Computed tomography indicated calcification of the L4-5 disc (Figure 1). The symptoms were refractory to conservative management, and the patient was scheduled for surgery. The patient underwent a 7-hour procedure with 2level lumbar decompression (L4-5 and L5-S1) and scoliosis correction by posterolateral instrumentation from T12 to S1 under general anesthesia in the
Figure 2. Right proptosis, periocular hyperemia, chemosis, and mydriasis were noted right after turning the patient from prone to supine position.
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prone position. Her head was positioned over an O-shaped soft headrest with the left side of the face up. The patient received transfusion of one unit of packed erythrocytes. At the end of surgery, right after turning the patient from prone to supine position, periocular hyperemia, corneal edema, and a tense orbit on the right side were noted. Complete internal and external ophthalmoplegia was observed on examination. Funduscopy could not be performed owing to corneal edema. No abnormal findings in the left eye were apparent (Figure 2). Urgent orbital CT demonstrated right proptosis, enlargement and stretching of the optic nerve, and intraorbital muscle edema (Figure 3). Mannitol, corticosteroids, and acetazolamide were initiated. Orbital signs progressively worsened over a few hours, and the patient complained of pain in the right orbit (Figure 3). The patient underwent digital subtraction angiography, which revealed occlusion of the right ophthalmic artery (Figure 4). No aneurysms or cavernous sinus thrombosis was documented. Operation and Postoperative Course After consultation with an ophthalmologist, bony orbital decompression was performed 26 hours after spinal surgery, in which the lateral wall of the orbit was removed (Figure 5). After orbital surgery,
WORLD NEUROSURGERY, https://doi.org/10.1016/j.wneu.2017.11.111
CASE REPORT JORGE LUIZ AMORIM CORREA AND MARCUS ANDRÉ ACIOLY
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Figure 3. (A) Orbital computed tomography revealed extraocular muscle enlargement, periocular soft tissue edema, and blurring of orbital fat. (B) Symptoms progressed over a few hours, and the patient developed severe proptosis and chemosis.
the globe progressively softened, and proptosis slightly subsided. During the following days, improvement of swelling and proptosis was gradual, taking several months for complete resolution. The patient was followed for 5 months; at her last follow-up consultation, the treated eye remained blind, but a marked resolution of complete ophthalmoplegia was observed (Figure 6). DISCUSSION Hollenhorst et al.17 were potentially the first to call attention to the phenomenon
of POVL during posterior cervical spine surgeries in the prone position. In 1954, they described a series of 8 patients affected by different degrees of orbital and ocular signs and performed a detailed experimental study on monkeys.17 Ocular lesions could be produced by lowering the blood pressure and by applying compression to the orbital contents, showing that their patients and experimental models shared the same pathophysiologic substrate for the occurrence of the condition.17 Apart from hypotension and ocular globe compression, several preoperative
Figure 4. Digital subtraction angiography of the right internal carotid artery (lateral view) demonstrating complete occlusion of the right ophthalmic artery (arrow).
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and intraoperative factors have been implicated in the development of POVL.1-3,21 The best evidence available indicates that preoperative anemia, vascular risk factors (e.g., hypertension, diabetes, peripheral artery disease, and coronary artery disease), obesity, tobacco consumption, prolonged surgery, and substantial intraoperative blood loss may be associated with POVL.22 An American Society of Anesthesiologists Advisory considers high-risk patients as patients undergoing surgery in the prone position, in whom prolonged procedures and substantial blood loss might be expected.22 The prone position is particularly involved in the setting in which most POVL is observed.3 This occurs because of the significant increase in intraocular pressure22 in anesthetized patients, especially in the Trendelenburg position.14,23 Given that ocular perfusion pressure is regulated by the difference between mean arterial blood pressure and intraocular pressure, any significant decrease in mean arterial blood pressure or increase in intraocular pressure may lead to visual loss. If external ocular globe compression also figures in this scenario, in addition to retinal and anterior chamber ischemia, ischemia of extraocular muscles is noted.4 In that situation, visual loss may occur because of direct damage to the optic nerve or the vasa nervorum, which leads to ION, or even to the retina, when intraorbital pressure surpasses central retinal artery pressure, thereby leading to CRAO.13 When external pressure is released, reperfusion results in transudation of fluids into the tissue spaces, which causes even more intraorbital compartmental pressure and ultimately leads to proptosis, extraocular muscle damage, and chemosis.4,17 This has been a major source of diagnostic controversy since the clinical and experimental study by Hollenhorst et al.17 Five of their patients experienced not only the characteristic findings of CRAO on funduscopy but also signs of increased intraorbital pressure, such as proptosis, ophthalmoplegia, and chemosis, which are typical of OCS.17 This has led to several equivocal descriptions of CRAO after spinal surgery in the prone position, in which the orbital signs were interpreted as a part of the clinical picture.14-16,18,19 In
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Figure 5. (A and B) Intraoperative photographs of bony decompression (A), demonstrating bulging orbital fat through the lateral orbital wall at the end of the procedure (B). (C)
fact, patients can have either ION or CRAO together with OCS, depending on individual susceptibility. From the clinical standpoint, ION is typically characterized by painless visual loss noted right after awaking from surgery or within 48 hours of surgery.4 Funduscopy helps differentiate anterior from posterior ION, as anterior ION demonstrates optic disc edema, with or without peripapillary flame-shaped hemorrhage, whereas funduscopy appears normal with posterior ION.1,4 CRAO also manifests with painless, sudden visual loss with distinctive macular and/or retinal edema and cherry-red spots on funduscopy.1,4,12 Afferent pupillary reflex and pupillary light reflex are noticeably reduced or absent in both ION and CRAO.1,4,12 Imaging is not useful for diagnosis and is mainly used to rule out pituitary apoplexy or occipital lobe infarction.2
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Postoperative computed tomography with three-dimensional reconstruction demonstrates extent of bony removal.
The clinical picture in OCS is much more apparent and includes orbital symptoms in addition to vision loss.13 Patients complain of sudden onset of decreased vision, painful periorbital edema, or proptosis.13 OCS typically develops following blunt trauma to the face or recent ocular surgery13,24 and is very rare in the scope of spinal surgeries in the prone position. To the best of our knowledge, only 3 other patients affected by OCS were reported in the literature after lumbar spine surgeries (Table 1).9-11 Symptoms were mostly recognized a few hours after surgery9-11 except in the present case, in which hyperemia of the eyelids was noted before the patient awoke. Although management of ION and CRAO is generally conservative and supportive by trying to restore ocular perfusion, OCS is an ophthalmologic emergency and should be promptly decompressed with
Figure 6. At 5 months after spinal surgery, eyelid swelling and proptosis resolved and marked improvement in ophthalmoplegia was noted, but there was still ptosis.
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canthotomy and cantholysis even before further imaging to minimize visual loss.13,24 This is in line with the fact that patients who undergo decompression within 2 hours after facial trauma experience maximal visual recovery.24 After this time window, visual recovery is far from satisfactory.24 Mannitol and acetazolamide can be used before decompression as well as corticosteroids, although their role in OCS has not been assessed in a systematic fashion.13 If canthotomy and cantholysis fail to restore retinal and optic nerve perfusion, the insertion of the superior limb of the lateral canthal tendon or even the orbital septum may be released.9,13 Bony decompression is recommended as the last resort of surgical treatment.13 In such situations, emergent orbital computed tomography is indicated, as it is often immediately available, to rule out large intraorbital hematomas.13 Orbital imaging may reveal posterior globe tenting, which is illustrated by the conical shape adopted by the ocular globe, indicating a rise in intraorbital pressure.13,25 In cases with suspected vascular anomalies, magnetic resonance angiography or cerebral angiography should be performed.13 Analyzing the present report and previous descriptions,9,11 it is worth noting that patients underwent imaging investigation before definitive treatment, suggesting that OCS diagnosis is still underrecognized in the scope of POVL. Two patients underwent canthotomy and cantholysis,9,11 whereas our patient was operated on for bony decompression. Timing of decompression was generally late in the course of disease, taking >24 hours for definitive treatment.11 We decided on bony decompression as the first measure because of the time required for surgical
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CASE REPORT JORGE LUIZ AMORIM CORREA AND MARCUS ANDRÉ ACIOLY
ORBITAL COMPARTMENT SYNDROME IN THE PRONE POSITION
Table 1. Summary of Reported Cases of Orbital Compartment Syndrome After Lumbar Surgery in the Prone Position
Study
Age (years)/ Risk Sex Factors
Surgery Length (hours)
Perioperative Forehead Events Side Numbness Ophthalmoplegia Proptosis
Treatment
Outcome
Leibovitch et al., 20069
80/M
No
8
Not reported
L
Not reported
Internal and external
Yes
Canthotomy, MP, ACTZ
Blind, no ocular movements, ptosis
Tachfouti et al., 200710
45/M
No
4
Not reported
L
Not reported
Internal and external
Yes
Corticosteroid
Blind, complete recovery of ophthalmoplegia, ptosis
Yu et al., 200811
68/M
DM, HTN
4
Blood and plasma transfusion
R
Not reported
Internal and external
Yes
Mannitol, canthotomy, MP, ACTZ
Blind, no ocular movements, ptosis
Present study
55/F
DM, HTN, Graves
7
Blood transfusion
R
Yes
Internal and external
Yes
Mannitol, bony decompression, MP, ACTZ
Blind, marked recovery of ophthalmoplegia, ptosis
M, male; L, left; MP, methylprednisolone; ACTZ, acetazolamide; DM, diabetes mellitus; HTN, hypertension; R, right; F, female; Graves, Graves ophthalmopathy.
decision making. We attributed the symptoms initially to CRAO, but with time the diagnosis of OCS became clear, with the development of proptosis and chemosis. Any further delay in our patient could increase the likelihood of permanent injury to the optic nerve or extraocular muscles if we were willing to respect the above-mentioned stepwise OCS surgical management. Although visual outcome was generally dismal in all 4 reports,9-11 our patient experienced marked improvement in extraocular muscle function. This suggests that surgical management should not be ruled out, even in the case of late disease, as treatment goals should also include recovery of extraocular muscle function. Despite all efforts to treat POVL, total or partial permanent visual loss occurs in most cases. The following preventive strategies should be carefully applied in all patients who are candidates for spine surgery in the prone position: continuous monitoring of mean arterial blood pressure during the entire procedure to avoid hypotension; keeping the head in neutral position with the globe freely located and elevated above the trunk to facilitate venous return; balancing of fluid replacement with crystalloid and colloids; routinely monitoring hematocrit and hemoglobin with blood transfusion if needed; and staging the surgical procedure, even with increased rates of surgical infection.5 This last issue is relevant. In retrospect, our patient was affected by a
segmental disease in the context of degenerative scoliosis with several medical comorbidities. Thus, we might have performed a limited or staged procedure to reduce the risks of POVL.
CONCLUSIONS OCS is a rare, but underreported additional mechanism of visual loss during prolonged spinal surgery in the prone position. All spine surgeons and anesthesiologists should be aware of its occurrence, as prompt recognition and management are of utmost importance for visual and extraocular muscle function outcomes. The inclusion of orbital signs in the clinical picture of ION and CRAO is not only incorrect but also gives the impression of therapeutic futility, thereby preventing successful orbital decompression in a timely fashion. Preventive measures are a key issue and should be adopted to reduce the risks of POVL. REFERENCES 1. Lee LA, Roth S, Posner KL, Cheney FW, Caplan RA, Newman NJ. The American Society of Anesthesiologists postoperative visual loss registry. Anesthesiology. 2006;105:652-659. 2. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol. 2008;145: 604-610. 3. Nickels TJ, Manlapaz MR, Farag E. Perioperative visual loss after spine surgery. World J Orthop. 2014; 5:100-106.
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4. Roth S. Perioperative visual loss: what do we know, what can we do? Br J Anaesth. 2009; 103(suppl 1):i31-i40. 5. Apfelbaum JL, Roth S, Connis RT, Domino KB, Lee LA, Nickinovich DG, et al. Practice advisory for perioperative visual loss associated with spine surgery: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Anesthesiology. 2012;116: 274-285. 6. Patil CG, Lad EM, Lad SP, Ho C, Boakye M. Visual loss after spine surgery: a population-based study. Spine (Phila Pa 1976). 2008;33:1491-1496. 7. Shen Y, Drum M, Roth S. The prevalence of perioperative visual loss in the United States: a 10year study from 1996 to 2005 of spinal, orthopedic, cardiac, and general surgery. Anesth Analg. 2009;109:1534-1545. 8. Stevens WR, Glazer PA, Kelley SD, Lietman TM, Bradford DS. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976). 1997;22: 1319-1324. 9. Leibovitch I, Casson R, Laforest C, Selva D. Ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Ophthalmology. 2006;113:105-108. 10. Tachfouti S, Karmane A, El Moussaif H, Boutimzine N, Daoudi R. Orbital ischemia syndrome after surgical intervention of the spine. A case report [in French] Bull Soc Belge Ophtalmol. 2007;305:27-30. 11. Yu YH, Chen WJ, Chen LH, Chen WC. Ischemic orbital compartment syndrome after posterior spinal surgery. Spine (Phila Pa 1976). 2008;33: E569-E572. 12. Varma DD, Cugati S, Lee AW, Chen CS. A review of central retinal artery occlusion: clinical presentation and management. Eye (Lond). 2013;27: 688-697.
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13. Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D. Orbital compartment syndrome: the ophthalmic surgical emergency. Surv Ophthalmol. 2009;54:441-449. 14. Asok T, Aziz S, Faisal HA, Tan AK, Mallika PS. Central retinal artery occlusion and ophthalmoplegia following spinal surgery in the prone position. Med J Malaysia. 2009;64:323-324. 15. Chung MS, Son JH. Visual loss in one eye after spinal surgery. Korean J Ophthalmol. 2006;20:139-142. 16. Delattre O, Thoreux P, Liverneaux P, Merle H, Court C, Gottin M, et al. Spinal surgery and ophthalmic complications. A French survey with review of 17 cases. J Spinal Disord Tech. 2007;20: 302-307. 17. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness occurring during anesthesia for neurosurgical operations. AMA Arch Ophthalmol. 1954;52: 819-830.
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18. Stambough JL, Cheeks ML. Central retinal artery occlusion: a complication of the knee-chest position. J Spinal Disord. 1992;5:363-365. 19. Wolfe SW, Lospinuso MF, Burke SW. Unilateral blindness as a complication of patient positioning for spinal surgery. A case report. Spine (Phila Pa 1976). 1992;17:600-605. 20. Kumar N, Jivan S, Topping N, Morrell AJ. Blindness and rectus muscle damage following spinal surgery. Am J Ophthalmol. 2004;138:889-891. 21. Ho VT, Newman NJ, Song S, Ksiazek S, Roth S. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol. 2005;17:38-44. 22. Cheng MA, Todorov A, Tempelhoff R, McHugh T, Crowder CM, Lauryssen C. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology. 2001;95:1351-1355. 23. Ozcan MS, Praetel C, Bhatti MT, Gravenstein N, Mahla ME, Seubert CN. The effect of body inclination during prone positioning on intraocular
pressure in awake volunteers: a comparison of two operating tables. Anesth Analg. 2004;99:1152-1158. 24. Sun MT, Chan WO, Selva D. Traumatic orbital compartment syndrome: importance of the lateral canthomy and cantholysis. Emerg Med Australas. 2014;26:274-278. 25. Dalley RW, Robertson WD, Rootman J. Globe tenting: a sign of increased orbital tension. AJNR Am J Neuroradiol. 1989;10:181-186. Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 31 July 2017; accepted 20 November 2017 Citation: World Neurosurg. (2018) 110:309-314. https://doi.org/10.1016/j.wneu.2017.11.111 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.
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