
==== Front
Int J Surg Case Rep
Int J Surg Case Rep
International Journal of Surgery Case Reports
2210-2612
Elsevier

S2210-2612(24)00964-7
10.1016/j.ijscr.2024.110183
110183
Case Report
Suspected cavernous sinus thrombosis and blindness after lumbar spine surgery: A rare case report and literature review
Yuan Hao 1
Tian Yanjie fygeneral@sina.com
2⁎
Li Xuemin lxmlxm66@sina.com
⁎2
Department of Ophthalmology, Peking University Third Hospital, No.49 Huayuan North Road, Haidian District, Beijing 100191, People's Republic of China
Beijing Key Laboratory of Restoration of Damaged Ocular Nerve, No.49 Huayuan North Road, Haidian District, Beijing 100191, People's Republic of China
⁎ Corresponding authors at: Department of Ophthalmology, Peking University Third Hospital, Beijing Key Laboratory of Restoration of Damaged Ocular Nerve, No 49 Huayuan North Road, Haidian District, Beijing 100191, People's Republic of China. fygeneral@sina.comlxmlxm66@sina.com
1 The first author.

2 They contributed equally to the study.

15 8 2024
9 2024
15 8 2024
122 11018330 6 2024
11 8 2024
14 8 2024
© 2024 Published by Elsevier Ltd on behalf of IJS Publishing Group Limited.
2024

https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Introduction and importance

Postoperative visual loss (POVL) is a relatively rare but devastating complication. We reported a case of POVL after spine surgery caused by ischemia of retina and optic nerve, and firstly introduced the possibility of cavernous sinus thrombosis in POVL development.

Case presentation

A 67-year-old woman diagnosed with “lumbar spinal stenosis” was admitted to undergo posterior lumbar spinal canal decompression surgery because of the persistent lumbago and numbness. The operation was performed in the prone position under general anesthesia uneventfully. On the second day, the visual acuity of her right eye suddenly decreased to no light perception. The ophthalmic examination indicated edematous eyelid, chemosis, ptosis, ophthalmoplegia, relative afferent pupillary defect and higher orbital pressure in her affected eye, and funduscopic examination revealed pale optic disc, diffuse retinal welling and attenuated arteries. Cerebral magnetic resonance angiography implied the stenosis of cavernous sinus segment of right internal carotid artery. Aseptic cavernous sinus thrombosis and the secondary combined occlusion of central retinal and optic nerve vessels were suspected. Therefore, anticoagulation, vasodilation, oxygen and anti-inflammation treatment were timely administrated. One month after the treatment, swelling eyelid and ocular motion had markedly improved. However, there was no remarkable improvement in the patient's visual acuity.

Clinical discussion

Postoperative visual loss (POVL) after spine surgery is regarded as a serious complication with irreversible vision damage. It was alarming that cavernous sinus thrombosis might be a possible cause of POVL. High-volume fluid replacement, unstable hemodynamic parameters, prone position and prolonged surgical duration might bring about microvascular diseases and hypercoagulable state, contributing to the occurrence of POVL.

Conclusion

Our study firstly implied the possibility of cavernous sinus thrombosis in the POVL development. Detailed assessment, fluids management, hemodynamic stabilizing and duration optimization were proposed for POVL prevention.

Highlights

• The first case of permanent visual loss after prone-position spine surgery, which was contributed by the optic nerve infarction and central retinal artery occlusion secondary to suspected cavernous sinus thrombosis postoperatively;

• Indicating the possibility of cavernous sinus thrombosis in the development of POVL which could broaden our current cognition of POVL causes;

• POVL prevention strategies were systematically reviewed and summarized.

Keywords

Cavernous sinus thrombosis
Hypercoagulability
Ischemia
Postoperative complications
Spinal stenosis
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pmc1 Introduction

Postoperative visual loss (POVL), a relatively rare but devastating complication, has been described after spine, cardiac, and head-neck surgeries, with variably reported incidences lying between 0.017 % and 0.2% [[1], [2], [3]]. Generally, the occurrence of POVL is attributable to ischemic optic neuropathy (ION), central retinal artery occlusion (CRAO) or cortical blindness [2]. Various risk factors, including long surgical duration, high venous pressure, excessive blood loss, high-volume fluid replacement, prone posture and poor head positioning, might bring about intraoperative hemodynamic compromise and microvascular impairment, contributing to the hypercoagulable state and the occurrence of POVL together [[1], [2], [3], [4]]. However, the exact pathophysiologic mechanism of POVL has not yet been clearly determined.

Despite the concerns were voiced increasingly, as to our knowledge, POVL contributed by cavernous sinus thrombosis has not been reported. We herein describe a woman who was considered to develop suspected cavernous sinus thrombosis after spine surgery in the prone position under general anesthesia, which secondarily led to her persistent unilateral vision loss with combined ischemia of retina and optic nerve. The case was reported in line with the SCARE criteria [5]. Meanwhile, the presentation, possible causes and risk factors of POVL after spine surgery were being discussed to help avoid this complication in future.

2 Case presentation

A 67-year-old woman (body mass index 24.39 kg/m2) was admitted to undergo L3–4-5-S1 posterior lumbar spinal canal decompression because of the persistent lumbago and the development of repeated numbness and debility in her both legs. She had a medical history of type II diabetes mellitus for 17 years, hypertension for 5 years and hyperlipidemia for 2 years, and all these basic diseases were badly controlled. Besides, she had been diagnosed with acute myocardial infarction 2 years ago, and been giving antiplatelet treatment (aspirin and clopidogrel) after coronary stent implantation treatment. Physical examination revealed both-sided tenderness at L2 to S1 with reduced sensation, muscle weakness, diminished reflexes and positive raising test. Preoperative carotid ultrasonography revealed that the patient exhibited atherosclerotic plaques in the carotid at both sides, and his left carotid artery had been totally occluded. No other abnormalities were found, including visual abnormalities or cerebral infarction. Most of his laboratory examination findings were within the reference ranges. Spinal computed tomography (CT) indicated lumbar disc herniation from L2 to S1. The diagnosis of “lumbar spinal stenosis” was confirmed.

The patient was then scheduled to undergo posterior lumbar spinal canal decompression. The operation was done in the prone position under general anesthesia. The surgery lasted for 150 min and blood loss was estimated to be 600 mL. During the intraoperative period, the total fluid input was 1800 mL, and the total urine output was 250 mL. Four units of packed red blood cells were transfused during the operation. The patient's intraoperative blood pressure fluctuated between 200/110 and 110/60 mmHg. The whole procedure was uneventful.

Two hours postoperatively, on fully waking up from general anesthesia, the patient was found showing periorbital swelling, eyelid erythema, conjunctival congestion and slight chemosis in her right eye. Extraocular movements were limited in all directions of gaze. Considering that the visual acuity was normal and the pupillary light reflex was sensitive, no special treatment was given. However, on the second day, the patient reported sudden vision loss in her right eye, without complain of pain, fever, headache and tinnitus. An on-call team immediately performed further ophthalmic and neurologic examinations at the bedside. The ophthalmic examination indicated that the patient's left eye was totally normal and for her right eye, the visual acuity decreased to no light perception. Her right eyelid and bulbar conjunctiva were severely edematous, and ptosis and ophthalmoplegia were both detected. With absent direct light pupillary reflex and insensitive indirect light reflex in right eye, relative afferent pupillary defect (RAPD) was present. The right orbital pressure was remarkable higher than the left side, but the intraocular pressure (IOP) was normal. Funduscopic examination revealed pale optic disc with blurred margins, diffuse retinal welling with “cherry-red” macula. Arteries showed severe narrowing and attenuation, whereas veins were grossly engorged. Pulsatile exophthalmos and vascular bruit were not detected. The neurologic examination showed no abnormalities in facial and periorbital sensation as well as the corneal reflex, and the meningeal irritation was absent.

Radiological imaging was then administered. Orbital computed tomography scanning showed diffuse edema process of extraocular muscles, periorbital soft tissue and optic nerve sheath of right eye, without remarkable intra-orbital space occupied including the orbital apex position. Cerebral magnetic resonance angiography (MRA) implied the stenosis of cavernous sinus segment of right internal carotid artery, indirectly reflecting the possibility of cavernous sinus thrombosis (CST) formation. Ocular doppler showed absence of retrobulbar perfusion with elevated resistance index in her right eye. The laboratory examinations revealed reduced hemoglobin of 101 g/L and hematocrit of 28.4 % compared with those prior to surgery (hemoglobin of 114 g/L and hematocrit of 37.3 %). The total protein was also decreased from 59.6 g/L to 52.8 g/L postoperatively. C-reactive protein and D-dimer were both in the normal range. The immunological examinations showed no abnormalities. Other counts were normal.

Synthesizing all above indications, aseptic cavernous sinus thrombosis was firstly suspected. And on the basis of fundus findings, the combined occlusion of central retinal and optic nerve vessels secondary to the elevated intra-orbital pressure might be the most likely explanation of the patient's dramatic vision loss. Therefore, 6000 IU enoxaparin was immediately injected subcutaneously to initiate anticoagulation treatment. Aiming to restore the blood perfusion of retina and optic nerve, 10 μg alprostadil was administered to dilate the artery. Given the normal intraocular pressure, the patient therefore received no intraocular pressure-lowering medications. The patient was also treated with high-flow oxygen inspiration and adequate fluid infusion. At the same time, in consideration of optic nerve inflammation and orbital congestion, the patient received pulsed intravenous injections of 500 mg methylprednisolone for 3 days, subsequently switched to oral prednisolone. 50 g mannitol was infused to eliminate orbital edema.

After two-week treatment, the patient's visual acuity recovered to light perception and the swelling of her right eyelid had markedly decreased. One month after the treatment, the motion of the extraocular muscles was significantly improved. However, after 12-month follow-up, there was no remarkable further improvement in the patient's visual acuity. Further fundus examination revealed that retinal edema had been absorbed, with pale optic disc and slim arteries. Fluorescein fundus angiography (FFA) showed grossly delayed filling of retina vessels with prolonged arm-to-retina circulation time. The choroidal background fluorescence was also slowly perfused. In the later phase of FFA, a small amount of fluorescein leakage was present on the margin of the optic disc. Optical coherence tomography (OCT) implied the thinning of retinal neuroepithelium and diffuse diminishing of inner retina structure (Fig. 1).Fig. 1 A: Optical coherence tomography of right eye implied the thinning of retinal neuroepithelium and diffuse diminishing of inner retina structure. The structure of all retina layers was atrophic and confused. B: Optical coherence tomography of left eye was roughly normal.

Fig. 1

3 Discussion

Postoperative visual loss (POVL) after spine surgery is regarded as a serious complication that greatly reduces quality of life, which has recently been gaining increasing recognition and special emphasis [6]. Generally, it could pose irreversible vision damage and serious threat to the patient's visual function [1]. Therefore, it is of much importance to figure out the possible etiology of POVL, so as to prevent and early identify this complication. According to the data provided by the American Society of Anesthesiologists (ASA), the three most recognized causes of POVL were ischemic optic neuropathy (ION), central retinal artery thrombosis (CRAO) and cortical blindness, and nearly 80 % of POVL was diagnosed as ION [2,7]. Herein, we firstly reported a case of permanent visual loss after prone-position spine surgery, which was contributed by the optic nerve infarction and central retinal artery occlusion secondary to suspected cavernous sinus thrombosis postoperatively, broadening our current cognition of potential causes of POVL.

In our case, the patient's clinical manifestations could be divided into two stages. In the first stage, immediately on regaining consciousness, the complain of periorbital swelling, lid erythema, exophthalmos and chemosis revealed the acute obstruction of venous drainage and increased venous pressure in the orbit [8]. Meanwhile, ptosis and complete external ophthalmoplegia implied the innervation dysfunction of the cranial nerve III, IV and VI [9]. Therefore, given the simultaneous involvement of orbital venous and cranial nerves, we considered that the primary lesion should be located in orbital apex or cavernous sinus. The subsequent radiological imaging was then preformed to further distinguish the specific pathological location. On the one hand, orbital CT scanning did not show remarkable space occupying, fracture incarceration or local inflammation involved in orbital apex. Meanwhile, our patient showed normal periorbital sensation and sensitive cornea reflex, revealing the unimpaired function of CN V, which was always susceptible in orbital apex syndrome but least affected in CST [9]. On the other hand, despite the lack of direct signs (such as lateral margin bulging and filling defects), MRA implied the narrowing of flow void of the intra-cavernous segment of right internal carotid artery (ICA) in our case, which could indirectly prove the formation of cavernous sinus thrombosis [10]. Horizontal segment of ICA is an important component that traverses the cavernous sinus and can be significantly affected in a number of cavernous sinus lesions [10]. Mee et al. evaluated cavernous sinus lesions on CT and MRI, and demonstrated that ICA encasement was the second most frequent radiologic finding in cavernous sinus thrombosis [11]. Moreover, considering the absence of pulsatile exophthalmos and vascular bruit, the diagnosis of carotid cavernous fistula was also excluded. Therefore, compared with the orbital apex syndrome, these findings were much more likely to support the diagnosis of cavernous sinus thrombosis. Additionally, given the absence of systemic toxic symptoms (headache, fever, vomiting) and un-elevated white blood cells, the thrombosis was regarded as aseptic related to the spinal surgery.

In the second stage, the patient reported sudden painless vision loss of her right eye, with the visual acuity of only light perception. The dramatically decreased VA, nonreactive pupil reaction and RAPD all verified the occurrence of severe afferent disorder. Diffuse retinal swelling, “cherry-red” macula and attenuated retinal artery revealed the acute retinal ischemic pathologic changes. In addition to the retina, the edematous and pale optic papilla also implied the blocked blood supply of optic nerve. Given the existence of cavernous sinus thrombosis, we speculated that, with the development of thrombosis and aggravated orbital swelling, the increased orbital pressure finally contributed to the simultaneous obstruction of branch vessels of the ophthalmic artery that supplied retina and optic nerve, the condition that was similar to a ‘compartment syndrome of the eye’ [12]. A resultant compartment syndrome at the optic nerve head may be a likely explanation for the combined occlusion. Further FFA proved our speculation with the delayed perfusion filling of retina and optic nerve, and OCT implied the atrophic and confused structure of all retina layers.

Generally, cavernous sinus thrombosis (CST) is regarded as an infectious thrombophlebitis caused by regional infections, but may also present aseptically, predominantly occurring following surgery, pregnancy or trauma [9]. Several previous studies have reported the accidental occurrence of CST after various operations, including the prone-position spinal, dental and maxillofacial surgeries [[13], [14], [15]]. Due to the rarity and heterogeneity, the risk factor of postoperative CST has not been determined clearly. However, the postoperative vein thrombosis has been explored widely, and the common contributory factors described are mainly microvascular diseases and intraoperative hemodynamic compromise [16]. In our case, in terms of the patient's basic condition, there are multiple patient-specific risk factors for the development of venous thrombosis, such as advanced age, obesity, hypertension, hyperlipidemia and diabetes, which contributed to the endothelium impairment and blood stagnation [17]. Besides, the history of myocardial infarction and carotid atherosclerosis both represented hypercoagulable and thrombophilia state, leaving the patient susceptible to active thrombosis formation.

On the other hand, the spinal operation also played an essential role in thrombosis formation. Firstly, the patient lost about 600 mL of blood and 250 mL of urine, and his intraoperative fluid input was about 1800 mL of crystalloids. Wang et al. concluded that massive intraoperative bleeding was independently associated with the occurrence of postoperative venous thrombosis, especially when bleeding volume was more than 2000 mL [18]. The combination of excessive blood loss and large quantities of fluid administration led to the patient's unstable hemodynamic parameters, with the fluctuated intraoperative blood pressure ranged from 200/110 to 110/60 mmHg. Meanwhile, the resultant fluid vortex will bring with blood stasis, especially in the reticular and tortuous “cavernous” structure filled with venous blood. The vascular shear stress could also do damage to the vascular endothelium, thus leading to the coagulation cascade activation [19].

Secondly, four units of packed red blood cells were transfused during the operation. Katsios et al. demonstrated that transfusing red cell was an independent risk factor associated with the occurrence of postoperative venous thrombosis [20]. It was speculated that patients actually lost whole blood during the surgery, but for improving oxygenation and maintain hemoglobin, red blood cell suspension was generally infused, which was not a physiological state and thus increased the blood viscosity [20]. Moreover, PIOVELLA et al. demonstrated that the reduction of nitric oxide level in stored red blood cells led to vasoconstriction, and the increase of lactic acid promoted the release of inflammatory cytokines, which would affect coagulation system and enhance hypercoagulable state [19].

Thirdly, the patient held the prone position during surgery, which directly applied the pressure on the abdomen and obstructed the venous drainage. Prone position is another recognized risk factor for the venous thrombosis after spinal surgery [21]. Obstruction of venous return elevated the venous pressure and restricted the blood flow, which increased the blood viscosity and promoted thrombosis formation [8]. Meanwhile, Sun et al. compared the IOP changes among different surgical positions in non-ocular surgeries, and found that larger head-down angle was accompanied by higher intraoperative IOP [22]. Ripa et al. found that increases in IOP and subsequent risk for postoperative vision loss were strictly related to the intraoperative Trendelenburg position (25–45° head-down tilt) [23]. Head-down angle interfering with the surgical operation bed, would increase venous pressure in the head and face, causing the obstruction of venous return and resulting in the pressure increase in episcleral vein, leading to pressure increase in IOP [22,24]. Therefore, they proposed inadequate head position played an important role in postoperative blindness due to high intraocular pressure, which would lead to reduced blood perfusion of retina and optic nerve. This demonstrated that eye cushioning device, including bolster and pillow, and positioning frame like Wilson or Jackson frame, might be helpful to avoid direct ocular compression. Additionally, Kim et al. suggested that the prolonged operation time in spinal surgery was independently associated with the occurrence of thrombosis [25]. Sebastian et al. found that, there was a positive correlation between the incidence of postoperative thrombosis and the number of vertebral segments involved in the surgery [26]. Due to the involving of multiple vertebrae (L2 ∼ S1), the surgery in our case lasted for 150 min, which consequently resulted in prolonged anesthesia time and increased intraoperative bleeding. Moreover, with the prolonged incision exposure time and more traumatic damage, the long operation duration might have a disposition to the accumulation of inflammatory factors and activation of coagulation cascade, promoting the hypercoagulable state [26].

Generally, vision impairment in CST often occurred as a result of corneal ulcerations (secondary to loss of the corneal reflex), ophthalmic or central retinal artery occlusion, ischemic optic neuropathy and orbital congestion [27,28]. With the incidence of 8–15 %, the vision loss is actually less often a complication of CST [9]. We supposed that our patient's optic nerve might be more susceptible to the compression of orbital congestion and ischemia injury, contributing to the occurrence and worsening of this rare complication. On the one hand, the patient lost about 600 mL of blood and his intraoperative fluid input was about 1800 mL of crystalloids. Although the fluid volume was not large, colloids were lacking, which was a contributing factor for aggravating periorbital swelling and increasing orbital pressure. Moreover, intraoperative crystalloid overload and colloid shortage contributes to the perfusion pressure reduction of optic nerve and retina. On the other hand, a patient undergoing spinal surgery was accompanied by IOP rise on account of direct pressure on the globe, raised central venous pressure and prone positioning [8]. Raised IOP superimposed with intraoperative anemia and hypotension can lead to ischemia of the optic nerve and retina. Therefore, the patient in our case was more prone to the infarction of optic nerve and vision loss.

The overall visual outcome of POVL, in general, is very poor as a result of limited treatment options and unclear pathogenesis. By exploring the Scoliosis Research Society (SRS) Database, Jamal et al. revealed that merely less than half (47.6 %) of POVL cases could recovered completely, and the majority of whom were cortical blindness [29]. Patients suffering ION and CRAO usually experienced irreversible vision loss and poor visual prognosis [29]. In our case, owing to the simultaneous involving of retina and optic nerve, although given the timely combined treatments, the patient still received no remarkable improvement in her visual acuity.

Rarity of the condition as well as lack of definite clinical diagnosis may be responsible for inability to adequately treat this complication, so prevention might play a more important role than treatment. Measures such as detailed pre-operative assessment, fluids management, anemia correction, vasopressors utilizing, blood pressure stabilizing and optimization of surgery duration have been proposed by American Society of Anesthesiologists Task Force, to avoid perioperative blindness in patients undergoing spine surgery [2]. In addition, the proper patient positioning with a head-holder was recently recommended. Jamal et al. concluded that intraoperative head support and Trendelenburg head positioning were associated with complete resolution and better visual prognosis [29].

This study had some limitations. First, although the stenosis of cavernous sinus segment of ICA is regarded as an indirect sign for CST, no direct imaging evidence was obtained in our case to confirm whether CST was present. However, the diagnosis of CST was basically made on clinical grounds, and in this case, it was appropriately proved by combining the patient's complaint, ophthalmic signs and indirect radiological finding. Secondly, the patient was lost for long-term follow up after the treatment. No further MRI was performed for comparation to evaluate the development of thrombosis after the anticoagulation treatment. Another limitation is that the patient was not examined by FFA in a timely manner, which should be immediately performed. Although further FFA revealed attenuated retinal artery and pale optic disc, the best chance to confirm vessel occlusion was lost. However, despite the lack of the abovementioned examinations, the infraction of retina and optic papilla were confirmed by the fundus findings and optical coherence tomography results.

4 Conclusions

Our study firstly implied the possibility of cavernous sinus thrombosis in the development of POVL. The high-volume fluid replacement, unstable hemodynamic parameters, prone position and prolonged surgical duration might bring about microvascular diseases and hypercoagulable state, contributing to the occurrence of POVL together. Detailed assessment, fluids management, hemodynamic stabilizing and duration optimization were proposed for POVL prevention.

Authorship

All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.

Disclosures

The authors have nothing to disclose.

Ethical approval

The studies involving human participants were reviewed and approved by the Ethics Committee of Peking University Third Hospital, Beijing, China on 9 October 2022 (M2022563). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Funding

This project was supported by Talent Project Foundation of Peking University Third Hospital (BYSYZD2021044 ) and 10.13039/501100004826 Beijing Municipal Natural Science Foundation (7202229 ) from Beijing Municipal Science and Technology Commission.

Author contribution

All authors listed have made a substantial, direct, and intellectual contribution to the work and approved it for publication.

Guarantor

Yanjie Tian and Xuemin Li are the guarantors.

Research registration number

1. Name of the registry: our research is not ‘First in Man’ studies.

2. Unique identifying number or registration ID: our research is not ‘First in Man’ studies.

3. Hyperlink to your specific registration (must be publicly accessible and will be checked): our research is not ‘First in Man’ studie.

Conflict of interest statement

The authors have no conflicting interests to declare.
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