Cortical blindness after percutaneous vertebroplasty: a case report and comprehensive review of the literature

ABSTRACT Objective Many complications but cortical blindness after percutaneous vertebroplasty has been rarely reported. Here, we describe a case who developed cortical blindness after percutaneous vertebroplasty. We also reviewed the literature to find the possible causes of this complication and its treatment. Methods Case report and literature review. Results A 71-year-old woman experienced cortical blindness after percutaneous vertebroplast. She developed dizziness, nausea, sweating, blood pressure changes, and vision loss during the procedure. MRI confirmed bilateral cerebral infarctions. The patient recovered with conservative treatment. Conclusions Percutaneous vertebroplasty, though helpful, carries a rare risk of cortical blindness. Surgeon awareness is crucial for informing patients of this potential complication.


Introduction
Percutaneous vertebroplasty has been widely used for treating osteoporotic vertebral compression fractures, vertebral tumors (Diamond et al., 2006), Kummell's disease, etc.In this surgical procedure, bone cement is injected into the vertebral body to increase its stability through a minimally invasive puncture method.The main complications of percutaneous vertebroplasty are pedicle and rib fractures (Evans et al., 2003), infection (Walker et al., 2004), pulmonary embolism (Syed et al., 2006), nerve injury and spinal cord compression due to thermal damage and cement leakage (Garfin & Reilley, 2002), thrombotic embolism in the inferior vena cava and bilateral iliac veins (Hu et al., 2021), total spinal anesthesia (Wang et al., 2022).Postoperative visual loss (POVL), however, has been rarely reported.POVL was first reported by Slocum (SLOCUM et al., 1948) in 1948.It can occur after spinal, cardiac, head, or neck surgery.Surgeons are not yet fully familiar with this complication.A previous study (Shen et al., 2009) reported that the incidence of POVL after nonophthalmic procedures was 0.0008-0.0030%,but the incidence was 0.2% after spinal surgery.This complication can be attributed to several factors, including intraoperative massive hemorrhage, hypotension, ocular compression, prone position surgery, and long operation time.However, there is currently no consensus regarding its underlying cause and mechanism.

Case report
A 71-year-old female visited our hospital with a complaint of low back pain caused by a sprain about 2 weeks ago.She did not have a history of hypertension or diabetes.Physical examination revealed the following findings: blood pressure: 125/78 mm Hg; heart rate: 72 bpm; normal vision in both eyes; pain with limitation of the lumbar motion; apparent tenderness and percussion pain of the L1-L5 spinous processes, particularly L1, L4, and L5; normal sensation and movement of limbs; normal physiological reflex; and no pathological reflex.The patient showed normal results for blood and urine routine tests, liver and kidney function tests, blood lipid level, and electrocardiography (ECG).The D-dimer level was 2.164 mg/L.X-ray (Figure 1a) showed multisegmental compression of the spinal cord, and MRI (Figure 1b) revealed multiple vertebral compression fractures at the L1, L4, and L5 spinous processes.
The patient was scheduled to undergo percutaneous vertebroplasty on the following day.After inducing local anesthesia, puncture channels were established at both sides of lumbar vertebrae L1, the right side of lumbar vertebrae L4, and the left side of lumbar vertebrae L5.The bone cement was injected into the vertebral body at 4 min after preparation; 3 mL bone cement was injected into the L1 vertebral body, and 4 mL bone cement was injected into the L4 and L5 vertebral bodies (Figure 1c, d).Approximately 5 min after the injection, the patient complained of dizziness, nausea, and sweating.Intraoperative findings were as follows: blood pressure: 90/60 mm Hg, heart rate: 110 bpm, blood oxygen saturation level: 94%.After receiving intensive fluid infusion and oxygen inhalation, the patient's blood pressure increased to 110/70 mm Hg, and her blood oxygen saturation level increased to 97%.A decision was made to terminate the surgical procedure, which lasted for approximately 1 h.After the operation, the patient reported that her low back pain had significantly alleviated.However, she expressed feeling dizzy and was hesitant to open her eyes.
After the patient returned to the ward, she complained of binocular vision loss and right upper limb weakness.Physicians in the ophthalmology and neurology departments were immediately consulted.In the ophthalmic examination, the patient's uncorrected visual acuity was 20/20, indicating only light perception.However, there was no evidence of hyperemia or edema of the conjunctiva, and the cornea was transparent.The intraocular pressure was normal, and the pupillary light reflex was intact.Bilateral fundus examination showed no abnormality (Figure 2f, g).Physical examination revealed the following findings: blood pressure: 125/70 mm Hg, heart rate: 95 bpm, blood oxygen saturation level: 99%.The right shoulder and elbow joint exhibited a passive range of motion.The right wrist and finger extensor muscle strength was Grade 0, the elbow flexor muscle strength was Grade 1, and the sensation level of the extremities was normal.An enhanced MRI scan of the head (Figure 3i, j) revealed cerebral infarction in the bilateral frontal-parietal-occipital lobe.Orbital MRI showed no abnormality (Figure 3h).Cerebral computed tomography angiography (Figure 2e) showed calcified plaques in the intracranial segment of the internal carotid artery.The patient received a combination of medications, including methylprednisolone (80 mg/qd), edaravone (10 mg/qd), butylphthalide sodium chloride qd injection (25 mg/qd), urinary kallidinogenase (0.15PNA/qd), and mecobalamin (0.5 mg/qd), for treating her health condition.
On postoperative day 3, the patient's visual acuity was largely restored, and the patient exhibited Grade 1 extensor muscle strength in her right wrist and right finger dorsum and Grade 3 elbow flexor muscle strength.The rehabilitation department then performed bedside rehabilitation treatment for the patient.Re-examination of the patient's head by MRI 1 week after the operation revealed no significant abnormalities.The patient's vision and muscle strength of the right hand had completely recovered, and the patient was discharged from the hospital.

Discussion
Currently, the cause of POVL is not fully understood.The development of POVL may be attributed to the following factors: (1) central retinal artery occlusion (Nickels et al., 2014); (2) ischemic optic neuropathy; (3) cortical blindness (Gupta et al., 2013); (4) eyeball compression; and (5) posterior reversible encephalopathy syndrome.Cortical blindness is a rare type of POVL (Nickels et al., 2014).Cortical blindness after spinal surgery has been rarely reported; however, it is known to occur after cerebral arteriography, with an incidence of 0.1-0.3%(Newman et al., 2011).Cortical blindness is a central visual dysfunction resulting from vasospasm ischemia-or toxin-induced damage to the  (5) normal retinal structure in fundus examination; and (6) presence of aphasia, hemiplegia, hemiparesthesia, and other positioning signs.The clinical manifestations of our patient were consistent with those of cortical blindness.
Cortical blindness may occur due the following conditions: (1) vertebrobasilar artery thrombosis; (2) reversible posterior leukoencephalopathy syndrome; (3) toxic encephalopathy; (4) brain metastases; and (5) traumatic encephalopathy.Vertebrobasilar thrombosis is the most common cause of acute cortical blindness (Savitz & Caplan, 2005).The vertebrobasilar circulation plays a crucial role in supplying blood to the visual cortex.Binocular visual loss can occur following the development of lesions in the bilateral temporal, parietal, and occipital lobes.This is mainly caused by stenosis or arteriosclerosis of the vertebrobasilar artery, resulting in low perfusion.Fortunately, most of these injuries are reversible, and following the development of collateral circulation in the parieto-occipital junction region, visual acuity can be partially or completely restored.Niimi analyzed four patients with cortical blindness probably related to vasospasm during the surgery.After symptomatic treatment, the four patients showed good prognosis (Niimi et al., 2008).Arterial emboli in the posterior circulation can lead to bilateral ischemic infarction of the visual cortex and visual loss.Marden FA reported a case of death due to the failure of thrombectomy in a patient who underwent vertebroplasty that resulted in bone cement embolism of the left cerebral artery (Marden & Putman, 2008).During the surgery, the patient experienced a temporary decrease in blood pressure.Postoperative arterial CTA did not reveal any apparent formation of an embolus.Therefore, we concluded that cerebral infarction was likely caused by transient vasospasm that occurred during the surgery.
Intraoperative hypotension is closely related to the occurrence of cortical blindness (Goyal et al., 2019).Therefore, intraoperative monitoring of blood pressure and maintenance of fluid balance are extremely important.Presently, a decrease in intraoperative blood pressure is considered to be caused by the following risk factors: (1) Bone cement implantation syndrome: The main manifestations of this syndrome are hypoxemia, hypotension, or sudden loss of consciousness after bone cement implantation (Donaldson et al., 2009).Huang Chengjun et al. reported that two patients who underwent percutaneous vertebroplasty experienced sudden disturbances of consciousness and a decrease in blood pressure following the injection of bone cement.The surgical procedure was immediately halted, and the patients received timely symptomatic treatment, which restored consciousness and blood pressure levels.Follow-up examinations revealed no clinical symptoms or sequelae (Chenjun & Fuyu, 2007); (2) Use of muscle relaxants: Muscle relaxants are commonly administered during spinal surgery.However, it should be noted that these drugs can trigger histamine release, which may subsequently cause hemodynamic changes, arrhythmia, and a reduction in blood pressure; (3) Hypotension due to prone positioning: Improper placement of a cushion can frequently lead to mechanical compression of the chest, resulting in insufficient cardiac output.Additionally, when a patient is in the prone position, blood is more likely to accumulate in the vessels below the heart plane because of gravity, which can decrease blood pressure; and (4) Blood loss: excessive intraoperative blood loss may lead to a decrease in blood pressure; in our present case, the intraoperative blood loss was minimized through local anesthesia.However, a temporary reduction in intraoperative blood pressure was observed following bone cement injection.This phenomenon strongly suggests the presence of bone cement implantation syndrome.
Presently, for postoperative cortical blindness, there is no single treatment method that encompasses the main principles involving expansion of cerebral blood vessels, reduction of cerebral edema, expansion of volume, hormone supplementation, and nerve enrichment.The commonly used drugs for treating patients with postoperative cortical blindness include nimodipine, mannitol, methylprednisolone, mecobalamin, etc.In a previous study, patients with transient cortical blindness experienced a gradual recovery of their visual acuity over a period of 4 days.The visual acuity and symptoms of most patients recovered within 1 month.Some researchers have suggested that cortical blindness is a benign and self-healing process that does not require special treatment (Li et al., 2019).

Conclusions
Cortical blindness is a rapidly occurring and rare complication of percutaneous vertebroplasty, and it can have psychological effects on patients.To minimize the risk of this complication during the surgery, the following preventive measures should be adopted: (1) preoperative prediction of the likelihood of this complications can help reduce patient anxiety post-surgery; (2) during the intraoperative bone cement injection process, it is important to administer the cement slowly while closely monitoring patient's blood pressure to prevent the occurrence of bone cement implantation syndrome; and (3) We should pay more attention to the decline of postoperative vision of patients.For patients experiencing visual loss after percutaneous vertebroplasty, the etiology should be identified as soon as possible, and treatment should be initiated at the earliest.Most patients with postoperative acute cortical blindness can achieve good results; however, because of the limited number of cases, many deficiencies need to be resolved through further in-depth studies.

Figure 1 .
Figure 1.a, b: preoperative X-ray and MRI showed multiple compression fractures of the lumbar vertebrae L1, L4, and L5; c, d: review of the lumbar vertebrae after percutaneous vertebroplasty.

Figure 2 .
Figure 2. e: cerebral CTA showed calcified plaques in the intracranial segment of the internal carotid artery; f and g: bilateral fundus examination showed no abnormality.

Figure 3 .
Figure 3. h: orbital MRI showed normal results; i and j: enhanced MRI of the head showed cerebral infarction in the bilateral frontal-parietal-occipital lobe.