Asian Spine J Search

CLOSE


Asian Spine J > Volume 6(4); 2012 > Article
Goni, Tripathy, Goyal, Tamuk, Panda, and BK: Cortical Blindness Following Spinal Surgery: Very Rare Cause of Perioperative Vision Loss

Abstract

A 38-year-old man was operated with posterior spinal decompression and pedicle screw instrumentation for his L2 fracture with incomplete neurological deficit. In the recovery, he complained of blindness in both eyes after twelve hours. Computed tomographic scan and magnetic resonance angiography revealed bilateral occipital lobe infarcts. He remained permanently blind even after three years follow-up. Though rare, perioperative vision loss is a potential complication following spine surgery in prone position. We report a rare occurrence of cortical blindness following lumbar spine surgery.

Introduction

Vision loss is a very rare but devastating complication of nonocular surgeries, and reported incidence is 0.003% to 0.0008% in the general surgical population [1]. The risk of perioperative vision loss (POVL) has been commonly noted after cardiac and spinal surgeries. The incidence as reported in literature is 8.64/10,000 for cardiac surgeries and 3.09/10,000 for spinal fusions [2].
Most cases of perioperative vision loss following spine surgery are mentioned as case reports in literature [3-8]. The specific pathogenesis of POVL remains elusive in most cases, with much controversy surrounding patient and surgical risk factors. Important causes of POVL include ischemic optic neuropathy (ION), retinal vascular occlusion (RVO) and cortical blindness. Among these major causes, cortical blindness is the rarest cause of POVL [7-9]. Myers et al. [7] reported only three cases of cortical ischemia leading to blindness while reviewing 37 patients of POVL after spine surgery. Because of the rarity of occurrence and as most of the data are retrospective, it is difficult to establish definite cause-effect relationship for the cortical blindness. In this article we report a case of POVL secondary to cortical ischaemia in a 38-year-old man following lumbar spinal fusion without any predisposing factors for vaso-occlusive disease.

Case Report

A 38-year-old manual labourer was brought to the emergency after a high energy motor vehicle accident. He was hemodynamically stable at the time of admission. On primary and secondary survey a lumbar spine fracture possibility was suspected. Radiographic evaluation confirmed our diagnosis and X-ray showed fracture of the second lumbar vertebra (Fig. 1A). Neurologically he had diminished power in both lower limbs (motor power of grade 3 or less around hip, knee and ankle joints). He had complete loss of bladder and bowel sensations, but no sensory impairment was elicited in the lower limbs.
His past medical history was not suggestive of any neurological problems, vision problems, diabetes, hypertension, coronary artery disease, deep vein thrombosis, peripheral vascular disease, collagen vascular disorder or previous chest or heart problems. He was a non smoker and a social drinker. His body mass index was 32.4.
Magnetic resonance imaging of the lumbar spine was performed to better delineate the severity of spinal cord injury and compression (Fig. 1B). He was operated after 72 hours of injury. Surgery was carried out with posterior decompression and fusion using pedicle screw instrumentation in the prone position under general anaesthesia (Fig. 2). Constant monitoring of the arterial blood pressure was performed during the surgery. Total duration of surgery was 105 minutes. Perioperative blood loss was 420 ml. Systolic blood pressure throughout the surgery was in the range of 90 to 110 mm Hg. The oxygen saturation as measured by pulse oxymeter was above 98% at all times. There was no other anaesthetic or surgical complication intraoperatively. In the recovery, patient complained of complete loss of vision after twelve hours. He was evaluated by an ophthalmologist, neurologist and a cardiologist. His ocular examination revealed complete bilateral loss of vision with preservation of papillary and corneal reflexes and normal ocular movements. Intraocular pressure and fundus examination were within normal limits. There was no new neurological deficit occurring after surgery and his cerebellar functions were intact. His postoperative haemoglobin was 10.6 g and he did not require any blood transfusion in the perioperative period.
The computed tomographic scan and magnetic resonance angiography of the brain revealed infarcts in bilateral occipital lobes (Fig. 3). Electrocardiography and echocardiography evaluation for underlying cardiac problem did not reveal any cardiac source of emboli. He was treated by the ophthalmologist, but no recovery in vision was observed even after three years follow-up.

Discussion

The article by Berg et al. [10] was surprising to the spine surgeons where they mentioned that the incidence of POVL following ocular surgeries is much lower than that seen in nonocular surgeries. Incidence estimates for POVL after nonocular surgery range from 0.013% for all surgeries up to 0.2% following spine surgery. Ischemic optic neuropathy is the most common cause of POVL accounting for more than 81%, followed by retinal artery thrombosis. Cortical blindness is the rarest cause of POVL with a handful of cases in the literature [11].
Work up of a patient with perioperative visual loss involves consideration of anatomy of the visual pathway. Anterior ischemic optic neuropathy and retinal vascular occlusion reveal remarkable changes on fundus examination, but no such changes are observed in posterior ischemic optic neuropathy (PION). The diagnosis in PION can be made by contrast enhancement seen in the optic nerve on ocular magnetic resonance imaging. Cortical blindness is diagnosed by looking for the ischemic changes in the occipital lobe on intracranial imaging. In our case, the diagnosis was made by cortical occipital changes seen on magnetic resonance imaging with the absence of fundoscopic examination findings.
Despite numerous efforts and explanations, pathogenesis of POVL is still elusive. Various aetiologies' such as fall in systemic blood pressure, anaemia, direct ocular compression, hypercoagulable states, embolism, increased venous pressure, prone positioning during surgery and increased cerebrospinal fluid pressure have been elucidated but none has proved so far [12-15]. Two important factors in cortical blindness are generalised cerebral hypoperfusion and embolism. It has been suggested that more than one factor may be working in any patient making this a multifactorial event [7,10]. Pathogenesis in cardiac surgery is relatively easy to explain. Embolisation may take place due to cardiac and great vessel manipulation, atrial or ventricular fibrillation [7]. The source of emboli in spinal surgery is difficult to explain. It is also unclear why this phenomenon is commoner in surgeries carried out in the prone position. Direct pressure on eye, raised intraocular pressure or vascular congestion does not explain cortical infarcts, but may explain other causes of vision loss such as ION and RVO. Intraoperative hypotension, hypoxia, blood loss and anaemia are contributory factors, but are not found in this patient. Further, they should classically affect the watershed areas of blood supply in the brain which innervate the proximal muscles of upper and lower limb. Also, it has been shown that the use of deliberate hypotensive anaesthesia during spine surgery does not increase chances of POVL [7]. Huber and Grob [8] suggested that abnormal posture of the neck when the patient is being positioned prone for surgery could be a contributory factor for reducing perfusion in the vertebra-basilar area manifesting as stroke. This is purely hypothetical thought and cannot be definitively proved. It has been recommended to keep the neck at the level of heart or above in a neutral forward position at the time of surgery to avoid chances of hypoperfusion due to vertebra-basilar compression. The bilateral infarction as in the present case does not support the hypothesis. Review of POVL following general surgeries include many procedure carried out in the lower limb in prone position [7,16]. Irrespective of the types of surgeries, the prone position itself is a predisposing factor for POVL. Shen et al. [2] found some important finding on perioperative visual loss following spinal surgeries. Incidences were higher for age less than 18 or more than 65 years, male gender, anaemia, and posterior approach. Many cases occur in patients who have no identified preoperative risk factors, although hypertension, smoking, diabetes, and vascular disease appear to lead to increased risk. None of these risk factors was present in this patient. He had no cardio-pulmonary comorbidities and he had no fluctuation in hemodynamic status in the perioperative period as well. Considering these situations, other than the prone position we could not find any predisposing condition in our case.
Most of patients with cortical blindness have a partial vision loss. They often have other associated symptoms such as cerebellar signs and other focal neurological deficits, depending upon the area of infarct. This patient had purely vision loss with no other deficit. There is no definite treatment for cortical blindness. No drugs including steroids have shown to reduce morbidity in these cases and most postoperative visual deficits do not show significant improvement with time. There is a hope of some improvement in initial months, but once the window time period has passed there is no hope of any further improvement.
This case report warns the spine surgeon about such fatal complication following spine surgery in prone position. Extreme cautions at every step should be taken to prevent the development of perioperative visual loss. Despite these precautions, some cases may still land up with visual loss and the patient should be explained about the grievous situation well before the surgical procedure.

References

1. Warner ME, Warner MA, Garrity JA, MacKenzie RA, Warner DO. The frequency of perioperative vision loss. Anesth Analg 2001 93:1417–1421. PMID: 11726416.
crossref pmid
2. Shen Y, Drum M, Roth S. The prevalence of perioperative visual loss in the United States: a 10-year study from 1996 to 2005 of spinal, orthopedic, cardiac, and general surgery. Anesth Analg 2009 109:1534–1545. PMID: 19713263.
crossref pmid
3. Grossman W, Ward WT. Central retinal artery occlusion after scoliosis surgery with a horseshoe headrest. Case report and literature review. Spine (Phila Pa 1976) 1993 18:1226–1228. PMID: 8362331.
crossref pmid
4. Hoski JJ, Eismont FJ, Green BA. Blindness as a complication of intraoperative positioning. A case report. J Bone Joint Surg Am 1993 75:1231–1232. PMID: 8354684.
crossref pmid
5. Katzman SS, Moschonas CG, Dzioba RB. Amaurosis secondary to massive blood loss after lumbar spine surgery. Spine (Phila Pa 1976) 1994 19:468–469. PMID: 8178240.
crossref pmid
6. Lee AG. Ischemic optic neuropathy following lumbar spine surgery: case report. J Neurosurg 1995 83:348–349. PMID: 7616283.
crossref pmid
7. Myers MA, Hamilton SR, Bogosian AJ, Smith CH, Wagner TA. Visual loss as a complication of spine surgery: a review of 37 cases. Spine (Phila Pa 1976) 1997 22:1325–1329. PMID: 9201835.
crossref pmid
8. Huber JF, Grob D. Bilateral cortical blindness after lumbar spine surgery: a case report. Spine (Phila Pa 1976) 1998 23:1807–1809. PMID: 9728383.
crossref pmid
9. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008 145:604–610. PMID: 18358851.
crossref pmid pmc
10. Berg KT, Harrison AR, Lee MS. Perioperative visual loss in ocular and nonocular surgery. Clin Ophthalmol 2010 4:531–546. PMID: 20596508.
pmid pmc
11. Kamming D, Clarke S. Postoperative visual loss following prone spinal surgery. Br J Anaesth 2005 95:257–260. PMID: 15951324.
crossref pmid
12. Remigio D, Wertenbaker C. Post-operative bilateral vision loss. Surv Ophthalmol 2000 44:426–432. PMID: 10734242.
crossref pmid
13. Stevens WR, Glazer PA, Kelley SD, Lietman TM, Bradford DS. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976) 1997 22:1319–1324. PMID: 9201834.
crossref pmid
14. Stambough JL, Dolan D, Werner R, Godfrey E. Ophthalmologic complications associated with prone positioning in spine surgery. J Am Acad Orthop Surg 2007 15:156–165. PMID: 17341672.
crossref pmid
15. Roth S. Perioperative visual loss: what do we know, what can we do? Br J Anaesth 2009 103:i31–i40. PMID: 20007988.
crossref pmid pmc
16. Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995 80:1018–1029. PMID: 7726399.
pmid
Fig. 1
Radiograph (A) and magnetic resonance imaging (B) of the lumbar spine showing fracture of the L2 vertebra (arrow).
asj-6-287-g001
Fig. 2
Radiogarphs (antero-posterior and lateral views) after posterior spinal decompression and pedicle screw fixation for L2 vertebra fracture.
asj-6-287-g002
Fig. 3
Magnetic resonance angiography of brain reveals bilateral infarction of occipital lobe.
asj-6-287-g003
TOOLS
Share :
Facebook Twitter Linked In Google+ Line it
METRICS Graph View
  • 7 Crossref
  • 6 Scopus
  • 241 View
  • 5 Download
Related articles in ASJ


ABOUT
ARTICLE CATEGORY

Browse all articles >

BROWSE ARTICLES
EDITORIAL POLICY
FOR CONTRIBUTORS
Editorial Office
Department of Orthopedic Surgery, Uijeongbu St. Mary’s Hospital, College of Medicine, The Catholic University of Korea,
271 Cheonbo-ro, Uijeongbu 11765, Korea
Tel: +82-31-820-3578    Fax: +82-31-847-3671    E-mail: spinepjb@catholic.ac.kr                

Copyright © 2019 by Korean Society of Spine Surgery. All rights reserved.

Developed in M2community

Close layer
prev next