Abstract

Background:Postoperative visual loss (POVL) following prone spine surgery occurs in from 0.013% to 1% of cases and is variously attributed to ischemic optic neuropathy (ION: anterior ION or posterior ION [reported in 1.9/10,000 cases: constitutes 89% of all POVL cases], central retinal artery occlusion [CRAO], central retinal vein occlusion [CRVO], cortical blindness [CB], direct compression [horseshoe, prone pillows, and eye protectors Dupaco Opti-Gard]), and acute angle closure glaucoma (AACG).

Methods:Risk factors for ION include prolonged operative times, long-segment spinal instrumentation, anemia, intraoperative hypotension, diabetes, obesity, male sex, using the Wilson frame, microvascular pathology, decreased the percent of colloid administration, and extensive intraoperative blood loss. Risk factors for CRAO more typically include improper positioning during the surgery (e.g., cervical rotation), while those for CB included prone positioning and obesity.

Results:POVL may be avoided by greater utilization of crystalloids versus colloids, administration of α-2 agonists (e.g., decreases intraocular pressure), avoidance of catecholamines (e.g., avoid vasoconstrictors), avoiding intraoperative hypotension, and averting anemia. Patients with glaucoma or glaucoma suspects may undergo preoperative evaluation by ophthalmologists to determine whether they require prophylactic treatment prior to prone spinal surgery and whether and if prophylactic treatment is warranted.

Conclusions:The best way to avoid POVL is to recognize its multiple etiologies and limit the various risk factors that contribute to this devastating complication of prone spinal surgery. Furthermore, routinely utilizing a 3-pin head holder will completely avoid ophthalmic compression, while maintaining the neck in a neutral posture, largely avoiding the risk of jugular vein and/or carotid artery compromise and thus avoiding increasing IOP.

Keywords: Blindness, central retinal artery occlusion, cortical blindness, eye diseases, glaucoma, ischemic optic neuropathy, prone position, spinal surgery, visual loss

INTRODUCTION

Postoperative visual loss (POVL) following prone spine surgery occurs in from 0.013% to 1% of cases, and the most frequently quoted risk is 0.2% [Tables 1 – 4 ].[ 14 40 ] POVL is variously attributed to ischemic optic neuropathy (ION: Anterior ION [AION] or posterior ION [PION reported in 1.9/10,000 cases: constitutes 89% of all POVL cases]), central retinal artery occlusion [CRAO], central retinal vein occlusion [CRVO], cortical blindness [CB], direct compression [horseshoe, prone pillows, and eye protectors Dupaco Opti-Gard]), acute angle closure glaucoma (AACG), rarely epidural spine injections, and occasional other factors (e.g., right-left atrial shunt with microvascular embolization).

Table 1

Case studies: Summary literature of blindness with spine surgery

Table 2

Case series: Summary literature of blindness with spine surgery

Table 3

Review articles: Summary of literature of blindness with spine surgery

Table 4

Summary of articles

The preoperative recognition of risk factors may protect against the development of POVL. The multiple factors contributing to ION may include; prolonged operative times, long-segment spinal instrumentation, anemia, intraoperative hypotension, diabetes, obesity, male sex, the Wilson frame, greater estimated blood loss (EBL), microvascular pathology, and decreased percent colloid administration. Risk factors for CRAO typically include improper positioning during the surgery (e.g., cervical rotation), while those for CB included prone positioning and obesity.

Limiting the risk of POVL may warrant greater utilization of crystalloids versus colloids, administration of α-2 agonists (e.g., decreases intraocular pressure [IOP]), avoidance of catecholamines (e.g., avoid vasoconstrictors), and avoiding excessive intraoperative blood loss/anemia, hypotension, and hypovolemia. Patients at risk for AACG may undergo preoperative ophthalmologic evaluation and prophylactic treatment where indicated. Most critically, routinely utilizing a 3-pin head holder for prone positioning completely avoids ophthalmic compression, and maintains the neck in a neutral posture, avoiding the potential for jugular venous congestion or carotid artery occlusion/embolization/compromise.

SUMMARY OF CASE STUDIES OF POSTOPERATIVE VISUAL LOSS

Of the 21 single case studies reviewed, the etiology of the POVL included: AACG (three patients), ION (three patients) CB (three patients), CRAO (four patients), ischemic orbital compartment syndrome/compression (one patients), CRA branch occlusion (one patient), or general POVL/unspecified etiology (six patients) [Tables 1 and 4 ].[ 1 4 9 10 12 14 15 16 18 21 23 26 29 30 31 34 36 37 39 40 ] They variously cited a 0.28–0.2% versus 0.01–1% frequency of POVL following prone surgery, most commonly noting that hypotension was the major contributor.[ 14 40 ] However, other risk factors for POVL included; prolonged spine surgery, extensive instrumentation, increased intraoperative blood loss, anemia, cancer, use of catecholamines or nefopam, patent foramen ovale (right to left shunt), use of a prone view pillow, and application of Dupaco Opti-Gard eye goggles.

Acute angle closure glaucoma after lumbar spine surgery

Five days following lumbar surgery performed in the prone position, Stewart et al. (2016) presented a patient who developed AACG due to an acute increase in IOP that had occurred intraoperatively [Tables 1 and 4 ].[ 36 ] POVL with prone spinal surgery was usually attributed to ION although prior cases of bilateral AACG had rarely been reported. The authors noted how critical it was to recognize postoperative AACG and to immediately treat it with laser iridotomy. They recommended targeted preoperative screening and treatment for those with significant risk factors for AACG with prone spinal surgery.

Postoperative visual loss in prone orthopedic spine surgery

Pin-On and Boonsri in 2015 reported on a patient with POVL due to ION occurring during prone spinal surgery [Tables 1 and 4 ].[ 29 ] They reviewed the pathophysiology and risk factors predisposing to POVL/ION as described by the American Association of Anesthesiology task force.

Cortical blindness following posterior lumbar decompression fusion

Agarwal et al. in 2014 noted that a 60-year-old paraparetic female developed POVL following an L2–L4 laminectomy for partial resection of a metastatic adenocarcinoma [Tables 1 and 4 ].[ 1 ] Intraoperatively, the patient had become severely anemic, and the resultant severe intraoperative hypotension had led to bilateral occipital lobe infarcts (posterior cerebral artery thromboembolism) leading to permanent cortical blindness.

Transient cortical blindness attributed to posterior spinal surgery in a child

Nathan et al. in 2013 noted the multiple factors that contribute to POVL following prone spine surgery; these vary from direct ocular ischemia (compression/venous occlusion) to CRAO, ION, or occipital cortical ischemia (infarction) [ Table 1 ].[ 23 ] They presented an 11-year-old female who developed transient CB following posterior spinal fusion for scoliosis performed under hypotensive anesthesia.

Unilateral visual loss after excision of an extradural hematoma in the prone position

Ooi et al. in 2013 presented a patient who developed blindness attributed to CRAO following excision of an epidural spinal hematoma performed in the prone position [Tables 1 and 4 ].[ 26 ] This deficit was attributed to poor positioning of the head, leading to direct mechanical compression of the eyes. They recommended that future precautions be taken to provide adequate eye protection when patients undergo prone spinal surgery. This should include using a 3-pin head holder to eliminate focal mechanical eye compression while also limiting the potential for carotid or jugular compromise (e.g., avoid rotation).

Cortical blindness following spinal surgery

In Goni et al. study in 2012, a 38-year-old male undergoing a laminectomy with pedicle screw instrumentation for an L2 fracture developed bilateral CB attributed to occipital lobe infarcts (computed tomography and magnetic resonance confirmed) within 12 h of surgery [Tables 1 and 4 ].[ 10 ] The patient was followed for 3 postoperative years, during which time the deficit remained permanent and irreversible.

Transient bilateral postoperative visual loss following spinal surgery

Quraishi et al. in 2012 reviewed the general incidence and etiology of POVL following prone spinal surgery while also presenting one case of bilateral POVL that resolved within 48 postoperative hours [Tables 1 and 4 ].[ 30 ]

Bilateral angle closure glaucoma after general anesthesia

Gayat et al. in 2011 discussed a patient who developed POVL attributed to bilateral postoperative AACG following prone cervical spine surgery [Tables 1 and 4 ].[ 9 ] AACG was variously attributed to the use of ephedrine, nefopam, and/or the prone surgical position.

Amaurosis after prone spine surgery

Zimmerer et al. in 2011 discussed the 0.028–0.2% frequency of POVL following prone spine surgery [Tables 1 and 4 ].[ 40 ] They noted two major risk factors prolonged procedures and the performance of complex spinal fusions They presented 73-year-old male who developed POVL following prone surgery for a lumbar disc herniation. His comorbid factors included hypertension (HTN), arterial sclerosis, diabetes, elevated blood lipids, and a history of prostate cancer. Intraoperatively, the patient had developed acute hypotension treated with catecholamines and using the Trendelenburg positioning; 3 h later, he developed POVL in the right eye (e.g., complete amaurosis).

Persistent cortical blindness after a thoracic epidural test dose of bupivacaine

Visser et al. in 2010 observed that following administration of a test dose of bupivacaine for thoracic epidural anesthesia (e.g., administered through an epidural catheter) in a patient about to undergo lung surgery, the patient developed persistent CB [Tables 1 and 4 ].[ 37 ]

Acute visual loss after prone spinal surgery

Hoff et al. in 2010 reported acute left-eye ION in a 56-year-old male undergoing prone cervical spine surgery [Tables 1 and 4 ].[ 12 ] At 6 postoperative weeks, there was only partial recovery; at 6 postoperative months, the ocular coherence tomography showed a marked reduction of the “retinal nerve fiber layer thickness around the optic nerve head.” The authors emphasized the preventive steps that may be taken during prone spinal surgery to avoid ION.

Bilateral acute angle closure glaucoma as a complication of facedown spine surgery

Singer and Salim in 2010 reported that prone spine surgery increased IOP “in individuals susceptible to AACG” [Tables 1 and 4 ].[ 34 ] They noted that ophthalmologists could perform provocative “prone tests” to determine whether glaucoma patients were at increased risk for AACG. The authors presented a 68-year-old Caucasian female who developed bilateral AACG while undergoing a multilevel lumbar decompression with fusion; postoperatively, she required bilateral laser iridotomies. The authors emphasized that ophthalmologists prior to prone spine surgery could screen patients with glaucoma or others at risk for AACG.

Ischemic orbital compartment syndrome after prone spinal surgery

Yu et al. in 2008 presented a patient undergoing prone spine surgery who developed “ischemic orbital compartment syndrome (e.g., due to compression)” warranting urgent intervention [Tables 1 and 4 ].[ 39 ] Unfortunately, 3 months later, the patients remained blind.

Unilateral postoperative visual loss due to the central retinal artery occlusion following prone cervical spine surgery

Nakra et al. in 2007 reported a patient who developed unilateral POVL due to CRAO following prolonged spine surgery performed in the prone position [Tables 1 and 4 ].[ 21 ]

Visual loss after prone spine surgery in patient using a foam headrest and eye goggles

Roth et al. 2007 described a patient who developed CRAO following prone spine surgery utilizing a foam headrest and goggles to protect the eyes (the Dupaco Opti-Gard) [Tables 1 and 4 ].[ 31 ] Together the two devices resulted in direct eye compression; the increase in IOP resulted in CRAO/irreversible blindness. This report highlighted the need to avoid both of these devices. Notably, these risks may be completely avoided using a 3-pin head holder for head immobilization in the prone position.

Prone spinal surgery leads to central retinal retinal artery occlusion and unilateral visual loss

Chung and Son in 2006 reported on a 60-year-old male who developed CRAO after prone spine surgery [Tables 1 and 4 ].[ 4 ] Postoperative medical treatment did not resolve his unilateral blindness. The authors emphasized that prolonged prone spinal surgery may contribute to sufficient mechanical eye compression to result in CRAO.

Monocular blindness due to prone cervical spine surgery

Kasodekar and Chen in 2006 documented a 0.05–1% risk of POVL with cardiac or prone spine (including prone cervical spine) surgery [Tables 1 and 4 ].[ 15 ] The authors presented a 62-year-old male with cervical myelopathy who following a C3–C6 laminectomy with lateral mass plating, developed unilateral blindness (POVL: Right eye).

Postoperative visual loss following prone spinal surgery

Kamming and Clarke in 2005 identified the incidence of POVL during nonocular surgery as ranging from 0.01% to 1% [Tables 1 and 4 ].[ 14 ] They also presented a patient who following a lengthy, prone spine operation was blind in one eye. The authors discussed the multiple etiologies of POVL following prone spine surgery and also discussed methods for avoiding this complication.

Visual field defect/postoperative visual loss after posterior spine fusion

Katz and Karlin in 2005 reviewed the literature and presented a case in which POVL followed prone scoliosis surgery [Tables 1 and 4 ].[ 16 ] This patient had a right-to-left atrial shunt responsible for a paradoxical micro-embolus that resulted in branch CRAO (quadrant defect). The authors reviewed this and multiple other etiologies of POVL occurring during prone spine surgery; they included ophthalmic compression, hypotension, excessive blood loss, and anemia.

Blindness and rectus muscle damage following prone spinal surgery

Kumar et al. in 2004 discussed a 16-year-old female who following prone surgery for scoliosis, developed ocular compression responsible for both POVL and rectus muscle damage [Tables 1 and 4 ].[ 18 ] The loss of vision in the right eye was attributed to direct “compression of the globe against the medial wall of the orbit;” this resulted in retinal/optic nerve ischemia, with a permanent loss of vision."

CASE SERIES AND LITERATURE REVIEW

The five case series involving between 2 and 55 patients per study, and recounted the multiple etiologies of POVL attributed to prone spine surgery [Tables 2 and 4 ].[ 5 7 13 17 20 ] In three series, the etiology of POVL included posterior reversible encephalopathy syndrome (PRES: 2 patients), ION (55 patients), and CRAO (17 patients).[ 5 7 17 ] In the fourth study, POVL was due to ION alone (six patients), while in the fifth study, there were multiple etiologies of POVL: ION (19 patients), CRAO (three patients), and CB (five patients).[ 13 20 ] Risk factors for POVL attributed to prone spinal surgery included; prolonged instrumented spinal fusions, improper positioning (e.g., compressive complications of the eyes, jugular vein, and carotids), anemia, hypotension, and transfusions. Remedies included rapid reversal of anemia, hypotension, and hypovolemia. In addition, Emery et al. study recommended elevating the head 10° to decrease intraoperative IOP during prone procedures.[ 7 ] Furthermore, placement of a 3-pin head holder would avoid direct pressure on the eyes, along with jugular/carotid compression (avoid neck rotation).

Temporary postoperative visual loss/posterior reversible encephalopathy syndrome following spinal deformity surgery

Kueper et al. in 2015 evaluated two patients presenting with PRES contributing to temporary POVL following prone spinal deformity surgery [Tables 2 and 4 ].[ 17 ] A 78-year-old female underwent a posterior T10 to pelvis fusion with transpsoas lumbar interbody fusion (L1–L4); on postoperative day 7, she developed confusion and bilateral visual loss. A second 51-year-old female following a posterior T3 to pelvis fusion with interbody L4–S1 (fusions; presacral interbody) device placement also developed bilateral POVL on postoperative day 15. Fortunately, both patients fully recovered after successful medical management of PRES (e.g. treatment of hypokalemia and HTN). Notably, avoiding such extensive instrumented fusions, particularly in older patients (e.g., the 78-year-old), would have eliminated this complication entirely.

Effect of head position on intraocular pressure during lumbar spine fusion

Emery et al. in 2015 noted that ION resulted from decreased perfusion attributed to increased IOP and/or hypotension occurring during prone spinal surgery [Tables 2 and 4 ].[ 7 ] In this randomized prospective trial, the authors studied the impact on IOP of elevating the head of bed 10 degrees in 55 patients (ages 18–80) undergoing prone lumbar fusions; results were compared with comparable control patients whose heads were positioned neutral/parallel to the ground. The multiple variables studied included; IOP, blood pressure, PCO₂, and changes in IOP. Elevating the head significantly lowered the mean IOP, improved optic nerve perfusion, and reduced the risk of perioperative blindness.

Postoperative visual loss following lumbar spine surgery: A review of risk factors by diagnosis

Li et al. in 2015 also noted that POVL rarely occurs following lumbar spine surgery performed in the prone position [Tables 2 and 4 ].[ 20 ] They evaluated the multiple perioperative risk factors likely contributing to the three main types of POVL; ION (19 cases), CRAO (three cases), and CB (five cases). Utilizing PubMed and Google literature searches, they identified the following risk factors in four large-scale studies; prolonged operative times, anemia, hypotension, and blood transfusion. Risks factors for CRAO mostly included improper positioning, while those for CB included both prone positioning and obesity. Notably, different types of POVL could be largely avoided through the routine use of an arterial line (e.g., avoidance of intraoperative hypotension/anemia/hypovolemia), and the 3-pin head holder (e.g. avoid direct eye compresssion and cervical spine rotation).

Visual loss after orthopedic procedures

Kaeser and Borruat in 2011 discussed six patients who developed ION (five of six cases bilateral blindness) following various orthopedic procedures (joint/fracture surgery); for some patients, deficits only partially recovered [Tables 2 and 4 ].[ 13 ] The authors emphasized the importance of rapidly diagnosing ION and its immediate treatment. Risk factors for ION included; intraoperative anemia, systemic hypotension, or hypovolemia.

Spinal surgery and ophthalmic complications: A review of 17 cases

Delattre et al. in 2007 noted that in 13 of 15 case reports, POVL due to prone spine surgery were due to ophthalmic compression [Tables 2 and 4 ].[ 17 ] However, in four review articles involving 66 cases of POVL following prone spine surgery, only 10 cited compression as the cause. Here, the authors utilized a 2-page survey of 28 French spine orthopedic centers asking about their incidence of POVL with prone spine surgery. They identified the following preoperative risk factors; “eyelid/conjunctival edema, periorbital numbness, or paresthesias;” intraoperative risks largely included head position. The etiology of 13 of 17 cases of POVL included ocular compression (nine cases-unilateral blindness due to CRAO), and internal carotid thromboembolism (four cases-head rotation toward the ipsilateral side leading to ION). The authors suggested modifying the horseshoe headrest and avoiding lateral rotation of the head, especially in patients with known carotid atheromata as this would effectively reduce/eliminate POVL. Rather than using a headrest at all, I would recommend using a 3-pin head holder; it completely eliminates all eye compression, and maintains the neck in a neutral posture.

REVIEW ARTICLES ON POSTOPERATIVE VISUAL LOSS WITH PRONE SPINE SURGERY

The 15 review articles from 2004 to 2015 cited the various types of POVL; ION (AION/PION), CRAO (including CRA-branch occlusion), CRVO, AACG, and CB (occipital lobe infarcts) [Tables 3 and 4 ]. The etiologies of POVL included direct compression (head rest/eye goggles), hypotension, excessive blood loss, anemia, glaucoma, HTN, use of catecholamines/ephedrine during surgery, prolonged prone spine surgery/deformity surgery, use of colloid rather than crystalloid fluid replacement intraoperatively, diabetes mellitus (DM), extensive use of instrumentation, obesity, history of multiple comorbidities, hypoxia, and male gender. Recommendations for avoiding POVL included; ophthalmological evaluation for patients with significant glaucoma histories, elevation of the head of the bed 10° to reduce IOP, avoidance of hypotension, hypovolemia, anemia, and greater use of colloids. In addition, the routine use of an arterial line would avoid hypotension/anemia/hypovolemia, while the 3-pin head holder would eliminate direct pressure on the eyes and avoid cervical rotation (e.g., jugular/carotid compression/manipulation).

Complications associated with prone positioning in elective spinal surgery

DePasse et al. in 2015 noted that POVL following prone spinal surgery was most frequently attributed to ischemia of the optic nerve, retina, or cerebral cortex, and rarely, AACG and amaurosis [Tables 3 and 4 ].[ 6 ] This article looked at ways in which spine surgeons could limit this complication.

Perioperative visual loss after spine surgery

Nickels et al. in 2014 evaluated POVL attributed to either prone spine or cardiac surgery [Tables 3 and 4 ].[ 25 ] The American Society of Anesthesiologists (ASA) POVL Registry noted that POVL following prone spine surgery was most commonly due to PION (e.g., comprised 89% of cases involving blindness). Other pathologies of POVL with prone spine surgery included retinal ischemia (CRAO, CRVO), CB, and PRES. Risk factors contributing to ION for patients undergoing prone spinal fusions included; “obesity, male sex, Wilson frame use, longer anesthetic duration, greater EBL, and decreased percent colloid administration.” Factors contributing to ION included; increased venous pressure/interstitial edema resulting in direct mechanical compression or venous infarction. As POVL is typically permanent/irreversible, it should be avoided by controlling the associated risks factors (e.g., greater utilization of crystalloids versus colloids) and α-2 agonists (e.g., decreases IOP).

Incidence and risk factors for perioperative visual loss after spinal fusion

Nandyala et al. in 2014 found that POVL was a rare complication of prone spine fusion surgery [Tables 3 and 4 ].[ 22 ] Utilizing the nationwide inpatient sample (NIS) database, the authors studied 541,485 patients undergoing spinal fusions, along with their preoperative risk factors and postoperative outcomes (e.g., length of stay [LOS], hospital costs, and mortality). POVL occurred in 1.9/10,000 cases; 56.2% of these patients underwent spinal deformity surgery, and LOS and hospital costs doubled. Risk factors contributing to POVL included; deformity surgery, DM with end organ damage, and paralysis. Studies like this should also ask why so many and such extensive spinal fusions are being performed in the first place.

Ischemic optic neuropathy after carotid body tumor resection

Özkiris et al. in 2014 noted that POVL followed any surgery in 0.013% of cases, but up to 0.2% of spine operations performed in the prone position [Tables 3 and 4 ].[ 27 ] The most frequent etiologies of POVL included AION or PION. ION was variously attributed to long prone operations, increased blood loss, anemia/hemodilution, and infusion of large volumes of crystalloid versus colloids. This study focused additionally on a single case of ION after resection of a carotid body tumor.

Postoperative visual loss in nonocular surgery

Pandey et al. discussed in 2014 various etiologies of POVL following prone spine surgery; this included ION, CRAO or branch retinal artery occlusion, and CB largely due to microvascular pathology and/or intraoperative hypotension [Tables 3 and 4 ].[ 28 ] This study uniquely presented POVL following a cesarean section.

The risks of epidural and transforaminal steroid injections in the spine

Epstein discussed in 2013 how the various types of spinal injections (e.g., epidural/translaminar, transforaminal, or facet injections) are increasingly and typically unnecessarily being performed in multiples of three by pain management specialists (radiologists, physiatrists, and anesthesiologists) [Tables 3 and 4 ].[ 8 ] Nevertheless, they are not approved by the Food and Drug Administration and expose patients to major risks/complications that are typically underreported; meningitis, stroke, paralysis, death, spinal fluid leaks (0.4–6%), positional headaches (28%), adhesive arachnoiditis (6–16%), hydrocephalus, air embolism, urinary retention, allergic reactions, intravascular injections (7.9–11.6%), stroke, blindness (occipital strokes associated with cervical injections typically inadvertently penetrating the vertebral artery), neurological deficits/paralysis, hematomas, seizures, and death. Furthermore, they have no documented long-term efficacy in the treatment of spinal pathology.

Perioperative visual loss and anesthetic management

Lee in their 2013 review discussed the frequency of ION/POVL due to prone spine surgery [Tables 3 and 4 ].[ 19 ] They reviewed the ASA recommendations regarding how to manage patients at increased risk for ION. They identified the following risk factors; “male sex, obesity, the Wilson spinal frame, longer anesthetic duration, greater blood loss, and a lower percentage of colloid in the nonblood fluid administration.”

Perioperative vision loss

Grover and Jangra in 2012 noted POVL occurred following prone spine surgery and cardiothoracic surgical procedures; it was variously attributed to ION, CRAO, CB, and occasionally, compressive ocular trauma [Tables 3 and 4 ].[ 11 ] Additional etiologies of these injuries included microvascular diseases and intraoperative hypotension.

Perioperative visual loss in ocular and nonocular surgery

Berg et al. in 2010 discussed the frequency of POVL following nonocular surgery as ranging from 0.013% for all operations, but up to 0.2% following spine surgery [Tables 3 and 4 ].[ 3 ] After nonocular surgery, the authors identified 111 cases of AION (most due to cardiac surgery), 165 cases of PION (most due to prone spine surgery or radical neck dissection), and another 526 cases of either AION or PION. Other etiologies of POVL included 933 cases of CRAO, 33 cases of pituitary apoplexy, and 245 cases of CB. The frequency of POVL was much lower with ocular surgery; five cases of optic nerve trauma, 47 cases of AION, and five cases of PION.

Perioperative visual loss: What do we know, what can we do?

Roth in 2009 noted that POVL rarely occurred following nonocular surgery. Its various etiologies included; retinal vascular occlusion (RVO) and ION [Tables 3 and 4 ].[ 32 ] This study discussed the frequency, risks, diagnosis, and treatment of POVL.

Postoperative visual loss; 10-year study attributed to spinal, orthopedic, cardiac, and general surgery

Shen et al. in 2009 studied POVL over a 10-year period (1996–2005) in the US following eight nonocular operations performed on >5.6 million patients in the NIS [Tables 3 and 4 ].[ 33 ] Surgery included: knee, gall bladder, hip/femur, laminectomy (no fusion), spinal fusion, appendectomy, colorectal, coronary artery bypass grafting, and cardiac valve procedures (1996–2005). POVL postoperatively was variously attributed to: ION, CB, or RVO. The highest rates of POVL occurred in cardiac (8.64/10,000) procedures, followed by spinal fusions (3.09/10,000), and orthopedic surgery. Those under 18 years of age showed a higher rate of CB, while those over 50-years-old exhibited more ION and RVO. Risk factors for POVL included; male gender, a higher Charlson comorbidity index, anemia, and the need for blood transfusion.

Perioperative visual loss after nonocular surgeries

Newman in 2008 discussed the risk of POVL in patients ages 5–81 undergoing nonocular surgery as varying from 0.002% to 0.2%; the majority occurred in cardiac and spine surgeries [Tables 3 and 4 ].[ 24 ] Most commonly, AION was seen bilaterally with cardiac surgery, while PION correlated with prone spine surgery. Risk factors included; long prone spine surgery, excessive blood loss, hypotension, anemia, hypoxia, high volume fluid replacement, use of vasoconstrictors, high venous pressure, and poor head positioning (rotation, orbital compression). Although the authors recommended urgent postoperative evaluation by ophthalmology for establishing the diagnosis of ION, most treatment modalities appeared to be largely ineffective.

Vision loss after spine surgery: review of the literature and recommendations

Baig et al. in 2007 reviewed the higher incidence of POVL (0.028–0.2%) due to the more frequent and complex instrumented spine versus cardiac operations [Tables 3 and 4 ].[ 2 ]

Ophthalmologic complications associated with prone positioning in spine surgery

Stambough et al. in 2007 discussed the most common eye injury occurring during prone spine surgery: a corneal abrasion [Tables 3 and 4 ].[ 35 ] Risk factors for ION included; surgery over 7 h, acute anemia, hypotension, and hypoxia. Other factors resulting in CRAO included; direct compression raising IOP. CB was attributed to hypoxia and cerebral embolism (e.g. occipital cortical infarct). Outcomes for ION and CRAO were poor, whereas those for CB may improve. The authors suggested multiple prophylactic measures to avoid these complications.

Postoperative blindness

Williams in 2002 looked at the various etiologies and of POVL (frequency 0.05–1%) that followed anesthesia for largely cardiac bypass or spine surgery [Tables 3 and 4 ].[ 38 ] Although direct compression may cause POVL, more frequent etiologies included ION, CRAO, CRVO, and CB.

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Conflicts of interest

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