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INTRODUCTION — Postoperative visual loss (POVL) is a rare complication of surgery, with increased prevalence after cardiac, spine, head and neck, and some orthopedic procedures. The most common cause of postoperative ocular injury is corneal abrasion, which may or may not be associated with visual loss. The most common causes of permanent POVL are central retinal artery occlusion, ischemic optic neuropathy, and cerebral vision loss.
POVL can occur after injury at any site in the visual pathway, from the cornea to the occipital lobe; the pathophysiology of POVL is often incompletely understood. Disability from POVL can range from transient blurring or loss of vision to devastating, permanent bilateral blindness.
This topic will discuss the types of postoperative visual disturbances, what is known about etiology, and recommendations for prevention and treatment as they relate to anesthesia care. Acute visual loss in other settings is discussed separately. (See "Approach to the adult with acute persistent visual loss" and "Approach to acute vision loss in children" and "Optic neuropathies".)
INCIDENCE — The exact incidence of postoperative visual loss (POVL) is unknown. POVL is a rare complication of surgery, with increased prevalence after cardiac, spine, head and neck, and some orthopedic procedures. Data come largely from retrospective studies and case series.
Estimates of the rate of POVL by type of surgery from a large national database were as follows :
●Appendectomy – 0.12 per 10,000
●Laminectomy without fusion – 0.86 per 10,000
●Knee surgery – 1.08 per 10,000
●Hip surgery – 1.86 per 10,000
●Spinal fusion – 3.09 per 10,000 for all fusions, 0.66 per 10,000 with anterior approach only, 5.50 per 10,000 with posterior approach
●Cardiac surgery – 8.64 per 10,000
Studies from single centers report low rates as well, with the following approximate rates [2,3]:
●All nonocular procedures – 5.4 per 10,000 for transient POVL and 0.16 per 10,000 for permanent POVL
●Noncardiac procedures – 4.3 per 10,000 patients for transient POVL and 0.08 per 10,000 patients for POVL lasting more than 30 days
Permanent POVL associated with spine surgery has been reported in as many as 1 in 500 operations (0.2 percent) from data obtained from three centers that performed over 3400 spine surgeries .
URGENT EVALUATION OF VISUAL LOSS — Any complaint of postoperative visual loss (POVL) should be taken seriously, rather than attributing symptoms to residual sedation or anesthesia. Some diagnoses that result in POVL, such as corneal abrasions, require minimal treatment, while others are medical emergencies, as complete and permanent vision loss may ensue within a few hours. Complaints of visual loss should prompt urgent ophthalmologic consultation so that an expeditious evaluation, diagnosis, and treatment plan can be developed to salvage as much vision as possible. The approach to the patient with visual loss is discussed more fully separately. (See "Approach to the adult with acute persistent visual loss" and "Approach to the adult with acute persistent visual loss", section on 'Approach to the patient'.)
For procedures associated with a high risk of POVL, such as cardiac procedures, prone spine surgery, head and neck procedures, and hip/femur surgery, we recommend a gross vision examination for each eye as soon as possible after emergence from anesthesia (eg, having the patient count fingers in each eye and assessing pupillary light reactions). Regardless of the type of surgical procedure, when a patient complains of postoperative visual changes, performance of a gross eye examination and obtaining a brief history will be helpful prior to consulting an ophthalmologist. Evaluation while waiting for ophthalmology consultation should include review of the following signs, symptoms, and historical features. Associated factors, clinical presentation, and indicated workup for various types of POVL are shown in the table (table 1).
●Pain – Eye pain, especially with foreign body sensation, is suggestive of corneal abrasion. Eye pain can also occur with acute glaucoma and retrobulbar hematoma, which are ophthalmologic emergencies. Headache occurs in almost all cases of pituitary apoplexy and acute angle-closure glaucoma, and may occur with Posterior Reversible Encephalopathy Syndrome (PRES). (See 'Corneal abrasion' below and 'Acute angle-closure glaucoma' below and 'Retrobulbar hematoma' below and 'Posterior reversible encephalopathy syndrome' below.)
●Erythema – Red eye often occurs with corneal abrasion and sometimes with acute angle-closure glaucoma.
●Visual deficit – Complete loss of vision or a visual field deficit may occur with central retinal artery occlusion, anterior and posterior ischemic optic neuropathy, damage to the intracranial visual pathways, and retrobulbar hematoma, which may be unilateral or bilateral. In cases of pituitary apoplexy and PRES, the visual deficit may be similar or limited to blurred vision. Intermittent blurring of vision with halos may occur with acute angle-closure glaucoma. Transient blurred vision usually occurs with glycine-induced visual loss and may occur with corneal abrasion. (See 'Postoperative ischemic optic neuropathy' below and 'Cerebral visual loss' below and 'Central retinal artery occlusion' below and 'Retrobulbar hematoma' below and 'Glycine-induced visual loss' below and 'Pituitary apoplexy' below and 'Posterior reversible encephalopathy syndrome' below.)
●Pupillary light reflexes – Unilateral central retinal artery occlusion, ischemic optic neuropathy, and retrobulbar hematoma result in a poor or absent pupillary response to light (“direct” response) with a normal response when light is directed to the other pupil (“indirect” response); this “relative afferent pupillary defect” is revealed when tested with the swinging flashlight maneuver; if these processes are bilateral, there will be poor or absent direct pupillary responses and a relative afferent pupillary defect if asymmetric. Mid-dilated and nonreactive pupils are consistent with acute angle-closure glaucoma, while sluggish to fixed and dilated pupils are seen with glycine-induced visual loss. Pupillary light reflexes are normal in cases of corneal abrasion, cerebral or cortical visual loss, and in cases of PRES. Examination of pupils is discussed more fully separately. (See "The detailed neurologic examination in adults".)
Evaluation by the ophthalmologist typically includes a past medical history, perioperative events, ocular complaints and an eye examination with visual acuity, color vision, pupillary light reflex testing, visual field testing, slit-lamp biomicroscopy, intraocular pressure measurement, and a dilated funduscopic examination unless acute glaucoma is suspected. Based on the findings, further diagnostic testing may include computed tomography (CT) or magnetic resonance imaging (MRI) of the head with attention to the visual pathways to screen for infarctions, hemorrhages, and pituitary apoplexy; visual evoked potentials to evaluate optic nerve function; and occasionally electroretinograms if there is any concern about retinal function (as with glycine toxicity).
MOST COMMON CAUSES — The most common causes of ocular complaints postoperatively are corneal abrasion, postoperative ischemic optic neuropathy, cerebral visual loss, and central retinal artery occlusion. Clinical features, associated factors, workup, and treatment of the various causes of postoperative visual loss (POVL) are shown in the table (table 1).
Corneal abrasion — The most common cause of postoperative visual complaint is corneal abrasion. Single-center studies have found an incidence ranging from 0.9 events per 10,000 to 1 event per 1000 general anesthetics [3,5]. Diagnosis and management of corneal abrasion are discussed more fully separately. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis" and "Corneal abrasions and corneal foreign bodies: Management".)
Etiology — Possible etiologies in the perioperative period include corneal drying, with exposure of the cornea compounded by decreased tear production during general anesthesia, or direct trauma to unprotected eyes during airway management from monitoring equipment (eg, pulse oximetry probe, electrocardiogram cables), from loose tape over the eyes with incomplete lid closure, or from drapes or other materials near the face. In addition, corneal injury can occur when patients rub their eyes while sedated after emergence from anesthesia.
Diagnosis — A presumptive diagnosis of corneal abrasion is often made postoperatively in a patient with eye pain, a foreign body sensation, and photophobia. Visual acuity may be subnormal if the abrasion is in the visual axis but generally recovers quickly. Residual anesthetic, analgesics, and sedatives may alter patient symptoms, making diagnosis difficult. The diagnosis can be confirmed at bedside by the use of fluorescein stain with a cobalt blue penlight, but if vision is involved or pain is severe, a slit-lamp examination and further care by an ophthalmologist are preferable (picture 1).
Mistaken diagnoses of corneal abrasions postoperatively have delayed urgently needed treatment for acute angle-closure glaucoma to prevent permanent loss of vision . One review of the literature on acute angle-closure glaucoma after anesthesia noted the onset of symptoms to correct diagnosis ranged from several hours to five days . For patients diagnosed with corneal abrasion, lack of significant improvement in symptoms by the next day should prompt further consultation with ophthalmology to investigate other causes of visual loss. As an example, corneal abrasions may accompany other ocular injuries such as central retinal artery occlusion, which requires a dilated funduscopic examination for diagnosis.
Diagnosis of corneal abrasion is discussed more fully separately. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis".)
Management — Treatment of corneal abrasion usually consists of administration of topical antibiotics, with healing expected within 24 hours. Management of corneal abrasion is discussed more fully separately. (See "Corneal abrasions and corneal foreign bodies: Management".)
Some hospitals and anesthesiology departments have specific diagnostic and treatment protocols in place for presumptive corneal abrasions, which primarily consist of diagnosis with fluorescein stain and cobalt blue light and treatment with prophylactic antibiotic and lubricant drops for two to three days, with expected complete resolution in that time. Patients with significant visual loss or symptoms that suggest other causes of ocular injury are not appropriate for these protocols and should have an urgent ophthalmologic consult to investigate other causes of visual loss. For patients treated for presumed corneal abrasion, lack of significant improvement by the next day should also prompt an ophthalmology consultation (table 1). (See "Corneal abrasions and corneal foreign bodies: Management", section on 'Indications for subspecialty consultation or referral'.)
Prevention — Prevention of perioperative corneal abrasions includes prompt taping of eyelids after the patient is induced for general anesthesia, making sure that the lids are fully closed . Use of lubricants, ointments, and gels prior to taping the eyes is controversial, as some studies have shown no additional benefit, while the gel and ointment may cause a foreign-body sensation in the eye and promote eye rubbing in the sedated postoperative state . The anesthesia clinician should check the face frequently during surgery to make sure the eye covering is in place and that there is no pressure on the eyes.
Postoperative ischemic optic neuropathy — Ischemic optic neuropathy (ION) is the most common cause of permanent POVL in adults after nonocular surgery. It is more common after cardiac, spine, and orthopedic procedures compared with abdominal surgery , and it has been reported after bilateral radical neck procedures  and in cases performed in the steep Trendelenburg position, such as laparoscopic gynecologic and urologic procedures .
National data from cardiac, spinal fusion, abdominal, and nonfusion orthopedic procedures demonstrate a twofold increased risk in men and a more than 1.5-fold risk for patients over the age of 50 years after multivariable analysis . Rates of ION vary among centers for the same category of procedures, possibly related to the invasiveness of procedures performed, specific practice patterns, or susceptibility of populations from different geographic regions. Major tertiary care centers that perform extensive spinal reconstruction and revision procedures report rates of ION ranging from 0.28 to 1.2 per 1000 spine surgeries [4,11]. National estimates are significantly lower and have decreased from 1.63/10,000 patients between the years 1998 and 2000 to 0.6/10,000 from 2010 to 2012 . This decrease occurred during the period when major research and education were focused on risk factors for ION associated with spinal fusion surgery.
In contrast, ION associated with cardiac surgery studied over a similar time period (1998 to 2013) using the same national database found no significant change over time with an average yearly incidence of 1.43 per 10,000 procedures . Risk factors for cardiac surgery included male sex, carotid artery stenosis and stroke as well as many ocular diseases including hypertensive retinopathy, cataracts, macular degeneration, diabetic retinopathy, and glaucoma. Perioperative data on fluid administration, blood pressure, lowest hematocrit, and use of vasopressors is limited in this national database, making it difficult to ascertain peri-procedural risk factors in this study.
ION may be arteritic (eg, giant cell arteritis) or nonarteritic. Postoperative ION is always nonarteritic and is of two types: anterior ischemic optic neuropathy (AION), affecting the optic disc; and posterior ischemic optic neuropathy (PION), which is retrobulbar or posterior to the lamina cribrosa. PION is believed to result from an infarction of the retrobulbar optic nerve and is distinguished clinically from AION by a normal-appearing optic nerve head in the first several weeks after surgery. It is unclear whether the risk factors for postoperative AION and PION differ for the same type of procedure where the same physiologic perturbations occur and no other discernible differences in patient characteristics or perioperative events exist. Ischemic optic neuropathy of both types is discussed more fully separately. (See "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis" and "Nonarteritic ischemic optic neuropathy: Prognosis and treatment" and "Posterior ischemic optic neuropathy" and "Optic neuropathies" and "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies".)
Postoperative anterior ION — Much of the information on postoperative AION comes from case reports and case series, so risk factors are not well defined. Postoperative nonarteritic AION is most common after cardiac surgery but also occurs after major vascular procedures in the supine position, prone spinal fusion surgery, and head and neck procedures . AION is more common in patients with risk factors for vascular disease and often occurs in the setting of vasopressor use, anemia, and hypotension. It is unclear, however, whether the risk of AION relates to the surgical procedure and associated physiological perturbations; the cardiovascular risk factors; an underlying individual predisposition for AION, in particular the congenitally small and crowded optic nerve head (so-called “disc at risk”); or a combination of factors.
●Diagnosis – While most patients with ION have vision loss as soon as they are conscious following anesthesia, patients with AION will not uncommonly have onset of visual loss a day or so after surgery, which is often sudden in onset, either unilateral or bilateral, and progressive over the course of several days. The diagnosis of AION in the majority of patients is clinical, based upon age, presence of vasculopathic risk factors, association with a preceding high-risk operation, temporal onset of visual loss, pupillary light reactions, presence of visual field defects, and presence of a swollen disc (table 1). Several weeks to months after the precipitating event, the only abnormality on funduscopic examination will be optic nerve pallor. (See "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis", section on 'Diagnosis'.)
Magnetic resonance imaging (MRI) will be normal but should be performed to rule out pituitary apoplexy and other causes of POVL.
●Management – No proven beneficial treatment has been identified. Normalization of blood pressure and transfusions are sometimes recommended by ophthalmologic consultants. High-dose steroids and hyperbaric oxygen have been used without consistent results. (See "Nonarteritic ischemic optic neuropathy: Prognosis and treatment", section on 'Treatment'.)
Some recovery is possible, but rarely is it substantial.
Postoperative posterior ION
Risk factors — Postoperative PION most commonly occurs after prone spinal fusion surgery, bilateral head and neck procedures, and after prolonged procedures in the head-down position (eg, robotic urologic and gynecologic procedures) and other procedures where elevated venous pressures may exist [9,14,15], as well as after cardiac surgery. It can occur in all ages, with several reports in children after major scoliosis surgery in the prone position with long duration, high blood loss, and large fluid resuscitation [11,16]. It occurs in men more commonly than women. Other associated factors reported in case reports and case series include hypotension, anemia, use of vasopressors, and patient coexisting diseases, although several case-control studies have not identified these as independent risk factors [17-19]. Their contribution to PION remains unclear. It is possible that individual patient vascular anatomy or physiology or genetic differences may also predispose patients to this injury. (See 'Strategies for prone spine surgery' below.)
The location of perioperative PION in histopathologic studies is in the portion of the posterior optic nerve from anterior to the optic canal to several millimeters posterior to the lamina cribrosa (figure 1) where the vascular supply to the optic nerve has vulnerable watershed areas relative to the most anterior portion of the optic nerve. Damage may be related to ischemia from edema and compression of the small pial vessels in this area of optic nerve, venous infarction, or direct damage from elevated interstitial pressure .
Diagnosis — Most patients with postoperative PION present with painless bilateral vision loss upon awakening from anesthesia. However, the diagnosis may be delayed if patients are kept intubated and mechanically ventilated overnight  or are sedated and not alert to their surroundings. Pupillary light reactions and visual field deficits are similar to AION (table 1). The funduscopic examination is normal within the first several weeks, and visual symptoms do not usually progress [14,21]. Within several weeks, optic nerve pallor will appear on funduscopic examination and will be indistinguishable from AION at that point. (See "Posterior ischemic optic neuropathy", section on 'Clinical presentation' and "Posterior ischemic optic neuropathy", section on 'Diagnosis'.)
The diagnosis of PION may be difficult because of the initially normal-appearing optic nerves. Beyond funduscopic examination, further evaluation should exclude cerebral infarction, pituitary apoplexy, and other possible causes for optic neuropathies [4,18,21-24]. Diffusion weighted imaging with magnetic resonance imaging may reveal abnormalities of the intraorbital optic nerve and should be performed to rule out pituitary apoplexy and other causes of POVL. (See "Posterior ischemic optic neuropathy", section on 'Differential diagnosis'.)
Management — Management is similar to postoperative nonarteritic anterior ischemic optic neuropathy (AION) and usually consists of attempts to normalize hemodynamics and hemoglobin. Head elevation is of theoretical benefit in cases with significant facial edema, such as after prone spinal fusion surgery. However, these maneuvers as well as other therapies such as high-dose steroids, hyperbaric oxygen, and mannitol remain unproven . (See "Nonarteritic ischemic optic neuropathy: Prognosis and treatment", section on 'Treatment'.)
Some recovery is possible with postoperative PION, but as with postoperative AION, it is rarely substantial [17,20,25].
ION associated with spine surgery — The American Society of Anesthesiologists (ASA) created a national registry, the ASA POVL Registry, in 1999 to collect cases of POVL occurring after nonocular surgery so that common perioperative characteristics could be identified to guide future research. Despite the much higher rate of POVL in cardiac surgery, the majority of submissions of cases to the ASA POVL Registry were related to prone spinal fusion surgery. The most common diagnosis associated with POVL after spinal fusion surgery was ION, with approximately 23 percent AION, 67 percent PION, and the remainder unknown ION .
Subsequently, a case control study compared 80 adult patients with ION from the ASA registry with 315 control patients to identify risk factors for ION after spine surgery . The controls were patients who had similar surgical procedures but did not develop POVL. Independent risk factors identified after multivariate regression analysis included male sex; obesity; use of the Wilson frame (figure 2), which keeps the head at a level lower than the heart; prolonged duration of procedure/anesthesia; and high estimated blood loss. Use of colloid fluids was found to be protective against the development of ION. This model accounted for approximately 80 percent of the ION cases; therefore, other risk factors remain unidentified. The lowest hematocrit was not significantly different between cases and controls. Within an acceptable range for adequate oxygen delivery, the exact hematocrit may be less important than whether the patient is euvolemic with a normal cardiac output, and perhaps what type of fluid (colloid versus crystalloid) is used to replace the blood loss that resulted in a lower hematocrit.
With the exception of male sex, the other risk factors are congruent with the theory that elevated venous pressure in the head and subsequent development of interstitial edema contribute to the occurrence of ION, although this theory remains speculative.
Based on findings from this study, the ASA convened a task force to develop recommendations for prevention of POVL associated with spine surgery. Because of the low level of evidence available on prevention of this complication, an ASA Practice Advisory for Perioperative Visual Loss Associated with Spine Surgery was created in 2006 and updated in 2012 (table 2) . The recommendations lack absolute target ranges of parameters because of the lack of strong evidence to support them. As an example, the ASA task force did not state the optimal hemoglobin or hemodynamics for prevention of POVL because of the absence of any evidence-based medicine in the literature on this issue. However, in the absence of evidence, it seems prudent to avoid extreme physiologic perturbations when possible.
Strategies for prone spine surgery — The following anesthetic approach has not been studied with respect to specific risk and benefit outcome measures for the development of ION. Some of these strategies are utilized for other purposes, including optimization of spinal cord perfusion and minimization of airway edema. Special patient conditions may preclude specific elements of this suggested anesthetic management. For patients who undergo prolonged spine surgery with the expectation of significant blood loss, the following approach is utilized by one of the authors (LAL):
●Inform patients expected to have prolonged spine surgery in the prone position, with or without substantial blood loss, of the risk of POVL.
●Position the head in a neutral position at or above the level of the heart.
●Perform frequent eye checks throughout the case to avoid direct pressure on the globe in order to prevent central retinal artery occlusion (CRAO). Avoid the use of the horseshoe headrest because of its close proximity to the eyes, the numerous reports of CRAO with its use, and the difficulty of checking the eyes for cervical spine procedures.
●Monitor blood pressure with an intraarterial catheter to allow beat-to-beat blood pressure monitoring, assessment of volume status, and frequent laboratory sampling for acid–base status, oxygenation, hematocrit or hemoglobin levels, glucose, and electrolyte concentrations. We do not utilize deliberate hypotensive anesthesia to reduce blood loss for patients having surgery with a high risk of POVL. We typically aim for a mean arterial pressure (MAP) within 20 to 25 percent of the preoperative baseline blood pressure, when possible, to optimize the spinal cord perfusion pressure. If evoked potential neuromonitoring signals deteriorate significantly during the case, then we raise the MAP to baseline or slightly above baseline preoperative MAP, as well as perform other troubleshooting maneuvers.
●Use colloids along with crystalloids to maintain euvolemia for patients who have substantial blood loss. The exact ratio of crystalloid to colloid that will protect against development of ION has not been determined ; however, utilizing colloid in the fluid resuscitation during prone spine surgery will also lessen airway edema formation compared with crystalloid administration alone, in our experience. Though colloid was found to be protective against ION in our multicenter case-control study for major prone spine surgery, ION can still occur when it is administered in cases with massive blood loss and resuscitation .
●Monitor hemoglobin or hematocrit periodically in cases with substantial blood loss. Case-control studies have not identified low hematocrit as a risk factor for ION. Therefore, the following recommendations are made irrespective of the risk of ION. The target threshold transfusion trigger should be made on a case-by-case basis with consideration of the rate and quantity of expected blood loss, the coexisting illnesses of the patient, institutional availability of blood and blood products, and the fact that patients who have had a high estimated blood loss (EBL) will typically lose 500 mL or more of blood from the wound drains in the immediate postoperative period. Setting a transfusion threshold means that a hematocrit lower than the threshold will have to occur before transfusion is triggered.
●Possible staging of very prolonged procedures, such as anterior-posterior procedures expected to take more than 10 to 12 hours, should be discussed with the surgeon. Staging may be considered for shorter procedures, depending on patient comorbidities and anticipated blood loss. These decisions must be made on a case-by-case basis, taking into account the potential increase in complications and cost from a prolonged or second hospital admission. We discuss the possibility of staging with the surgeon during the operation if there is significant difficulty maintaining normal acid–base status, acceptable coagulation parameters, and MAP target, or if there is difficulty keeping up with blood loss.
●Assess postoperative vision in high-risk patients as soon as they are cooperative.
●Obtain an urgent ophthalmology consult if there is any concern of POVL.
●Consider magnetic resonance imaging (MRI) to rule out intracranial causes of POVL.
Cerebral visual loss
Incidence and etiology — Cerebral or cortical visual loss is one of the more common types of POVL. A study of over 5.6 million surgical procedures, using the Nationwide Inpatient Sample, found that POVL due to cerebral visual loss occurred in 0.38 per 10,000 discharges after cardiac, spinal fusion, nonfusion orthopedic, and abdominal surgery . Postoperative cerebral visual loss was more common in patients less than 18 years of age, occurring in 4.3 per 10,000 cases. After adjusting for other risk factors, the risk of cerebral visual impairment in patients <18 years old was increased 64-fold over that of patients >18 years old . Because the Nationwide Inpatient Sample does not allow temporal associations of procedures and diagnoses, it is not certain that the cerebral visual loss in the pediatric age group was not present prior to the spinal fusion procedure.
Other risk factors identified from national data include a 19-fold increased risk with spinal fusion surgery, a more than 12-fold increased risk with cardiac surgery, and a fivefold increased risk with nonfusion orthopedic surgery when compared with abdominal surgery . Higher comorbidity burden, as assessed by the Charlson comorbidity score, was associated with increased risk of development of cerebral visual loss. A Charlson Comorbidity Index score of 1 doubled the risk of cerebral visual loss, and a score of 2 or more increased the risk more than fivefold when compared with a Charlson score of 0 (table 3).
Cerebral visual loss is usually caused by emboli, resulting in infarction of the posterior cerebral artery territories, or less commonly by profound hypotension with watershed infarctions in the parietooccipital regions. Embolism and/or hemodynamic instability can occur during cardiac, spinal fusion, and nonfusion orthopedic surgery.
Diagnosis and management — With bilateral infarction, the patient may be completely blind or have only small areas of preserved central vision. With unilateral infarction, the patient presents with a contralateral homonymous hemianopia (figure 3) . Pupillary light reflexes and funduscopic examination are normal. Computed tomography (CT) or magnetic resonance imaging (MRI) of the head shows infarction in the occipital cortex (typically unilateral) or in the parietooccipital watershed zones (usually bilateral). (See "Approach to the adult with acute persistent visual loss", section on 'Cortical blindness'.)
As some of these infarctions are caused by profound hypotension, normalization of blood pressure, cardiac output, and oxygen delivery are primary treatment goals. Optimal hemoglobin for oxygen-carrying capacity has not been identified in these patients. No definitive outcome data regarding effective treatment are available for this rare complication, and reestablishing euvolemia and normal cardiac output and blood pressure are likely more important for recovery than a specific hemoglobin level above 7 to 8 g/dL. Cerebral visual loss from emboli has no specific treatment, assuming that the emboli were thought to be related to the surgical procedure and not intrinsic to the patient.
Some recovery is possible with cerebral visual loss, but only rarely is there complete resolution of the visual field defects.
Prevention — The most common cause of cerebral visual loss perioperatively is embolus, and for most procedures there are no proven preventative measures. Some studies have shown a reduction in emboli during cardiopulmonary bypass with the use of specialized filters. For the rarer cause of cerebral visual loss, prevention is aimed at avoiding prolonged hypoperfusion by avoiding excessive hypotension, hypovolemia, or both. Optimal perfusion pressure for prevention of watershed infarction is not known but may depend on comorbidities, the type of surgical procedure, and individual patient anatomy and physiology. Although the optimal blood pressure parameters have not been defined for prevention of cerebral visual loss or for the prevention of ischemic optic neuropathy, we do not utilize deliberate hypotensive anesthesia to reduce blood loss for patients having surgery with a high risk of POVL. The lower limit of cerebral autoregulation in most human (adult) studies is approximately 70 mmHg, correlating to a cerebral perfusion pressure of 55 to 60 mmHg. 
Central retinal artery occlusion — Central retinal artery occlusion (CRAO) is the most commonly reported retinal cause of visual loss after nonocular surgery. CRAO has occurred after head and neck procedures, cardiac surgery, and prone spine procedures.
Etiology — The etiology of CRAO is presumed to be embolic in cardiac and head and neck surgery; however, CRAO after prone spine surgery is frequently associated with periorbital trauma, suggesting that in those cases the etiology may be sustained globe compression . During nasal or sinus surgery, injection of local anesthetic with epinephrine or corticosteroid, or surgical trauma near the retinal vasculature, may cause vasospasm, embolism, or direct injury to the vasculature [29,30].
A rare cause of CRAO relates to the use of nitrous oxide in patients who have had recent placement of gas expansion bubbles during vitrectomy for retinal detachment surgery . These gas bubbles may remain in the eye for 10 to 14 days when sulfur hexafluoride is injected, and up to 55 to 65 days when perfluorocarbon is injected . Because nitrous oxide readily diffuses into the bubble, the bubble may increase in size and raise the intraocular pressure to levels that occlude central retinal artery flow. Permanent damage to the retina and optic nerve may occur with nitrous oxide administration for more than one to two hours. In a series of five patients with CRAO after gas bubble therapy, the time interval from placement of the gas bubble to anesthesia with nitrous oxide was 2 to 30 days, and four of five patients sustained permanent optic nerve damage . The patient who did not sustain permanent damage was 25 days from insertion of the gas bubble and had a one-hour general anesthetic.
For prone procedures, the horseshoe headrest may increase the risk of CRAO , as the edges of the headrest are very close to the eyes, and slight movement of the head can cause globe compression. CRAO from this etiology was described as early as 1954 in a series of eight patients who developed unilateral blindness after prone spine surgery on a horseshoe headrest (picture 2) .
Diagnosis and management — Postoperative CRAO is almost always unilateral, and patients typically complain of severe loss of vision in one eye immediately after awakening from anesthesia. The clinical context suggests possible etiologic diagnosis. As an example, associated periorbital trauma such as corneal abrasion, supraorbital numbness or bruising, ophthalmoplegia, proptosis, and ptosis may be present, consistent with a mechanism of globe compression after prone surgery. The pupillary light reflex is sluggish or absent, and patients will exhibit a relative afferent pupillary defect (RAPD). Urgent ophthalmologic consultation should be arranged and funduscopic examination performed if CRAO is suspected (picture 3A-B). CRAO has distinct funduscopic findings of an ischemic retina and a classic cherry red spot at the macula (table 1). (See "Central and branch retinal artery occlusion", section on 'Acute clinical features'.)
Partial recovery of vision is possible [15,33], but prognosis is generally poor, as there is no known beneficial postoperative treatment for CRAO. Animal studies in rhesus monkeys indicate that irreversible damage starts occurring after 105 minutes of occlusion and complete optic nerve and retinal destruction at 240 minutes . Conservative measures that may be of benefit include the inhalation of a mixture of 95 percent oxygen and 5 percent carbon dioxide (carbogen), anterior chamber paracentesis, and administration of acetazolamide. Intraarterial thrombolysis is controversial and carries significant risk. This is discussed in more detail separately. (See "Central and branch retinal artery occlusion", section on 'Acute treatment'.)
Prevention — Prevention of postoperative CRAO is aimed at preventing pressure on the globe, including avoidance of headrests in the prone position where the eyes cannot be adequately checked and protected (ie, use of skull pins with the Mayfield apparatus or soft foam cushion with large cutouts for the eyes) and performance and documentation of frequent eye checks throughout the procedure. Additional goals include minimizing embolism if possible (eg, use of filters during cardiopulmonary bypass procedures) and avoidance of nitrous oxide for anesthesia for patients who have had intraocular gas bubbles placed within two to three months before surgery.
Branch retinal artery occlusion — Branch retinal artery occlusion (BRAO) is a milder version of CRAO whereby a branch of the retinal artery is affected, resulting in a sectoral loss of retina and a partial visual field defect. Retinal emboli are common with BRAO. If the diagnosis is unclear, fluorescein angiography can be performed and will show filling defects of the central or branch retinal artery. Electroretinograms will have abnormal/flattened b-waveforms. (See "Central and branch retinal artery occlusion".)
LESS COMMON CAUSES — Rare causes of postoperative visual loss (POVL) include acute angle-closure glaucoma, retrobulbar hematoma, pituitary apoplexy, posterior reversible encephalopathy syndrome, and glycine-induced visual loss.
Acute angle-closure glaucoma — Acute angle-closure glaucoma is a very rare postoperative ocular injury, but it is considered a medical emergency because it requires urgent treatment to prevent permanent loss of vision. One review reported two cases of acute angle-closure glaucoma in 25,000 nonocular procedures . A review of the literature cited 32 cases published as of 2011 , but its true incidence is probably much higher.
●Etiology – Acute angle-closure glaucoma is also known as primary angle-closure glaucoma. Nonsurgical risk factors include genetic predisposition (Asian race), hyperopia (farsightedness), and advanced cataracts. Some medications that are commonly administered perioperatively are associated with acute angle-closure glaucoma (table 4), including over-the-counter decongestants, antihistamines, antiepileptics (eg, topiramate), antiparkinsonian medications, antispasmodic drugs, mydriatic agents, adrenergic agents (eg, ephedrine), antipsychotics, antidepressants, and anticholinergic agents (eg, scopolamine, atropine). (See "Angle-closure glaucoma".)
●Diagnosis – Patients typically present with unilateral or bilateral ocular pain that is boring in nature, nausea, vomiting, ipsilateral or bilateral headache, and intermittent or persistent blurring of vision with halos. Characteristic findings on the physical examination include fixed and mid-dilated pupils, edematous eyelids and cornea, injected conjunctiva, and elevated intraocular pressures (picture 4). If acute angle-closure glaucoma is suspected, urgent ophthalmologic consultation is necessary, and dilated funduscopic examination is contraindicated. (See "Angle-closure glaucoma", section on 'Clinical presentation' and "Angle-closure glaucoma", section on 'Diagnosis'.)
●Management – Treatment consists of topical and systemic medications that lower the intraocular pressure and, if necessary, peripheral iridotomy. Because glaucomatous damage may occur in hours and is generally not reversible, prognosis is dependent on time to diagnosis and effective treatment. (See "Angle-closure glaucoma", section on 'Management'.)
●Prevention – Prevention is theoretical and includes avoidance of medications known to be associated with this complication, when possible, in individuals who have a history of narrow angles (however, if a patient is known to have narrow angles, they will likely have already had prophylactic peripheral iridotomies, making them no longer at risk).
Retrobulbar hematoma — Retrobulbar hematoma is another medical emergency that leads to permanent loss of vision with optic nerve compression within hours.
●Etiology – Retrobulbar hematoma is most commonly associated with orbital trauma, repair of orbital floor fractures, ocular surgery, endoscopic sinus surgery, retrobulbar injections, and other head and neck procedures, including blepharoplasty where bleeding may occur in proximity to the globe. Rarely, it occurs in susceptible individuals after general anesthesia as a result of coughing, straining, vomiting, or extremely elevated blood pressure, particularly in the presence of anticoagulation. Incidence varies among surgical procedures, occurring in 0.04 percent of blepharoplasties , 0.43 percent of endoscopic sinus surgeries , and in up to 3.2 percent of orbital floor fractures .
●Diagnosis – Onset of symptoms typically occurs within three hours of surgery and the vast majority within 24 hours; however, onset may occur as many as nine days after surgery [40,41]. Clinicians should have a high index of suspicion for this complication after head and neck procedures, especially after orbital floor repair [15,29-32].
The clinical presentation may be dramatic in appearance, and the diagnosis is made based on clinical signs and symptoms (picture 5). Proptosis with severe stabbing pain, vision loss, and a sensation of pressure are common. Patients may also experience nausea and vomiting, diplopia, and visual flashes. External examination of the eye may reveal eyelid hematoma or ecchymosis, subconjunctival hemorrhage, proptosis, or ophthalmoplegia. If the optic nerve is compromised, pupillary light reflexes will be abnormal, with a relative afferent pupillary defect. Emergency ophthalmology consultation is indicated if the diagnosis is suspected.
●Management – Definitive treatment is surgical. Immediate decompression with a lateral canthotomy and inferior cantholysis is the treatment of choice and may be performed at the bedside with local anesthesia. Emergent surgical decompression should not be delayed for imaging or administration of topical or systemic medications aimed at lowering intraocular pressure. Evacuation of the hematoma may be performed subsequent to decompression. Prognosis for vision is dependent on the time from the onset of symptoms to decompression, with poor outcomes reported in symptom-to-treatment intervals as short as four hours. Retrobulbar hematoma is responsible for almost half of all cases of visual loss associated with repair of orbital floor fractures .
●Prevention – Prevention includes primarily surgical hemostasis, avoidance of excessive coughing and straining with emergence, and retching in the recovery room [15,29-32].
Pituitary apoplexy — Pituitary apoplexy is a life-threatening condition caused by sudden hemorrhage or infarction within the pituitary gland, frequently associated with a pituitary tumor. It is an exceedingly rare cause of POVL but is discussed here because its clinical presentation may overlap with postoperative posterior ischemic optic neuropathy (PION) and is one of the reasons that further imaging is required in cases suspected of having PION. It has been reported after cardiac surgery and transurethral resection of the prostate [42,43]. (See 'Postoperative ischemic optic neuropathy' above.)
●Etiology – Most cases of pituitary apoplexy occur in patients with pituitary adenomas, often unrecognized . Risk factors include reduced blood flow in the pituitary gland (eg, increases in intracranial pressure, severe hemorrhagic hypotension, head trauma, pituitary irradiation), sudden increase in blood flow to the pituitary gland, stimulation of the pituitary gland by hormonal manipulation, and anticoagulation.
●Diagnosis – Clinical presentation occurs immediately to several months postoperatively, though most occur within 48 hours of surgery. The symptoms include a diffuse, severe headache in the vast majority of patients. Most patients with pituitary apoplexy have nausea, decreased visual acuity, ophthalmoplegia, and visual field deficits . Cranial nerve III is most commonly involved and may manifest as a unilaterally dilated, fixed pupil with ptosis. Altered mental status and Addisonian crisis may occur as well. Urgent magnetic resonance imaging should be performed to confirm hemorrhage into the sella turcica. (See "Causes of hypopituitarism", section on 'Pituitary apoplexy'.)
●Management – Treatment consists of surgical decompression for cases with visual changes or altered mental status, but less severe cases may be managed with high-dose corticosteroids and endocrine replacement therapy alone. (See "Treatment of hypopituitarism".)
●Prevention – Anesthesia clinicians should recognize the risk of pituitary hemorrhage when a patient with a known pituitary adenoma presents for surgery, especially if significant blood loss is expected. Invasive blood pressure monitoring and tighter hemodynamic control may be helpful in preventing severe hypoperfusion or shock in patients with a known pituitary tumor undergoing procedures with an expected high estimated blood loss (EBL), though preventative measures for this rare complication have not been determined.
Glycine-induced visual loss — Transient perioperative visual loss can occur after absorption of glycine solution used as a nonelectrolyte bladder irrigant during transurethral resection of the prostate (TURP) or as uterine irrigant during hysteroscopy. Neurologic signs and symptoms related to glycine absorption are discussed more fully separately. (See "Hyponatremia following transurethral resection or hysteroscopy", section on 'Clinical manifestations'.)
●Etiology – Rapid absorption of glycine from the bladder or uterus can cause a constellation of symptoms, known as TURP syndrome (mental status changes, seizures, hypotension, visual symptoms, fluid overload with pulmonary edema, bradycardia, hypoxia, brainstem herniation, or death). Visual symptoms can include a self-limited decrease in visual acuity, blurred vision, or blindness [45-47]. Neurologic symptoms may be caused by the hyponatremia that results from absorption of large quantities of irrigant, or by neurotoxic effects of glycine and some of its metabolites. Glycine crosses the blood brain barrier where it depresses retinal neurons, with the greatest effect on the amacrine cells. Serine, ammonia, glyoxylate, and other metabolites may also play a role. (See "Hyponatremia following transurethral resection or hysteroscopy", section on 'Pathogenesis of neurologic symptoms'.)
●Diagnosis – Onset of symptoms may occur intraoperatively to several hours postoperatively. Nausea usually occurs first as a result of the hyponatremia that accompanies the absorption of irrigant. Visual symptoms often begin with blurred vision if the patient is awake in the operating room but may progress to complete blindness. Pupillary light reflexes vary from sluggish to nonreactive and dilated and may depend on the severity of glycine toxicity and associated hyponatremia. Funduscopic exam is normal. Electroretinogram, while not required for diagnosis, will be abnormal with loss of the oscillatory potentials. Serum electrolytes show hyponatremia.
●Management – If not associated with severe hyponatremia and severe glycine toxicity, symptoms abate spontaneously within 2 to 24 hours, as the half-life of glycine varies from 26 to 245 minutes [48,49]. Associated severe hyponatremia, other neurologic manifestations, hypoxia and cardiac dysfunction require specific treatment. (See "Hyponatremia following transurethral resection or hysteroscopy", section on 'Management'.)
●Prevention – Prevention of glycine toxicity is aimed at minimizing the absorption of glycine and includes :
•Avoid Trendelenburg position as it increases the potential for irrigant absorption
•Limit operative time to <60 minutes
•During TURP, intraprostatic vasopressin injection can minimize open dilated vessel absorption
•Use of low-pressure irrigation
•Laser or Holmium laser technique that minimizes bleeding and absorption of irrigant
•Halt procedure if ≥1000 mL of irrigant is absorbed
Posterior reversible encephalopathy syndrome — Posterior reversible encephalopathy syndrome (PRES), also known as reversible posterior leukoencephalopathy syndrome, is characterized by headache, altered consciousness, seizures, and visual disturbance. Cerebral visual loss may occur as part of PRES. Visual symptoms may include hemianopia, visual neglect, auras, visual hallucinations, and cerebral blindness [51,52].
Although this syndrome is not usually seen in the perioperative period, it has appeared in single-case reports after thoracoscopic wedge resection , lumbar fusion , and hysterectomy . PRES may occur in patients with preeclampsia or eclampsia. PRES is discussed more fully separately. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Clinical manifestations'.)
SUMMARY AND RECOMMENDATIONS — Postoperative visual loss (POVL) is a rare complication of nonocular surgery, which may result from injury to any of the different areas of the visual pathways (table 1). With the exception of uncomplicated, minor corneal abrasion, an urgent ophthalmology consultation is required. Most causes of POVL other than corneal abrasions can result in permanent visual loss.
●The most common perioperative ocular injury after nonocular surgery is a corneal abrasion, which almost always has an excellent outcome, is typically self-limiting, and usually results in, at most, transient blurred vision. The eyes of all patients who have general anesthesia should be covered with dressings that keep the lids closed to prevent corneal injury. Patients should be positioned to eliminate pressure on the globe. Lack of symptomatic improvement by the next day should prompt an urgent ophthalmologic consultation. (See 'Corneal abrasion' above.)
●POVL otherwise requires urgent ophthalmologic consultation for diagnosis and treatment of potentially reversible causes of visual loss. Immediate evaluation should include an assessment of pain, visual deficits, and pupillary light reflex. Medical emergencies include (see 'Urgent evaluation of visual loss' above):
•Acute angle-closure glaucoma can result in rapidly progressive, potentially preventable permanent loss of vision. Acute angle-closure glaucoma presents with ocular pain, fixed and mid-dilated pupils, edematous eyelids and cornea, and injected conjunctiva. It may be misdiagnosed as corneal abrasion. (See 'Acute angle-closure glaucoma' above and 'Retrobulbar hematoma' above.)
•Retrobulbar hematoma is most commonly associated with orbital trauma or head and neck surgery and can result in permanent loss of vision with optic nerve compression within hours. Symptoms develop within hours to days and include proptosis with severe stabbing pain, vision loss, nausea, vomiting, and diplopia. Definitive treatment is surgical. (See 'Retrobulbar hematoma' above.)
●Ischemic optic neuropathy (ION) is associated with cardiac bypass, prone spinal fusion, nonfusion orthopedic procedures, head and neck procedures, and prolonged procedures performed in steep Trendelenburg position. Risk factors identified for prone spine surgery patients with ION include male sex, obesity, use of the Wilson spine frame, prolonged surgery duration, and high blood loss. (See 'Postoperative ischemic optic neuropathy' above.)
●For patients who undergo prolonged prone spine surgery with the expectation of significant blood loss, one of the authors (LAL) uses the following approach, which includes strategies to optimize spinal cord perfusion, decrease airway edema, and possibly prevent development of ION (see 'Strategies for prone spine surgery' above):
•Position the head in a neutral position at or above the level of the heart. Perform frequent eye checks throughout the case to avoid direct pressure on the globe to prevent central retinal artery occlusion.
•We aim for a mean arterial pressure (MAP) within 20 to 25 percent of preoperative baseline primarily to maintain adequate spinal cord perfusion pressure.
•We typically utilize invasive hemodynamic monitoring with an intraarterial catheter to assess volume status with pulse pressure variation and to assess laboratory values at regular intervals for oxygenation and ventilation, serum hemoglobin concentration, acid–base status, lactate, electrolytes, glucose, and coagulation parameters. Urine output (approximately 0.5 mL/kg/h) is also used to assess volume status.
•We use colloids along with crystalloids to maintain euvolemia for patients who have substantial blood loss. For major spine operations, a specific transfusion threshold that would prevent ION has not been established, and case-control studies indicate no difference in the lowest hematocrit between patients with and without ION. The risks of transfusion must be weighed against the potential benefits. (See 'Strategies for prone spine surgery' above.)
•Staging very prolonged procedures should be discussed with the surgeon.
•Assess postoperative vision in high-risk patients as soon as they are cooperative, and obtain an urgent ophthalmology consult if there is any concern for POVL.
●Cerebral visual loss is most common in procedures with high embolic loads or profound hypotension such as cardiac bypass, prone spinal fusion, or nonfusion orthopedic surgery. (See 'Cerebral visual loss' above.)
●Central retinal artery occlusion is caused by embolic phenomena or by globe compression and should be suspected in the patient who awakens from anesthesia with severe unilateral visual loss with or without periorbital trauma. (See 'Central retinal artery occlusion' above.)
●Very rarely, POVL may be caused by pituitary apoplexy, absorption of glycine irrigant during transurethral resection of the prostate or hysteroscopy, or posterior reversible encephalopathy syndrome. (See 'Less common causes' above.)
- 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.
- Warner ME, Warner MA, Garrity JA, et al. The frequency of perioperative vision loss. Anesth Analg 2001; 93:1417.
- Roth S, Thisted RA, Erickson JP, et al. Eye injuries after nonocular surgery. A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology 1996; 85:1020.
- Stevens WR, Glazer PA, Kelley SD, et al. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976) 1997; 22:1319.
- Vetter TR, Ali NM, Boudreaux AM. A case-control study of an intraoperative corneal abrasion prevention program: holding the gains made with a continuous quality improvement effort. Jt Comm J Qual Patient Saf 2012; 38:490.
- Lentschener C, Ghimouz A, Bonnichon P, et al. Acute postoperative glaucoma after nonocular surgery remains a diagnostic challenge. Anesth Analg 2002; 94:1034.
- Fazio DT, Bateman JB, Christensen RE. Acute angle-closure glaucoma associated with surgical anesthesia. Arch Ophthalmol 1985; 103:360.
- Cucchiara RF, Black S. Corneal abrasion during anesthesia and surgery. Anesthesiology 1988; 69:978.
- Pazos GA, Leonard DW, Blice J, Thompson DH. Blindness after bilateral neck dissection: case report and review. Am J Otolaryngol 1999; 20:340.
- Weber ED, Colyer MH, Lesser RL, Subramanian PS. Posterior ischemic optic neuropathy after minimally invasive prostatectomy. J Neuroophthalmol 2007; 27:285.
- Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: the Johns Hopkins Hospital Experience. Spine (Phila Pa 1976) 2005; 30:1299.
- Rubin DS, Parakati I, Lee LA, et al. Perioperative Visual Loss in Spine Fusion Surgery: Ischemic Optic Neuropathy in the United States from 1998 to 2012 in the Nationwide Inpatient Sample. Anesthesiology 2016; 125:457.
- Rubin DS, Matsumoto MM, Moss HE, et al. Ischemic Optic Neuropathy in Cardiac Surgery: Incidence and Risk Factors in the United States from the National Inpatient Sample 1998 to 2013. Anesthesiology 2017; 126:810.
- Roth S. Postoperative blindness. In: Miller’s Anesthesia, 6th ed, Miller RD (Ed), Elsevier, New York 2004. p.3001.
- Lee LA, Roth S, Posner KL, et al. The American Society of Anesthesiologists Postoperative Visual Loss Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006; 105:652.
- Kim JW, Hills WL, Rizzo JF, et al. Ischemic optic neuropathy following spine surgery in a 16-year-old patient and a ten-year-old patient. J Neuroophthalmol 2006; 26:30.
- Postoperative Visual Loss Study Group. Risk factors associated with ischemic optic neuropathy after spinal fusion surgery. Anesthesiology 2012; 116:15.
- Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery. A review of 37 cases. Spine (Phila Pa 1976) 1997; 22:1325.
- Holy SE, Tsai JH, McAllister RK, Smith KH. Perioperative ischemic optic neuropathy: a case control analysis of 126,666 surgical procedures at a single institution. Anesthesiology 2009; 110:246.
- Ho VT, Newman NJ, Song S, et al. Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol 2005; 17:38.
- Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008; 145:604.
- Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80:1018.
- Baig MN, Lubow M, Immesoete P, et al. Vision loss after spine surgery: review of the literature and recommendations. Neurosurg Focus 2007; 23:E15.
- Gill B, Heavner JE. Postoperative visual loss associated with spine surgery. Eur Spine J 2006; 15:479.
- Sadda SR, Nee M, Miller NR, et al. Clinical spectrum of posterior ischemic optic neuropathy. Am J Ophthalmol 2001; 132:743.
- American Society of Anesthesiologists Task Force on Perioperative Visual Loss. 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.
- Lee LA, Newman NJ, Wagner TA, et al. Postoperative ischemic optic neuropathy. Spine (Phila Pa 1976) 2010; 35:S105.
- Patel P, Drummond J. Cerebral Physiology and the Effects of Anesthetic Drugs. In: Miller’s Anesthesia, 7th ed, Miller RD (Ed), Churchill Livingstone/Elsevier, Philadelphia 2010. p.305.
- Rettinger G, Christ P, Meythaler FH. [Blindness caused by central artery occlusion following nasal septum correction]. HNO 1990; 38:105.
- Whiteman DW, Rosen DA, Pinkerton RM. Retinal and choroidal microvascular embolism after intranasal corticosteroid injection. Am J Ophthalmol 1980; 89:851.
- Fu AD, McDonald HR, Eliott D, et al. Complications of general anesthesia using nitrous oxide in eyes with preexisting gas bubbles. Retina 2002; 22:569.
- Silvanus MT, Moldzio P, Bornfeld N, Peters J. Visual loss following intraocular gas injection. Dtsch Arztebl Int 2008; 105:108.
- HOLLENHORST RW, SVIEN HJ, BENOIT CF. Unilateral blindness occurring during anesthesia for neurosurgical operations. AMA Arch Ophthalmol 1954; 52:819.
- Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004; 78:723.
- Eldor J, Admoni M. Acute glaucoma following nonophthalmic surgery. Isr J Med Sci 1989; 25:652.
- Gayat E, Gabison E, Devys JM. Case report: bilateral angle closure glaucoma after general anesthesia. Anesth Analg 2011; 112:126.
- DeMere M, Wood T, Austin W. Eye complications with blepharoplasty or other eyelid surgery. A national survey. Plast Reconstr Surg 1974; 53:634.
- Stankiewicz JA, Chow JM. Two faces of orbital hematoma in intranasal (endoscopic) sinus surgery. Otolaryngol Head Neck Surg 1999; 120:841.
- Gosau M, Schöneich M, Draenert FG, et al. Retrospective analysis of orbital floor fractures--complications, outcome, and review of literature. Clin Oral Investig 2011; 15:305.
- Hass AN, Penne RB, Stefanyszyn MA, Flanagan JC. Incidence of postblepharoplasty orbital hemorrhage and associated visual loss. Ophthal Plast Reconstr Surg 2004; 20:426.
- Teng CC, Reddy S, Wong JJ, Lisman RD. Retrobulbar hemorrhage nine days after cosmetic blepharoplasty resulting in permanent visual loss. Ophthal Plast Reconstr Surg 2006; 22:388.
- Mattke AF, Vender JR, Anstadt MR. Pituitary apoplexy presenting as Addisonian crisis after coronary artery bypass grafting. Tex Heart Inst J 2002; 29:193.
- Biousse V, Newman NJ, Oyesiku NM. Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry 2001; 71:542.
- Randeva HS, Schoebel J, Byrne J, et al. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol (Oxf) 1999; 51:181.
- Mizutani AR, Parker J, Katz J, Schmidt J. Visual disturbances, serum glycine levels and transurethral resection of the prostate. J Urol 1990; 144:697.
- Radziwill AJ, Vuadens P, Borruat FX, Bogousslavsky J. Visual disturbances and transurethral resection of the prostate: the TURP syndrome. Eur Neurol 1997; 38:7.
- Karci A, Erkin Y. Transient blindness following hysteroscopy. J Int Med Res 2003; 31:152.
- Wang JM, Creel DJ, Wong KC. Transurethral resection of the prostate, serum glycine levels, and ocular evoked potentials. Anesthesiology 1989; 70:36.
- Hahn RG. Dose-dependent half-life of glycine. Urol Res 1993; 21:289.
- Hawary A, Mukhtar K, Sinclair A, Pearce I. Transurethral resection of the prostate syndrome: almost gone but not forgotten. J Endourol 2009; 23:2013.
- Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996; 334:494.
- Lysandropoulos AP, Rossetti AO. Postictal cortical visual impairment: a symptom of posterior reversible encephalopathy. Epilepsy Behav 2010; 17:276.
- Eran A, Barak M. Posterior reversible encephalopathy syndrome after combined general and spinal anesthesia with intrathecal morphine. Anesth Analg 2009; 108:609.
- Yi JH, Ha SH, Kim YK, Choi EM. Posterior reversible encephalopathy syndrome in an untreated hypertensive patient after spinal surgery under general anesthesia -A case report-. Korean J Anesthesiol 2011; 60:369.
- Kim TK, Yoon JU, Park SC, et al. Postoperative blindness associated with posterior reversible encephalopathy syndrome: a case report. J Anesth 2010; 24:783.