Perioperative Vision Loss

Etiology

The risk of POVL has consistently been shown to be highest during cardiac and spine surgery. However, it can occur in non-spine orthopedic surgeries and abdominal surgery.[2] The estimated incidence of POVL is around .03% for spine fusion and .09% for cardiac surgery.[3] Spine surgery from a posterior approach may have the highest rate of POVL. Spine surgery for scoliosis correction and posterior lumbar fusion have rates of POVL around (0.28%) and (.14%) respectively.[4] 

Ischemic optic neuropathy is the most common subtype of POVL for prone spine surgery, the estimates of which range from (0.017%) to (0.1%). Statistically significant risk factors other than patient-related characteristics associated with ischemic optic neuropathy following prone spine surgery include the use of the Wilson frame, anesthesia duration (as a surrogate for the surgical duration), estimated blood loss, and a lower ratio of colloid to crystalloid in administered nonblood perioperative fluid.[5]

Epidemiology

Most patients diagnosed with POVL following spine surgery were classified by the American Society of Anesthesiologists as grade I or II, indicating a low risk of anesthesia-related complications.[6] Therefore, the anesthesia risk assessment strategy for POVL is distinct from that of typical anesthesia risk stratification. There is a sex predilection for males without a clear, identifiable explanation.[3] POVL can occur at all ages; however, it is uncommon in patients younger than 12.[7] Overall, ischemic optic neuropathy is the most common specific diagnosis associated with POVL. The risks of the other subtypes of POVL vary by age. In the pediatric population (<18 years of age), cortical blindness is the most common etiology. Patients over 50 may be at higher risk for central retinal artery occlusion.[3]

Reports on obesity, defined as body mass index (BMI) greater than or equal to 30 kg/m, are conflicting. In theory, increased intraabdominal pressure leading to increased central venous pressure in the prone position should affect eye circulation; however, there are some reports where BMI did not significantly increase the risk of POVL.[7] Regarding preoperative comorbidities, the risk of POVL is twice as high in patients with peripheral vascular disease.[4] Evidence for preoperative hypertension and smoking have yielded contradictory results for POVL risk.[7][8] Other common medical conditions, including coronary artery disease, myocardial infarction, diabetes mellitus, prior ischemic stroke, hyperlipidemia, and kidney disease, are associated with an elevated risk of POVL.[7][6] Further studies are needed to delineate if preexisting eye disease is a risk factor for POVL.

Pathophysiology

The proposed common underlying mechanism among the causes of POVL is insufficient vascular perfusion to critical components of the visual pathway. In many patients, there is insufficient vascular perfusion to the essential structures of the eye itself. Insufficient vascular perfusion in the perioperative setting can be related to increased venous pressure and subsequent development of interstitial edema. The prone position places patients at risk for decreased venous return and stroke volume secondary to increases in intra-abdominal and intra-thoracic pressure. Larger abdominal girth, as seen in obesity, can further increase central venous pressure due to increased intraabdominal pressure.

In addition to body habitus, surgical positioning can also affect vascular perfusion to the visual pathways. The Wilson frame is used widely in lumbar spine surgery, positioning patients with the benefit of flexing the lumbosacral spine, widening the interspinous spaces, and providing easier access to pathology.[9] Due to the associated thoracic elevation with the Wilson frame, the headrests are considerably lower than the heart. This may result in increased venous pressure within the head.

Increased anesthetic time, particularly after 5 to 6 hours, leads to accumulated interstitial edema due to a prolonged decrease in venous return. POVL is also associated with higher blood loss, which is related to a reduction in cardiac output and perfusion, as well as increased inflammation, fluid shifts, capillary leak, and lowering oncotic pressure when replaced with crystalloid, increasing the risk of ischemic optic neuropathy.[10] Replacement of blood loss with colloid causes a smaller decrease in oncotic pressure with theoretically less edema formation. This may explain why anemia alone is not an independent risk factor, as anemia may instead serve as a surrogate marker for low oncotic pressure.[10] The underlying pathophysiology of POVL is not entirely understood and requires further research for validation.

History and Physical

Anterior Ischemic Optic Neuropathy

Patients may initially have normal vision after awakening from anesthesia for a few days, followed by painless, unilateral, or bilateral progressive vision loss. Relative afferent pupillary defect (RAPD) if unilateral or absent pupillary reflexes of involved optic nerves. Visual complaints may include scotoma, absent light perception, or altitudinal field cuts. On early funduscopic examination, there is an edematous optic disc with a background of attenuated vessels and peripapillary hemorrhages. On late funduscopic examination, the edema has resolved, the vessels appear normal, and there is no evidence of optic nerve pallor.

Posterior Ischemic Optic Neuropathy

In posterior ischemic optic neuropathy, patients experience painless and typically bilateral vision loss present immediately after awakening from anesthesia. RAPD is unilateral or absent pupillary reflexes of involved optic nerves. Visual complaints may include scotoma, absent light perception, or altitudinal field cuts.[10] On early funduscopic examination, the fundus is normal, with evidence of optic nerve pallor on a late funduscopic exam.

Orbital Compartment Syndrome

Patients complain of painful visual loss present upon awakening from anesthesia, which may progress over the following days. The painful vision loss is associated with acute periocular edema, conjunctival swelling, and proptosis.

Corneal Abrasion

Patients complain of painful unilateral or bilateral vision loss present upon awakening from anesthesia accompanied by tearing, the sensation of a foreign body, and photophobia. Visible abrasion or a foreign body may be visible on the inspection with fluorescein staining.

Central Retinal Artery Occlusion

Patients experience unilateral vision loss present upon awakening from anesthesia—sluggish or absent pupillary light reflex. On early funduscopic examination, patients may have a cherry-red spot at the macula in the background of the whitened ischemic retina. On late funduscopic examination, patients may have optic nerve pallor in the setting of a reperfused retina.[10]

Cortical Blindness

Cortical blindness involves vision loss upon awakening from anesthesia. If a unilateral cerebral hemisphere is involved, contralateral homonymous hemianopsia may be present with or without macular sparing. If bilateral cerebral hemispheres are involved, expect complete vision loss with or without macular sparing. In posterior reversible encephalopathy syndrome, altered consciousness presenting as agitation, confusion, or coma may be present.[11] Nausea, vomiting, and seizures may also be present.

Pituitary Apoplexy

In pituitary apoplexy, the vision loss, if present, is present upon awakening from anesthesia. The typical pattern is bitemporal hemianopsia or a junctional scotoma. In addition to visual loss, headache, nausea, vomiting, meningeal signs, altered mental status, and ophthalmoplegia may be present.[12]

Evaluation

Prevention and immediate recognition of POVL are paramount. Most delays are likely due to delayed recognition rather than deterioration following initially normal postoperative vision. Emergent ophthalmologic consultation is recommended for a more thorough ocular examination and to localize the anatomic lesion along the visual pathway.[12] If there is a concern for cortical visual loss, neurology consultation and stroke activation should be initiated, which may begin with a non-contrast computed tomography (CT) of the head to rule out an intracranial hemorrhage, then possibly followed by CT angiography of the head to rule out large vessel occlusion and ultimately magnetic resonance imaging (MRI) of the brain to delineate the extent of ischemic stroke.

Regarding intraoperative evaluation, real-time flash visual evoked potentials (VEP) are currently under investigation as a potentially useful tool for monitoring visual function during prone spine surgery.[13] The anesthetic regimen used during surgery can influence the stability of intraoperative VEP recording. A small study found that total intravenous (TIVA) is associated with higher VEP amplitude and shorter latencies than balanced anesthesia. This suggests that TIVA could be the most efficient anesthesia regimen when using VEP monitoring.[14]

Treatment / Management

Unfortunately, no treatment is effective for central retinal artery occlusion or ischemic optic neuropathy. Suppose the perioperative vision loss is secondary to cortical visual loss and on imaging. In that case, the patient is found to have occlusion of a cerebral artery contributing to deficits within the defined time-sensitive window. If not contraindicated, intravascular clot retrieval or thrombolysis may play a role.[15] 

Due to the inherent risk of POVL occurring more frequently in patients with prolonged operations greater than 5 or 6 hours, it is unlikely that many patients would be candidates for thrombolysis within the defined 3- to 4-hour window. In major surgery, such as posterior spine surgery, the risk of thrombolysis must also be weighed with the elevated risk of surgical site hemorrhage, which may lead to cord compression and paralysis. Management of cortical vision loss secondary to posterior reversible encephalopathy syndrome includes prompt control of seizures and blood pressure and discontinuation of possible responsible medications and other contributing factors.[16] If pituitary apoplexy is recognized on cranial imaging, prompt neurosurgical consultation is recommended, as urgent surgical evacuation within 48 hours can improve visual outcomes.[17] For suspected corneal abrasion, the treatment is to remove the foreign body if present and supportive ocular care.(B3)

Differential Diagnosis

The differential diagnoses for perioperative vision loss include the following:

• Ischemic optic neuropathy: Classified as either anterior or posterior ischemic optic neuropathy if ischemia is to the optic nerve head or posterior portion of the optic nerve, respectively
• Orbital compartment syndrome: Seen in conjunction with traumatic injury to the eye; direct eye compression may cause venous congestion with associated elevation in orbital pressure, compromising circulation to the orbit and adjacent intraocular structures [18]
• Corneal abrasion: May occur if the eye sustains direct trauma intraoperatively
• Central retinal artery occlusion: A retinal stroke due to decreased retinal perfusion, typically related to direct eye compression; the severity of vision loss depends on the occluded vessel territory, but in most patients, it is extensive [19]
• Cortical blindness: Can result from ischemic stroke involving the cerebral visual cortex or subcortical edema within the parietooccipital regions, resulting from a condition referred to as posterior reversible encephalopathy syndrome (PRES); cerebral ischemia may result from an altered hemodynamic state or embolism [20][21] 
  • The hypothesized etiology of posterior reversible encephalopathy syndrome is endothelial damage resulting in dysregulation of cerebral vasculature with transplant medications, such as tacrolimus and cyclosporine, increasing the risk.[22]
• Pituitary apoplexy: Results from spontaneous infarction or hemorrhage into a pituitary tumor or pituitary parenchyma
  • Although rare, it has been reported in the setting of spine surgery.[23] In the operative setting, it may be precipitated by anticoagulation, hemodynamic fluctuations, or the hemodilutional effect of fluid replacement.[8]

Prognosis

Ischemic optic neuropathy is the most common subtype of POVL in most patients. Consequently, most patients have not discovered an effective treatment, and the prognosis is poor.[24][25] Prevention is, therefore, the most effective treatment strategy. Although rare, spontaneous, full vision recovery is possible and has been reported.[26] Subtypes of POVL with a more favorable outcome, unfortunately, include the less common causes of POVL, which include pituitary apoplexy, cortical blindness secondary to PRES, and corneal abrasion.

Most patients with pituitary apoplexy who undergo surgery within 48 hours of the presentation will improve visual deficits.[17] The prognosis of cortical vision loss depends on the extent of cerebral ischemia. A typically reversible condition in PRES is not characterized by extensive ischemia but subcortical edema. Therefore, complete resolution results in most patients.[11] The prognosis for a corneal abrasion is also promising, with early recognition and appropriate supportive care.

Complications

POVL results in increased disability in patients who may already have a pre-operative disability, particularly within the spine population. Associated disability and decreased quality of life can significantly hinder rehabilitation and survival. Further studies are needed to quantify the impact of POVL on patient outcomes.