Ocular, oropharyngeal, dental, nerve, and extravasation injuries represent a notable source of perioperative complications that can be debilitating. Even minor postoperative complications are important to patients, and better efforts to prevent and treat such complications should lead to improved postoperative recovery and patient satisfaction.

I. Perioperative Ocular Injury can affect the anterior chamber of the eye (cornea and conjunctiva) or the posterior chamber of the eye, its blood supply, and the optic nerve. Severity ranges from transient blurring of vision to irreversible blindness. Transient blurring of vision can be attributed to cycloplegia from anticholinergic medications, use of ocular lubricants, excessive corneal drying, or a corneal abrasion. The most common perioperative ocular injury is corneal abrasion, which typically does not result in permanent visual changes. However, injuries affecting the posterior chamber, the optic nerve, and its blood supply, such as Ischemic Optic Neuropathy (ION) or Central Retinal Artery Occlusion (CRAO), usually result in some degree of permanent visual changes or blindness. In an ASA closed claims report, ocular injury accounted for 3% of all anesthetic claims.

A. Corneal Abrasions

Corneal abrasions occur due to disruption of the corneal epithelium and underlying corneal layers.

1. Epidemiology

a. Incidence. Corneal abrasion is the most common ocular injury in the perioperative period, with reported incidences ranging from 0.17% to 44%. In an ASA closed claims report, corneal abrasions accounted for 1.2% of all claims and 35% of eye injury claims.

b. Risk factors include:

1. Patient-related risk factors: advanced age

2. Surgical-related risk factors: Trendelenburg and prone positioning, large-volume blood loss, urologic surgery

3. Anesthesia-related risk factors: general anesthesia, greater length of PACU stay, use of oxygen during transport/recovery

2. Pathophysiology

The cornea forms the anterior portion of the globe and is composed of five layers. The outermost layer is a delicate epithelium that is continuous with the conjunctiva. The cornea is protected by a tear film that functions to prevent evaporation, lubricate the eyelids, supply dissolved oxygen to the cornea, irrigate the cornea of debris, and supply immunologic factors to the corneal surface. This protective film is regenerated by blinking. Corneal abrasions occur when the corneal epithelium and underlying layers are damaged. Mechanisms of injury include direct trauma, chemical injury, corneal drying resulting from failure of the eyelids to close properly (lagophthalmos), and pressure
on the globe leading to decreased oxygen delivery and corneal edema, which in turn leads to desquamation of the corneal epithelium. General anesthesia decreases tear production and normal protective reflexes, which further predispose patients to corneal abrasions.

3. Clinical significance

The corneal epithelium is self-regenerating, and the majority of corneal abrasions resolve within days to weeks without long-term sequelae. It is important to avoid secondary infection of the compromised cornea, because these can lead to permanent corneal ulceration. In an ASA closed claims analysis, corneal abrasions were associated with fewer permanent injuries (16%) and lower median claim payments than other ocular injuries.

4. Signs/symptoms include eye pain, blurry vision, increased tear production, eye redness, photophobia, excessive squinting, and foreign body sensation.

5. Diagnosis is based on clinical history, symptoms, and uptake of fluorescein dye by the corneal epithelium on slit-lamp examination.

6. Management consists of a combination of artificial tears and antibiotic ointment (erythromycin or bacitracin eye ointment QID × 48 hours). Ophthalmology consultation should be considered, particularly if symptoms do not resolve within 24 hours.

7. Prevention

Strategies to prevent corneal abrasions include careful covering of the eyes (with tape or eye patches) after induction of anesthesia, mindfulness of dangling objects over the patients’ face, and attention to patients emerging and recovering from anesthesia.

8. Outcome

In the majority of cases, corneal abrasions are not permanent injuries. In two retrospective studies, there were no cases of permanent injury resulting from perioperative corneal abrasions; however, of the corneal abrasions submitted to the ASA closed claims database, 16% resulted in permanent injuries.

9. Subsequent care

If the patient is asymptomatic after 48 hours, there is typically no follow-up required; however, if symptoms persist, the patient should follow up with an ophthalmologist.

B. Postoperative Visual Loss

1. Overall incidence

In retrospective studies, the overall incidence of postoperative visual loss (POVL) following nonocular surgery has ranged from 1 in 60,000 to 1 in 125,000. Spine and cardiac surgery are associated with higher incidence of POVL.

2. Ischemic optic neuropathy

a. Incidence. In retrospective studies, the incidence of ION following spine surgery has ranged from 0.028% to 0.1%, whereas ION following cardiac surgery has varied between 0.06% and 1.3%.

b. Risk factors. In prone spine surgery, factors found to confer higher risk of ION include male gender, obesity, anesthesia duration, large-volume blood loss, and low ratio of colloid to crystalloid fluid resuscitation. In cardiac surgery, risk factors include longer cardiopulmonary bypass times, low postoperative hemoglobin, transfusion of RBC or non-RBC blood components, and severe vascular disease.

c. Pathophysiology. There are two types of ION—anterior ION (AION) and posterior ION (PION). AION is more common among cardiac surgery, whereas PION is more common following spine surgery.
ION is thought to be caused by a decrease in O₂ delivery to the optic nerve because of hypoperfusion or embolism. The anterior optic nerve derives its blood supply primarily from the posterior ciliary arteries, whereas the posterior optic nerve is supplied by penetrating pial arteries and branches of the central retinal artery. Ischemic insult to the optic nerve initially causes optic nerve edema and later atrophy, leading to visual loss.

d. Clinical significance. Roughly 30% of patients will show some improvement following diagnosis, but ION usually results in some degree of permanent visual loss.

e. Signs/symptoms. Hallmark symptom of ION is painless visual loss.

1. AION—Symptom onset may not be evident until more than 24 hours postoperatively. Signs/symptoms of AION include altitudinal visual field deficit, central scotoma, blindness, and afferent pupil defect or nonreactive pupils with bilateral symptoms in more than half of the cases.

2. PION—Symptom onset is typically within 24 hours postoperatively. Signs/symptoms include blindness, altitudinal visual field deficit, central scotoma, afferent pupil defect or nonreactive pupils with bilateral involvement in two-thirds of the cases.

f. Workup. Ophthalmology consultation should be sought for anyone with postoperative visual changes.

1. Fundoscopic examination. With AION, initial fundoscopic exam reveals optic disc edema that progresses to disc pallor and atrophy within 2 to 3 weeks. In PION, the optic disc is normal, with disc pallor and atrophy becoming evident in 6 to 8 weeks.

2. Fluorescein fundus angiography is used to evaluate the circulation of the retina and choroid. If preformed shortly after symptom onset, this examination reveals a filling defect in the prelaminary region in AION, but is normal in PION.

g. Management. There is no proven treatment for ION; however, advocated treatments have included diuretics (mannitol, furosemide, and acetazolamide), high-dose steroids, surgical optic nerve decompression (in AION), and correction of hypotension and anemia.

h. Prevention. The ASA Task Force on Perioperative Visual Loss with Spine Surgery published an updated Practice Advisory in 2012. Advisory statements include the following:

1. Blood pressure should be monitored continually in high-risk patients, and deliberate hypotension be used on a case-by-case basis.

2. Colloids should be used along with crystalloids in patients with substantial blood loss.

3. Direct pressure on the eye should be avoided.

4. The patient’s head should be positioned at or above the level of the heart when possible.

5. Consideration should be given to staged spine surgeries to minimize time in the prone position.

i. Outcomes. Following initial diagnosis of AION, roughly 50% of patients have no improvement or worsening of visual symptoms, whereas 30% improve. In PION, results are similar: roughly 45% of patients have no improvement and 30% improve; however, PION is typically associated with more severe visual loss upon diagnosis.

3. Retinal artery occlusion

a. Epidemiology

1. Incidence. The overall incidence of retinal artery occlusion (RAO) is unclear; however, it seems to be highest in cardiac,
lower extremity joint, and spine fusion surgeries, with incidences of 0.06%, 0.009%, and 0.007%, respectively.

2. Risk factors. Because of limited available data, no firm risk factors have been established; however, retinal vascular occlusion has been associated with increasing age, male gender, blood transfusion, use of a horseshoe headrest, and anemia as well as cardiac, orthopedic, and spinal surgery.

3. Pathophysiology. Retinal vascular occlusion encompasses CRAO, which decreases blood supply to the entire retina, and branch retinal artery occlusion (BRAO), which decreases blood supply to only a portion of the retina. Mechanisms that have been described include: decreased arterial supply to the retina, retinal artery embolism, external compression of the eye, impaired venous drainage of the retina, and arterial thrombosis. The most common cause is thought to be external compression because of poor intraoperative positioning, which increases intraocular pressure and subsequently occludes the arterial circulation.

4. Signs/symptoms. Symptoms include painless visual loss, blindness (CRAO) or scotoma with intact peripheral vision (BRAO), and abnormal pupillary reactivity. Fundoscopic exam reveals a normal optic disc initially that later becomes atrophic and whitening of the retina with a cherry red macula.

5. Workup. Urgent ophthalmology consultation should be sought if RAO is suspected.

6. Management. No treatment has proven effective for RAO. Advocated treatments include acetazolamide or mannitol, local hypothermia, ocular massage, inhaled CO₂ for retinal artery vasodilation, hyperbaric oxygen therapy, and systemic as well as localized thrombolysis.

b. Prevention.

1. See Prevention of ION above.

2. Avoid external compression on the orbit and the horseshoe headrest.

3. Frequent checking of eyes during prone surgery.

c. Outcome. There are no outcome data available for perioperative RAO, but most cases result in permanent visual loss.

4. Cortical blindness refers to infarction of the parietal-occipital areas of the cortex, responsible for reception and integration of visual input, resulting in visual loss.

a. Epidemiology

1. Incidence. In one retrospective study analyzing the eight most commonly performed surgeries in the United States, the incidence of cortical blindness was 0.0038%, occurring most commonly among spinal fusion, cardiac, and hip surgery. In this study, cortical blindness was more common among patients less than 18 years of age. Other retrospective and prospective studies of cortical blindness following cardiac surgery have reported incidences between 0.2% and 5%.

2. Risk factors

a. No concrete risk factors have been established, but associated factors have included those that put patients at risk of stroke: age, diabetes, prior CVA/TIA, history of CAD and previous CABG, and history of vascular disease.

b. Surgical and anesthetic-associated factors include cardiac, hip, and spine surgery (see above) as well as cardiopulmonary bypass, hypotension, anemia, and hemodilution.

3. Pathophysiology. Cortical blindness results from infarction of the parietal-occipital areas of the cortex, which ultimately occurs due to decreased O₂ delivery and neuronal cell death. Mechanisms include hypoperfusion (global ischemia, cardiac arrest, hemorrhage, local ischemia, and watershed infarctions) as well as thrombotic or embolic events, intracranial hypertension, and vasospasm. In cardiac surgery, the major culprit of cortical blindness is thought to be embolism, particularly from aortic atherosclerosis. Paradoxical emboli have been described as a source of cortical blindness in patients with congenital heart disease, allowing a right-to-left shunt.

4. Clinical significance. Cortical blindness is frequently accompanied by other neurologic deficits. Following cardiac surgery, CNS dysfunction such as stroke (including cortical blindness) increases ICU length of stay and perioperative mortality.

5. Signs/symptoms. Cortical blindness is associated with

a. Painless visual loss with an intact pupillary response to light, which indicates that lesion is distal to the optic chiasm (and the pathways of the light reflex).

b. An unremarkable fundoscopic exam (normal optic disc, retina, macula, etc.)

c. Lack of response to visual threat

d. Normal eye movement

e. Depending upon the location of the lesion, the patient may have complete blindness (rare), which necessitates infarction of the bilateral parietal-occipital cortex, or unilateral blindness produces homonymous hemianopia.

f. Often accompanied by other neurologic deficits (other areas of cortex affected by the stroke)

6. Workup. Radiologic imaging with CT or MRI reveals the area of infarction. Ophthalmology and/or neurology consultation should be obtained.

7. Management. Visual recovery occurs over time. Treatment is supportive and aimed at minimizing stroke and cardiovascular risk factors as well as further neurologic insults.