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Causes of postoperative ocular complaints

	Associated factors (not necessarily causal)	Clinical presentation	Duration of POVL	Workup	Treatment
Visual loss with pain
Corneal abrasion^[1-5]	Any type of surgery Prolonged surgery Exposure of cornea Trauma Surgery in non-supine position Increased age	Onset immediate after emergence from anesthesia Usually unilateral Painful Foreign body sensation Conjunctival erythema, tearing, photophobia Normal pupillary reflexes Blurred vision to no visual deficit	24 to 48 hours	History Symptoms External eye exam Pupillary light reflexes Fluorescein stain and slit lamp exam Topical proparacaine*	Prophylactic antibiotic and lubricant eye drops
Acute angle closure glaucoma^[6-9]	Any type of surgery General anesthesia Drugs: adrenergic, anticholinergic, antihistamines, antiparkinsonian, mydriatic, cholinergic, antidepressants Genetic/anatomic predisposition Female Hypermetropia	Onset may be delayed >12 hours postop Unilateral > bilateral Pain: boring quality with ipsilateral headache Intermittent blurring of vision with halos Nausea, vomiting Mid-dilated nonreactive pupil Conjunctival erythema Corneal epithelial edema IOP >21 mmHg	Until IOP controlled Treatment required within a few hours of onset to prevent permanent vision loss	History Symptoms External eye exam IOP >21 mmHg Avoid dilated funduscopic exam as it may worsen symptoms	Topical and systemic medication to reduce IOP Iridotomy for refractory ↑ IOP Temporizing maneuvers (ie, anterior chamber paracentesis) Avoid eye patch or other Rx that dilates pupils
Retrobulbar hematoma^[10-14]	Orbital trauma Head and neck procedures May occur (rarely) with other surgical procedures when other associated risk factors are present: orbital floor fracture and s/p repair, anticoagulation, uncontrolled hypertension, straining or Valsalva, sneezing, vomiting	Most vision loss within 3 to 24 hours, but may be delayed up to seven to nine days Unilateral Severe, stabbing pain; pressure Visual loss from hematoma causing optic nerve ischemia, direct compression, or central retinal artery occlusion Nausea, vomiting Diplopia, ophthalmoplegia Visual flashes Relative afferent pupillary defect or absent pupillary reflex Eyelid hematoma/ecchymosis Subconjunctival hemorrhage Proptosis	Depends on time to effective treatment Treatment required within a few hours of onset to prevent permanent vision loss	History External eye exam with pupillary light reflexes Imaging if necessary, but may delay Rx	Surgical emergency if visual loss present Lateral canthotomy or inferior cantholysis May give topical medications to lower IOP if surgery delayed
Pituitary apoplexy^[15-17]	Cardiac surgery; one case report after transurethral prostate surgery Reduced blood flow to pituitary: severe hemorrhagic hypotension, head trauma, pituitary irradiation Sudden increase in blood flow to the pituitary Stimulation of the pituitary Anticoagulation	Onset immediate to delayed by three months Severe headache Blurred vision to visual field defect to blindness Cranial nerve III commonly involved with dilated, nonreactive pupil Ophthalmoplegia Altered mental status Possible Addisonian crisis	Full recovery to permanent blindness (especially for chiasmal injuries)	CT/MRI imaging of head Lab: electrolytes, glucose, pituitary hormones	Surgical decompression for visual changes or altered mental status Endocrine replacement as necessary including high-dose corticosteroids
Posterior reversible encephalopathy^[18-22]	Preeclampsia, eclampsia Not commonly associated with surgery Immunosuppressants Chemotherapy Infection Vascular disease Renal disease	Three postoperative cases: onset immediate after emergence from anesthesia May have diffuse headache Blurred vision, homonymous hemianopia, blindness Nausea, vomiting Seizures Brainstem symptoms Hemiplegia Altered mental status Normal pupillary light reflexes Normal funduscopic exam Brisk DTRs Positive Babinski	Average seven days; range from one day to permanent if progresses to infarction	DWI MRI brain showing vasogenic edema posterior circulation, especially subcortical white matter	Antihypertensives Antiseizure medications for seizures Mannitol for cerebral edema Magnesium sulfate for preeclampsia/eclampsia
Visual loss without pain
Anterior ischemic optic neuropathy^[23-28]	Cardiac surgery Prone spine surgery Head and neck surgery Older age Vascular risk factors Anemia Vasopressor use Hypotension Small optic nerve cup-to-disc ratio Aberrant physiology or anatomy in the setting of reduced perfusion pressure	Onset immediate; may be delayed to POD one to three Bilateral > unilateral Progresses for a few days before stabilizing Altitudinal field cuts, scotoma to complete loss of vision with no light perception Relative afferent pupillary defect if asymmetric or amaurotic pupils Funduscopic examination: optic disc swelling, attenuated vessels, splinter hemorrhages	Usually permanent; may have small degree of recovery	History Symptoms Pupillary light reflexes External eye exam Dilated funduscopic exam	None proven Theoretical: optimized hemodynamics, glucocorticoids, mannitol, hyperbaric O₂
Posterior ischemic optic neuropathy^[23-29]	Prone spinal procedures Bilateral head and neck procedures Cardiac surgery Prolonged duration in position with increased venous pressure in head: prone, Trendelenburg, Wilson frame Large blood loss Large fluid resuscitation, high crystalloid/colloid ratio Wilson frame Male sex Obesity in prone position	Onset usually immediate after emergence from anesthesia, no progression Bilateral >> unilateral Altitudinal field cuts, scotoma to complete loss of vision with no light perception Relative afferent pupillary defect if asymmetric or amaurotic pupils Funduscopic exam normal	Usually permanent; may have small degree of recovery	History Symptoms Pupillary light reflexes External eye exam Dilated funduscopic exam	None proven Theoretical: optimized hemodynamics, glucocorticoids, mannitol, hyperbaric O₂
Cerebral or cortical visual loss^{[23,24,27,28]}	Spine fusion Cardiac surgery Nonfusion orthopedic surgery <18 years old Charlson risk index >0 Infarction due to emboli or hypotension	Onset immediate after emergence from anesthesia Bilateral: total blindness or small area preserved central vision Unilateral: contralateral homonymous hemianopia Pupillary light reflexes normal Funduscopic exam normal	Some recovery possible; rarely complete Treatment required within a few hours of onset to prevent permanent vision loss	CT or MRI	Acute stroke reperfusion therapy. Thrombolysis may be contraindicated in postoperative patients. Mechanical thrombectomy may be possible in some patients. Normalization of blood pressure, cardiac output, oxygenation
Central retinal artery occlusion^{[23-25,27,30,31]}	Prone procedures, especially spine Cardiac surgery Head and neck surgery Emboli Horseshoe headrest Intraocular gas bubbles within two months of GA with nitrous oxide	Onset immediate after emergence from anesthesia Unilateral Complete or nearly complete loss of vision in the affected eye Pupillary light reflex sluggish to absent; relative afferent pupillary if caused by globe compression; may have signs of periorbital trauma Retinal whitening on funduscopic exam	Usually permanent, severe visual loss in affected eye If treatment is attempted, it must be performed within a few hours of onset to prevent permanent vision loss	External eye exam IOP measurement Pupillary light reflexes Funduscopic exam	None proven Theoretical: inhaled O₂ with 5% CO₂, acetazolamide Controversial, especially in postoperative setting: thrombolysis
Glycine-induced visual loss^[32-37]	Transurethral prostate surgery Hysteroscopy Long operative time Large irrigant absorption Increased height of irrigation bag High-pressure irrigation Head-down position	Onset intraoperative if awake; up to several hours postoperatively Blurred vision Sluggish to fixed and dilated pupils Funduscopic exam normal	<24 hours; may be longer if severe hyponatremia and other neurological/cardiac dysfunction	History Lab: serum glycine and ammonia levels	Correct volume overload and electrolyte abnormalities Supportive

IOP: intraocular pressure; Rx: treatment; CT: computerized tomography; MRI: magnetic resonance imaging; DWI: diffused weighted imaging; GA: general anesthesia.

* For patients with suspected corneal abrasion and eye pain/discomfort, topical proparacaine may be used to make a presumptive diagnosis. After examining the eye to ensure the absence of a foreign body and confirming normal pupil reactivity, one drop of ophthalmic proparacaine 0.5% is instilled into the affected eye. Immediate relief of pain is consistent with the diagnosis of corneal abrasion, though relief will also occur if pain is caused by dry cornea or a small undetected foreign body. Ophthalmology should be consulted urgently for abnormal pupil reactivity, or if pain is not relieved within one minute after administration of proparacaine^[5].

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