Shu Yi Teh

Introduction

Postoperative visual loss (POVL) is a rare complication of surgery. The spectrum of disability from POVL can range between transient blurring of vision, to permanent visual loss. Permanent POVL are most commonly attributed to central retinal artery occlusion, ischemic optic neuropathy, and cerebral vision loss, whilst other postoperative ocular injury can include corneal abrasion, which may or may not be associated with visual loss. The underlying mechanisms of POVL (postoperative visual loss) are not always fully understood, but it can arise from damage at any point along the visual pathway, from the cornea to the occipital lobe. The incidence for temporary POVL and permanent POVL of non-ocular procedures are 5.4 per 10,000 and 0.16 per 10,000 respectively, with the most prevalent cases occurring post cardiac surgery and spinal fusion (1,2).

Aetiology

The most common causes of ocular complaints postoperatively are corneal abrasion, postoperative ischemic optic neuropathy, cerebral visual loss, and central retinal artery occlusion. On the other hand, rare causes of postoperative visual loss can be due to acute angle-closure glaucoma, retrobulbar hematoma, pituitary apoplexy, glycine-induced visual loss and posterior reversible encephalopathy syndrome (1).

Corneal abrasion

Corneal abrasion is the leading cause of postoperative visual complaints. The potential mechanism during the perioperative period includes corneal drying due to corneal exposure compounded with reduced tear production from general anaesthesia. Direct trauma to unprotected eyes such as loose tape over the eyes or drapes over the face with incomplete lid closure and contact with monitoring equipment like ECG cables or pulse oximetry probes during airway management may also cause injury to the cornea. Sedated patients may rub their eyes after waking from anaesthesia, which can result in trauma to the cornea as well. Studies have also shown increased risk of corneal abrasion in older age patients, longer duration of surgery or anaesthesia, and surgery done in non-supine positions (3,4).

Postoperative ischemic optic neuropathy

The most common cause of permanent POVL in adults following non-ocular surgeries is ischemic optic neuropathy (ION), and is more frequently associated with cardiac, spinal, and orthopaedic surgeries compared to abdominal procedures (1). Some risk factors include male gender, age over 50, carotid artery stenosis, history of stroke, and various eye conditions such as hypertensive retinopathy, cataracts, glaucoma, diabetic retinopathy, and macular degeneration.

ION can be either arteritic (as seen in giant cell arteritis) or non-arteritic. Postoperative ION is always non-arteritic and is categorised into anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). The former affects the optic disc and the latter occurs behind the lamina cribrosa in the retrobulbar region. PION is thought to result from an infarction of the retrobulbar optic nerve and can be clinically differentiated from AION with a normal appearing optic nerve head in the first few weeks post-surgery.

Cerebral visual loss

Cerebral or cortical visual loss is one of the more common types of POVL. It is more prevalent in patients less than 18 years of age and is identified to have increased risk of 19-fold with spinal fusion surgery, more than 12-fold with cardiac surgery, and a 5-fold risk with non-fusion orthopaedic surgery when compared with abdominal surgery (1).

The pathophysiology is typically results from infarction of the posterior cerebral artery territories, caused by emboli, or less commonly from severe hypotension leading to watershed infarctions in the parieto-occipital areas. Consequently, these embolism and hemodynamic instability can occur during surgeries leading to cerebral visual loss (1).

Central retinal artery occlusion

Central retinal artery occlusion (CRAO) is the most frequently reported retinal cause of vision loss following non-ocular surgeries. It has been observed after head and neck procedures, prone spinal and cardiac surgeries. In cardiac and head and neck surgeries, CRAO is thought to be caused by emboli, while in prone spine surgeries, it is often linked to periorbital trauma, suggesting that globe compression may be the cause in these cases (5).

Risk factors for CRAO include those predisposing to vascular disease and hypercoagulability. The horseshoe headrest in prone procedures contributes to risk of CRAO as well (6), as slight movement of the head can cause globe compression due to close proximity of the headrest edges to the eyes. Emergency spinal fusion surgeries also pose an elevated risk (7).

Besides that, CRAO can result from vasospasm, embolism, or direct injury to retinal vessels in nasal or sinus procedures, caused by local anaesthetic injections containing epinephrine or corticosteroids, or from surgical trauma near the retinal vasculature (8,9). The use of nitrous oxide in patients who have recently undergone vitrectomy with gas bubble placement for retinal detachment is another rare cause of CRAO. Expansion of these bubbles can raise intraocular pressure and potentially block central retinal artery flow (10).

Branch retinal artery occlusion

Branch retinal artery occlusion (BRAO) is a less severe form of CRAO, where only a branch of the retinal artery is impacted, leading to a sectoral loss of retina and a partial visual field defect. BRAO are often due to retinal emboli. Fluorescein angiography can be used to demonstrate filling defects in the central or branch retinal artery to confirm diagnosis. Optical coherence tomography (OCT) can also reveal thickened, swollen, and hyperreflective inner retinal layers in the area supplied by the affected branch retinal artery (1).

Acute angle-closure glaucoma

Acute angle-closure glaucoma is a very rare postoperative eye injury, but it is a medical emergency that requires prompt treatment to prevent permanent vision loss (1). Non-surgical risk factors include genetic susceptibility (particularly individuals of Asian descent), hyperopia, and advanced cataracts. Several medications used perioperatively that may contribute to acute angle-closure glaucoma include over-the-counter decongestants, antihistamines, mydriatics, adrenergic drugs (like ephedrine), antiepileptic drugs (like topiramate), and anticholinergics (like scopolamine and atropine).

Retrobulbar hematoma

Retrobulbar hematoma is also a medical emergency that can result in permanent vision loss within hours due to optic nerve compression. It can be associated with endoscopic sinus surgery and also may occur in susceptible individuals after general anaesthesia but rarely, due to coughing, vomiting, straining or extreme blood pressure elevation, particularly with concurrent use of anticoagulation (1).

Pituitary apoplexy

Pituitary apoplexy is another life-threatening condition that has been reported following cardiac surgery and transurethral resection of the prostate. It is frequently associated with pituitary tumour and may lead to sudden pituitary gland haemorrhage or infarction (11). Risk factors include sudden increased blood flow to the pituitary gland, pituitary gland stimulation with hormonal manipulation, anticoagulation, or reduced blood flow in the pituitary gland due to raised intracranial pressure and severe haemorrhagic hypotension. It is an exceedingly rare cause of POVL, and because of the overlapping clinical presentation with PION, and further imaging is required to rule out in cases of suspected PION.

Glycine-induced visual loss

Transient perioperative visual loss can occur following the absorption of glycine solution, commonly used as a uterine irrigant during hysteroscopy or as a nonelectrolyte bladder irrigant during transurethral resection of the prostate (TURP). Rapid absorption of glycine from the uterus or bladder can lead to a range of symptoms collectively known as TURP syndrome, which includes mental status alterations, visual disturbances, seizures, hypotension, bradycardia, hypoxia, pulmonary oedema, brainstem herniation, or even death. Glycine crosses the blood-brain barrier to inhibit retinal neurons, particularly affecting the amacrine cells, resulting in visual symptoms such as a temporary decrease in visual acuity, blurred vision, or blindness (12,13).

Posterior reversible encephalopathy syndrome

Posterior reversible encephalopathy syndrome (PRES), also referred to as reversible posterior leukoencephalopathy syndrome, is marked by symptoms such as headache, altered consciousness, seizures, and visual disturbances. Visual symptoms can manifest as hemianopia, visual neglect, auras, visual hallucinations, and cerebral blindness (14). This syndrome is typically not observed during the perioperative period, but individual cases following procedures like thoracoscopic wedge resection, lumbar fusion, and hysterectomy have been reported (15-17).

References

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