Postoperative Visual Loss

Dr. Deepak Ruparel
Assistant Professor,
Department of Anaesthesiology,
GMC, Nagpur

Perioperative visual loss after anaesthesia is rare but devastating complication that appears particularly after spine, cardiac and orthopaedic surgery. This review will discuss about incidence, suspected risk factors, diagnoses and management of POVL in non ocular surgery. Primary causes of perioperative visual loss includes central or branch retinal artery occlusion (CRAO or BRAO), ischemic optic neuropathy (ION), cortical blindness and acute glaucoma. However glycine toxicity after transurethral resection of prostate and patient receiving nitrous oxide after vitrectomy with vitreal gas bubble tamponade are also infrequent causes of POVL. Spine and cardiac surgery are associated with more frequent occurrence of    POVL with reported incidence of 0.03% and 0.086% in spine and cardiac surgery respectively. Although perioperative ION is rare two large retrospective studies showed incidence of approximately 1 in 60,000 to 1in 1,25,000.

Types of POVL:

Retinal Ischemia: Branch and central retinal artery occlusion: Central retinal artery occlusion affects blood supply        of entire retina while branch arterial occlusion is localised injury affecting part of it. Four causes have been implicated 1)External compression of     eye: It is most common cause and is due to improper positioning producing rise in intraocular pressure leading to stoppage of flow of central retinal artery E.g. spine    surgery 2) Decreased arterial supply to retina due to arterial embolism as may occur during cardiac surgery. 3) Impaired venous drainage of retina as it may follow radical neck dissection and jugular vein ligation 4) Arterial thrombosis due to systemic coagulation disorders.

Central Retinal Artery Occlusion (CRAO):
The cause of CRAO in most cases is external compression on eye         causing sufficiently rise in IOP to occlude retinal arterial circulation. Improper      head positioning or unintended head movement especially when horseshoe head rest is used may place eye in contact with head rest leading to occlusion of retinal artery flow. This is more common in patients with prone position as in spine surgery. Patient characteristics may       add to increase risk of CRAO as in altered facial anatomy, in osteogenesis imperfect where sclera and cornea are unusually thin and exophthalmos is common. POVL in CRAO is usually unilateral. Signs      and symptoms include paresthesia of supra orbital region ptosis, proptosis, eye lid oedema, chemosis, hazy or cloudy cornea, afferent pupil defect with loss of light perception. Fundoscopic examination reveals macular oedema with cherry red spot and attenuated vessels. Early orbital CT  or MRI shows proptosis and extra ocular muscle swelling. Ischemic ocular compartment syndrome usually found with retrobulbar haemorrhage after nasal sinus surgery has also been reported with spine surgery done in prone position and is believed to be due to external compression of eye. This       is also   seen in orbital emphysema and intra orbital bacitracin ointment during sinus surgery. This is an acute     ophthalmic emergency requiring prompt decompression to reduce IOP.

Branch Retinal Artery Occlusion (BRAO):
This is usually a result of emboli either from intravascular injection or circulating embolic material from surgical field or cardio-pulmonary bypass equipment in cardiac surgery, specially when bubble oxygenator was used. Injection of carmustine into internal carotid artery for treatment of glioma or fat injection into orbit for cosmetic purposes have been rarely reported to cause visual loss due   to RAO.

Retinal artery vasospasm in rare instances can cause BRAO as it may occur with local infiltration of anaesthesia with lidocaine or bupivacaine with epinephrine. Clinically it can lead to partial visual field loss or small scotoma in visual field. Management: In most cases, treatment is not satisfactory and leads to permanent loss of vision. Ocular massage to decrease IOP and dislodge an embolus can be given, but should not be attempted in glaucoma. Intravenous Acetazolamide can be administered to increase retinal blood flow. Five percent carbon dioxide in O2 can be given to enhance dilation and increase O2 delivery from retinal and choroidal vessels. Fibrinolysis through a catheter in the ophthalmic artery within 6 to 8 hours after spontaneous CRAO was associated with improved visual outcome. Localised application of hypothermia to the affected eye may decrease injury. Prevention as it is most  often caused by unintended application of     external pressure to the eye, steps must be taken to avoid compression of the globe. Pressure on the eye from anaesthetic masks is avoidable. If surgery is near the face, the surgeon’s arm must not be allowed to rest on the patient’s eye. In patients positioned prone for surgery, a foam headrest should be    used with the eyes properly placed in the opening of the headrest; the position of the head and eyes must be checked every 20 minutes. In the    setting of cervical spine surgery with the patient prone, the most effective method for preventing head movement is to place the head in pins and if horseshoe headrest is used, patient must be positioned prone with great caution. The head should be positioned straight in neutral position. The eyes and nose is to be placed in open portion of headrest so as to check them intermittently.

The Prone View is useful because it combines a foam headrest with a mirror immediately below, which enables the eyes to be seen easily during surgery. The use of goggles to cover the eyes is not advised when the head is positioned prone in a conventional square foam headrest. In nasal and sinus surgery and in neuroradiologic procedures, the most important principles are avoidance of inadvertent injections into, or compromise of, the ocular circulation. After endoscopic sinus surgery, patients should be checked for signs of acutely elevated IOP suggestive of orbital haemorrhage. If present, immediate ophthalmologic consultation should be obtained.        

Ischemic Optic Neuropathy:
Perioperatively, non arteritic ischemic optic neuropathy is more common, occurring in adults and most cases occurring after cardio      thoracic surgery, spinal fusion surgery, orthopaedic joint surgery, head and neck surgery and surgery on the nose and paranasal sinuses.

Patient characteristics: Two types of ION occur perioperatively: Anterior (AION) and posterior (PION). Anterior ION most frequently occurs after cardiac surgery while most cases of PION have been reported after spine surgery. Most cases of PION occurring after spine surgery are bilateral. The onset of visual loss is usually within first 24 to 48 hours after surgery and is noted on awakening. However later onset have also been reported particularly in patients who were mechanically ventilated postoperatively. Signs and symptoms include painless loss of vision, decreased or absent colour vision, complete visual loss, no light perception, afferent pupil defect or non-reactive pupils, or visual field defects. Optic disc oedema and haemorrhage are seen in AION while optic disc is normal in PION. Optic disc atrophy develops over period    of weeks to months. MRI is frequently inconclusive however, few reports have described as nerve enlargement or peri-neural enhancement suggestive of oedema. Visual evoked potential is abnormal while electroretinogram is unaffected. Possible pathogenic factors: Factors implicated in perioperative ION are long surgery; hypotension; blood loss; anaemia or hemodilution; altered venous hemodynamics; flow of CSF in optic nerve; abnormal auto regulation in the optic nerve; anatomical variation in blood supply of nerve; male gender; small cup-to-disc ratio; use of vasopressor; presence of systemic vascular risk factors, including hypertension, diabetes, atherosclerosis, hyperlipidemia, obesity and smoking history; prone position; lengthy surgery for spinal fusion; nature of intravascular fluid resuscitation; and other existing systemic abnormalities, such as sleep apnoea and hyper coagulability. Hypotension, lengthy surgery, blood loss, and large amounts of fluid administration occur frequently in many patients undergoing complex spinal surgery. Possibly, combination of these factors, together with abnormal auto regulation in posterior optic nerve, prothrombotic tendencies, and other patient specific factors, lead to decrease in oxygen delivery to the optic nerve sufficient to cause ischemic injury.

• Length of Surgery and Blood Loss: In study by Myers and associates as well as by Postoperative Visual Loss study group, length of surgery and blood loss were higher in patients with postoperative blindness after spine surgery. So patients undergoing anticipated long duration surgery with large blood loss are at higher risk and therefore staging of spinal fusion procedure may be advisable. In uncontrolled haemorrhage in which blood volume is not maintained, decreased O2 delivery to the optic nerve could result in either AION or PION. But how low or for how long the haemoglobin concentration must decrease to lead to this complication is unknown.
• Intraoperative Hypotension: Hypotension can potentially lead to decreases in perfusion pressure in the optic nerve and to ischemic injury because of either anatomic variation in the circulation or abnormal autoregulation and an inability to adequately compensate for decreased perfusion pressure. The degree of hypotension that is potentially dangerous is difficult to quantify because of the lack of data in the literature.
• Intravascular Fluid Replacement: Massive fluid resuscitation during lengthy complex spine surgery associated with substantial blood loss could be pathogenic in perioperative ION. Fluid administration could result in increased IOP, accumulation of fluid in the optic nerve, or both. Because the central retinal vein exits out of the optic nerve, an internal compartment syndrome may occur in the optic nerve. Alternatively, fluid accumulation in the vicinity of the lamina cribrosa may compress axons as they transit this region. CSF pressure may increase with fluid resuscitation and this relatively high CSF pressures in the intra orbital optic nerve can result in compression of optic nerve. However this isn’t proved yet. Use of crystalloids rather than colloids had increased risk of developing optic nerve oedema and visual loss. It is possible that the use of colloids may decrease oedema in the optic nerve during surgery, particularly when the patient is placed prone for surgery. However, at present, such oedema has not yet been demonstrated. So fluid administration could be a pathogenic factor in ION, especially in patients positioned prone or undergoing cardiac surgery, but the mechanisms involved, as well as the amounts and nature of fluid required, remain undefined.
• Anatomic variation in the circulation of the optic nerve may potentially predispose patients to the development of ION. The location of potential watershed zones in the anterior and         posterior circulation and the presence of disturbed auto-regulation, even in normal patients, are of concern. Human studies generally show preserved blood flow at clinically used or even lower ranges of perfusion pressure, but these studies have focused primarily on the anterior portion of the optic nerve. Measurement of blood flow is not feasible in retro laminar optic nerve. In animal studies, blood flow is preserved in various layers of the optic nerve, including the retrolaminar area, at a mean arterial blood pressure as low as 40 mmHg.
• Vasopressor: Hayreh and associates theorised that AION is related to excessive secretion of vasoconstrictors, which in turn could lower optic nerve perfusion to dangerously low levels. This theory was based on development of AION in patients who sustained massive blood loss and vasopressors are used to maintain blood pressure of the patient as after cardiac surgery. However,        α-adrenergic receptors are not found in optic nerve. Also the blood-brain barrier prevents entry of systemically administered agents, except possibly in the pre-laminar zone of the nerve. Therefore, a role of vasopressor use in ION remains unclear.
• Medical History: Medical history of hypertension, diabetes, coronary artery disease and cerebrovascular disease and use of drugs for erectile dysfunction has all been correlated but none has definite association. Although basis for association between atherosclerosis and ION postulated is that optic nerve vasculature would respond abnormally to changes in perfusion pressure but has not been studied in humans. Also it is        wise to discontinue erectile dysfunction drugs 24 to 48 hours prior to surgery due to possible risk of increased ION.
• Surgery on Nose and Paranasal Sinuses: Retrobulbar haemorrhage may follow surgical damage to the fragile lateral wall of ethmoidal cells, the lamina papyracea. Blindness can also occur after endoscopic sinus surgery as a result of direct surgical damage to the optic nerve, but indirect damage by compression from retrobulbar hematoma leading to ION is more common. Ocular compartment syndrome may occur requiring immediate decompression.

Prognosis, Treatment and Prevention: No proved treatment exists for ION. In their review of perioperative PION reports in the literature, Buono and Foroozan summarised the lack of proof that treatment altered the course of PION. In few cases, increasing blood pressure or haemoglobin, or applying hyperbaric O2 improved visual outcome. Acetazolamide decreases IOP and may improve flow to optic nerve and retina. Similarly, diuretics like mannitol and furosemide reduces oedema but with unproven benefits. Increasing ocular perfusion pressure or haemoglobin concentration may be appropriate when ION is found in conjunction with significant decreases in blood pressure and haemoglobin concentration. Maintaining the patient in a head-up position if increased ocular venous pressure is suspected may be advantageous, but its use must be balanced against decreased arterial supply with head-up posture.

Few general recommendations can be given for prevention of ION but with unproven benefits. The head should be positioned neutral relative to the back, and head-down positioning is discouraged. Arterial blood pressure should be maintained close to baseline in patients with poorly controlled hypertension or suspected atherosclerosis. Risks and benefits must be weighed when against possible surgical needs of deliberate hypotension in order to reduce blood loss. Hypertensive patients treated with Angiotensin converting enzyme inhibitors or angiotensin II receptor blocker, often together with beta blockers or calcium channel blockers frequently become hypotensive intraoperatively and might require vasopressors as patients may be refractory to ephedrine and phenyl epinephrine. Systemic risks exist for increasing blood pressure with vasoactive agents or by infusion of intravenous fluids, such as decreased renal, liver, and intestinal perfusion, congestive heart failure, and myocardial ischemia.

These risks are important considerations in deciding appropriate range for blood pressure and fluid resuscitation requirements. Whether hematocrit should be maintained at or near its baseline value is controversial. However, simultaneous deliberate hypotension and hemodilution to a hematocrit of less than 25% should be done with caution. Use of minimally invasive surgical techniques towards lumbar spine surgery and fusion, staging of complex spine procedures may reduce amount of blood loss and fluid requirements.

Cortical Blindness: Complete cortical blindness is bilateral visual loss with an absence of optokinetic nystagmus and of the lid reflex response to threat. The papillary response, eye motility, retina and optic nerve are normal. Damage to bilateral occipital cortex leads to complete blindness while localised injury produces homonymous hemianopia. Because the visual pathway travels through the parietotemporal lobes, a perioperative cerebrovascular accident affecting the internal carotid, middle, basilar, or posterior cerebral arteries is the common cause of cortical blindness while total blindness from bilateral occipital infarction is rare. Most reported cases have followed cardiac or thoracic surgery. It is usually accompanied by signs of stroke in parieto-occipetal region. Patient is unable to interpret sensory stimuli and papillary reflexes are preserved. In most cases vision improves over time with incomplete lesion in visual field and visual disorientation.

Pathophysiology: Cortical blindness can result from global ischemia, cardiac arrest,       hypoxemia, intracranial hypertension and exsanguinating haemorrhage, focal ischemia, vascular occlusion, thrombosis, intracranial haemorrhage, vasospasm and emboli. CABG is most common surgery associated with cortical blindness and major source of damage      to brain and vision is considered to be embolism from surgical field which may be fat or atheroma. Another suspected factor is transient decreases in blood flow to border zones of perfusion between the middle and posterior cerebral arteries, especially in patients with pre-existent cerebrovascular disease.

Prognosis, Treatment and Prevention: Visual recovery may be delayed but previously healthy adults show considerable recovery. Therefore, when cortical blindness is accompanied          by focal neurologic signs, treatment should be directed towards preventing progression of stroke. Strategies to prevent neurological injury during cardiac surgery includes decrease manipulation of aorta and embolisation, adequate removal of air and particulate matter from heart during valvular surgery, use of arterial line filter during CPB to reduce number of micro-emboli and maintenance of       adequate perfusion pressure to prevent episodes of hypoperfusion in patients with cerebrovascular episode.

Acute Glaucoma: Incidence of upto 0.1% have been reported by Gartner and Billet in patients undergoing spinal or general anaesthesia. Acute angle closure glaucoma occurs when passage of aqueous humor from the posterior to the anterior chamber is obstructed by apposition  of the     iris to the anterior surface of the lens. The    pupil is mid-dilated, with an associated papillary block. Patient has painful red eye, blurred vision, headache, nausea and vomiting and condition is usually bilateral. Treatment is usually with β-adrenergic antagonists, α-adrenergic agonists, carbonic anhydrase inhibitors, cholinergic agonists and corticosteroids.

American Society of Anaesthesiologists 2012 Task Force Summary of Advisory Statements

1. Pre-operative Considerations
   •  At this time there were no identifiable preoperative patient characteristics that predispose patients to perioperative posterior ischemic optic neuropathy (ION).
   • There is no evidence that an ophthalmic or neuro-ophthalmic evaluation would be useful in identifying patients at risk for peri-operative visual loss.
   • The risk of perioperative ION may be increased in patients who undergo prolonged procedures, have substantial blood loss or both.
   • Prolonged procedures, substantial blood loss or both are associated with a small, unpredictable risk of perioperative visual loss.
   • Because the frequency of visual loss after spine surgery of short duration is infrequent, the decision to inform patients who are not anticipated to be “high risk” for visual loss should be determined on a case-by-case basis.
2. Intra-operative Management
   Blood Pressure Management:
   • Arterial blood pressure should be monitored continually in high-risk patients.
   • The use of deliberate hypotensive techniques during spine surgery can be associated with the development of perioperative visual loss. Therefore, the use of deliberate hypotension for these patients should be determined on a case-by-case basis.
   • Central venous pressure monitoring should be considered in high-risk patients.
   • Colloids should be used along with crystalloids to maintain intravascular volume in patients who have substantial blood loss.
     
   • Management of Anaemia:
     Haemoglobin or hematocrit values should be monitored periodically during surgery in high-risk patients who experience substantial blood loss. A transfusion threshold that would eliminate the risk of perioperative visual loss related to anaemia cannot be established at this time.
     
   • Use of Vasopressors:
     There is insufficient evidence to provide guidance for the use of α-adrenergic agonists in high-risk patients during spine surgery.
     
   • Patient Positioning:
     The Task Force believes that there is no pathophysiologic mechanism by which facial oedema can cause perioperative ION. There is no evidence that ocular compression causes isolated perioperative anterior ION or posterior ION. However, direct pressure on the eye should be avoided to prevent central retinal artery occlusion (CRAO).
   • The high-risk patient should be positioned so that the head is level with or higher than the heart when possible.
3. Staging of Surgical Procedures:
   Although the use of staged spine surgery procedures in high-risk patients may entail additional costs and patient risks (e.g. infection, thromboembolism or neurologic injury), it may, also decrease these risks and the risk of perioperative visual loss in some patients.
4. Postoperative Management
   • The consensus of the Task Force is that a high-risk patient’s vision should be assessed when the patient becomes alert.
   • If there is concern regarding potential visual loss, an urgent ophthalmologic consultation should be obtained to determine its cause.
   • There is no role for anti-platelet drugs, steroids or intraocular pressure-decreasing drugs in the treatment of perioperative ION.

Conclusion: Visual loss can result in the perioperative period from retinal arterial occlusion, ION, cortical blindness or acute glaucoma. Visual loss after TURP     is transient; visual loss in patients anaesthetised with N2O after a vitrectomy and placement of a gas bubble tamponade may be permanent. In most of these cases visual prognosis is poor. Most of these cases are occurring after spine, cardiac or orthopaedic surgery. Risk factors for ION remains completely unexplained.

Reference:  
1. Millers Anaesthesia 8^th edition.