Conference Lectures

                                   Perioperative  Vision  Loss
Dr Gautam Saha
Sr. Consultant ( Anesthesiology and Critical Care )
Bokaro General Hospital
Steel Authority Of India

Introduction
Perioperative vision loss is a rare but devastating complication which follows non ocular surgery.  Perioperative visual loss refers to the permanent impairment or total loss of sight associated with spine procedure   when general anesthesia is administered.( As per practice advisory of American Society of Anesthesiologists ). The perioperative period  includes  the time period from immediate preoperative assessment through discharge from acute health care facility. Conditions included under POVL are  : ( 1). Central Retinal Artery Occlusion and ( 2.) Ischemic Optic Neuropathy  (ION ) . High risk patients are defined as those who undergo prolonged   spine procedure in a prone position  and experience substantial blood loss.
Branch and Central Retinal Artery Occlusion
Central retinal artery occlusion ( CRAO ) decreases blood supply to the entire retina while occlusion of a retinal artery branch ( BRAO ) is a localized injury affecting a portion of the retina. In most instances this injury is unilateral  . Following causes have been identified which impair the blood flow to the retina  :

  • External compression of the eye.
  • Decreased blood supply to the retina due to Embolism or any other systemic cause.
  • Impaired venous drainage from the retina.

The most common cause of perioperative retinal artery occlusion is improper patient positioning resulting in external compression of the eye that produces sufficient intra ocular pressure ( IOP ) to prevent flow in the central retinal artery.
Emboli blocking flow in the central retinal artery or its branches may occur during open heart surgery. Impaired venous flow as a cause of CRAO  may  occur during radical neck surgery subsequent to Jugular vein ligation.
Clinical Features in Central Retinal Artery Occlusion
The clinical features in CRAO are as follows :

  • Painless vision loss.
  • Abnormal pupillary reaction.
  •  Fundoscopy show whitening of the retina and narrowing of the retinal   arteries.
  • BRAO is characterized by cholesterol emboli ( bright yellow glistening on fundoscopy ) or in case of in case of calcific emboli fundus gives a white non , glistening appearance.
  • Retinal arteries appear to be narrow on fundus examination.
  • A cherry red macula against a white ground glass background is the classic diagnostic sign of CRAO.

Patient Characteristic which may which may increase the risk of CRAO are :

  • Osteogenesis imperfect :  These patients have thin fibrous coat of the eye which make them more susceptible to raised IOP and there by CRAO.
  • Patients of Asian descent have a lower nasal bridge , which may increase the risk of external compression of the eye during prone position.

Prevention of CRAO
Following simple measures can go a long way to prevent to prevent CRAO :

  • Proper use of head positioning device such as square or circular foam head rests with cut outs for the eye as well as mirror to view the eye in the prone position.
  • Avoid horseshoe headrest.
  • Check the eye position at regular interval.
  • Place the patient in pin head holder if possible.
  • Pad the eye and eye to the extent possible.
  • Place a mirror below the operating table if transparent head piece is in use.
  • After endoscopic sinus  surgery  , patients should be checked for the signs of  acutely elevated IOP , suggestive of orbital hemorrhage.

  Mechanism of Retinal Ischemia

  • Findings of increased extracellular glutamate concentration during retinal ischemia and attenuation of ischemic injury in vitro and in vivo by glutamate receptor agonist  support a role of excitotoxicity. It is believed that an increased intracellular calcium ion concentration as a result of enhanced glutamate release ultimately initiates mechanisms that result in cellular destruction.
  • Two distinct blood flow pattern have emerged after a period of ischemia. In cats both retinal and choroidal blood flow increases dramatically ( hyperemia ) immediately after the end of ischemia. Hyperemia is of clinical relevance in reperfusion after a period of ischemia , increasing the blood flow when the vessels or the blood – retinal barrier is damaged might lead to macular edema .
  • Hypoperfusion is the other extreme in blood flow derangement. Delayed retinal hypoperfusion 1 to 4 hours after a period of ischemia has been shown in adult rats. The mechanism of change in the blood flow is not fully understood , although depletion of vasodilators such as adenosine and nitric oxide may be responsible. Most of these animal model experiments were carried out by ligating the central retinal artery. The retina still maintained some perfusion from choroidal vessels . Injury to the retina from increased external pressure is more severe than ligation of central retinal artery  , because with external pressure both the source of blood supply to the retina , from central retinal artery and choroidal vessels are obliterated.

  Branch Retinal Artery Occlusion

  • BRAO usually leads to permanent partial ischemic retinal damage. BRAO is primarily due to emboli but vasospasm has been reported in a few cases.
  • Emboli is usually from the surgical field or from cardio – pulmonary by pass equipment in cardiac surgery .Retinal fluorescing angiography reveals micro emboli during cardiopulmonary bypass.

Treatment
Currently available methods of treatment are not satisfactory . The treatment modalities currently in use are :

  • Occular massage to lower the IOP and thereby dislodge the emboli .
  • Intravenous acetozolamide administration helps in increasing the retinal blood flow.
  • Inhalation of 5% CO2 in oxygen helps in arteriolar dilation and increased delivery of blood to the retinal choroidal vessels .
  • Fibrinolysis through a catheter in the ophthalmic artery within 6to 8 hours of CRAO was associated with improved outcome.
  • Localized application of hypothermia is associated with decreased injury in animal studies.

 Ischemic Optic Neuropathy
Ischemic optic neuropathy (ION ) primarily presents spontaneously without warning signs , is a leading cause of sudden visual loss in patients 50 years of age or older  . ION is of 2  types ,anterior AION or posterior PION. AION or PION can be arteritic or non arteritic .  Arteritic ION , caused by temporal arteritis responds well to steroids .

  • Non arteritic ION more common than arteritic , is found in the perioperative setting . It has been reported after variety of operations but most commonly after instrumented spinal fusion surgery , cardiothoracic surgery , head and neck surgery and surgery of nose and sinuses.

 Mechanism of ION
Stimulated ischemia in optic nerve axons in vitro , culminates in axonal destruction. When oxygen delivery decreases , ATP is depleted leading to membrane depolarization , influx of sodium and calcium through specific voltage gated channel and reversal of Na+ -Ca2+ exchange pump. Calcium ion overload damages the cells due to activation of proteolytic and other enzymes . Disruption of the blood brain barrier due to the above event is an early event in AION , and fluorescein angiography in the affected patient shows dye leakage in the optic nerve .
 Patient Characteristics and Presentation

  • Most cases occurring after spine surgery are PION and usually bilateral. AION is more frequently reported after cardiac surgery.
  • Visual loss was typically within 24 to 48 hrs. of surgery.
  • The vision loss is usually painless with afferent pupil defect or non reactive pupil. There may be complete visual loss , no light perception or visual field defect .
  • In AION altitudinal visual field defect may be present.
  • Optic disc edema and hemorrhage are seen on symptom onset in AION whereas in PION optic disc appears normal even though the patient complains of visual loss .
  • Optic disc atrophy develops over several weeks.

Possible Pathogenic Factors

  • Prone position : IOP increases in prone position . It is advisable to position the patients head level or above the heart , where possible and in a neutral position during spine surgery performed in a prone position.
  • Length of surgery and hypotension : Surgery was longer in patients with post operative blindness after spine surgery versus unaffected patients. Hypotension may play a role either because of anatomic circulatory variation or abnormal autoregulation and inability to adequately compensate for decreased perfusion pressure.
  • Blood loss :  With uncontrolled hemorrhage where blood volume is not maintained , decreased oxygen delivery to optic nerve cold result in AION or PION. Just how long or how low the hemoglobin concentration must decrease to lead to this complication is not known.
  • Fluid replacement : ION has been reported in the setting of massive fluid replacement , probably due to altered haemodynamics within the optic nerve. Because central retinal vein exits out of the optic nerve , an internal compartment syndrome occur in the optic nerve due to fluid overload .
  • Vasopressors : Studies have shown an association between prolonged epinephrine infusion or long bypass time and ION in patients undergoing open heart surgery.
  • Erectile dysfunction drugs : AION has been described in patients who use these agents , but the cause and effect has been debated.

Treatment/ Prevention of ION

  • Diuretics : Acetozolamide lowers IOP and may increase flow to the optic nerve head . Mannitol and Furesemide may be helpful as they reduce edema.
  • Maintaining head up position may be helpful if increased ocular venous pressure is suspected.
  • Maintain the head in a neutral position with relative to the back .
  • Vasopressor treatment may be needed in patients who develop severe hypotension , especially who are on anti hypertensive like ACE inhibitors and Angiotensin II receptor blocker as these patients have a tendency to develop severe hypotension during general anesthesia.
  • Maintain caution while simultaneously instituting deliberate hypotension and hemodilution.

 Conclusion :
Much is unknown about about perioperative ION . The above review article outlines in brief the possible strategies an anesthesiologist may employ in the perioperative period while providing general anesthesia to patients undergoing spine surgery, although there no conclusive scientific evidence that above mentioned measures can prevent or treat ION.
References :
1.Millers Anesthesia , seventh edition.
2. Br . J . Anesth. (2009) 103 (suppl 1 ) : 131-140
3. Practice advisory by ASA task force  for  perioperative visual loss associated with spine surgery.