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Care of the eye during anaesthesia and intensive care
retina, while the choroidal circulation supplies the outer layers of the retina. Two or three posterior ciliary arteries arise from the ophthalmic artery, each of which divides into one long posterior ciliary artery and between eight and ten short posterior ciliary arteries. The short posterior ciliary arteries pierce the sclera and form the choriocapillaris, which supplies the anterior part of the optic nerve, the lamina cribosa and the choroid posterior to the equator. The choriocapillaris is composed of small lobules supplied by a terminal arteriole. Each lobule has draining venules at the periphery. The long posterior ciliary arteries travel forward in the suprachoroidal space to the ciliary body where they combine with the anterior ciliary arteries to form the major arterial arcade. Recurrent branches of the long posterior ciliary arteries supply the choroid anterior to the equator and anastomose with the short posterior ciliary arteries. Age-related arteriosclerotic changes in the orbital arteries are more severe in the most proximal vessels, which are similar to the rest of the arterial tree. In particular, arteriosclerotic changes tend to be most marked where the ophthalmic artery enters the orbit and at the origins of the posterior ciliary arteries and central retinal artery.3 Watershed zones are believed to occur between: • the choroidal and retinal circulation • the long posterior ciliary arteries • the short posterior ciliary arteries • the long posterior ciliary arteries and the anterior ciliary arteries • the choriocapillaris lobules Hence in the event of ischaemia the pattern of visual disturbance is variable.
Emert White Don B David
Abstract Perioperative eye injuries and blindness are rare but important complications of anaesthesia. The three most common ocular complications after general anaesthesia are corneal abrasion, ischaemic optic neuropathy and central retinal artery thrombosis; the latter two are important causes of postoperative blindness. This article aims to improve the readers’ knowledge of orbital anatomy, ocular physiology and the mechanisms of perioperative eye injuries.
Keywords central retinal artery occlusion; corneal abrasion; intraocular pressure; ischaemic optic neuropathy
Perioperative eye injuries and blindness are rare but important complications of anaesthesia. Eye injuries account for 2% of negligence claims against anaesthetists.1 The three main problems are ischaemic optic neuropathy, central retinal artery thrombosis, and corneal abrasion. A better understanding of orbital anatomy and ocular physiology, and the mechanisms of ocular injuries during anaesthesia may help to reduce their incidence.
Ocular blood flow and perfusion Ocular blood flow (OBF) is determined by the pressure difference between mean arterial pressure (Pa) and mean venous pressure (Pv), and the resistance to that flow (R).
Arterial supply to the optic nerve and retina The ophthalmic artery enters the orbit through the optic canal enclosed within the dural sheath of the optic nerve, and its first branch within the orbit, the central retinal artery, runs along the inferior aspect of the optic nerve, exiting from the dural sheath of the optic nerve approximately 10 mm behind the globe. The vascular supply to this posterior part of the optic nerve is from pial branches of the ophthalmic artery and the central retinal artery.2 The central retinal artery divides into four major vessels at the optic disc, each supplying one quadrant of the retina. The retinal vessels are distributed within the inner two-thirds of the
OBF =
Retinal blood flow is approximately 170 ml/100 g/min. Choroidal blood flow is high, (around 2000 ml/100 g/min) and accounts for between 60 and 80% of the retinal oxygen supply. Retinal blood vessels autoregulate in response to changes in arterial PaO2, PaCO2, arterial blood pressure, and perfusion pressure. The choroidal circulation responds to changes in PaO2, PaCO2 and arterial blood pressure, but not to increases in intraocular pressure (i.e. perfusion pressure). Inhalation of 100% oxygen causes retinal vasoconstriction, which reduces retinal blood flow by 60%. However, this reduction is not sufficient to prevent an overall increase in retinal pressure of oxygen (PO2). Inhalation of carbon dioxide causes retinal vasodilatation. Retinal blood flow increases by 3% for each 1 mm Hg increase in PaCO2. In most patients a stable retinal blood flow is maintained by autoregulation, over a wide range of perfusion pressures. However, in a significant proportion of patients (aound 20%) autoregulation fails to occur, which results in a progressive reduction in retinal blood flow at the onset of an increase in intraocular pressure or hypotension. As a result of the lack of
Emert White, FRCA, is Consultant Anaesthetist at Warwick Hospital, Warwick, UK. He qualified from the University of Birmingham and trained in anaesthesia in Nottingham and Southampton, UK, and Sydney, Australia, and Ann Arbor, USA. His research interest is ocular physiology. Don B David, FRCOphth, is Consultant Ophthalmologist at Warwick Hospital, Warwick, UK. He qualified from the University of Alberta, Canada and trained in ophthalmology in Liverpool, Bristol and Birmingham, UK, and Brisbane, Australia. His research interest is oculoplastic surgery.
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Pa − Pv R
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choroidal autoregulation during increases in intraocular pressure, the PO2 in the choroid and outer retina decreases. In primates irreversible damage occurs if ocular ischaemia exceeds 100 minutes, but in humans there is little correlation between occlusion time and visual outcome. In the upright position the pressure within the artery entering the eye is 60–70 mm Hg, while the intraocular pressure is 10–15 mm Hg, which under normal conditions provides a perfusion pressure of approximately 50 mm Hg. The episcleral venous pressure is approximately 3–7 mm Hg (7–8 mm Hg lower than the intraocular pressure), and increases by 3–4 mm Hg in the supine position. If large increases in episcleral venous pressure occur, part of this pressure will be transmitted into the intraocular veins, causing congestion with reduced perfusion pressure. An increase in volume of the intraocular vascular bed of 1–4 μl will increase the intraocular pressure by 1–2 mm Hg. Intraocular pressure varies with posture.4 Clinically significant increases have been observed in both awake and anaesthetized patients positioned prone. There have been two studies of the effect of the prone position in anaesthetized patients.5,6 Both studies found that the intraocular pressure increased markedly when the patient was turned prone, and that there was a tendency for increasing intraocular pressure with time. The cause of the observed increase in intraocular pressure is uncertain, but probably reflects increased intraorbital venous pressure: an intraorbital ‘compartment syndrome’.
The probable mechanism of ischaemic optic neuropathy following bilateral radical neck dissection is a reduction of perfusion pressure caused by an increase in venous pressure due to ligation of veins in the neck, and arterial hypotension. There are multiple reasons for postoperative visual loss after cardiac surgery: embolic, changes in oncotic pressure, ischaemic, thrombotic and surgical technique. The American Society of Anesthesiologists postoperative visual loss registry recently published its analysis of 93 cases of POVL after spinal surgery in the prone position.9 Ischaemic optic neuropathy occurred in 83 of the 93 patients. Of these patients PION was diagnosed in 56 cases. In 55 patients with ischaemic optic neuropathy, visual loss affected both eyes. The average duration of general anaesthesia for patients with ischaemic optic neuropathy was 9.8 hours, with a median blood loss of 2 litres. Of particular interest is that 70% of affected patients were male. Central retinal artery occlusion was the cause of unilateral visual loss in 10 patients (11%) in the registry. The average duration of general anaesthesia was 6.5 hours for these patients, with a median blood loss of 0.75 litres. Head rests (including horseshoe head rests) were used in all cases (in contrast to a 20% use of Mayfield pins ensuring the eyes were free of pressure in patients with ischaemic optic neuropathy). Stigmata of peri ocular trauma were present in 70% of patients with central retinal artery occlusion: • decreased supraorbital sensation • unilateral erythema • periorbital oedema • ptosis • corneal abrasion • ophthalmoplegia • proptosis. These findings suggest that central retinal artery occlusion tends to follow globe compression in prone patients. In contrast, the causes of ischaemic optic neuropathy seem to be multifactorial. There is no safe lower limit for either arterial blood pressure or haematocrit to avoid postoperative vision loss. Hypotension associated with increases in venous pressure, raised intraocular pressure and intraorbital pressure, and poor positioning when prone, can jeopardize the eye, especially in patients with vascular risk factors (smoking, hypertension, diabetes, atherosclerosis, polycythaemia). When patients are anaesthetized in the prone position, it is imperative that anaesthetists regularly check for globe compression and that only head rests specifically designed for the prone posture are used. There is currently no published protocol that recommends frequency of eye checks during anaesthesia. The eyes should be checked whenever a patient’s position is altered (table tilt for instance). We do not know how much pressure needs to be applied (or for how long) to cause retinal ischaemia. The most certain method of preventing globe compression during anaesthesia is by suspending the head by skull pins (Mayfield™). Face-contoured systems such as the Proneview™ device may represent an improvement on pillows and rings.10 The main risk factors for ischaemic optic neuropathy are listed below: • prone position • male sex
Optic nerve ischaemia: the causes of optic nerve ischaemia are listed below: • arterial hypotension (hypotensive anaesthesia, haemorrhage) • elevated venous or intraocular pressure (prone position) • increased resistance to flow (atherosclerosis, diabetes mellitus, hypertension, cigarette smoking, polycythaemia) • decreased oxygen delivery (anaemia). Postoperative visual loss There are two main causes of postoperative visual loss (POVL): ischaemic optic neuropathy and central retinal artery thrombosis. The former causes painless visual loss and is most often seen after prolonged spinal surgery in the prone position. The latter is believed to be the result of external pressure on the eye or emboli. Cortical blindness due to ischaemia of the occipital cortex is a rare cause of POVL.7 Ischaemic optic neuropathy is classified into either anterior ischaemic optic neuropathy (AION) or posterior ischaemic optic neuropathy (PION). AION is characterized by infarction at watershed zones (described above), a visual field defect, a pale oedematous optic disc, flame-shaped retinal haemorrhages, and oedema of the optic nerve in the posterior scleral foramen. PION occurs when the pial branches of the ophthalmic artery become occluded. Blood flow in the posterior part of the optic nerve is significantly less than that in the anterior part of the optic nerve. These pial vessels are end arteries that are not capable of autoregulatory control, and therefore this part of the optic nerve is more vulnerable to ischaemia in the event of a fall in perfusion pressure or anaemia.8 PION is characterized by a slower onset of visual field defect and mild optic-disc oedema. The incidence of ischaemic optic neuropathy varies between 1 in 30,000 and 60,000 operations. High-risk procedures are spinal surgery, cardiopulmonary bypass and bilateral neck dissection.
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• large blood loss • hypotension. The main risk factors for central retinal artery thrombosis are external pressure on the eye and a source of emboli. Ischaemic optic neuropathy and central retinal artery thrombosis should be suspected in patients who complain of visual loss on emergence from anaesthesia. An urgent referral to an ophthalmologist for advice on diagnosis and treatment should be sought. Patients with central retinal artery occlusion should have an echocardiogram and carotid ultrasounds to exclude an embolic source. Depending on the cause of postoperative visual loss, the treatment options are to reduce optic nerve fibre oedema as it passes through the posterior scleral foramen with steroids or osmotic diuretics, and optimizing oxygen delivery by maintaining a normal arterial blood pressure, alleviating the obstruction and
reventing damage to the retina. Treatment options for retinal p artery occlusion are: • ocular massage, which may dislodge the embolus to a point further down the arterial tree and improve retinal perfusion11 • anterior chamber paracentesis (removal of 0.1–0.4 ml of aqueous humour decreases intraocular pressure to 3 mm Hg) • intravenous methylprednisolone to reduce optic nerve fibre oedema • increasing perfusion pressure (carbonic anhydrase inhibitor and/or mannitol) • lateral canthotomy and cantholysis • vasodilator therapy or carbogen therapy (5% carbon dioxide, 95% oxygen) • thrombolysis. The prognosis for postoperative visual loss is poor.
Methods of eye protection during general anaesthesia Method
Advantages
Disadvantages
Manual closure of the eyelids
• Avoids trauma to the eye and eyelids • Avoids chemical injuries associated with tapes, gels and ointments • Protects the eye from exposure keratopathy, chemical injury and trauma
• Ineffective in 59% of patients because of lagophthalmus • Unsuitable for operations on the head and neck, and on patients in the lateral or prone position • Inadequate taping results in exposure keratopathy • Possibility of placing the tape directly onto the cornea • Trauma to eyelashes and eyelids on tape removal • Does not adequately protect the eye from chemical injury or trauma • Unsuitable for operations on the head and neck, and on patients in the lateral or prone position • Inadequate application results in exposure keratopathy • Possibility of placing the bio-occlusive dressing directly onto the cornea • Trauma to eyelashes and eyelids on removal of the dressing • Reports of chemical injuries to eyes following the use of ointments containing the preservatives, methylparaben and chlorambutanol • Causes blurred vision in 55–75% of patients • Causes a foreign body sensation in 25–62% of patients
Taping the eyelids closed Tape applied across the upper eyelid only
• Protects the eye from exposure keratopathy
Bio-occlusive dressings
• Protects the eye from exposure keratopathy, chemical injury and trauma
Ophthalmic ointment
• Equally effective at preventing corneal abrasions as taping the eyelids closed • Allows continuous perioperative monitoring of the eye during nasolacrimal and functional endoscopic sinus surgery • Long ocular retention time • Equally effective at preventing corneal abrasions as taping the eyelids closed and ointments • Increase in tear-film stability • Allows continuous perioperative monitoring of the eye during nasolacrimal and functional endoscopic sinus surgery • Reduces the risk of mechanical injury
Methylcellulose and hydro gels
Hydrogel dressing
Eye pads, with or without shields Hydrophilic contact lenses
Suture tarsorrhaphy
• Equally effective at preventing corneal abrasions as taping the eyelids closed and ointments • Increase in tear-film stability • Protects the eye from exposure keratopathy, chemical injury and trauma, particularly during head and neck procedures
• Relatively short ocular retention times • Causes a foreign body sensation in 2–3% of patients
• Not as effective as ointment in preventing corneal abrasions • Dressing becomes adherent to underlying tissues if permitted to dry out • Must be used with either taping the eyes closed or instillation of ointment/gel to adequately protect the eye • Risk of trauma on insertion and removal of the lens
• Causes trauma to the eyelids • Limits compensatory proptosis of the eyeball in the event of periorbital oedema
Table 1
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There are several methods to protect the eye during surgery and anaesthesia. No single method is completely effective and the various protective strategies may be associated with morbidity (Table 1). Vigilance regarding the perioperative care of the eye is required to reduce these rare but potentially devastating complications. ◆
Perioperative corneal abrasions The most common ocular complication associated with general anaesthesia is corneal abrasion. Its incidence varies between 0.03% and 0.17%, depending on the method of reporting. Prolonged surgery, lateral or prone positioning during surgery and operations on the head and neck are the main risk factors.12 Corneal abrasions are most commonly caused by exposure kerato pathy, chemical injury and direct trauma. General anaesthesia reduces the tonic contraction of the orbicularis oculi muscle, which causes lagopthalmos in up to 59% of patients. If the anaesthetist does not ensure that the eyes are fully closed, exposure keratopathy may occur in 27–44% of patients. Anaesthesia inhibits the protective mechanism afforded by Bell’s phenomenon (in which the eyeball turns upwards during sleep, hence protecting the cornea), decreases tear production, and tear-film stability. This combination of effects may lead to corneal epithelial drying and loss of lysosomal protection.13 Chemical injury can be caused by cleaning materials on the facemask and inadvertent spillage of antiseptic skin preparations onto the eye. The only antiseptic skin preparation that is not toxic to the cornea is preservative-free povidone-iodine 10% in aqueous solution.14 It is the agent of choice when antimicrobial skin preparation of the face is required. Antiseptic solutions with detergent readily penetrate the corneal epithelium, causing damage to the underlying iris, ciliary body, lens and blood vessels, leading to ischaemia. Chlorhexidine, cetrimide, aqueous povidone-iodine containing phenol and alcoholic antiseptic solutions cause oedema and de-epitheliali zation of the cornea. Trauma to the eyes can occur at any time during the perioperative period. During induction of anaesthesia it can be caused by ill-fitting facemasks, the laryngoscope, the anaesthetist’s fingers, watchstrap, identification badge or stethoscope. After induction of anaesthesia, trauma to the eyes has been caused by surgical drapes, surgical instruments and patient repositioning. In the postoperative anaesthetic care unit, the patient’s fingers, pulse oximeter probe, pillow, Hudson mask and removal of the occlusive tape from the eyelid may injure the eye. Patients often rub their eyes on emergence from anaesthesia. Placing the pulse oximeter probe on either the little or ring finger of the non-dominant hand can reduce the risk of trauma to the eye. Removal of occlusive tape from the eyelid at the end of surgery should be from the upper eyelid to the lower. Removal of the tape from the lower eyelid to upper causes the upper eyelid to open, potentially exposing the cornea to mechanical trauma and exposure keratopathy.
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References 1 The National Health Service Litigation Authority. Reports and Accounts. London: The Stationery Office, 2003. 2 Hart WM, ed. Adler’s physiology of the eye, 9th edn. St Louis: Mosby, 1992. 3 Kaiser HJ, Flammer J, Hendrickson P, eds. Ocular blood flow: new insights into the pathogenesis of ocular diseases. Basel: Karger, 1996. 4 Ozcan MS, Praetel C, Bhatti MT, et al. The effect of body inclination during prone positioning on intraocular pressure in awake volunteers: a comparison of two operating tables. Anesth Analg 2004; 99: 1152–8. 5 Cheng MA, Todorov A, Tempelhoff R, et al. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001; 95: 1351–5. 6 Hunt K, Bajekal R, Calder I, et al. Changes in intraocular pressure in anesthetized prone patients. J Neurosurg Anesthesiol 2004; 16: 287–90. 7 Chaudhry T, Chamberlain MC, Vila H. Unusual cause of postoperative blindness. Anesthesiology 2007; 106: 869–70. 8 Williams EL, Hart WM, Templehoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80: 1018–29. 9 Lee LA, Roth S, Posner KL, et al. The American Society of Anesthesiologists postoperative visual loss registry. Analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006; 105: 625–9. 10 Atwater BI, Wahrenbrock E, Benumof Jl, et al. Pressure on the face while in the prone position: proneview™ versus prone positioner™. J Clin Anesth 2004; 16: 111–16. 11 Huang E, Gordon K. Retinal artery occlusion. eMedicine. http://www. emedicine.com/emerg/topic777.htm (accessed 23 April 2007). 12 Roth S, Thisted RA, Erickson JP, et al. Eye injuries after nonocular surgery: a study of 60,965 anesthetics from 1988 to 1992. Anesthesiology 1996; 85: 1020–7. 13 White E, Crosse MM. The aetiology and prevention of peri-operative corneal abrasions. Anaesthesia 1998; 53: 157–61. 14 Morgan JP, Haug RH, Kosman JW. Antimicrobial skin preparations for the maxillofacial region. J Oral Maxillofac Surg 1996; 54: 89–94.
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