North Zone Ophthalmological Society :NZOS

Vol.13 No. 1, October 2003

OCULAR COMPLICATIONS OF ANESTHESIA

Dr. Bashir Ahmad, Dr. Imtiyaz Ahmad

INTRODUCTION

Just as ocular drugs can have dramatic ramifications in their interaction with anesthetics, so also can anesthetic drugs and methods affect intraocular dynamics. Factors such as ocular pathologic lesions, anesthetic depth, arterial carbon dioxide partial pressure, pupillary size, change in extraocular muscle tone, hydration and use of adjuvant drugs such as muscle relaxants interact to determine the overall effect of anesthesia on the eye. ¹

The choice of anesthetic technique, principally between local and general anesthesia, must be individualized. General considerations include the nature and duration of the surgical procedure, coagulation status, the patients ability to communicate and cooperate and the surgeons personal preference. Of course, local anesthesia is not an ideal choice for patients who are deaf or speak a foreign language and those who have problems such as claustrophobia, excessive anxiety or confusion. Other relative contraindications include chronic cough, tremors and an inability to lie flat. Local anesthesia, however, is more frequently employed as it produces little risk, is easy to perform, has got rapid onset of action and is more economical in developing countries like India with large number of cataract cases.

Almost all major ocular surgeries like cataract extraction, glaucoma surgery, keratoplasty, iridectomy, squint and retinal detachment surgeries can be performed in adults under the effect of local anesthetics. However before a local anesthesia is given, an intravenous line should be started and patient should be put on a pulse-oximeter and preferably a cardiac monitor.

The main aims of local anesthesia for successful intra-ocular surgery include globe and conjunctival anesthesia, orbicularis akinesia, ocular akinesia and low intraocular pressure. These goals can be achieved by local anesthesia comprising surface anesthesia, facial block and retrobulbar block or a combination of surface anesthesia and peribulbar block.

(A)    COMPLICATIONS OF RETROBULBAR / PERIBULBAR BLOCK

The complications associated with peribulbar / retrobulbar technique, although rare (approximately 1 in 500 blocks), usually occur within 15 minutes of injection and are the result of apprehension, pain, over-sedation, local anesthetic toxicity, the method of needle placement or injection of local anesthetic.

Hypotension, bradycardia, cardiac arrest, diaphoresis and nausea are usually responses to fear or pain of injection or to manipulation of eyeball.

i)    Retrobulbar hemorrhage

This is a rare complication of retrobulbar / peribulbar block. Edge et al² in a study of 12500 consecutive retrobulbar blocks documented an incidence of retrobulbar hemorrhage of 0.44%. Acquired vascular disease was a significant risk factor. it can be recognized by severe ocular pain, proptosis, subconjunctival hemorrhage, eyelid ecchymosis and elevated intraocular pressure.

Investigations include intraocular pressure measurement and ophthalmoscopy to check the retinal circulation if the media are sufficiently clear. CT or ultrasound of the orbit can confirm the diagnosis.

Management may include osmotic diuresis, anterior paracentesis to lower IOP and lateral canthotomy for blood drainage. More extensive surgical decompression of the orbit is indicated when proptosis is progressive or if there is deterioration of the visual acuity. Surgery must be postponed for atleast two weeks.

ii)    Perforation of globe

This complication is more likely to occur in patients with elongated myopic eyes. Globe perforation can result from peribulbar or retrobulbar injection of local anesthetics. ³ The use of blunt needles reduces the risk.

Perforation may go unnoticed, or may be suspected in the presence of hypotony, poor red reflex and vitreous hemorrhage. Indirect ophthalmoscopy confirms the diagnosis if the media are clear. Retinal detachment is a common sequelae of this complication. The prognosis is good if the perforation is recognized and treated immediately.

iii)    Accidental central neuraxial injection

An initially insidious but potentially lethal complication also arises when the local anesthetic gains access to cerebrospinal fluid as a result of perforation of the meningeal sheaths that surround the optic nerve. Symptoms range from drowsiness, contralateral blindness and inappropriate shivering to more severe complications such as progressive respiratory depression, apnea, hemiplegia, aphasia, seizure, unconsciousness and cardiopulmonary arrest. ⁴ in a prospective series of 6000 consecutive retrobulbar blocks by Nicoll et al, the incidence of symptoms suggesting local anesthetic spread to the brain was 0.27%, with life-threatening complication occurring in 0.13% of patients. ⁵

Prevention involves using a block needle no longer than 3 cm ⁶ and performing the block with the eye in neutral gaze or looking infero-nasally, to render the optic nerve sheath less vulnerable to penetration.⁷

iv)    Post-operative vertical diplopia

Post-operative vertical diplopia resulting from muscle fibre degeneration in the inferior rectus muscle has been reported following regional local anesthetic injection for cataract extraction with an incidence of 1.4%. ⁸ Diplopia may be temporary or permanent. Possible causes include traumatic injection, myotoxicity of local anesthetic solution, bridle suture, surgical trauma, ocular compression. ⁹

v)    Post-operative ptosis

Post-operative ptosis following cataract surgery is reported with an incidence as high as 13%. This is speculated to result from myotoxic effects of the local anesthetics on the levator palpabrae muscle. However, that myotoxicity cannot be isolated as the sole factor is underscored by the observation that post-surgical ptosis is seen in patients who received general anesthesia.

vi)    Oculocardiac reflex

The oculocardiac reflex, a vagal response manifested by cardiac arrhythmias and hypotension may be elicited by pain, pressure on the conjunctiva, orbital structures or extraocular muscles. It also may be due to retrobulbar block ¹⁰, ocular trauma and direct pressure on tissue remaining in the orbital apex after enucleation ¹¹.

This reflex may appear during local or general anesthesia, irrespective of depth, but hypercapnia or hypoxemia is said to increase its incidence and severity. The reported incidence of the reflex varies considerably from 16% to 82% ¹². Commonly, the reports citing a higher incidence involve children because they have increased vagal tone.

Treatment requires administration of oxygen, Trendelenburg positioning, intravenous administration of crystalloid, discontinuation of pressure or muscle traction at eyeball (e.g., release of pinky ball) and on occasion intravenous administration of atropine.

(B)    COMPLICATIONS OF GENERAL ANESTHESIA

General anesthesia is fraught with the risk of elevating IOP at every phase, from the simple event of endotracheal intubation associated with laryngeal spasm, coughing and wheezing, which may be associated with a sudden increase in IOP and expulsion of the contents of an open globe ¹³, to the emotional stress of general anesthesia, resulting in a sympathetic discharge and pupillary dilation. The latter, in turn, may place the eye at risk to an attack of angle-closure glaucoma¹⁴. In stage two of general anesthesia pupillary dilation may place the eye at risk for an acute attack of angle-closure glaucoma.

Various techniques and drugs used in general anesthesia alter the IOP significantly, thereby putting the eye at risk of various complications.

i)    Inhalational agents

These are said to cause dose-related decreases in IOP ¹⁵. The precise mechanisms responsible for this purported decrease remains to be established, but hypothesized causes include depression of a central nervous system control center probably located in the diencephalic region, reduction of aqueous humor production, facilitation of aqueous humor outflow, or relaxation of extraocular muscle tension. However investigators maintain that if patients are well sedated before baseline measurements are obtained, the introduction of inhalational agents will not change IOP.

ii)    Central nervous system depressant agents

These agents in general decrease the IOP. Sedative doses of barbiturates lower IOP; thiopental reduces IOP in normal and glaucomatous eyes. Neuroleptanalgesia produces a 12% decrease in IOP in normocapnic patients. Intramuscular morphine produces a small decrease in IOP in normal and glaucomatous eyes, presumably by facilitating aqueous outflow.

iii)    Ketamine

Administered intravenously or intramuscularly, ketamine initially was said to increase the IOP significantly, as measure by indentation tonometry ¹⁶. In more recent studies using applanation tonometry and diazepam-meperidine preanesthetic medication, Ketamine produces no change in IOP when given to adults and a 25% decrease when given intramuscularly to children. However ketamine's propensity to trigger nystagmus and blepharospasm makes it a suboptimal agent for many types of ophthalmic evaluations or surgery.

iv)    Hypoventilation and Temperature

Hypercapnia and hypoxia increase IOP, whereas hyperventilation reduces it. These effect appear to be associated with changes in intracranial pressure consequent to vasodilatation or vasoconstriction. Hypothermia is thought to lower IOP by means of decreased formation of aqueous humor as well as vasoconstriction.

v)    Succinylcholine

Succinylcholine increase the IOP. Lincoff and colleagues ¹⁷, in 1955 were the first to report extrusion of vitreous after succinylcholine administration intraoperatively in the presence of an open eye. An average peak IOP increase of 8 mmHg occurs within 7 minutes. Postulated mechanisms for the ocular hypertensive effect of succinylcholine include tonic contraction of extraocular muscles, choroidal vascular dilatation and relaxation of orbital smooth muscle. A recent study suggests that the ocular hypertensive effect may be primarily the result of the cycloplegic action of succinylcholine producing a deepening of the anterior chamber and increased outflow resistance. ¹⁸

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