Chapter 36: Anesthesia for Ophthalmic Surgery

Ophthalmic surgery poses unique problems, including regulation of intraocular pressure, control of intraocular gas expansion, prevention of the oculocardiac reflex and management of its consequences, and management of systemic effects of ophthalmic drugs. Mastery of general and sedation anesthesia techniques for ophthalmic surgery and a thorough understanding of potentially complicating issues—including the comorbidities of an increasing geriatric patient population—are necessary for optimal perioperative outcomes. In addition, the majority of ophthalmic procedures are performed under topical or regional anesthesia. The anesthesiologist must be familiar with their potential complications, including those of the accompanying sedation, even if not personally administering the topical anesthetic or the block.

Physiology of Intraocular Pressure

The eye can be considered a hollow sphere with a rigid wall. If the contents of the sphere increase, the normal intraocular pressure of 12 to 20 mm Hg will rise. For example, glaucoma is caused by an obstruction to aqueous humor outflow. Similarly, intraocular pressure will rise if the volume of blood within the globe is increased. A rise in venous pressure will increase intraocular pressure by decreasing aqueous drainage and increasing choroidal blood volume. Any event that alters arterial blood pressure or ventilation (eg, laryngoscopy, intubation, airway obstruction, coughing, Trendelenburg position) can also affect intraocular pressure (Table 36–1).

Alternatively, compressing the globe without a proportional change in the volume of its contents will increase intraocular pressure. Pressure on the eye from a malpositioned mask, improper prone positioning, or retrobulbar hemorrhage can lead to a marked increase in intraocular pressure, possible eye pain, and temporary or permanent visual changes.

Intraocular pressure helps to maintain the shape and the optical properties of the eye. Temporary variations in pressure are normally well tolerated. For example, blinking raises intraocular pressure by 5 mm Hg, and squinting (forced contraction of the orbicularis oculi muscles) may transiently increase intraocular pressure greater than 50 mm Hg. However, even brief episodes of increased intraocular pressure in patients with underlying low ophthalmic artery pressure (eg, from systemic hypotension, arteriosclerotic involvement of the retinal artery) may cause retinal ischemia.

When the globe is opened by surgical incision (Table 36–2) or traumatic perforation, intraocular pressure approaches atmospheric pressure. Any factor that increases intraocular pressure in the setting of an open globe may cause drainage of aqueous or extrusion of vitreous through the wound, serious complications that can permanently worsen vision.

Effect of Anesthetic Drugs on Intraocular Pressure

Most anesthetic drugs either reduce intraocular pressure or have no effect (Table 36–3). Intraocular pressure decreases with inhalational anesthetics in proportion to anesthetic depth. There are multiple causes for this: A drop in blood pressure reduces choroidal volume, relaxation of the extraocular muscles lowers wall tension, and pupillary constriction facilitates aqueous outflow. Intravenous anesthetics also decrease intraocular pressure, with the exception of ketamine, which usually raises arterial blood pressure and does not relax extraocular muscles.

Topically administered anticholinergic drugs result in pupillary dilation (mydriasis), which may precipitate or worsen angle-closure glaucoma. Systemically administered atropine or glycopyrrolate for premedication are not associated with intraocular hypertension, even in patients with glaucoma.

Succinylcholine increases intraocular pressure by 5 to 10 mm Hg for 5 to 10 min after administration, principally through prolonged contracture of the extraocular muscles. However, in studies of hundreds of patients with open eye injuries, no patient experienced extrusion of ocular contents after administration of succinylcholine. Thus, succinylcholine is not contraindicated in cases of open eye injuries. Nevertheless, dogma often trumps data and ophthalmic surgeons may request that it not be administered in certain circumstances. Unlike other skeletal muscle, extraocular muscles contain myocytes with multiple neuromuscular junctions, and depolarization of these cells by succinylcholine causes prolonged contracture. The resulting increase in intraocular pressure may have several effects: it will cause spurious measurements of intraocular pressure during examinations under anesthesia in glaucoma patients, potentially leading to unnecessary surgery, and prolonged contracture of the extraocular muscles may result in an abnormal forced duction test, a maneuver utilized in strabismus surgery to evaluate the cause of extraocular muscle imbalance and to determine the type of surgical correction. Nondepolarizing neuromuscular blockers (NMBs) do not increase intraocular pressure, and we advocate that succinylcholine be reserved for rapid-sequence induction.

Traction on extraocular muscles, pressure on the eyeball, administration of a retrobulbar block, and trauma to the eye can elicit a wide variety of cardiac arrhythmias ranging from bradycardia and ventricular ectopy to sinus arrest or ventricular fibrillation. This reflex consists of a trigeminal (V₁) afferent and a vagal efferent pathway. The oculocardiac reflex is most commonly encountered in children undergoing strabismus surgery, although it can be evoked in all age groups and during a variety of ocular procedures. In awake patients, the oculocardiac reflex may be accompanied by nausea.

Routine prophylaxis for the oculocardiac reflex is controversial, especially in adults. Anticholinergic medication is often helpful in preventing the oculocardiac reflex, and intravenous atropine or glycopyrrolate immediately prior to surgery is more effective than intramuscular premedication. However, anticholinergic medication should be administered with caution to any patient who has, or may have, coronary artery disease, because of the potential for increase in heart rate sufficient to induce myocardial ischemia. Ventricular tachycardia and ventricular fibrillation following administration of anticholinergic medication has also been reported. Retrobulbar blockade or deep inhalational anesthesia may also be of value in preempting the oculocardiac reflex, although administration of a retrobulbar block may itself initiate the oculocardiac reflex.

Management of the oculocardiac reflex includes (1) immediate notification of the surgeon and cessation of surgical stimulation until heart rate increases; (2) confirmation of adequate ventilation, oxygenation, and depth of anesthesia; (3) administration of intravenous atropine (10 mcg/kg) if bradycardia persists; and (4) in recalcitrant episodes, infiltration of the rectus muscles with local anesthetic.

A gas bubble may be injected by the ophthalmologist into the posterior chamber during vitreous surgery. Intravitreal air injection will tend to flatten a detached retina and facilitate anatomically correct healing. Nitrous oxide administration is contraindicated in this circumstance: The bubble will increase in size if nitrous oxide is administered because nitrous oxide is 35 times more soluble than nitrogen in blood (see Chapter 8). Thus, it tends to diffuse into an air bubble more rapidly than nitrogen (the major component of air) is absorbed by the bloodstream. If the bubble expands after the globe is closed, intraocular pressure will rise.

Sulfur hexafluoride is an inert gas that is less soluble in blood than is nitrogen—and much less soluble than nitrous oxide. Its longer duration of action (up to 10 days) compared with an air bubble can provide a therapeutic advantage. The bubble size doubles within 24 h after injection, because nitrogen from inhaled air enters the bubble more rapidly than the sulfur hexafluoride diffuses into the bloodstream. Even so, unless high volumes of pure sulfur hexafluoride are injected, the slow bubble expansion does not typically raise intraocular pressure. If the patient is breathing nitrous oxide, however, the bubble will rapidly increase in size and may lead to intraocular hypertension. A 70% inspired nitrous oxide concentration will almost triple the size of a 1-mL bubble and may double the pressure in a closed eye within 30 min. Subsequent discontinuation of nitrous oxide will lead to reabsorption of the bubble, which has become a mixture of nitrous oxide and sulfur hexafluoride. The consequent fall in intraocular pressure may precipitate another retinal detachment.

Complications involving the intraocular expansion of gas bubbles can be avoided by discontinuing nitrous oxide at least 15 min prior to the injection of air or sulfur hexafluoride, or by avoiding the use of nitrous oxide entirely. Nitrous oxide should be avoided until the bubble is absorbed (5 days after air and 10 days after sulfur hexafluoride injection). Avoiding nitrous oxide seems the simplest approach in these patients.

Topically applied eye drops are systemically absorbed by vessels in the conjunctival sac and the nasolacrimal duct mucosa (see Case Discussion, Chapter 13). One drop (typically, approximately 1/20 mL) of 10% phenylephrine contains approximately 5 mg of drug. Compare this dose with the intravenous dose of phenylephrine (0.05–0.1 mg) used to treat an adult patient with acute hypotension. Medications applied topically to mucosa are absorbed systemically at a rate intermediate between absorption following intravenous and subcutaneous injection. The two patient populations most likely to require eye surgery, pediatric and geriatric, are at particular risk of the toxic effects of topically applied medications and should receive at most a 2.5% phenylephrine solution (Table 36–4).

Echothiophate (phospholine iodide) is an irreversible cholinesterase inhibitor used in the treatment of glaucoma. Topical application leads to systemic absorption and an inhibition of plasma cholinesterase activity. Because succinylcholine is metabolized by this enzyme, echothiophate will prolong its duration of action. Paralysis usually will not exceed 20 to 30 min and postoperative apnea is unlikely. The inhibition of cholinesterase activity lasts for 3 to 7 weeks after discontinuation of echothiophate drops. Muscarinic side effects of echothiophate, such as bradycardia during induction, can be prevented with intravenous anticholinergic drugs (eg, atropine, glycopyrrolate).

Epinephrine eye drops can cause hypertension, tachycardia, and ventricular arrhythmias; the arrhythmogenic effects are potentiated by halothane. Direct instillation of epinephrine into the anterior chamber of the eye has not been associated with cardiovascular toxicity.

Timolol, a nonselective β-adrenergic antagonist, reduces intraocular pressure by decreasing production of aqueous humor. Topically applied timolol eye drops, commonly used to treat glaucoma, will often result in reduced heart rate. In rare cases, timolol has been associated with atropine-resistant bradycardia, hypotension, and bronchospasm during general anesthesia.

The choice between general and local anesthesia should be made jointly by the patient, anesthesiologist, and surgeon. Patients may refuse to consider local anesthesia due to fear of being awake during the operation, fear of the eye block procedure, or unpleasant recall of a previous eye block or local eye procedure. General anesthesia is indicated in children and uncooperative patients, as even small head movements can prove disastrous during microsurgery.

PREMEDICATION

Patients undergoing eye surgery may be apprehensive; however, premedication must be administered with caution and only after careful consideration of the patient’s medical status. Adult patients are often elderly, with systemic illnesses such as hypertension, diabetes mellitus, and coronary artery disease, and pediatric patients may have associated congenital disorders.

INDUCTION

The choice of induction technique for eye surgery usually depends more on the patient’s other medical problems than on the patient’s eye disease or the specific operation contemplated. One exception is the patient with a ruptured globe. The key to inducing anesthesia in a patient with an open eye injury is controlling intraocular pressure with a smooth induction. Specifically, coughing during intubation must be avoided by first achieving a deep level of anesthesia and profound paralysis. The intraocular pressure response to laryngoscopy and endotracheal intubation can be moderated by prior administration of intravenous lidocaine (1.5 mg/kg), an opioid (eg, remifentanil 0.5–1 mcg/kg or alfentanil 20 mcg/kg), or esmolol (0.5–1.5 mg/kg). A nondepolarizing muscle relaxant or succinylcholine may be used. Many patients with open globe injuries have full stomachs and require a rapid-sequence induction technique to avoid aspiration (see the later Case Discussion); despite theoretical concerns, succinylcholine does not increase the likelihood of vitreous loss with open eye injuries.

MONITORING & MAINTENANCE

Eye surgery often necessitates positioning the anesthesia provider away from the patient’s airway, making close monitoring of pulse oximetry and the capnograph particularly important. Endotracheal tube kinking, breathing circuit disconnection, and unintentional extubation may be more likely because of the surgeon working near the airway. Kinking and obstruction can be minimized by using a preformed oral RAE (Ring-Adair-Elwyn) endotracheal tube (Figure 36–1). The possibility of arrhythmias caused by the oculocardiac reflex increases the importance of closely monitoring the electrocardiogram. In contrast to most other types of pediatric surgery, infant body temperature may rise during ophthalmic surgery because of head-to-toe draping and minimal body surface exposure. End-tidal CO₂ analysis helps to differentiate this situation from malignant hyperthermia.

The pain and stress evoked by eye surgery are considerably less than during a major surgical procedure. “Lighter” anesthesia might be attractive if the consequences of patient movement were not so potentially catastrophic. The lack of cardiovascular stimulation inherent in most eye procedures combined with the need for adequate anesthetic depth can result in hypotension in elderly individuals. This problem is usually avoided by ensuring adequate intravenous hydration and by administering small doses of intravenous vasoconstrictors. Administration of nondepolarizing muscle relaxants to avoid patient movement is often used in such circumstances in order to allow reduced depth of general anesthesia.

Emesis caused by vagal stimulation is a common postoperative problem following eye surgery, particularly with strabismus repair. The Valsalva effect and the increase in central venous pressure that accompany vomiting can be detrimental to the surgical result. Intraoperative intravenous administration of drugs that prevent postoperative nausea and vomiting is strongly recommended.

EXTUBATION & EMERGENCE

A smooth emergence from general anesthesia is important in order to minimize the risk of postoperative wound dehiscence. Coughing or gagging due to stimulus from the endotracheal tube can be minimized by extubating the patient at a moderately deep level of anesthesia. As the time of extubation approaches intravenous lidocaine (1.5 mg/kg) may be given to blunt cough reflexes temporarily. Extubation proceeds 1 to 2 min after the lidocaine administration and during spontaneous respiration with 100% oxygen. Proper airway maintenance is crucial until the patient’s cough and swallowing reflexes return.

Severe discomfort is unusual following eye surgery. Scleral buckling procedures, enucleation, and ruptured globe repair are the most painful operations. Modest incremental doses of intravenous opioid usually provide sufficient analgesia. The surgeon should be alerted if severe pain is noted following emergence from general anesthesia, as it may signal intraocular hypertension, corneal abrasion, or other surgical complications.

Options for local anesthesia for eye surgery include topical application of local anesthetic or placement of a retrobulbar, peribulbar, or sub-Tenon (episcleral) block. All of these techniques are commonly combined with intravenous sedation. Local anesthesia is preferred to general anesthesia for eye surgery because local anesthesia involves less physiological trespass and is less likely to be associated with postoperative nausea and vomiting. However, eye block procedures have potential complications and may not provide adequate ophthalmic akinesia or analgesia. Some patients may be unable to lie perfectly still for the duration of the surgery. For these reasons, appropriate equipment and qualified personnel required to treat the complications of local anesthesia and to induce general anesthesia must be readily available.

RETROBULBAR BLOCKADE

In this technique, local anesthetic is injected behind the eye into the cone formed by the extraocular muscles (Figure 36–2), and a facial nerve block is utilized to prevent blinking (Figure 36–3). A blunt-tipped 25-gauge needle penetrates the lower lid at the junction of the middle and lateral one-third of the orbit (usually 0.5 cm medial to the lateral canthus). Awake patients are instructed to stare supranasally as the needle is advanced toward the apex of the muscle cone. Commonly, patients undergoing such eye blocks will receive a brief period of deep sedation or general anesthesia during the block (using such agents as etomidate, propofol, or remifentanil). After aspiration to preclude intravascular injection, 2 to 5 mL of local anesthetic is injected, and the needle is removed. Choice of local anesthetic varies, but lidocaine 2% or bupivacaine (or ropivacaine) 0.75% are common. Addition of epinephrine may reduce bleeding and prolong the anesthesia. A successful retrobulbar block is accompanied by anesthesia, akinesia, and abolishment of the oculocephalic reflex (ie, a blocked eye does not move during head turning).

Complications of retrobulbar injection of local anesthetics include retrobulbar hemorrhage, perforation of the globe, optic nerve injury, intravascular injection with resultant convulsions, oculocardiac reflex, trigeminal nerve block, respiratory arrest, and, rarely, acute neurogenic pulmonary edema. Forceful injection of local anesthetic into the ophthalmic artery causes retrograde flow toward the brain and may result in an instantaneous seizure. The postretrobulbar block apnea syndrome is probably due to injection of local anesthetic into the optic nerve sheath, with spread into the cerebrospinal fluid. The central nervous system is exposed to high concentrations of local anesthetic, leading to mental status changes that may include unconsciousness. Apnea occurs within 20 min and resolves within an hour. Treatment is supportive, with positive-pressure ventilation to prevent hypoxia, bradycardia, and cardiac arrest. Adequacy of ventilation must be constantly monitored in patients who have received retrobulbar anesthesia.

The adjuvant hyaluronidase is frequently added to local anesthetic solutions used in eye blocks to enhance the spread and density of the block. Patients may rarely experience an allergic reaction to hyaluronidase. Retrobulbar hemorrhage, cellulitis, occult injury, and contact allergy to topical eye drops must be ruled out in the differential diagnosis. Retrobulbar injection is usually not performed in patients with bleeding disorders or receiving anticoagulation therapy because of the risk of retrobulbar hemorrhage, extreme myopia because the elongated globe increases the risk of perforation, or an open eye injury because the pressure from injecting fluid behind the eye may cause extrusion of intraocular contents through the wound.

PERIBULBAR BLOCKADE

In contrast to retrobulbar blockade, in the peribulbar blockade technique, the needle does not penetrate the cone formed by the extraocular muscles. Advantages of the peribulbar technique include less risk of penetration of the globe, optic nerve, and artery, and less pain on injection. Disadvantages include a slower onset and an increased likelihood of ecchymosis. Both techniques will have equal success at producing akinesia of the eye.

The peribulbar block is performed with the patient supine and looking directly ahead (or possibly under a brief period of deep sedation). After topical anesthesia of the conjunctiva, one or two transconjunctival injections are administered (Figure 36–4). As the eyelid is retracted, an inferotemporal injection is given halfway between the lateral canthus and the lateral limbus. The needle is advanced under the globe, parallel to the orbital floor; when it passes the equator of the eye, it is directed slightly medial (20°) and cephalad (10°), and 5 mL of local anesthetic is injected. To ensure akinesia, a second 5-mL injection may be given through the conjunctiva on the nasal side, medial to the caruncle, and directed straight back parallel to the medial orbital wall, pointing slightly cephalad (20°).

Sub-Tenon (Episcleral) Block

Tenon’s fascia surrounds the globe and extraocular muscles. Local anesthetic injected beneath it into the episcleral space spreads circularly around the sclera and to the extraocular muscle sheaths (Figure 36–4). A special blunt curved cannula is used for a sub-Tenon block. After topical anesthesia, the conjunctiva is lifted along with Tenon’s fascia in the inferonasal quadrant with forceps. A small nick is then made with blunt-tipped scissors, which are then slid underneath to create a path in Tenon’s fascia that follows the contour of the globe and extends past the equator. While the eye is still fixed with forceps, the cannula is inserted, and 3 to 4 mL of local anesthetic is injected. Complications with sub-Tenon blocks are significantly less than with retrobulbar and peribulbar techniques. Globe perforation, hemorrhage, cellulitis, permanent visual loss, and local anesthetic spread into cerebrospinal fluid have been reported.

FACIAL NERVE BLOCK

A facial nerve block prevents squinting of the eyelids during surgery and allows placement of a lid speculum. There are several techniques of facial nerve block: van Lint, Atkinson, and O’Brien (Figure 36–3). The major complication of these blocks is subcutaneous hemorrhage. The Nadbath technique blocks the facial nerve as it exits the stylomastoid foramen under the external auditory canal, in close proximity to the vagus and glossopharyngeal nerves. This block is not recommended because it has been associated with vocal cord paralysis, laryngospasm, dysphagia, and respiratory distress.

TOPICAL ANESTHESIA OF THE EYE

Simple topical local anesthetic techniques have been used for anterior chamber (eg, cataract) and glaucoma operations, and, increasingly, the trend has been to eliminate local anesthetic injections entirely. A typical regimen for topical local anesthesia consists of application of 0.5% proparacaine (also known as proxymetacaine) local anesthetic drops, repeated at 5-min intervals for five applications, followed by topical application of a local anesthetic gel (lidocaine plus 2% methyl-cellulose) with a cotton swab to the inferior and superior conjunctival sacs. Ophthalmic 0.5% tetracaine may also be utilized. Topical anesthesia is not appropriate for posterior chamber surgery (eg, retinal detachment repair with a buckle), and it works best for faster surgeons with a gentle surgical technique that does not require akinesia of the eye.

INTRAVENOUS SEDATION

Many techniques of intravenous sedation are available for eye surgery, and the particular drug used is less important than the dose. Deep sedation, although sometimes used during placement of ophthalmic nerve blocks, is almost never used intraoperatively because of the risks of apnea, aspiration, and unintentional patient movement during surgery. An intraoperative light sedation regimen that includes small doses of midazolam, with or without fentanyl or sufentanil, is recommended. Doses vary considerably among patients but should be administered in small increments.

Patients may find administration of eye blocks uncomfortable, and many anesthesia providers will administer small incremental doses of propofol to produce a brief state of unconsciousness during the regional block. Some will substitute a bolus of opioid (remifentanil 0.1–0.5 mcg/kg or alfentanil 375–500 mcg) to produce a brief period of intense analgesia during the eye block procedure.

Administration of an antiemetic should be considered if an opioid is used. Regardless of the anesthetic technique, American Society of Anesthesiologists standards for basic monitoring must be employed, and equipment and drugs necessary for airway management and resuscitation must be immediately available.