Current concepts in retrobulbar anesthesia

Current concepts in retrobulbar anesthesia

SURVEY OF OPHTHALMOLOGY VOLUME 30 * NUMBER 2 * SEPTEMBER-OCTOBER 1985 DIAGNOSTIC AND SURGICAL TECHNIQUES STEVEN G. KRAMER, EDITOR Current Concep...

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SURVEY OF OPHTHALMOLOGY

VOLUME 30 * NUMBER 2 * SEPTEMBER-OCTOBER

1985

DIAGNOSTIC AND SURGICAL TECHNIQUES STEVEN

G. KRAMER,

EDITOR

Current Concepts in Retrobulbar Anesthesia ROBERT

M. FEIBEL,

M.D

Department of Ophthalmology, Washington University School of Medicine, St. Louis, Missouri

Abstract. Recently there have been major advances in the field of retrobulbar anesthesia. New agents which allow prolonged anesthesia and akinesia have been introduced. Several new techniques to administer retrobulbar anesthesia have been developed. The toxicity of local anesthetics and the complications arising from such injections have been studied, and ways to avoid and manage them have been expanded. (Surv Ophthalmol 30: 102-l 10, 1985)

Key words. bupivacaine etidocaine retinal vascular occlusion retrobulbar anesthesia retrobulbar hemorrhage scleral perforation toxicity of local anesthetics l

l

l

l

l

l

For over

100 years

performed esthesia

ophthalmic

surgery

has been

under local anesthesia.

Indeed,

local an-

was discovered

the summer ophthalmology, anesthesic cocaine

Carl

in the systemic ingested

numbed tongue -

the

the mucous

Austrian

Koller,

for eye surgery. by his friend

terested often

by an ophthalmologist.

of 1884 a young

resident

posterior part of the globe. Five minutes later the eyeball was removed in the usual way. The divisions of the recti tendons caused slight pain; that of the optic nerve and the dissection of the posterior part of the globe, none or almost none. When the ball was removed, the branches of the toothed forceps were thrust an inch deep through the wound into the orbital tissue, of which the patient felt nothing. The bleeding was scant. Recovery undisturbed.43

In in

set out to find a local He was introduced

Sigmund

Freud,

to

who was in-

effects of the drug. Both men drug,

and

membranes

observed of the

a fact that had been previously

that lips noted

it and by

However,

the injection

small amount

necessary

resulted

in serious

and

of cocaine,

even

for retrobulbar even

fatal

in the

anesthesia,

complications.

several other scientists, but ignored. Koller realized the significance of this observa-

Thus,

tion. He prepared aqueous solutions of cocaine and proved its anesthetic potency in animal and human eyes. This discovery was announced in the fall of

ophthalmology fell into disrepute. By the time procaine was introduced in 1905, ophthalmologists had come to reply on topical anesthesia from the repeat-

1884 and the news swept around the world.“” In December of that year, Hermann Knapp of New York was the first to describe retrobulbar anes-

ed instillation of cocaine. At first, the use of procaine was confined to the surgery of the ocular adnexa, and later subconjunctival procaine was used to sup-

thesia:

plement the sensory anesthesia of topical cocaine. In 1914, van Lint popularized the use of procaine injections for lid akinesia. Only in the 1930s did the retrobulbar injection of procaine for anesthesia and akinesia become widespread.“g Retrobulbar injections have been used to intro-

Enucleation of an eyeball under anaesthesia from injecting cocaine into the post-ocular connective tissue. The conjunctiva was first anaesthetized by instilling the solution. Then the globe was strongly drawn toward the nose by means of a forceps, and six minims of a 4% solution (painlessly) injected into the orbital tissue close to the

the use of cocaine

duce a variety 102

of drugs

for injectable

anesthesia

to the eye and surrounding

in

RETROBULBAR

103

ANESTHESIA

tissues - anesthetics, antibiotics, steroids, vasodilators, alcohol and other compounds. This review will concentrate on new techniques and agents for retrobulbar anesthesia which have been developed since this subject was last reviewed in 1974, both in this journal”’ and elsewhere.ti

New Agents ETIDOCAINE Etidocaine (Duranes?) is a local anesthetic of the amide type and is similar in structure to both lidoCaine and bupivacaine. However, it has a greater lipid solubility and protein binding capacity than lidocaine, which seems to account for its longer duration of action. Its metabolism is similar to that of other amide anesthetics in that it is broken down in the liver and its metabolites are excreted by the kidneys. In the laboratory, the potency of etidocaine is four times that of lidocaine. Studies suggest that its dosage should be about half that of lidocaine in order to obtain the long duration of action without increasing potential toxicity. Etidocaine has as rapid an onset as lidocaine, which is remarkable as longer acting anesthetics tend to have slower onset of action, e.g. hupivacaine. In general, the duration of analgesia and akinesia of etidocaine is twice that of lidocaine. An early study of 1% etidocaine showed that the average duration of a retrobulbar block was 9 hours, 55 minutes compared to 6 hours, 10 minutes for lidocaine.” Thus, the sensory block was 61% longer in duration, and no patient receiving etidocaine for cataract surgery required post-operative analgesia. The lid block for etidocaine was 7 hours, 28 minutes compared to 2 hours, 17 minutes for lidocaine. Smith and Kimb” found the mean onset of analgesia and akinesia to be approximately 3 minutes for either 1% etidocaine or 2% lidocaine. The mean duration of sensory anesthesia was 5 hours for etidoCaine and 3 hours, 19 minutes for lidocaine. The lid and globe akinesia was also significantly longer in the etidocaine group. Less postoperative analgesia was needed in the etidocaine patients. Smith and Smith6” showed that the addition of epinephrine did not increase the duration of the analgesia as compared to plain etidocaine. Another comparison of etidocaine with 1% mepivacaine showed similar lindings.6g Only one study”’ found fault with etidocaine, reporting that unsatisfactory anesthesia was more common with it than with lidocaine. However, in cases in which the anesthesia was initially satisfactory, the study again confirmed that less post-operative analgesia was necessary in the etidocaine group. In all but one of these studies,6q hyaluronidase

was added to the etidocaine (hyaluronidase and epinephrine were added to the lidocaine). Thus, use of 1% etidocaine with added hyaluronidase should be expected to produce a rapid onset of analgesia and akinesia of the globe with a signilicantly longer duration of action than lidocaine. Etidocaine does not require epinephrine, providing a decided advantage over lidocaine which requires epinephrine to maximize its duration of action. No complications were reported with the use of etidocaine, and excessive burning sensation during injection was not noted. BUPIVACAINE Bupivacaine (Marcaine@), an amide-type of anesthetic like lidocaine, was synthesized in 1957. It was first used for retrobulbar anesthesia in 1966 in a double-masked study that compared 0.5% bupivaCaine to 2% mepivacaine. This study did not find either the delayed onset or the prolonged duration of anesthesia which was noted in ail later studies.14 The next clinical study of bupivacaine in the ophthalmic literature did not appear until 1972. Again, 0.5% bupivacaine was compared to 2% mepivaCaine. Bupivacaine anesthesia had a duration about 1.5 times longer than mepivacaine, that is, 5 hours with bupivacaine compared to 3i/r hours with mepivacaine. Also, the globe akinesia lasted from 6-10 hours for the former compared to 4-6 hours for the latter. The slower onset of action was first noted as the major disadvantage of bupivacaine.” Bupivacaine was approved for use in the United States in 1973 and gained wide acceptance as a longacting anesthetic. Smith and Linn”” published a preliminary report in 1974, the same year that CaroIan et al” described the first major American series of retrobulbar anesthesia with bupivacaine. The duration of anesthesia of 0.75% bupivacaine was 3 hours and increased to 4% hours if epinephrine was added. The time of onset was in the range of 5-10 minutes and was not influenced by the addition of epinephrine; all injections had added hyaluronidase. These authors concluded that 0.5% bupivaCaine was not potent enough for retrobulbar block and that 0.75% should be used for complete akinesia of skeletal muscles. The only complication noted was significant burning and irritation when injection was given subcutaneously for lid block. No patient experienced severe postoperative pain and most had little discomfort; one patient complained of prolonged numbness after surgery.” Also in 1974, Gills and Rudisil12” used a combination of bupivacaine and mepivacaine, the latter being added to hasten the onset of action of bupivaCaine. They found that the combination produced anesthesia lasting for 6-8 hours, but that 0.75% bupivacaine alone produced anesthesia for 8-12

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FEIBEL

1985

hours. It was again concluded that only the 0.75% concentration of bupivacaine was adequate to produce satisfactory anesthesia and akinesia. The authors attributed the slower onset and incomplete akinesia found in earlier studies of bupivacaine to the use of the weaker 0.5% concentration. They also concluded that the combination of mepivacaine-bupivacaine was superior to that of lidocaine-bupivaCaine. They noted that hyaluronidase potentiated the effect of bupivacaine.28 Kennerdell et a13’ confirmed that the slow onset of bupivacaine akinesia was a limiting factor, but they found that the onset could be hastened with the use of a larger volume of the retrobulbar injection. The authors concluded that if plain bupivacaine was to be used, then 4 cc should be given. There was no correlation between the duration of the anesthesia and the volume of bupivacaine administered. They then used a mixture of 0.75% bupivacaine and 2% mepivacaine, and noted a more rapid onset of globe akinesia, the average being 5.7 minutes. The duration of the anesthesia was as long as that of plain bupivacaine (in contrast to Gill and Rudisill’s study28), and they felt that the combination was superior to plain bupivacaine.3g A carefully randomized and controlled study comparing 2% lidocaine to a combination of lidoCaine and bupivacaine again confirmed the longer duration of anesthesia in retinal detachment sur35 In this study, no hyaluronidase was added to gery . either solution (though epinephrine was) and a rapid onset of anesthesia and akinesia was noted. This was the only study in which hyaluronidase was not used. Chin and Almquist” reported that the addition of hyaluronidase quickened the onset of bupivacaine anesthesia, making it unnecessary to add lidocaine. They questioned whether the combination of lidoCaine and bupivacaine might reduce the effectiveness of both anesthetics. They noted that the addition of epinephrine did not increase the already long duration of bupivacaine. The duration of a 3 CC retrobulbar injection of 0.75% bupivacaine was 11 hours compared to 4 hours for lidocaine. Bupivacaine has been repeatedly shown to be an effective, long-acting, local anesthetic for retrobulbar anesthesia. Its main drawback, according to several studies, has been its prolonged and variable onset which may be reduced by the addition of hyaluronidase and the use of at least 3 cc of the 0.75% concentration. A mixture of bupivacaine and a short-acting anesthetic has worked in practice, but some studies show this is unnecessary. Theoretical objections to the use of this mixture are that the dilution might reduce the potency of each agent, and that, if a complication occurs, it would be diffi-

cult to determine

which

agent

is responsible.

New Techniques POSITIONING

OF THE GLOBE

Several new techniques for the administration of ophthalmic anesthesia have been introduced in the past few years. The first is a modification of the traditional Atkinson position of turning the globe upward and inward prior to the retrobulbar injection. Atkinson recommended this maneuver “to move the inferior oblique muscle and the fascia between the lateral and inferior rectus muscles forward and upward, out of the way,” He emphasized that only a blunted needle no longer than 35 mm should be employed. However, Unsold et al,‘O using computerized tomographic scanning of a cadaver orbit as the retrobulbar needle is introduced, have shown that in the Atkinson position, the optic nerve, the ophthalmic artery and its branches, the superior orbital vein, and the posterior pole of globe are all brought into close proximity to the tip of the needle. In addition, since the nerve is stretched, it may be more susceptible to puncture by the needle as it cannot move out of the way as easily. These authors recommend that the globe be positioned in either the primary position or in a slightly downward and outward position, and that the needle be directed not toward the orbital apex, as recommended by Atkinson, but slightly lower toward the inferior part of the superior orbital fissure. Other surgeons concur with this new recommendation. A recent report described 11 patients with complications presumed to arise from the retrobulbar needle or injection. Seven had visual loss: there were two cases of combined central retinal artery and vein occlusion, three cases of central retinal artery closure, and two cases of late optic atrophy. Four patients had central nervous system complications immediately after the injection: three cases of respiratory arrest and one grand ma1 seizure. All patients had been injected with the globe in the traditional Atkinson position, all but one with sharp needles. These authors also recommend keeping the globe in either the primary position or slightly downward and outward, using a needle no longer than 35 mm, and not crossing the midsagittal plane through the macula with the needle tip.* The major disadvantage to this technique is that since the ciliary ganglion and the nerves to the rectus muscle lie

*Grizzard WS, Pautler SE: Complications from retrobulbar injection. Poster 87, Annual Meeting, American Academy of Ophthalmology, 1984. Pautler SE, Grizzard WS, Thompson GE et al: Blindness from retrobulbar injection into the optic nerve. Personal communication.

RETROBULBAR

I 05

ANESTHESIA

inside the muscle cone, this maneuver in a greater frequency of incomplete

might blocks.

result

TYPE OF NEEDLE Many authors have expressed concern about the use of ultrasharp disposable needles for retrobulbar injection.“’ but note that they are more comfortable than blunted needles for repeated procedures in unsedated outpatients. This objection might be overcome by making a skin wheal ofanesthetic at the site of the lower lid injection site and waiting for anesthesia here before the blunted needle is used for the retrobulbar injection. Whether sharp or blunted needles are used, the use of the modified Atkinson ocular position will remind the surgeon of the proximity of the needle tip to the various orbital structures. One technique proposed to avoid the complications of retrobulhar anesthesia is the peribulbar block, in which the anesthetic is injected outside the musclr cone. The injections are given through the lids into the superior and inferior orbital tissues. These injections will also provide adequate lid block. The use of prolonged orbital pressure is necessary to allow complete anesthesia and akinesia.” This is a variation on the quadrantic block, which has been used to supplement retrobulbar injection. Another technique recently developed uses a modification of the retrobulbar injection to achieve akinesia ofthe orbicularis oculi muscles as well, thus obviating the need for a separate injection of the muscle or its nerve. Gills and Loyd” gave a regular injection of 5 cc of 0.75% bupivacaine by the transconjuctival route, preceded by a small injection of lidocaine to prevent the burning of the bupivacaine injection. Orbital pressure was then applied for 60 minutes. Presumably, enough of the solution diffuses into the lateral canthal area to paralyze the orhicularis muscle. Kimbrough et al”Ohave reported a variation of this technique. As the retrobulbar needle, inserted through the skin, is being withdrawn from the orbit, another injection is given into the subcutaneous space as the surgeon’s finger is pressed onto the lid just medial to the needle tip. This forces the anesthetic solution to flow toward the lateral canthus to paralyze the orbicularis. These techniques require at least 30 minutes of orbital pressure before the orbicularis block is apparent. This may be a disadvantage if the patient cannot be observed for this period of time. SOFTENING

OF THE EYE

Over the past 25 years, the concept of softening the eye prior to cataract surgery has emerged as an important safeguard. This was accomplished by the addition of hyaluronidase to the anesthetic, by or-

bital pressure, and by the use of either oral or parenteral osmotic agents. The classic paper on this subject by Everett et al” reported that the retrobulbar anesthetic accounted for 22% of the post-injection reduction in intraocular pressure (IOP), while orbital pressure accounted for most of the rest. The maximum reduction in IOP occurred within the first five minutes of the injection, and the magnitude of the fall was proportional to the degree of akinesia obtained. More recent studies have failed to confirm this finding. In two studies,“~‘” the use of a retrobulbar anesthetic did not produce a statistically or clinically significant fall in IOP. The reason for this discrepancy is not known. The use ofhyaluronidase for retrobulbar anesthesia was popularized by Atkinson as an aid in producing a more rapid and complete block. This suggestion has withstood the test of time. Not only have many authors given their clinical impression of this finding, a recent controlled study showed that hyaluronidase increased the speed of onset of both the facial and retrobulbar block of 2% mepivacaine compared to mepivacaine without hyaluronidase. However, the use of hyaluronidase did not increase the success rate of complete blocks.” The value of adding hyaluronidase to bupivacaine has also been confirmed. “J* USE OF CATHETER Several recent reports have described techniques for placement of a retained flexible catheter in the retrobulbar space to allow repetilive injection of anesthetics for prolonged anesthesia.“‘.“* These procedures are modifications of a technique originally described in 1956.“0 This technique would seem to be of limited value with the present availability of bupivacaine for prolonged anesthesia during surgery, but it could be useful in cases where anesthesia might be required over a period of several days, e.g. for repeated paracenteses after traumatic hyphema. A recent note reminded us that the pain associated with the injection of local anesthetics may be reduced by warming the solution (often just removed from the refrigerator) to about 40” C.H

Complications of Local Anesthetics Retrobulbar anesthesia is the most common anesthetic procedure in ophthalmic surgery and, in the vast majority of cases, has no serious complications. However, since this technique involves the blind insertion of a needle into a space occupied by a number of delicate and vital neural and vascular structures, various complications due to direct trauma of these structures must be anticipated occasionally. Complications may be arbitrarily divided into

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1985

those arising from the anesthetic compound itself and those arising from the needle used to inject the anesthetic solution. A recent prospective study of 1000 consecutive operations performed under local anesthesia reported nine cases of significant cardiovascular or pulmonary problems associated with the anesthetic administration.2” There were eight cases of hypotension requiring intervention with pressor agents or other cardiovascular drugs. There was one case of respiratory arrest. Eight cases were associated with the use of bupivacaine-lidocaine mixture and one received mepivacaine alone. For many ophthalmic surgeons, even a 1% adverse reaction rate warrants the presence or easy access to anesthesiology personnel and equipment at the time of administration of ophthalmic anesthesia. The toxic effects of local anesthetics on the central nervous and cardiovascular systems are generally due to inadvertent intravenous injection. Although reactions can occur from rapid absorption from properly placed solutions, this mechanism is much less common. The maximum safe dosage of local anesthetics in any given patient is subject to many variables. In general, for a single dose peripheral nerve block in adults of any sex, weight, height, or underlying disease, up to 400 mgm of bupivacaine or 450 mgm of etidocaine is considered safe. These figures are derived from anesthesia other than in the orbit and all figures assume epinephrine has been added.5’ However, remembering that even 10 cc of 0.75% solution contains only 75 mgm of bupivaCaine, the doses used in retrobulbar anesthesia and facial nerve block are far below those generally considered toxic. The usual signs of toxicity to local anesthetics first involve the central nervous system. Initial signs are excitatory in nature, with tremors, agitation, and slurred speech progressing to generalized convulsions. This stage is then followed by nervous system depression, with respiratory depression and arrest, and finally cardiovascular collapse. Toxic effects seen following retrobulbar injection of bupivacaine are frequently different from those noted above. Although grand ma1 seizures after retrobulbar bupivacaine have been reported twice,47,52 this is not the usual clinical picture. The more common story is the sudden onset of respiratory depression, apnea and loss of consciousness, without the usual preceding convulsive state. There are nine well documented cases in the literature, as well as many other anecdotal cases. Many were relatively young patients, and live of the nine were diabetic. Six patients had received 6 cc or more of 0.75% bupivacaine, and three had received a mixture of bupivacaine and a shorter-acting agent. The pa-

FEIBEL tients became abruptly drowsy, unconscious, and showed respiratory depression preceding apnea. All patients were treated with mechanical ventilation until, after 15 to 20 minutes, spontaneous respirations resumed. All patients recovered uneventfully and no case proceeded to circulatory collapse. 6.7.47.51.58.63 The pathogenesis of this potentially lethal complication is not completely understood. Presumably the bupivacaine gains rapid access to the area of the respiratory nucleus (which lies superficially in the midbrain) and interferes with spontaneous respiration. This continues until the flow of cerebra-spinal fluid washes it away and respiration resumes. In one case where the retrobulbar anesthesia was a mixture of bupivacaine and mepivacaine, a spinal tap performed 15 minutes after the onset of apnea revealed 2.5 microgram/cc of mepivacaine and no measurable bupivacaine.“8 How the anesthetic solution gains access to the brain is unknown. Even an injection of 6 cc of 0.75% bupivacaine is a dose of only 45 mg, which is lower than the usual toxic dose given intravenously to normal human volunteers. In cases of respiratory arrest, the blood level of bupivacaine is well below that usually considered dangerous.* Thus, inadvertent intravenous injection is not a likely mechanism for this complication. A second possibility would be inadvertent intraarterial injection. Presumably the retrobulbar needle penetrates the ophthalmic artery or its branches, and the force of the injection causes the anesthetic solution to flow retrograde in the artery back to the internal carotid artery, where it then flows directly into the brain. This mechanism has been shown to occur in the area of the face and mouth in both to this baboons and monkeys. 2.3A major objection mechanism is that in no case was there blood in the syringe upon aspiration prior to injection, nor was there evidence of orbital hemorrhage from laceration of an orbital artery. However, cases have been reported where retrobulbarly injected steroids appeared in the central retinal or choroidal vessels without associated signs of retrobulbar hemorrhage.22~25 The third and most likely mechanism is direct injection into the central nervous system via the sheaths of the optic nerve. This route has been shown to occur in man following the injection of radio-opaque dye for positive-contrast orbitography”“.49,57 and in the cadaver.lg Another route for direct injection into the central nervous system would be via the superior orbital fissure. Similar

*Wittpenn

JR: Personal

communication.

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ANESTHESIA

cases have been reported following injection into the nasal passages34 and the pterygo-palatine fossa.“” In these reports, direct injection into the subarachnoid space was presumed to be the reason for the complication. Methods to reduce the chance of this complication include using a short needle with a blunted tip, aspirating the syringe prior to injection, reducing the volume of the injectate, and lessening the force with which it is injected. Patients receiving a retrobulbar anesthetic should have constant monitoring and the availability of persons and equipment for immediate cardiopulmonary resuscitation. In a prospective study, Wittpenn has shown that the incidence of respiratory arrest following retrobulbar bupivacaine was 8 cases during 3600 injections.* A striking finding was that this complication was much more frequent when the bupivacaine was mixed with 4% lidocaine than when the same amount of bupivacaine was mixed with 2% lidoCaine. This finding suggests that this syndrome is not specific to bupivacaine alone, but can result from other anesthetics. A unique complication of’ bupivacaine was reported in a series of patients undergoing cyclocryotherapy. A number of patients experienced prolonged pain (lasting an average of 15-30 days) while those having lidocaine anesthesia had an average duration of pain of only 3-4 days.’ This has also been reported anecdotally in patients after cataract surgery.5” All those cases had pure bupivacaine injected; this problem has not been reported with bupivacaine mixed with another anesthetic. It is difftcult to explain this observation. It has recently been proposed that the diplopia seen following retrobulbar anesthesia could be explained by a direct myotoxic effect of the anesthetic on the extraocular muscIe. This hypothesis has been demonstrated in rats following retrobulbar injection of the commonly used anesthetics.** Several surgeons have commented on the prolonged (up to 24 hours) anesthesia, akinesia, and amaurosis after bupivacaine injection.

Complications RETROBULBAR

of Retrobulbar

Injections

HEMORRHAGE

Orbital hemorrhage following retrobulbar injection is generally considered to be a minor annoyance that causes cancellation of elective intraocular surgery. However, severe visual loss may result from such a hemorrhage.

*Wittpenn

JR:

Personal

communiration.

**Rainin EA. Carlson BM: Postoperative diplopia and ptosis clinical hypothesis based on the myotoxicity of local anesthetics. Personal communication.

a

The incidence of hemorrhage from retrobulbar injections is estimated to be about ~‘Yo.“~Gifford, using a sharp 5 cm needle designed for deep orbital injection, noted an incidence of 5%.” This prompted him to switch to a blunt needle which reduced his rate to zero in the next 300 cases. Atkinson reported no retrobulbar hemorrhages in 20 years of practice using a blunted 3.5 cm needle.’ Other factors which might reduce this complication would be the accurate and gentle insertion of the needle, and slow injection of the solution as the needle pierces the orbital septum to push the blood vessels ahead of the needle. However, since the placement of the needle is done in blind manner, a hemorrhage will occasionally occur. Orbital hemorrhages vary in severity. Some are of venous origin and spread slowly. Signs of a severe hemorrhage of arterial origin are a rapid and taut orbital swelling, marked proptosis with immobility of the globe, inability to close the lids, and massive blood-staining of the lids and conjunctiva.‘s In a study of 28 patients having a retrobulbar hemorrhage, Kraushar et al” reported that two (7%) had much poorer vision after the episode. This was thought to be due to closure of the central retinal artery. In a study of 2750 cases of cataract surgery under retrobulbar anesthesia, Klecker’” found two cases of optic atrophy arising from an unspecified number of hemorrhages. The mechanism ofvisual loss from orbital hemorrhage is still unclear, and there may be multiple causes. Spasm of the artery has been implicated. More likely, the increased orbital pressure exceeds the mean arterial pressure in the ophthalmic artery.“’ This would explain those cases in which release of the orbital pressure caused a restoration of retinal circulation. Perhaps the rapid increase in intraocular pressure closes off the artery within the globe itself. This would explain those cases where paracentesis caused a prompt reversal of blindness.“4 Increased orbital pressure may tamponade the small nutrient vessels in the optic nerve, explaining those cases of profound visual loss in which the findings of retinal vascular occIusion were not seen and late optic atrophy developed. (,I” If retrobulbar hemorrhage occurs, careful observation of the eye must be emphasized. Since the optic nerve will have been anesthetized from the injection and the pupillary response abolished by either the injection or the preoperative dilation, ophthalmoscopic observation may be necessary to rule out ischemic damage to the optic nerve or retina. If the hemorrhage occurs in procedures without retrobulbar anesthesia, e.g., trauma, orbital surgery, or blepharoplasty, then vision and the pupillary response to light would be helpful. Measure-

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ment of the intraocular pressure with a portable tonometer would be extremely helpful in evaluating the severity of the hemorrhage and the risk to the circulation of the eye. If the central retinal vessels are seen to occlude, if the nerve becomes pale, if vision falls profoundly, or if dense opacity of the media precludes these observations, then treatment must be immediately started. Lateral canthotomy and lysis of the superior or inferior canthal tendons will relieve some of the orbital pressure and should be the first maneuver. If this is unsuccessful, then cutting the insertion of the orbital septum to the orbital rim in either the upper or lower lids may release the orbital pressure. When the hemorrhage results from lid or orbital surgery, opening the surgical wound and evacuating any clots, removing any implants, cauterizing the bleeding points, and inserting drains would seem indicated. In cases following retrobulbar injection, if the orbital pressure cannot be reduced by any of the techniques mentioned above and ischemic damage seems likely, then emergency decompression of the orbit by a transantral approach might be indicated.4 The use of anterior chamber paracentesis for visual loss during retrobulbar hemorrhage is controversial. Ophthalmoscopic observation should be helpful here. If the artery is seen to be patent but the optic nerve is pale, then paracentesis would not be indicated and efforts should be directed to reducing the orbital pressure. If the artery is seen to be closed or pulsating, then paracentesis should be performed also, as this will lower the intraocular pressure immediately. Intravenous mannitol or Diamox@ may not be helpful, as their effects will not be rapid enough. However, paracentesis carries the risk of either prolapse of the iris or intraocular hemorrhage from the sudden hypotony.33,72 RETINAL

VASCULAR

OCCLUSION

Retinal vascular occlusion may occur in the absence of clinically detectable retrobulbar hemorrhage. Recently, a number of cases of either central retinal artery or combined artery/vein occlusion were noted after retrobulbar anesthesia. In four cases, the patients had severe hematologic or vascular disease predisposing to decreased perfusion in either the retinal or ophthalmic arteries. Some cases were noted to occur prior to surgery (usually when the planned surgery was retinal photocoagulation), but most cases were not diagnosed until one or more days postoperatively.“‘x6’ One possible cause is direct trauma to the ophthalmic artery or the optic nerve by the retrobulbar needle. Compression of the artery from an intravaginal sheath hemorrhage is suggested by finding an enlargement of the optic nerve sheath as dem-

FEIBEL onstrated with ultrasonography or computerized scanning of the orbit.67 Hsrven36 observed that a retrobulbar injection of lidocaine with added epinephrine causes a 50% reduction in ophthalmic artery pulse pressure. This effect may be more from the epinephrine than from the anesthetic. This would suggest that epinephrine not be used for retrobulbar anesthesia in cases where optic nerve function or circulation is known to be weak.36 Apropos of these cases, reports of embolism and occlusion of the central retinal or choroidal vessels from the retrobulbar injection of steroids have been noted.22~25 In these cases, no retrobulbar hemorrhage had been observed. To prevent this complication, avoid deep orbital injection and use the techniques mentioned on pages 104-105. In cases with vascular, hematologic, or optic nerve disease, consider omitting the epinephrine and reducing the volume of the injectate. Most important, after the injection, check the retina with the indirect ophthalmoscope to be sure that the retinal vessels are patent. If not, then any possible orbital pressure from unsuspected hemorrhage should be sought and a paracentesis performed. An immediate computerized tomogram of the optic nerve to search for a dilated nerve sheath from hemorrhage should be done. If such a hemorrhage is found, then decompression of the optic nerve sheath may be considered.67 Late developing optic atrophy following cataract or other types of intraocular surgery has been reported and in many cases it is difficult, if not impossible, to implicate the retrobulbar injection as the cause.12 Indeed, eleven cases of profound visual loss due to optic atrophy were reported after retinal detachment surgery done with general anesthesia and no retrobulbar injections. Small vessel ischemia in the optic nerve was the presumed mechanism as visible change in the retinal vessels was not noted.37 Other proposed causes of late optic atrophy have been postoperative glaucoma or hypotony.32,7’ SCLERAL

PERFORATION

Perforation of the sclera may occur during retrobulbar injection. In one series of 4000 patients undergoing retinal surgery with local anesthesia, three cases were observed.56 All three eyes were highly myopic, thus having a longer antero-posterior diameter and presumably thinner sclera. Posterior staphyloma might increase the risk of perforation, although that was not present in these patients. Symptoms in one case included pain and agitation.62 Signs should include subconjunctival hemorrhage and hyptony, although occult cases obviously occur. If perforation seems likely, the pupil should be immediately dilated and the fundus checked with

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indirect ophthalmoscopy. In extracapsular cataract surgery, this is easier since the pupil is already dilated. If the sclera and retina have been perforated, then surgery on the anterior segment should be cancelled and retinal surgery to close the perforation sites with cryopexy or photocoagulation (with plombagr if indicated) should be done as soon as possible. If the media are too opaque to allow visualization of the posterior segment, then cataract surgery should be performed, preferably with the posterior capsule left intact and without an intraocular lens implant. The fundus can then be examined immediately and retinal repair performed. It would seem wise to consider indirect ophthalmoscopy in all cases ofretrobulbar anesthesia if the media are suff~iciently clear. This would allow the surgeon to check the patency of the central retinal vessels and be sure no posterior perforation has occurred. In three cases inadvertent injection of lidocaine into the vitreous caused no significant clinical problems or visual loss. In a fourth case, a permanent field defect developed from the subretinal hemorrhage. Injection of lidocaine into the vitreous of rabbits and cats produced no longlasting electroretinographic or histological damage.* INJECTION

INTO THE OPTIC

NERVE

SHEATH

Injection of the local anesthetic into the optic nerve sheaths and thus into the intracranial cavity has been proposed as the mechanism of action of certain central nervous system complications following retrobulbar injection (vide supra). This mechanism has been shown to occur in five cases of retrobulbar injection of contrast media for orbitography,lR.49..57 In all cases, the injection was thought to be uncomplicated. Only a transient loss of vision was noted, with some mild neurological signs and symptoms, all of which cleared without permanent sequelae. The contrast material was seen to outline the optic nerve, extend through the optic canal into the middle cranial fossa, and even flow over the clivus into the brainstem. The dye disappeared from optic nerve sheaths within ten minutes. In no case was there any permanent loss of vision, retrobulbar hemorrhage, or change in the appearance of the retinal vessels. The pathway has also been demonstrated in a cadaver.“’ It is of interest in these cases that there was no permanent damage to visual function where the

*Freeman M. Bonuik I, Okun E et al: Inadvertent lidocaine injection: a case report and experimental investigation. Poster 126, Annual Meeting, American Academy of Ophthalmology, 1984. Lincoff H, Zweifach P, Brodic S rt al: Intraocular injection of lidocainc. Personal communication.

needle was known to pierce the optic nerve or its sheaths. Since this mechanism has been presumed to cause optic atrophy with retrobulbar injection, perhaps there are varying degrees of penetration of the nerve or just the sheaths, or visual loss depends upon interruption of the vascular supply within the nerve itself.

Summary Retrobulbar anesthesia is the most common anesthetic procedure in ophthalmology. It is seldom associated with serious complications. However, complications can arise, either from the anesthetic compound itself or from the mechanical manipulation of the needle. I have reviewed toxic eff‘ects of the agents commonly used in retrobulbar injections and the possible mechanisms involved. I have also reviewed the mechanical complications (retrobulbar hemorrhage, retinal vascular occlusion, scleral perforation, and injection into the optic nerve sheath) and described current techniques to minimize the possibility of complications.

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