- Email: [email protected]
Inferior Oblique Muscle Injury from Local Anesthesia for Cataract Surgery
Inferior Oblique Muscle Injury from Local Anesthesia for Cataract Surgery David G. Hunter, MD, PhD, Geoffrey C. Lam, FRACO,l David L. Guyton, MD Background: Vertical rectus muscle injury is commonly cited as a cause of stra bismus after cataract surgery. Injury to the inferior oblique muscle or nerve as a com plication of cataract surgery has not been described previously. Methods: Four patients without pre-existing strabismus who had diplopia after cat aract surgery were studied. Analysis included prism and cover testing, Lancaster red green testing, and fundus torsion assessment. Results: Three patients had a delayed-onset hypertropia with fundus extorsion in the eye that underwent surgery, which is consistent with inferior oblique muscle over action secondary to presumed contracture. The fourth patient had an immediate-onset hypotropia with fundus intorsion in the eye that underwent surgery, which is consistent with inferior oblique muscle paresis. Damage to a vertical rectus muscle or "unmasking" of a pre-existing superior oblique muscle paresis could not explain the history and findings in this group of four patients. Conclusion: The inferior oblique muscle contracture observed in three patients may have been caused by local anesthetic myotoxicity, whereas the paresis observed in one patient may have been due to mechanical trauma or anesthetic toxicity directly to the nerve innervating the muscle. Inferior oblique muscle or nerve injury should be considered as another possible cause of postoperative strabismus, especially when significant fundus torsion accompanies a vertical deviation. Ophthalmology 1995;102:501-509
Diplopia after successful cataract surgery is disappointing for both patient and surgeon and can be difficult to man age in some cases. In most patients, persistent binocular diplopia is due to strabismus. 1•2 In a review of strabismus or binocular diplopia presenting after cataract extraction, Hamed 2 outlined the following four broad categories for Originally received: August I, 1994. Revision accepted: October 18, 1994. From The Wilmer Ophthalmological Institute, The Johns Hopkins Uni versity School of Medicine, Baltimore. Dr. Lam currently is affiliated with the Department of Pediatric Oph thalmology, Princess Margaret Hospital for Children, Subiaco, Western Australia. Presented at the Annual Meeting of the American Association for Pe diatric Ophthalmology and Strabismus, February 1993. Supported in part by the Knights Templar Eye Foundation, the National Children's Eye Care Foundation, and NIH EY06447 (Dr. Hunter). Reprint requests to David G. Hunter, MD, PhD, Wilmer Bl-35, The Johns Hopkins Hospital, Baltimore, MD 21287-9009.
the etiology of the strabismus or diplopia: ( 1) pre-existing conditions (e.g., thyroid eye disease) in which the mis alignment was masked by a dense cataract, (2) conditions secondary to the prolonged occlusion by the cataract (e.g., sensory deviations), (3) conditions leading to optically in duced deviations (e.g., spectacle correction of postoper ative anisometropia), and (4) surgical trauma to the ex traocular muscles or orbital soft tissues. Strabismus due to surgical trauma most likely is caused by extraocular muscle damage. An exception was a patient with post operative strabismus with possible scarring associated with injection of subconjunctival gentamicin reported by Kushner, 3 although the extraocular muscles appeared hy pertrophic on computed tomographic scanning, which would be more in agreement with thyroid eye disease. 4 Injury to extraocular muscles at the time of cataract surgery, in particular injury to the inferior rectus muscle, has received much attention in recent years. Inferior rectus muscle paresis5- 7 and restriction or contracture7- 10 have been postulated, although horizontal strabismus, 11 tran
501
Ophthalmology
Volume 102, Number 3, March 1995
sient pareses of other extraocular muscles, 12 and Brown syndrome 13 also have been described. Inferior oblique muscle injury as a complication of cataract surgery has not been described in the literature. In this report, four patients in whom vertical strabismus developed after cat aract surgery are described. The clinical findings in these patients were not consistent with vertical rectus muscle dysfunction; rather, the ocular motility abnormalities were most consistent with injury to the inferior oblique muscle or nerve caused at the time local anesthesia was admin istered.
Patients and Methods The four patients in this report were referred between February and November 1992 to the Division of Pediatric Ophthalmology and Strabismus of the Wilmer Ophthal mological Institute with vertical and torsional diplopia after cataract surgery. The patients had no history of stra bismus, diplopia, or other ocular disorders with the ex ception of refractive error and cataract. There was no pre existing abnormal head posture in any of the patients. None of the patients had a history of diabetes, thyroid eye disease, neuromuscular disorders, closed head injury, or ocular trauma. Each patient had undergone uneventful extracapsular cataract extraction with posterior chamber intraocular lens (IOL) implantation. Detailed information regarding the surgery was obtained from the surgeons performing the procedures. A different surgeon was involved in each case. The patients were referred from New York, Florida, Georgia, and Maryland. In cases 1, 2, and 3, a superior rectus bridle suture was used. None ofthe surgeons used an inferior rectus bridle suture. Retrobulbar anesthesia was used in cases 1, 2, and 3, whereas peri bulbar anesthesia was used in case 4. No supplemental superior orbital in jection was given in any case. The anesthetic was admin istered by the surgeon in each case. On presentation to the Strabismus Service, a complete eye examination was performed, including measurement of best-corrected visual acuity at distance and near. Stra bismic deviations were measured by the prism and alter nate cover test at 6 m with an accommodative target in at least five positions of gaze, with head tilt to the right and left, and at 0.33 m. Intraocular lens centration and conjunctival scarring were assessed by slit-lamp biomi croscopy. The Lancaster red-green test was performed at a distance of 1 m, with the horizontal and vertical gaze positions located 45 prism diopters (approximately 24 °) from primary position. Fundus examination was per formed after pupillary dilation, with particular attention paid to fundus torsion. 14• 15 Fundus torsion was graded using indirect ophthal moscopy by evaluating the vertical position of the fovea with respect to the optic disc. The level of the fovea was evaluated by extending imaginary horizontal lines through the optic disc. Normally, the fovea is at the level of the lower third of the disc. However, the indirect ophthal moscopic view is inverted and reversed, and it is less con
502
fusing for the examiner to assess torsion directly in this view-that is, normally, the fovea is at the level of the upper third of the disc in the indirect ophthalmoscopic view. To quantify fundus torsion, an imaginary horizontal line is extended through the top of the optic disc, and a second imaginary horizontal line is extended through the junction of the upper one third and the lower two thirds of the optic disc as seen in the indirect ophthalmoscopic view. The fovea is located normally within the area defined by these two lines. If the fovea is above the imaginary line through the top ofthe disc, the eye is extorted; ifthe fovea is below the lower imaginary line, the eye is intorted. If the fovea is located one-half disc diameter or more above the imaginary line through the top of the disc, the eye is considered to be 4+ extorted. If the fovea is one-half disc diameter or more below the bottom of the normal range, the eye is considered to be 4+ intorted. Each one eighth of a disc diameter of torsion in between is graded as 1+, 2+, and 3+. 14 • 15 The Lancaster red-green test particularly is useful for recording hyperdeviations, A and V patterns, and torsional deviations. 16 It is a two-target test where the eyes fixate on red and green vertical streak images, respectively, pro jected on a screen by hand-held projectors. The patient wears a pair of red-green glasses, with the red lens over the right eye by convention. The right eye sees only the red streak image, and the left eye sees only the green streak image. The examiner first projects one of the streaks on the screen in the desired direction ofgaze. In our method of performing this test, the examiner asks the patient if the streak is perfectly vertical in orientation. If not, the patient guides the examiner to straighten the streak. 14 The patient then is instructed to superimpose the second streak image on the first, and the examiner records the actual position and orientation of the streaks. Each of the nine diagnostic positions ofgaze is tested. The test is interpreted from the patient's vantage; that is, ifthe red streak is higher and slanted to the right, there is a right hypertropia with extorsion of the right eye. Testing is performed in near darkness to maximize dissociation. The measurements obtained with Lancaster red-green testing are sometimes different from those obtained with prism and alternate cover testing. This probably reflects different types of dis sociation: with Lancaster red-green testing, each eye has an object to view at the end point of measurement, whereas with prism and alternate cover testing, the two eyes never view the fixation object simultaneously.
Case Reports Case 1. A 75-year-old man underwent extracapsular cataract extraction with IOL implantation in the left eye. The best corrected preoperative visual acuity was 20/20- in the right eye and 20/40- in the left. The patient received a retrobulbar injection of a I: I mixture of0.5% bupivacaine and 2% lidocaine without epinephrine, with added hyaluronidase. Six weeks after surgery, the patient noted diplopia and image tilt. Various prisms were prescribed, but he remained symptomatic and was referred for further evaluation. On examination 18 months after cataract
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia
LHT10 LHT 11 LHT6 LHT7 LHT5 LHT5 Tilt Right LHT5
LHT10 LHT7 LHT5
Tilt Left LHT7
LHT2 LHT2 LHT2 LHT 1 LHT 1 Tilt Right LHT2
Tilt Left LHT2
Figure 1. Case 1, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
Figure 3. Case 2, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
extraction, the diplopia was still present, both vertical and torsional. Best-corrected visual acuity was 20/40+ in the right eye and 20/25+ in the left. Prism and alternate cover testing demonstrated 7 prism diopters of left hypertropia at distance and 5 prism diopters at near (Fig I). There was no hyperdeviation detected on downgaze at near other than on downgaze to the left. The left hypertropia measured 5 prism diopters with head tilt to the right and 7 prism diopters with head tilt to the left. Lancaster red-green testing (Fig 2A) showed a left hyperdeviation in all fields of gaze, with extorsion of the left eye on left gaze. Extorsion of the left fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis of left inferior oblique muscle overaction secondary to muscle contracture was made. The patient declined additional prism therapy and underwent
left inferior oblique muscle recession (under local anesthesia using a sub-Tenon's infusion technique 17 ) with resolution of symptoms (Fig 2B). Three months postoperatively, he remained asymptomatic. Case 2. A 78-year-old woman underwent extracapsular cataract extraction with IOL implantation in the left eye. The patient received a retrobulbar injection of a 1:7 mixture of0.5% bupivacaine and 2% lidocaine without epinephrine, with added hyaluronidase. Several weeks after surgery, she had double vision and noted that images in the left eye appeared to be intorted. She remained symptomatic after 14 months and was referred for further evaluation. Best-corrected visual acuity was 20/15 in the right eye and 20/25+ in the left. Prism and alternate cover testing demon-
''
j
r·
•
•••
f
••• •.
A
:1 • •
I• •
~
•
•
~
~
8
Figure 2. A, preoperative Lancaster red-green plot of case 1 shows left hyperdeviation and extorsion of the left eye especiaiiy on down and left gaze. B, postoperative Lancaster red-green plot of case 1 shows improvement, correlating with resolution of symptoms. Solid line = right eye; dashed line = left eye. Dots are separated by 15 prism diopters.
503
Ophthalmology
Volume 102, Number 3, March 1995
•
l I:• •• ••
••
•
'
·I
• •••
Figure 4. Lancaster red-green plot of case 2 shows a small V-esotropia and extorsion of the left eye in various gaze positions. Solid line = right eye; dashed line = left eye. Dots are separated by 15 prism diopters.
strated a 2-prism diopter left hypertropia (Fig 3), which did not change with head tilt to the right or left. Lancaster red-green testing (Fig 4) demonstrated 5o to 8 ° of extorsion of the left eye that was worst on left of downgaze. Six degrees of extorsion in primary position also was identified by double Maddox rod test ing. Extorsion of the left fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis ofleft inferior oblique muscle overaction secondary to contracture was made. The pa tient was successfully managed with vertical prisms. Case 3. An 84-year-old man underwent extracapsular cat aract extraction with IOL implantation in the right eye. Visual acuity was 20/40 in the right eye and 20/20 in the left I year before surgery and 20/100 in the right eye shortly before surgery. The patient received a retrobulbar injection of a I: I mixture of 0.5% bupivacaine and 2% lidocaine with epinephrine and hy aluronidase. The retrobulbar injection was given inferotempor ally, and the surgeon commented that the needle deliberately was aimed inferiorly, away from the orbital apex, to avoid the optic nerve. Six weeks after the procedure, the patient reported double vision. Seven months after cataract extraction, the patient remained symptomatic and was referred for further evaluation. Best-corrected visual acuity was 20/25 in the right eye and 20/20 in the left. Prism and alternate cover testing (Fig 5) dem onstrated an esotropia with a 9-prism diopter V pattern and a right hypertropia worse on left gaze. The right hypertropia mea sured 2 prism diopters with head tilt to the right and to the left. Lancaster red-green testing (Fig 6A) demonstrated the hyper tropia, the V-pattern esotropia, and extorsion of the right eye. Extorsion of the right fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis of right inferior oblique muscle overaction secondary to contracture was made. A com puted tomographic scan, thyroid function tests, and a medical evaluation were all unremarkable. The patient underwent reces sion of his right inferior oblique and right medial rectus muscles under local anesthesia using a sub-Tenon's infusion technique. Postoperatively, the patient reported subjective relief of symp
504
toms, and he remained asymptomatic with 8 months of follow up. Lancaster red-green testing (Fig 6B) demonstrated resolution of the vertical deviation and the fundus extorsion, along with a residual V-pattern esophoria largest in downgaze. On prism and cover testing, there was no shift in primary position, with a small residual esophoria in downgaze. Case 4. A 78-year-old woman underwent extracapsular cat aract extraction with IOL implantation in the left eye. The patient received a peribulbar injection ofa l:I mixture ofO.75% bupivacaine and 2% lidocaine with epinephrine, with added hyaluronidase, via an inferotemporal approach. An inflatable pressure-reducing device was used preoperatively. Immediately after surgery, she noticed vertical diplopia. Prism therapy was tried without success, and 12 months later she was referred for further evaluation. Best-corrected visual acuity was 20/20 in the right eye and 20/25- in the left. Prism and alternate cover testing demon strated a right hypertropia (left hypotropia), which was greater in downgaze and right gaze (Fig 7). The vertical deviation mea sured 25 prism diopters with head tilt to the right and 8 prism diopters with head tilt to the left. Lancaster red-green testing (Fig 8A) suggested slight extorsion in some gaze positions; how ever, indirect ophthalmoscopy demonstrated unequivocal in torsion of the left eye in primary position. Double Maddox rod testing also showed 5° of intorsion. The diagnosis ofleft inferior oblique muscle paresis was made. She underwent a tenotomy of the posterior two thirds of the left superior oblique tendon at its insertion and a left inferior rectus recession under local anes thesia using a sub-Tenon's infusion technique. Postoperatively, the patient was asymptomatic, and she remained asymptomatic with 6 months of follow-up. Results of examination after surgery showed a small residual vertical phoria consistent with repeat Lancaster red-green testing (Fig 88). The phoria was controlled by the patient without difficulty.
Discussion Many of the clinical features of the four patients in the current report were similar. All patients were 75 years of
RH4 ET8 RH2 ET 12 RH 1 ET 12
RHT4 ET8 RH3 ET 10 RH4 ET 17
Tilt Right RH2 ET9
RHT6 ET8 RH7 ET 17 RH3 ET22 Tilt Left RH2 ET9
Figure 5. Case 3, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
Hunter et al
Inferior Oblique Muscle Injury from Local Anesthesia
.: I•
1---~
l'-:•
"'-,, . -,
... ••
•
•
1---:
••
1----:
·1-----~
,. ,,
'-,,,
--,
A
•
~--i
•
J-------:
.~-----~
•
1-~-------i
8
Figure 6. A, preoperative Lancaster red-green plot of case 3 shows a V -esotropia with extorsion of the right eye and right hypertropia in downgaze. B, postoperative Lancaster red-green plot of case 3 shows resolution of extorsion and hypertropia and residual V-esodeviation. Solid line= right eye; dashed line = left eye. Narrow dashed line connects pairs of tracings in each gaze position. Dots are separated by 15 prism diopters.
age or older at the time of cataract extraction. No patient had findings suggesting optically induced diplopia, such as IOL decentration or anisotropia from spectacle cor rection of anisometropia. None had any head tilt, history of prism wear, or other indication of a pre-existing ocular motility disorder. Preoperatively, visual acuity was not impaired sufficiently to disrupt fusion 18 or to "mask" a pre-existing condition such as superior oblique muscle paresis 19 •20 or thyroid ophthalmopathy. 21 All patients re mained symptomatic for 7 to 18 months after cataract extraction, without worsening of symptoms, before ther apeutic intervention. In the patients requiring surgery, there was no evidence of orbital scarring or fibrosis, and
RHT 14 RHT 18 RHT12 RHT8 RHT30 Tilt Right RHT25
Tilt Left RHT8
Figure 7. Case 4, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
the strabismic deviation improved with weakening of the presumed contractured muscle (or the antagonist of the presumed paretic muscle). Thus, postoperative diplopia was due to strabismus, which was most likely secondary to surgical trauma to the inferior oblique muscle or nerve. While these clinical features were similar among the pa tients, the onset of symptoms and direction of the devia tions in cases 1 to 3 were very different from those in case 4 (Table 1). Most cases of vertical strabismus after cataract surgery are attributed to vertical rectus muscle injury. However, injury to the inferior oblique muscle or nerve may be more common than previously suspected. During the time period covered by this study, a total of 18 other patients with symptomatic diplopia after cataract surgery were ex amined on our service. Of those, three had nonstrabismic diplopia due to aniseikonia or related optical factors, whereas 15 had strabismus not involving the inferior oblique muscle.
Locating the Injured Muscle The Parks three-step test2 2 commonly is applied when evaluating cyclovertical deviations. This test exploits the marked and consistent incomitance present with an acute, isolated muscle paresis. However, the three-step test only helps to identify an isolated paretic cyclovertical muscle; it was not designed to identify a contractured muscle. The three-step test is also less helpful in cases ofchronic paresis, where vertical deviations tend to become comitant. 23 In
505
Volume 102, Number 3, March 1995
Ophthalmology
these cases, fundus torsion can provide important clues to the etiology of the vertical deviation. In primary po sition, the vertical rectus muscles have less torsional action than the oblique muscles. Most cases of inferior rectus muscle contracture that we have examined have had mild anatomic fundus torsion in primary position, and sub jective complaints of torsional diplopia have been rare. Thus, if significant fundus torsion or torsional diplopia is present in the setting of a vertical deviation, it is likely that oblique muscle dysfunction is present. An exaggerated traction tese 4 can help confirm the presence of oblique muscle contracture. This test is most reliable when performed under general anesthesia. Un fortunately, cases 1, 3, and 4 had strabismus surgery under local anesthesia, and exaggerated muscle traction testing was not performed. Case 2 did not require surgery. In cases 1 to 3, the hypertropia and fundus extorsion were most consistent with contracture of the inferior oblique muscle, which elevates the eye and has its greatest torsional action in abduction. Inferior rectus muscle pa resis could have caused the hypertropia but also would have caused mild intorsion rather than the observed marked extorsion. Although superior rectus muscle con tracture could have caused the hypertropia, the superior rectus muscle is a secondary intorter of the globe, which is inconsistent with the observed fundus extorsion. The presence of a V pattern in cases 2 and 3 is also consistent with inferior oblique muscle contracture. It is certain that these features were not caused by ipsilateral inferior rectus
I I
I
I
~
••
I! I .: .
.I i
•
I I
I I
I
J
I
•I
r•
I
I
••
~.
Cases 1-3
Case 4
Onset of diplopia Deviation of surgical eye Anatomic fundus torsion
Delayed H ypertropia
Immediate Hypotropia
Extorsion
Intorsion
muscle contracture, because a hypotropia would have been present. Also, extorsion caused by a tight inferior rectus muscle would have been greater in adduction; cases 1 and 2 definitely had greater extorsion in abduction. The fundus extorsion and V pattern might have been caused by superior oblique muscle weakness. However, superior oblique muscle injury is unlikely because there were no injections of anesthetic into the superior orbit of any pa tient in this series. Pre-existing superior oblique muscle paresis is unlikely based on the lack of an abnormal head posture before surgery and on the temporal relation of the onset of diplopia weeks after the cataract operation. Cases I to 3 did not demonstrate all of the physical findings that might be expected in a case ofinferior oblique muscle contracture. For example, in no case did the hy pertropia increase more than a few prism diopters in the vertical field of action of the inferior oblique muscle. However, isolated contracture of the inferior oblique muscle from presumed anesthetic myotoxicity has not
•
I I I I
.:
Clinical Finding
j
,l
I
I
Table 1. Clinical Features of Cases 1 to 4
I
I
II
••
.I• ••
••• •
I
•~
I I I I
• I
I
I
I I I
~
•••
I
I.
I
I
I I I I I
1
A
I I I I
I
I
.I
I
I
••• I
••• •
I.
I I I I I
\I
I I I I
I
~
••
8
Figure 8. A, preoperative Lancaster red-green plot of case 4 shows left hypotropia greatest in down and right gaze. B, postoperative Lancaster red green plot of case 4 shows improvement of the left hypotropia. Solid line = right eye; dashed line = left eye. Narrow dashed line connects pairs of tracings in each gaze position. Dots are separated by 15 prism diopters.
506
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia been specifically described, and it is likely that such a muscle will not behave the same as either a primarily overactive inferior oblique muscle or a secondarily "over active" inferior oblique muscle seen in cases of superior oblique muscle paresis. In case 3, there was apparent ex torsion in right gaze as well as in left gaze on Lancaster red-green testing. Nevertheless, although not all expected physical findings were demonstrated, the observations in these three patients were most consistent with inferior oblique muscle contracture. In case 4, the hypotropia, fundus intorsion, and head tilt findings were most consistent with paresis of the in ferior oblique muscle. In an acute inferior oblique muscle paresis, the hypotropia should be greatest in upgaze. Sec ondary "overaction" of the ipsilateral superior oblique muscle, however, can cause the hypotropia to be greatest in downgaze, as observed in case 4. Hypotropia might be caused by inferior rectus muscle contracture, especially since the deviation is greatest in downgaze, but the marked anatomic fundus intorsion and immediate onset of the deviation observed in this patient were not consistent with this diagnosis. Superior rectus muscle paresis would cause hypotropia with mild fundus extorsion rather than the observed intorsion. Superior oblique muscle injury is un likely because there were no injections of anesthetic into the superior orbit.
Mechanisms of Damage to Extraocular Muscles Injury to the inferior rectus muscle is the most commonly reported form of extraocular muscle damage after cataract surgery. 5-8 Possible consequences of extraocular muscle damage include paresis or contracture. Transient paresis is usually followed by full recovery and is seen after per imuscular injection of anesthetic agents. It has been pro posed that if the paresis is prolonged, the ipsilateral an tagonist muscle may develop contracture. 5- 7 Rainin and Carlson 25 observed postoperative strabismus in four pa tients who received injections of anesthetic directly into extraocular muscles. These authors initially attributed the strabismus in these patients to paresis, but they now be lieve that the strabismus after cataract surgery is more likely due to extraocular muscle contracture (E. A. Rainin and B. M. Carlson, personal communication). Hamed and Mancuso 9 found computed tomograpic or magnetic resonance imaging abnormalities consistent with damage to the inferior rectus muscles in eight patients with inferior rectus muscle contracture confirmed by forced duction testing. The extraocular myotoxicity of retrobulbar bupiva caine has been studied histologically in an animal model by Porter et al. 26 They found only a mild and very limited myopathic response that resolved by 27 days without per manent sequelae. They did not study the effect of direct injections of the anesthetic into the extraocular muscle. 26 In contrast, Carlson et al 27 injected saline or various local anesthetic agents directly into monkey extraocular mus cles. While the saline-injected muscles showed minimal damage, anesthetic-injected muscles had massive lesions which sometimes occupied the bulk of the cross-section
of the muscle. The damaged muscle fibers in the monkey were replaced by myoblasts, which formed into well-or ganized myofibrillar bundles by the end of the first week. Carlson et al 27 also performed histologic studies after in jection of saline or local anesthetic agents into human extraocular muscles. Again, saline-injected muscles showed no damage. Anesthetic-injected muscles of two subjects 79 and 80 years of age showed extensive damage. In contrast to the injected monkey muscles, the muscles from these elderly humans were filled with dense mats of fibroblastic cells with no significant muscle regeneration. The authors concluded that the patients' age may have contributed to the poor regeneration of injected human muscles compared with the rapid regeneration of injected monkey muscles. 27 Thus, permanent fibrous contracture of the muscle can be caused by myotoxicity of local anesthetic agents, es pecially ifthe anesthetic is injected directly into the muscle body. 27 Although bupivacaine is a more potent local an esthetic than lidocaine, both agents are myotoxic, and their relative myotoxicity has not been formally com pared.26·27 Hamilton et al 10 recently reported four cases of inferior rectus restriction in which lidocaine without bupivacaine was used by the anesthesiologist. While bridle suture placement has been implicated as a cause of con nective tissue fibrosis with subsequent strabismus in six reported cases, 20 ·28 permanent muscle injury is unlikely, considering that injection ofsaline into human extraocular muscle does not cause permanent structural changes.
Proposed Mechanism of Inferior Oblique Muscle Paresis The nerve innervating the inferior oblique muscle is vul nerable to trauma during anesthetic injection. This small branch of the inferior division of the oculomotor nerve is isolated from the other branches in a relatively exposed part of the inferior orbit (Fig 9). In case 4, the lack of involvement of the other rectus muscles supplied by the third cranial nerve, and the lack of pupillary involvement, are consistent with damage localized to this nerve. Damage was most likely in the distal part of the nerve, near the muscle, because a peribulbar needle was used in this case. There was no evidence ofciliary ganglion injury. Although Gonzalez 29 ·30 has documented the remarkable capacity of the nerve to the inferior oblique muscle to re-innervate the muscle after iatrogenic denervation, all of his patients were younger than 18 years of age (C. Gonzalez, personal communication). It is not known how the nerve of a 78 year-old woman would respond to the same insult, but it is possible that regeneration might not occur.
Etiology of Inferior Oblique Muscle Dysfunction Based on the clinical observations in cases 1 to 3 and the observations in human and animal models of anesthetic myotoxicity, 27 the following sequence of events is pro posed. At the time ofcataract surgery, the initial injection of anesthetic into the muscle caused a significant, but lo
507
Ophthalmology Figure 9. Artist's impression of mechanism of injury in case 4. A. View of the right orbit with the roof of the or bit, the levator muscle, and part of the superior rectus muscle removed. The nerve to the inferior oblique muscle is shown traversing the orbit inferiorly within the muscle cone in a postero-anterior di rection. The nerve is rela tively exposed and unpro tected in the retrobulbar area. The illustration depicts the injecting needle in the ret robulbar space threatening the nerve. B, view of the right orbit with the globe removed shows the four rectus muscles and the inferior oblique muscle. The nerve to the in ferior oblique is shown with the injecting needle threat ening.
Volume 102, Number 3, March 1995
Lateral ---'+-~-~.tv
rectus m.
m.
A
calized and subclinical, inferior oblique muscle lesion. While younger patients might have recovered from this insult, the damaged muscle fibers in these older patients were replaced by fibroblasts. As the fibroblasts proliferated, the inferior oblique muscle developed a progressive con tracture that finally became symptomatic weeks later, causing a hypertropia, fundus extorsion, and diplopia. The diplopia resolved when the contractured inferior oblique muscle was weakened in cases I and 3. In case 2, correc tion of the small vertical misalignment with prisms al lowed the patient to use sensory and motor cyclofusion mechanisms 31 to correct any residual torsional diplopia. In case 4, a different sequence of events is proposed. At the time of cataract surgery, the anesthetic needle may have severed the nerve to the inferior oblique muscle, or perhaps the anesthetic agent was injected directly into the nerve. This caused an immediate hypotropia and fundus intorsion in the affected eye. While a younger patient might have recovered from this insult, the nerve did not regenerate sufficiently tore-innervate the inferior oblique muscle in this 78-year-old woman, and she remained symptomatic. Her diplopia resolved when the left superior oblique muscle (the direct antagonist to the inferior oblique muscle) and the ipsilateral inferior rectus muscle were weakened.
Summary These four cases demonstrate that the inferior oblique muscle is susceptible to injury during administration of local anesthetic. Inferior oblique muscle dysfunction should be considered as a cause of vertical strabismus with fundus torsion and torsional diplopia after the ad ministration oflocal anesthetic to the inferior orbital area.
508
As more cases of this and other complications of local anesthesia for cataract surgery occur, cataract surgeons might consider adopting the sub-Tenon's infusion tech nique oflocal anesthetic administration, which eliminates the use of retrobulbar and peribulbar needles en tirely. 17.32,33
References 1. Hamed LM, Helveston EM , Ellis FD. Persistent binocular diplopia after cataract surgery. Am J Ophthalmol 1987; 103: 741-4. 2. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology 1991 ;98:247-52. 3. Kushner BJ. Ocular muscle fibrosis following cataract ex traction. Arch Ophthalmol 1988;106: 18-9. 4. Lubow M. Dr. Kushner's unneeded syndrome [letter]. Arch Ophthalmol 1988; 106: 1162. 5. de Faber J-THN, von Noorden GK. Inferior rectus muscle palsy after retrobulbar anesthesia for cataract surgery. Am J Ophthalmol 1991 ;112:209-11. 6. Grimmett MR, Lambert SR. Superior rectus muscle over action after cataract extraction. Am J Ophthalmol 1992; 114: 72-80. 7. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J Ophthalmol 1993;116:424-30. 8. Ong-Tone L, Pearce WG. Inferior rectus muscle restriction after retrobulbar anesthesia for cataract extraction. Can J Ophthalmol 1989;24: 162-5. 9. Hamed LM, Mancuso A. Inferior rectus muscle contracture syndrome after retrobulbar anesthesia. Ophthalmology 1991 ;98: 1506-12. 10. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia
II. 12. 13. 14. 15.
16. 17. 18. 19. 20. 21. 22.
cataract surgery. J Pediatr Ophthalmol Strabismus 1993;30: 288-91. Poland PJ , Hiatt RL. The correction of diplopia after cat aract extraction. Ann Ophthalmol 1993;25: 110-8. Rao VA, Kawatra VK. Ocular myotoxic effects oflocal an esthetics. Can J Ophthalmol 1988;23: 171-3. Erie JC. Acquired Brown's syndrome after peribulbar anes thesia. Am J Ophthalmol 1990; 109:349-50. Guyton DL. Clinical assessment of ocular torsion . Am Or thopt J 1983;33:7-15. Guyton DL, Weingarten PE. Sensory torsion as the cause of primary oblique muscle overaction/underaction and A and V-pattern strabismus. Binocular Vision Eye Muscle Surg Q 1994;9(Suppl):209-36. Lancaster WB. Detecting, measuring, plotting and inter preting ocular deviations. Arch Ophthalmol 1939;22:867 80. Cap6 H, Munoz M. Sub-Tenon 's lidocaine irrigation for strabismus surgery [letter]. Ophthalmic Surg 1992;23: 145. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol 1989; 107:23-6. Metz HS. Think superior oblique palsy. J Pediatr Ophthal mol Strabismus 1986;23: 166-9. Catalano RA, Nelson LB, Calhoun JH, eta!. Persistent stra bismus presenting after cataract surgery. Ophthalmology 1987;94:491-4. Hamed LM, Lingua RW. Thyroid eye disease presenting after cataract surgery. J Pediatr Ophthalmol Strabismus 1990;27: 10-15. Parks MM. Isolated cyclovertical muscle palsy. Arch Ophthalmol 1958;60: 1027-35.
23. Parks MM, Hamtil LW. Surgical management of isolated cyclovertical muscle palsy. J Pediatr Ophthalmol 1971 ;8: 145-52. 24. Guyton DL. Exaggerated traction test for the oblique mus cles. Ophthalmology 19H I ;HH : I 035-40. 25. Rainin EA, Carlson BM . Postoperative diplopia and ptosis: a clinical hypothesis based on the myotoxicity of local an esthetics. Arch Ophthalmol 1985; I 03:1337-9. 26 . Porter JD, Edney DP, McMahon EJ , Burns LA. Extra ocular myotoxicity of the retrobulbar anesthetic bupi vacaine hydrochlorid e. Invest Ophthalmol Vis Sci 1988;29: 163-74. 27. Carlson BM, Emerick S, Komorowski TE, eta!. Extraocular muscle regeneration in primates: local anesthetic-induced lesions. Ophthalmology 1992;99:582-9. 28. Burns CL, Seigel LA. Inferior rectus recession for vertical tropia after cataract surgery. Ophthalmology 1988;95: 1120 4. 29. Gonzalez C. Denervation of the inferior oblique: current status and long-term results. Trans Am Acad Ophthalmol Otolaryngol 1976;81 :OP899-906. 30. Gonzalez C. Reinnervation of the nerve to the inferior oblique after iatrogenic denervation. J Pediatr Ophthalmol Strabismus 1981; 18:21-4. 31. Guyton DL, von Noorden GK. Sensory adaptations to cy clodeviations. In: Reinecke RD, ed. Strabismus. New York: Grune & Stratton, 1978;399-403. 32. Mein CE, Woodcock MG. Local anesthesia for vitreoretinal surgery. Retina 1990;10:47-9. 33. Steele MA, Lavrich JB, Nelson LB, Koller HP. Sub-Tenon's infusion of local anesthetic for strabismus surgery. Ophthalmic Surg 1992;23:40-3.
509
Diplopia after successful cataract surgery is disappointing for both patient and surgeon and can be difficult to man age in some cases. In most patients, persistent binocular diplopia is due to strabismus. 1•2 In a review of strabismus or binocular diplopia presenting after cataract extraction, Hamed 2 outlined the following four broad categories for Originally received: August I, 1994. Revision accepted: October 18, 1994. From The Wilmer Ophthalmological Institute, The Johns Hopkins Uni versity School of Medicine, Baltimore. Dr. Lam currently is affiliated with the Department of Pediatric Oph thalmology, Princess Margaret Hospital for Children, Subiaco, Western Australia. Presented at the Annual Meeting of the American Association for Pe diatric Ophthalmology and Strabismus, February 1993. Supported in part by the Knights Templar Eye Foundation, the National Children's Eye Care Foundation, and NIH EY06447 (Dr. Hunter). Reprint requests to David G. Hunter, MD, PhD, Wilmer Bl-35, The Johns Hopkins Hospital, Baltimore, MD 21287-9009.
the etiology of the strabismus or diplopia: ( 1) pre-existing conditions (e.g., thyroid eye disease) in which the mis alignment was masked by a dense cataract, (2) conditions secondary to the prolonged occlusion by the cataract (e.g., sensory deviations), (3) conditions leading to optically in duced deviations (e.g., spectacle correction of postoper ative anisometropia), and (4) surgical trauma to the ex traocular muscles or orbital soft tissues. Strabismus due to surgical trauma most likely is caused by extraocular muscle damage. An exception was a patient with post operative strabismus with possible scarring associated with injection of subconjunctival gentamicin reported by Kushner, 3 although the extraocular muscles appeared hy pertrophic on computed tomographic scanning, which would be more in agreement with thyroid eye disease. 4 Injury to extraocular muscles at the time of cataract surgery, in particular injury to the inferior rectus muscle, has received much attention in recent years. Inferior rectus muscle paresis5- 7 and restriction or contracture7- 10 have been postulated, although horizontal strabismus, 11 tran
501
Ophthalmology
Volume 102, Number 3, March 1995
sient pareses of other extraocular muscles, 12 and Brown syndrome 13 also have been described. Inferior oblique muscle injury as a complication of cataract surgery has not been described in the literature. In this report, four patients in whom vertical strabismus developed after cat aract surgery are described. The clinical findings in these patients were not consistent with vertical rectus muscle dysfunction; rather, the ocular motility abnormalities were most consistent with injury to the inferior oblique muscle or nerve caused at the time local anesthesia was admin istered.
Patients and Methods The four patients in this report were referred between February and November 1992 to the Division of Pediatric Ophthalmology and Strabismus of the Wilmer Ophthal mological Institute with vertical and torsional diplopia after cataract surgery. The patients had no history of stra bismus, diplopia, or other ocular disorders with the ex ception of refractive error and cataract. There was no pre existing abnormal head posture in any of the patients. None of the patients had a history of diabetes, thyroid eye disease, neuromuscular disorders, closed head injury, or ocular trauma. Each patient had undergone uneventful extracapsular cataract extraction with posterior chamber intraocular lens (IOL) implantation. Detailed information regarding the surgery was obtained from the surgeons performing the procedures. A different surgeon was involved in each case. The patients were referred from New York, Florida, Georgia, and Maryland. In cases 1, 2, and 3, a superior rectus bridle suture was used. None ofthe surgeons used an inferior rectus bridle suture. Retrobulbar anesthesia was used in cases 1, 2, and 3, whereas peri bulbar anesthesia was used in case 4. No supplemental superior orbital in jection was given in any case. The anesthetic was admin istered by the surgeon in each case. On presentation to the Strabismus Service, a complete eye examination was performed, including measurement of best-corrected visual acuity at distance and near. Stra bismic deviations were measured by the prism and alter nate cover test at 6 m with an accommodative target in at least five positions of gaze, with head tilt to the right and left, and at 0.33 m. Intraocular lens centration and conjunctival scarring were assessed by slit-lamp biomi croscopy. The Lancaster red-green test was performed at a distance of 1 m, with the horizontal and vertical gaze positions located 45 prism diopters (approximately 24 °) from primary position. Fundus examination was per formed after pupillary dilation, with particular attention paid to fundus torsion. 14• 15 Fundus torsion was graded using indirect ophthal moscopy by evaluating the vertical position of the fovea with respect to the optic disc. The level of the fovea was evaluated by extending imaginary horizontal lines through the optic disc. Normally, the fovea is at the level of the lower third of the disc. However, the indirect ophthal moscopic view is inverted and reversed, and it is less con
502
fusing for the examiner to assess torsion directly in this view-that is, normally, the fovea is at the level of the upper third of the disc in the indirect ophthalmoscopic view. To quantify fundus torsion, an imaginary horizontal line is extended through the top of the optic disc, and a second imaginary horizontal line is extended through the junction of the upper one third and the lower two thirds of the optic disc as seen in the indirect ophthalmoscopic view. The fovea is located normally within the area defined by these two lines. If the fovea is above the imaginary line through the top ofthe disc, the eye is extorted; ifthe fovea is below the lower imaginary line, the eye is intorted. If the fovea is located one-half disc diameter or more above the imaginary line through the top of the disc, the eye is considered to be 4+ extorted. If the fovea is one-half disc diameter or more below the bottom of the normal range, the eye is considered to be 4+ intorted. Each one eighth of a disc diameter of torsion in between is graded as 1+, 2+, and 3+. 14 • 15 The Lancaster red-green test particularly is useful for recording hyperdeviations, A and V patterns, and torsional deviations. 16 It is a two-target test where the eyes fixate on red and green vertical streak images, respectively, pro jected on a screen by hand-held projectors. The patient wears a pair of red-green glasses, with the red lens over the right eye by convention. The right eye sees only the red streak image, and the left eye sees only the green streak image. The examiner first projects one of the streaks on the screen in the desired direction ofgaze. In our method of performing this test, the examiner asks the patient if the streak is perfectly vertical in orientation. If not, the patient guides the examiner to straighten the streak. 14 The patient then is instructed to superimpose the second streak image on the first, and the examiner records the actual position and orientation of the streaks. Each of the nine diagnostic positions ofgaze is tested. The test is interpreted from the patient's vantage; that is, ifthe red streak is higher and slanted to the right, there is a right hypertropia with extorsion of the right eye. Testing is performed in near darkness to maximize dissociation. The measurements obtained with Lancaster red-green testing are sometimes different from those obtained with prism and alternate cover testing. This probably reflects different types of dis sociation: with Lancaster red-green testing, each eye has an object to view at the end point of measurement, whereas with prism and alternate cover testing, the two eyes never view the fixation object simultaneously.
Case Reports Case 1. A 75-year-old man underwent extracapsular cataract extraction with IOL implantation in the left eye. The best corrected preoperative visual acuity was 20/20- in the right eye and 20/40- in the left. The patient received a retrobulbar injection of a I: I mixture of0.5% bupivacaine and 2% lidocaine without epinephrine, with added hyaluronidase. Six weeks after surgery, the patient noted diplopia and image tilt. Various prisms were prescribed, but he remained symptomatic and was referred for further evaluation. On examination 18 months after cataract
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia
LHT10 LHT 11 LHT6 LHT7 LHT5 LHT5 Tilt Right LHT5
LHT10 LHT7 LHT5
Tilt Left LHT7
LHT2 LHT2 LHT2 LHT 1 LHT 1 Tilt Right LHT2
Tilt Left LHT2
Figure 1. Case 1, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
Figure 3. Case 2, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
extraction, the diplopia was still present, both vertical and torsional. Best-corrected visual acuity was 20/40+ in the right eye and 20/25+ in the left. Prism and alternate cover testing demonstrated 7 prism diopters of left hypertropia at distance and 5 prism diopters at near (Fig I). There was no hyperdeviation detected on downgaze at near other than on downgaze to the left. The left hypertropia measured 5 prism diopters with head tilt to the right and 7 prism diopters with head tilt to the left. Lancaster red-green testing (Fig 2A) showed a left hyperdeviation in all fields of gaze, with extorsion of the left eye on left gaze. Extorsion of the left fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis of left inferior oblique muscle overaction secondary to muscle contracture was made. The patient declined additional prism therapy and underwent
left inferior oblique muscle recession (under local anesthesia using a sub-Tenon's infusion technique 17 ) with resolution of symptoms (Fig 2B). Three months postoperatively, he remained asymptomatic. Case 2. A 78-year-old woman underwent extracapsular cataract extraction with IOL implantation in the left eye. The patient received a retrobulbar injection of a 1:7 mixture of0.5% bupivacaine and 2% lidocaine without epinephrine, with added hyaluronidase. Several weeks after surgery, she had double vision and noted that images in the left eye appeared to be intorted. She remained symptomatic after 14 months and was referred for further evaluation. Best-corrected visual acuity was 20/15 in the right eye and 20/25+ in the left. Prism and alternate cover testing demon-
''
j
r·
•
•••
f
••• •.
A
:1 • •
I• •
~
•
•
~
~
8
Figure 2. A, preoperative Lancaster red-green plot of case 1 shows left hyperdeviation and extorsion of the left eye especiaiiy on down and left gaze. B, postoperative Lancaster red-green plot of case 1 shows improvement, correlating with resolution of symptoms. Solid line = right eye; dashed line = left eye. Dots are separated by 15 prism diopters.
503
Ophthalmology
Volume 102, Number 3, March 1995
•
l I:• •• ••
••
•
'
·I
• •••
Figure 4. Lancaster red-green plot of case 2 shows a small V-esotropia and extorsion of the left eye in various gaze positions. Solid line = right eye; dashed line = left eye. Dots are separated by 15 prism diopters.
strated a 2-prism diopter left hypertropia (Fig 3), which did not change with head tilt to the right or left. Lancaster red-green testing (Fig 4) demonstrated 5o to 8 ° of extorsion of the left eye that was worst on left of downgaze. Six degrees of extorsion in primary position also was identified by double Maddox rod test ing. Extorsion of the left fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis ofleft inferior oblique muscle overaction secondary to contracture was made. The pa tient was successfully managed with vertical prisms. Case 3. An 84-year-old man underwent extracapsular cat aract extraction with IOL implantation in the right eye. Visual acuity was 20/40 in the right eye and 20/20 in the left I year before surgery and 20/100 in the right eye shortly before surgery. The patient received a retrobulbar injection of a I: I mixture of 0.5% bupivacaine and 2% lidocaine with epinephrine and hy aluronidase. The retrobulbar injection was given inferotempor ally, and the surgeon commented that the needle deliberately was aimed inferiorly, away from the orbital apex, to avoid the optic nerve. Six weeks after the procedure, the patient reported double vision. Seven months after cataract extraction, the patient remained symptomatic and was referred for further evaluation. Best-corrected visual acuity was 20/25 in the right eye and 20/20 in the left. Prism and alternate cover testing (Fig 5) dem onstrated an esotropia with a 9-prism diopter V pattern and a right hypertropia worse on left gaze. The right hypertropia mea sured 2 prism diopters with head tilt to the right and to the left. Lancaster red-green testing (Fig 6A) demonstrated the hyper tropia, the V-pattern esotropia, and extorsion of the right eye. Extorsion of the right fundus in primary position was seen by indirect ophthalmoscopy. The diagnosis of right inferior oblique muscle overaction secondary to contracture was made. A com puted tomographic scan, thyroid function tests, and a medical evaluation were all unremarkable. The patient underwent reces sion of his right inferior oblique and right medial rectus muscles under local anesthesia using a sub-Tenon's infusion technique. Postoperatively, the patient reported subjective relief of symp
504
toms, and he remained asymptomatic with 8 months of follow up. Lancaster red-green testing (Fig 6B) demonstrated resolution of the vertical deviation and the fundus extorsion, along with a residual V-pattern esophoria largest in downgaze. On prism and cover testing, there was no shift in primary position, with a small residual esophoria in downgaze. Case 4. A 78-year-old woman underwent extracapsular cat aract extraction with IOL implantation in the left eye. The patient received a peribulbar injection ofa l:I mixture ofO.75% bupivacaine and 2% lidocaine with epinephrine, with added hyaluronidase, via an inferotemporal approach. An inflatable pressure-reducing device was used preoperatively. Immediately after surgery, she noticed vertical diplopia. Prism therapy was tried without success, and 12 months later she was referred for further evaluation. Best-corrected visual acuity was 20/20 in the right eye and 20/25- in the left. Prism and alternate cover testing demon strated a right hypertropia (left hypotropia), which was greater in downgaze and right gaze (Fig 7). The vertical deviation mea sured 25 prism diopters with head tilt to the right and 8 prism diopters with head tilt to the left. Lancaster red-green testing (Fig 8A) suggested slight extorsion in some gaze positions; how ever, indirect ophthalmoscopy demonstrated unequivocal in torsion of the left eye in primary position. Double Maddox rod testing also showed 5° of intorsion. The diagnosis ofleft inferior oblique muscle paresis was made. She underwent a tenotomy of the posterior two thirds of the left superior oblique tendon at its insertion and a left inferior rectus recession under local anes thesia using a sub-Tenon's infusion technique. Postoperatively, the patient was asymptomatic, and she remained asymptomatic with 6 months of follow-up. Results of examination after surgery showed a small residual vertical phoria consistent with repeat Lancaster red-green testing (Fig 88). The phoria was controlled by the patient without difficulty.
Discussion Many of the clinical features of the four patients in the current report were similar. All patients were 75 years of
RH4 ET8 RH2 ET 12 RH 1 ET 12
RHT4 ET8 RH3 ET 10 RH4 ET 17
Tilt Right RH2 ET9
RHT6 ET8 RH7 ET 17 RH3 ET22 Tilt Left RH2 ET9
Figure 5. Case 3, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
Hunter et al
Inferior Oblique Muscle Injury from Local Anesthesia
.: I•
1---~
l'-:•
"'-,, . -,
... ••
•
•
1---:
••
1----:
·1-----~
,. ,,
'-,,,
--,
A
•
~--i
•
J-------:
.~-----~
•
1-~-------i
8
Figure 6. A, preoperative Lancaster red-green plot of case 3 shows a V -esotropia with extorsion of the right eye and right hypertropia in downgaze. B, postoperative Lancaster red-green plot of case 3 shows resolution of extorsion and hypertropia and residual V-esodeviation. Solid line= right eye; dashed line = left eye. Narrow dashed line connects pairs of tracings in each gaze position. Dots are separated by 15 prism diopters.
age or older at the time of cataract extraction. No patient had findings suggesting optically induced diplopia, such as IOL decentration or anisotropia from spectacle cor rection of anisometropia. None had any head tilt, history of prism wear, or other indication of a pre-existing ocular motility disorder. Preoperatively, visual acuity was not impaired sufficiently to disrupt fusion 18 or to "mask" a pre-existing condition such as superior oblique muscle paresis 19 •20 or thyroid ophthalmopathy. 21 All patients re mained symptomatic for 7 to 18 months after cataract extraction, without worsening of symptoms, before ther apeutic intervention. In the patients requiring surgery, there was no evidence of orbital scarring or fibrosis, and
RHT 14 RHT 18 RHT12 RHT8 RHT30 Tilt Right RHT25
Tilt Left RHT8
Figure 7. Case 4, preoperative prism and cover testing (distance, with correction). Deviations given in prism diopters.
the strabismic deviation improved with weakening of the presumed contractured muscle (or the antagonist of the presumed paretic muscle). Thus, postoperative diplopia was due to strabismus, which was most likely secondary to surgical trauma to the inferior oblique muscle or nerve. While these clinical features were similar among the pa tients, the onset of symptoms and direction of the devia tions in cases 1 to 3 were very different from those in case 4 (Table 1). Most cases of vertical strabismus after cataract surgery are attributed to vertical rectus muscle injury. However, injury to the inferior oblique muscle or nerve may be more common than previously suspected. During the time period covered by this study, a total of 18 other patients with symptomatic diplopia after cataract surgery were ex amined on our service. Of those, three had nonstrabismic diplopia due to aniseikonia or related optical factors, whereas 15 had strabismus not involving the inferior oblique muscle.
Locating the Injured Muscle The Parks three-step test2 2 commonly is applied when evaluating cyclovertical deviations. This test exploits the marked and consistent incomitance present with an acute, isolated muscle paresis. However, the three-step test only helps to identify an isolated paretic cyclovertical muscle; it was not designed to identify a contractured muscle. The three-step test is also less helpful in cases ofchronic paresis, where vertical deviations tend to become comitant. 23 In
505
Volume 102, Number 3, March 1995
Ophthalmology
these cases, fundus torsion can provide important clues to the etiology of the vertical deviation. In primary po sition, the vertical rectus muscles have less torsional action than the oblique muscles. Most cases of inferior rectus muscle contracture that we have examined have had mild anatomic fundus torsion in primary position, and sub jective complaints of torsional diplopia have been rare. Thus, if significant fundus torsion or torsional diplopia is present in the setting of a vertical deviation, it is likely that oblique muscle dysfunction is present. An exaggerated traction tese 4 can help confirm the presence of oblique muscle contracture. This test is most reliable when performed under general anesthesia. Un fortunately, cases 1, 3, and 4 had strabismus surgery under local anesthesia, and exaggerated muscle traction testing was not performed. Case 2 did not require surgery. In cases 1 to 3, the hypertropia and fundus extorsion were most consistent with contracture of the inferior oblique muscle, which elevates the eye and has its greatest torsional action in abduction. Inferior rectus muscle pa resis could have caused the hypertropia but also would have caused mild intorsion rather than the observed marked extorsion. Although superior rectus muscle con tracture could have caused the hypertropia, the superior rectus muscle is a secondary intorter of the globe, which is inconsistent with the observed fundus extorsion. The presence of a V pattern in cases 2 and 3 is also consistent with inferior oblique muscle contracture. It is certain that these features were not caused by ipsilateral inferior rectus
I I
I
I
~
••
I! I .: .
.I i
•
I I
I I
I
J
I
•I
r•
I
I
••
~.
Cases 1-3
Case 4
Onset of diplopia Deviation of surgical eye Anatomic fundus torsion
Delayed H ypertropia
Immediate Hypotropia
Extorsion
Intorsion
muscle contracture, because a hypotropia would have been present. Also, extorsion caused by a tight inferior rectus muscle would have been greater in adduction; cases 1 and 2 definitely had greater extorsion in abduction. The fundus extorsion and V pattern might have been caused by superior oblique muscle weakness. However, superior oblique muscle injury is unlikely because there were no injections of anesthetic into the superior orbit of any pa tient in this series. Pre-existing superior oblique muscle paresis is unlikely based on the lack of an abnormal head posture before surgery and on the temporal relation of the onset of diplopia weeks after the cataract operation. Cases I to 3 did not demonstrate all of the physical findings that might be expected in a case ofinferior oblique muscle contracture. For example, in no case did the hy pertropia increase more than a few prism diopters in the vertical field of action of the inferior oblique muscle. However, isolated contracture of the inferior oblique muscle from presumed anesthetic myotoxicity has not
•
I I I I
.:
Clinical Finding
j
,l
I
I
Table 1. Clinical Features of Cases 1 to 4
I
I
II
••
.I• ••
••• •
I
•~
I I I I
• I
I
I
I I I
~
•••
I
I.
I
I
I I I I I
1
A
I I I I
I
I
.I
I
I
••• I
••• •
I.
I I I I I
\I
I I I I
I
~
••
8
Figure 8. A, preoperative Lancaster red-green plot of case 4 shows left hypotropia greatest in down and right gaze. B, postoperative Lancaster red green plot of case 4 shows improvement of the left hypotropia. Solid line = right eye; dashed line = left eye. Narrow dashed line connects pairs of tracings in each gaze position. Dots are separated by 15 prism diopters.
506
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia been specifically described, and it is likely that such a muscle will not behave the same as either a primarily overactive inferior oblique muscle or a secondarily "over active" inferior oblique muscle seen in cases of superior oblique muscle paresis. In case 3, there was apparent ex torsion in right gaze as well as in left gaze on Lancaster red-green testing. Nevertheless, although not all expected physical findings were demonstrated, the observations in these three patients were most consistent with inferior oblique muscle contracture. In case 4, the hypotropia, fundus intorsion, and head tilt findings were most consistent with paresis of the in ferior oblique muscle. In an acute inferior oblique muscle paresis, the hypotropia should be greatest in upgaze. Sec ondary "overaction" of the ipsilateral superior oblique muscle, however, can cause the hypotropia to be greatest in downgaze, as observed in case 4. Hypotropia might be caused by inferior rectus muscle contracture, especially since the deviation is greatest in downgaze, but the marked anatomic fundus intorsion and immediate onset of the deviation observed in this patient were not consistent with this diagnosis. Superior rectus muscle paresis would cause hypotropia with mild fundus extorsion rather than the observed intorsion. Superior oblique muscle injury is un likely because there were no injections of anesthetic into the superior orbit.
Mechanisms of Damage to Extraocular Muscles Injury to the inferior rectus muscle is the most commonly reported form of extraocular muscle damage after cataract surgery. 5-8 Possible consequences of extraocular muscle damage include paresis or contracture. Transient paresis is usually followed by full recovery and is seen after per imuscular injection of anesthetic agents. It has been pro posed that if the paresis is prolonged, the ipsilateral an tagonist muscle may develop contracture. 5- 7 Rainin and Carlson 25 observed postoperative strabismus in four pa tients who received injections of anesthetic directly into extraocular muscles. These authors initially attributed the strabismus in these patients to paresis, but they now be lieve that the strabismus after cataract surgery is more likely due to extraocular muscle contracture (E. A. Rainin and B. M. Carlson, personal communication). Hamed and Mancuso 9 found computed tomograpic or magnetic resonance imaging abnormalities consistent with damage to the inferior rectus muscles in eight patients with inferior rectus muscle contracture confirmed by forced duction testing. The extraocular myotoxicity of retrobulbar bupiva caine has been studied histologically in an animal model by Porter et al. 26 They found only a mild and very limited myopathic response that resolved by 27 days without per manent sequelae. They did not study the effect of direct injections of the anesthetic into the extraocular muscle. 26 In contrast, Carlson et al 27 injected saline or various local anesthetic agents directly into monkey extraocular mus cles. While the saline-injected muscles showed minimal damage, anesthetic-injected muscles had massive lesions which sometimes occupied the bulk of the cross-section
of the muscle. The damaged muscle fibers in the monkey were replaced by myoblasts, which formed into well-or ganized myofibrillar bundles by the end of the first week. Carlson et al 27 also performed histologic studies after in jection of saline or local anesthetic agents into human extraocular muscles. Again, saline-injected muscles showed no damage. Anesthetic-injected muscles of two subjects 79 and 80 years of age showed extensive damage. In contrast to the injected monkey muscles, the muscles from these elderly humans were filled with dense mats of fibroblastic cells with no significant muscle regeneration. The authors concluded that the patients' age may have contributed to the poor regeneration of injected human muscles compared with the rapid regeneration of injected monkey muscles. 27 Thus, permanent fibrous contracture of the muscle can be caused by myotoxicity of local anesthetic agents, es pecially ifthe anesthetic is injected directly into the muscle body. 27 Although bupivacaine is a more potent local an esthetic than lidocaine, both agents are myotoxic, and their relative myotoxicity has not been formally com pared.26·27 Hamilton et al 10 recently reported four cases of inferior rectus restriction in which lidocaine without bupivacaine was used by the anesthesiologist. While bridle suture placement has been implicated as a cause of con nective tissue fibrosis with subsequent strabismus in six reported cases, 20 ·28 permanent muscle injury is unlikely, considering that injection ofsaline into human extraocular muscle does not cause permanent structural changes.
Proposed Mechanism of Inferior Oblique Muscle Paresis The nerve innervating the inferior oblique muscle is vul nerable to trauma during anesthetic injection. This small branch of the inferior division of the oculomotor nerve is isolated from the other branches in a relatively exposed part of the inferior orbit (Fig 9). In case 4, the lack of involvement of the other rectus muscles supplied by the third cranial nerve, and the lack of pupillary involvement, are consistent with damage localized to this nerve. Damage was most likely in the distal part of the nerve, near the muscle, because a peribulbar needle was used in this case. There was no evidence ofciliary ganglion injury. Although Gonzalez 29 ·30 has documented the remarkable capacity of the nerve to the inferior oblique muscle to re-innervate the muscle after iatrogenic denervation, all of his patients were younger than 18 years of age (C. Gonzalez, personal communication). It is not known how the nerve of a 78 year-old woman would respond to the same insult, but it is possible that regeneration might not occur.
Etiology of Inferior Oblique Muscle Dysfunction Based on the clinical observations in cases 1 to 3 and the observations in human and animal models of anesthetic myotoxicity, 27 the following sequence of events is pro posed. At the time ofcataract surgery, the initial injection of anesthetic into the muscle caused a significant, but lo
507
Ophthalmology Figure 9. Artist's impression of mechanism of injury in case 4. A. View of the right orbit with the roof of the or bit, the levator muscle, and part of the superior rectus muscle removed. The nerve to the inferior oblique muscle is shown traversing the orbit inferiorly within the muscle cone in a postero-anterior di rection. The nerve is rela tively exposed and unpro tected in the retrobulbar area. The illustration depicts the injecting needle in the ret robulbar space threatening the nerve. B, view of the right orbit with the globe removed shows the four rectus muscles and the inferior oblique muscle. The nerve to the in ferior oblique is shown with the injecting needle threat ening.
Volume 102, Number 3, March 1995
Lateral ---'+-~-~.tv
rectus m.
m.
A
calized and subclinical, inferior oblique muscle lesion. While younger patients might have recovered from this insult, the damaged muscle fibers in these older patients were replaced by fibroblasts. As the fibroblasts proliferated, the inferior oblique muscle developed a progressive con tracture that finally became symptomatic weeks later, causing a hypertropia, fundus extorsion, and diplopia. The diplopia resolved when the contractured inferior oblique muscle was weakened in cases I and 3. In case 2, correc tion of the small vertical misalignment with prisms al lowed the patient to use sensory and motor cyclofusion mechanisms 31 to correct any residual torsional diplopia. In case 4, a different sequence of events is proposed. At the time of cataract surgery, the anesthetic needle may have severed the nerve to the inferior oblique muscle, or perhaps the anesthetic agent was injected directly into the nerve. This caused an immediate hypotropia and fundus intorsion in the affected eye. While a younger patient might have recovered from this insult, the nerve did not regenerate sufficiently tore-innervate the inferior oblique muscle in this 78-year-old woman, and she remained symptomatic. Her diplopia resolved when the left superior oblique muscle (the direct antagonist to the inferior oblique muscle) and the ipsilateral inferior rectus muscle were weakened.
Summary These four cases demonstrate that the inferior oblique muscle is susceptible to injury during administration of local anesthetic. Inferior oblique muscle dysfunction should be considered as a cause of vertical strabismus with fundus torsion and torsional diplopia after the ad ministration oflocal anesthetic to the inferior orbital area.
508
As more cases of this and other complications of local anesthesia for cataract surgery occur, cataract surgeons might consider adopting the sub-Tenon's infusion tech nique oflocal anesthetic administration, which eliminates the use of retrobulbar and peribulbar needles en tirely. 17.32,33
References 1. Hamed LM, Helveston EM , Ellis FD. Persistent binocular diplopia after cataract surgery. Am J Ophthalmol 1987; 103: 741-4. 2. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology 1991 ;98:247-52. 3. Kushner BJ. Ocular muscle fibrosis following cataract ex traction. Arch Ophthalmol 1988;106: 18-9. 4. Lubow M. Dr. Kushner's unneeded syndrome [letter]. Arch Ophthalmol 1988; 106: 1162. 5. de Faber J-THN, von Noorden GK. Inferior rectus muscle palsy after retrobulbar anesthesia for cataract surgery. Am J Ophthalmol 1991 ;112:209-11. 6. Grimmett MR, Lambert SR. Superior rectus muscle over action after cataract extraction. Am J Ophthalmol 1992; 114: 72-80. 7. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J Ophthalmol 1993;116:424-30. 8. Ong-Tone L, Pearce WG. Inferior rectus muscle restriction after retrobulbar anesthesia for cataract extraction. Can J Ophthalmol 1989;24: 162-5. 9. Hamed LM, Mancuso A. Inferior rectus muscle contracture syndrome after retrobulbar anesthesia. Ophthalmology 1991 ;98: 1506-12. 10. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for
Hunter et al · Inferior Oblique Muscle Injury from Local Anesthesia
II. 12. 13. 14. 15.
16. 17. 18. 19. 20. 21. 22.
cataract surgery. J Pediatr Ophthalmol Strabismus 1993;30: 288-91. Poland PJ , Hiatt RL. The correction of diplopia after cat aract extraction. Ann Ophthalmol 1993;25: 110-8. Rao VA, Kawatra VK. Ocular myotoxic effects oflocal an esthetics. Can J Ophthalmol 1988;23: 171-3. Erie JC. Acquired Brown's syndrome after peribulbar anes thesia. Am J Ophthalmol 1990; 109:349-50. Guyton DL. Clinical assessment of ocular torsion . Am Or thopt J 1983;33:7-15. Guyton DL, Weingarten PE. Sensory torsion as the cause of primary oblique muscle overaction/underaction and A and V-pattern strabismus. Binocular Vision Eye Muscle Surg Q 1994;9(Suppl):209-36. Lancaster WB. Detecting, measuring, plotting and inter preting ocular deviations. Arch Ophthalmol 1939;22:867 80. Cap6 H, Munoz M. Sub-Tenon 's lidocaine irrigation for strabismus surgery [letter]. Ophthalmic Surg 1992;23: 145. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol 1989; 107:23-6. Metz HS. Think superior oblique palsy. J Pediatr Ophthal mol Strabismus 1986;23: 166-9. Catalano RA, Nelson LB, Calhoun JH, eta!. Persistent stra bismus presenting after cataract surgery. Ophthalmology 1987;94:491-4. Hamed LM, Lingua RW. Thyroid eye disease presenting after cataract surgery. J Pediatr Ophthalmol Strabismus 1990;27: 10-15. Parks MM. Isolated cyclovertical muscle palsy. Arch Ophthalmol 1958;60: 1027-35.
23. Parks MM, Hamtil LW. Surgical management of isolated cyclovertical muscle palsy. J Pediatr Ophthalmol 1971 ;8: 145-52. 24. Guyton DL. Exaggerated traction test for the oblique mus cles. Ophthalmology 19H I ;HH : I 035-40. 25. Rainin EA, Carlson BM . Postoperative diplopia and ptosis: a clinical hypothesis based on the myotoxicity of local an esthetics. Arch Ophthalmol 1985; I 03:1337-9. 26 . Porter JD, Edney DP, McMahon EJ , Burns LA. Extra ocular myotoxicity of the retrobulbar anesthetic bupi vacaine hydrochlorid e. Invest Ophthalmol Vis Sci 1988;29: 163-74. 27. Carlson BM, Emerick S, Komorowski TE, eta!. Extraocular muscle regeneration in primates: local anesthetic-induced lesions. Ophthalmology 1992;99:582-9. 28. Burns CL, Seigel LA. Inferior rectus recession for vertical tropia after cataract surgery. Ophthalmology 1988;95: 1120 4. 29. Gonzalez C. Denervation of the inferior oblique: current status and long-term results. Trans Am Acad Ophthalmol Otolaryngol 1976;81 :OP899-906. 30. Gonzalez C. Reinnervation of the nerve to the inferior oblique after iatrogenic denervation. J Pediatr Ophthalmol Strabismus 1981; 18:21-4. 31. Guyton DL, von Noorden GK. Sensory adaptations to cy clodeviations. In: Reinecke RD, ed. Strabismus. New York: Grune & Stratton, 1978;399-403. 32. Mein CE, Woodcock MG. Local anesthesia for vitreoretinal surgery. Retina 1990;10:47-9. 33. Steele MA, Lavrich JB, Nelson LB, Koller HP. Sub-Tenon's infusion of local anesthetic for strabismus surgery. Ophthalmic Surg 1992;23:40-3.
509