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Incidence of ocular misalignment and diplopia after uneventful cataract surgery
Incidence of ocular misalignment and diplopia after uneventful cataract surgery Karl C. Golnik, MD, Constance E. West, MD, Elaine Kaye, Kevin T. Corcoran, OD, Robert J. Cionni, MD ABSTRACT Purpose: To evaluate the incidence of ocular misalignment and diplopia after uneventful cataract surgery. Setting: An outpatient private practice eye institute. Methods: One hundred thirty-eight patients referred to 1 cataract surgeon were prospectively evaluated. Orthoptic evaluations were performed within 1 month before and then 1 day, 1 week, and 1 month after cataract surgery. Anesthesia was by retrobulbar injection, and cataract extraction was done by phacoemulsification. Results: Cataract surgery was performed in 118 patients. Preoperatively, 16 patients had ocular misalignment; 10 were phoric, 4 were intermittently tropic, and 2 were tropic. Follow-up evaluation was obtained for 101 patients (86%) at 1 day, 91 (77%) at 1 week, and 88 (75%) at 1 month. A change in ocular alignment occurred in 22 of 101 patients (22%) at 1 day, 9 of 91 (10%) at 1 week, and 6 of 88 (7%) at 1 month. Only 1 patient who had a change in alignment at 1 month was symptomatic. Conclusions: A persistent change in ocular alignment after uneventful cataract surgery occurred in 7% of patients. However, symptomatic diplopia was uncommon (1 in 118; 0.85%) in this relatively small series. J Cataract Refract Surg 2000; 26:1205–1209 © 2000 ASCRS and ESCRS
D
iplopia after uneventful cataract surgery has been well documented.1–14 Patterns of ocular misalignment include ipsilateral hypotropia, ipsilateral hypertropia, exotropia, esotropia, and Brown’s syndrome. Hamed5 suggests that the etiology of misalignment in most patients falls into 1 of 4 categories: (1) pre-existing misalignment masked by the cataract (e.g., trochlear nerve palsy), (2) disorders precipitated by poor vision caused by the cataract (e.g., sensory deviations), (3) sur-
gical or anesthetic trauma to the extraocular muscles or orbital soft tissue, or (4) disorders related to aphakia/ pseudophakia and associated optical aberrations. The incidence of ocular misalignment after cataract surgery is unknown. We prospectively evaluated a consecutive series of patients before and after cataract surgery to ascertain the incidence of preoperative and postoperative ocular misalignment and diplopia.
Patients and Methods Accepted for publication January 6, 2000. Correspondence to Karl G. Golnik, MD, Cincinnati Eye Institute, 10494 Montgomery Road, Cincinnati, Ohio 22033-4003, USA. © 2000 ASCRS and ESCRS Published by Elsevier Science Inc.
Patients referred to 1 cataract surgeon (R.J.C.) at the Cincinnati Eye Institute Ambulatory Surgery Center between February and September 1996 were pro0886-3350/00/$–see front matter PII S0886-3350(00)00330-8
OCULAR MISALIGNMENT AND DIPLOPIA AFTER CATARACT SURGERY
spectively evaluated for preoperative and postoperative ocular misalignment. Patients were examined 1 to 4 weeks preoperatively and postoperatively at 1 and 6 to 8 days and 4 weeks. Each patient received a complete dilated eye examination. Ocular alignment was assessed by the cover/uncover test and alternate cover test at distance in at least 5 positions of gaze (primary, right, left, up, down) and at near in primary position and downgaze. Strabismic deviations were measured by the prism and alternate cover test. Measurements were made preoperatively and postoperatively with the patients wearing their current spectacles. Anesthesia was a retrobulbar injection of a mixture of 1.5 cc lidocaine 4%, 4.0 cc bupivacaine 0.75%, and 75 units hyaluronidase (Wydase威). All retrobulbar injections were given with a 27 gauge 1.5 inch needle over the inferotemporal orbital rim (3 to 4 cc) and in the superotemporal orbit (0 to 2 cc). A 13 ounce mercury bag was placed on the operative eye for 5 minutes after the retrobulbar injection(s). Phacoemulsification with posterior chamber intraocular lens (IOL) implantation was performed. Bridle sutures were not used. Gentamicin (0.3 cc, 40 mg/cc) was given subconjunctivally at 6 o’clock with a 30 gauge needle, and betamethasone (Celestone Soluspan威, 0.5 cc, 6 mg/cc) and dexamethasone (0.5 cc, 4 mg/cc) were injected through the inferior eyelid with a 27 gauge 5⁄8 inch needle at the end of the procedure.
Results One hundred eighteen consecutive patients had cataract surgery. No patient had a history of significant eye or head injury, thyroid ophthalmopathy, or neuromuscular condition. Mean age of the 47 men and 71 women at the time of surgery was 71 years (range 46 to 93 years). The right eye was operated on in 68 patients. Preoperative visual acuity ranged from 20/20 to hand motions (median 20/50). Patients with a visual acuity of 20/40 or better had significant worsening of acuity with glare testing. Preoperative phoria was present in 10 patients: 6 patients were esophoric at distance; 2 were exophoric at near; 2 were exophoric at distance and near. Preoperative tropia was present in 6 patients. Four patients had an intermittent tropia (exotropia at near, 3; esotropia at distance, 1), 1 patient had a concomitant congenital esotropia, and 1 had a mild abducens nerve palsy subsequently found to be caused by an intracavernous sinus internal carotid artery aneurysm. Intermittent preoperative binocular double vision was present in each of the tropic patients except for the patient with congenital esotropia (Figure 1). None of the 5 patients sought medical attention for the diplopia. Nine patients had constant monocular diplopia. In all patients cataract extraction and IOL implantation were uneventful. Both inferotemporal and su-
Figure 1. (Golnik) Patients with preoperative binocular diplopia; measurements are in prism diopters (E ⫽ esophoria; E(T) ⫽ intermittent esotropia; ET ⫽ esotropia; X ⫽ exophoria; X(T) ⫽ intermittent exotropia; orthoP ⫽ orthophoric).
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perotemporal anesthetic injections were given in 106 patients, 3 of whom required an additional superonasal injection. Twelve patients required only the inferotemporal injection. No patient had a decentered IOL. Follow-up orthoptic evaluation was available for 101 patients (86%) at 1 day, 91 (77%) at 1 week, and 88 (75%) at 1 month (Table 1). One day postoperatively, 22 of 101 patients (22%) developed a change in ocular alignment; most of these (16) had a nonspecific combination of horizontal and vertical misalignment and ophthalmoplegia. At 1 week, 9 of 91 patients (10%) and at 1 month 6 of 88 patients (7%) had a change in alignment from preoperatively. Of the 6 patients with a change in ocular misalignment at 1 month (Figure 2), 5 were phoric and asymptomatic. The sixth patient (patient 1, Figure 2) had a preoperative esophoria that became a symptomatic esotropia at distance only. Although formal motility examination at 1 month was not done by us in 30 of the 118 patients, they were examined by the referring physician; none of the 30 had diplopia. Thus, 0.85% (1 of 118) developed a change in alignment resulting in diplopia. Dipolpia resolved in each of the 9 patients with preoperative monocular diplopia.
Discussion Although there are numerous reports of patients who develop diplopia after cataract surgery, these studies are all retrospective and hampered by referral bias and the lack of thorough preoperative assessment of ocular motility. Our study is the first to prospectively evaluate patients having cataract extraction to determine the incidence of preoperative and postoperative ocular misalignment and diplopia.
Sixteen of our 118 patients had preoperative ocular misalignment. Five of the 16 experienced symptoms of intermittent diplopia: 3 had intermittent exotropia, 1 had intermittent esotropia, and 1 had abducens nerve palsy caused by an intracavernous sinus internal carotid artery aneurysm. None of the 5 patients sought medical attention for the diplopia. Only 1 of 16 patients with preoperative misalignment developed a persistent change in alignment postoperatively. She had an intermittent divergenceinsufficiency-type esotropia (patient 1, Figures 1 and 2). Preoperative visual acuity was 20/50 in both eyes with ⫹0.75 ⫹0.75 ⫻ 140 in the right eye and ⫹1.00 ⫹0.75 ⫻ 180 in the left eye. Five days postoperatively, uncorrected visual acuity was 20/25; a correction of – 0.50 diopters provided 20/20 acuity. Perhaps this patient’s asymmetric postoperative visual acuity precipitated the loss of alignment control. The other cataract was removed 2 months later; however, fusion was not regained. One day postoperatively, acquired ocular misalignment was common (22%). Ophthalmoplegia with nonspecific combined vertical and horizontal misalignment was most frequently observed; for example, an ipsilateral hypertropia worse on down-gaze, exotropia in adduction, and esotropia in abduction, indicating weakness of the inferior, medial, and lateral recti, respectively. These deviations had mostly resolved by 1 week postoperatively. We believe the pattern of misalignment and ophthalmoplegia with subsequent rapid resolution is most consistent with prolonged anesthetic action. Occurrence of postoperative diplopia at 1 day was not uncommon in a study comparing the efficacy of 2 retrobulbar anesthetic mixtures.15 It is possible that a slightly decentered IOL could have been responsible for some of the
Table 1. Acquired postoperative misalignment. Number of Patients Phoric
Tropic
Postoperative
Eso-
Exo-
Hyper-
Combo
Eso-
Exo-
Hyper-
Combo
1 day (n ⫽ 101)
—
—
—
—
4
—
2
16
1 week (n ⫽ 91)
4
3
—
—
—
—
1
1
1 month (n ⫽ 88)
2
3
—
—
1
—
—
—
Combo ⫽ combined vertical/horizontal misalignment
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OCULAR MISALIGNMENT AND DIPLOPIA AFTER CATARACT SURGERY
Figure 2. (Golnik) Summary of 6 patients with acquired misalignment at 1 month; measurements are in prism diopters (orthoP ⫽ orthophoric; X ⫽ exophoria; E ⫽ esophoria; E(T) ⫽ intermittent esotropia; ET ⫽ esotropia; int ⫽ intermittent).
small postoperative misalignments; however, we did not observe a decentered IOL in any eye. We did not perform patch testing before surgery. Thus, it is possible that a patient could have lost control of a previously well-controlled phoria. By 1 month, 6 patients had misalignment not present preoperatively; 5 had developed asymptomatic horizontal phorias. The sixth patient had preoperative intermittent diplopia at distance only with a divergenceinsufficiency-pattern esophoria. After surgery, this patient became persistently diplopic as a result of complete loss of control of this pre-existing phoria. No patient developed persistent, vertical misalignment. Except for a pre-existing esophoria in 1 patient, we could not identify any factor that predisposed these 6 patients to misalignment. Thus, in our small series, the incidence of acquired, persistent, postoperative binocular diplopia was 0.85% (1 of 118). Ocular misalignment after cataract surgery can occur by a variety of mechanisms. The strabismus may or may not be concomitant. Preoperative misalignment and breakdown of a pre-existing phoria can be ruled out by careful preoperative motility evaluation. Postoperative ocular misalignment may be caused by extraocular muscle paresis, restriction, or overaction related to bridle suture placement2; nerve or muscle damage 1208
by the anesthetic needle5; or anesthetic or antibiotic myotoxicity.1,12,16 –18 Postoperative diplopia associated with concomitant ocular misalignment most often results when the patient is unable to regain control of a preoperative sensory tropia that occurred because of the cataract.4,9,19 Occasionally, these patients have disruption of central fusion and cannot be successfully treated with a prism or surgery.4 To our knowledge, breakdown of a preoperative divergence-insufficiency-type intermittent esotropia has not been reported as a sequela of cataract surgery. This patient did have intermittent diplopia at distance before surgery. Thus, this symptom should alert the physician to the potential for persistent postoperative diplopia. In summary, preoperative diplopia (monocular or binocular) and ocular misalignment were not uncommon. Transient ocular misalignment occurred frequently after cataract surgery. Symptomatic, persistent ocular misalignment only occurred in 1 patient (0.85%) who had breakdown of a pre-existing divergence-insufficiency-type intermittent esotropia.
References 1. Rainin EA, Carlson BM. Postoperative diplopia and ptosis; a clinical hypothesis based on the myotoxicity of local anesthetics. Arch Ophthalmol 1985; 103:1337–1339
J CATARACT REFRACT SURG—VOL 26, AUGUST 2000
OCULAR MISALIGNMENT AND DIPLOPIA AFTER CATARACT SURGERY
2. Catalano RA, Nelson LB, Calhoun JH, et al. Persistent strabismus presenting after cataract surgery. Ophthalmology 1987; 94:491– 494 3. Hamed LM, Helveston EM, Ellis FD. Persistent binocular diplopia after cataract surgery. Am J Ophthalmol 1987; 103:741–744 4. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol 1989; 107:23–26 5. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology 1991; 98:247–252 6. Grimmett MR, Lambert SR. Superior rectus muscle overaction after cataract extraction. Am J Ophthalmol 1992; 114:72– 80 7. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for cataract surgery. J Pediatr Ophthalmol Strabismus 1993; 30:288 –291 8. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract surgery. Am J Ophthalmol 1993; 116:424 – 430 9. Sharkey JA, Sellar PW. Acquired central fusion disruption following cataract extraction. J Pediatr Ophthalmol Strabismus 1994; 31:391–393 10. Wylie J, Henderson M, Doyle M, Hickey-Dwyer M. Persistent binocular diplopia following cataract surgery: aetiology and management. Eye 1994; 8:543–546 11. Hunter DG, Lam GC, Guyton DL. Inferior oblique muscle injury from local anesthesia for cataract surgery. Ophthalmology 1995; 102:501–509
12. Capo´ H, Guyton DL. Ipsilateral hypertropia after cataract surgery. Ophthalmology 1996; 103:721–730 13. Capo´ H, Roth E, Johnson T, et al. Vertical strabismus after cataract surgery. Ophthalmology 1996; 103:918 – 921; discussion by DL Guyton, 921 14. Erie JC. Acquired Brown’s syndrome after peribulbar injection. Am J Ophthalmol 1990; 109:349 –350 15. Sarvela PJ, Paloheimo MPJ, Nikki PH. Comparison of pH-adjusted bupivacaine 0.75% and a mixture of bupivacaine 0.75% and lidocaine 2%, both with hyaluronidase, in day-case cataract surgery under regional anesthesia. Anesth Analg 1994; 79:35–39 16. Carlson BM, Emerick S, Komorowski TE, et al. Extraocular muscle regeneration in primates; local anestheticinduced lesions. Ophthalmology 1992; 99:582–589 17. Kushner BJ. Ocular muscle fibrosis following cataract extraction. Arch Ophthalmol 1988; 106:18 –19 18. Chapman JM, Abdelatif OMA, Cheeks L, Green K. Subconjunctival gentamicin induction of extraocular muscle myopathy. Ophthalmic Res 1992; 24:189 –196 19. Brent P. Cataract patients: pre-operative assessment for fusion potential. Am Orthopt J 1986; 36:135–139 From The Cincinnati Eye Institute (Golnik, Kaye, Corcoran, Cionni), the Departments of Ophthalmology & Neurosurgery, University of Cincinnati (Golnik), and Childrens Hospital Medical Center (West), Cincinnati, Ohio, USA. Presented in part as a poster at the annual meeting of the American Academy of Ophthalmology, San Francisco, California, USA, October 1997.
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D
iplopia after uneventful cataract surgery has been well documented.1–14 Patterns of ocular misalignment include ipsilateral hypotropia, ipsilateral hypertropia, exotropia, esotropia, and Brown’s syndrome. Hamed5 suggests that the etiology of misalignment in most patients falls into 1 of 4 categories: (1) pre-existing misalignment masked by the cataract (e.g., trochlear nerve palsy), (2) disorders precipitated by poor vision caused by the cataract (e.g., sensory deviations), (3) sur-
gical or anesthetic trauma to the extraocular muscles or orbital soft tissue, or (4) disorders related to aphakia/ pseudophakia and associated optical aberrations. The incidence of ocular misalignment after cataract surgery is unknown. We prospectively evaluated a consecutive series of patients before and after cataract surgery to ascertain the incidence of preoperative and postoperative ocular misalignment and diplopia.
Patients and Methods Accepted for publication January 6, 2000. Correspondence to Karl G. Golnik, MD, Cincinnati Eye Institute, 10494 Montgomery Road, Cincinnati, Ohio 22033-4003, USA. © 2000 ASCRS and ESCRS Published by Elsevier Science Inc.
Patients referred to 1 cataract surgeon (R.J.C.) at the Cincinnati Eye Institute Ambulatory Surgery Center between February and September 1996 were pro0886-3350/00/$–see front matter PII S0886-3350(00)00330-8
OCULAR MISALIGNMENT AND DIPLOPIA AFTER CATARACT SURGERY
spectively evaluated for preoperative and postoperative ocular misalignment. Patients were examined 1 to 4 weeks preoperatively and postoperatively at 1 and 6 to 8 days and 4 weeks. Each patient received a complete dilated eye examination. Ocular alignment was assessed by the cover/uncover test and alternate cover test at distance in at least 5 positions of gaze (primary, right, left, up, down) and at near in primary position and downgaze. Strabismic deviations were measured by the prism and alternate cover test. Measurements were made preoperatively and postoperatively with the patients wearing their current spectacles. Anesthesia was a retrobulbar injection of a mixture of 1.5 cc lidocaine 4%, 4.0 cc bupivacaine 0.75%, and 75 units hyaluronidase (Wydase威). All retrobulbar injections were given with a 27 gauge 1.5 inch needle over the inferotemporal orbital rim (3 to 4 cc) and in the superotemporal orbit (0 to 2 cc). A 13 ounce mercury bag was placed on the operative eye for 5 minutes after the retrobulbar injection(s). Phacoemulsification with posterior chamber intraocular lens (IOL) implantation was performed. Bridle sutures were not used. Gentamicin (0.3 cc, 40 mg/cc) was given subconjunctivally at 6 o’clock with a 30 gauge needle, and betamethasone (Celestone Soluspan威, 0.5 cc, 6 mg/cc) and dexamethasone (0.5 cc, 4 mg/cc) were injected through the inferior eyelid with a 27 gauge 5⁄8 inch needle at the end of the procedure.
Results One hundred eighteen consecutive patients had cataract surgery. No patient had a history of significant eye or head injury, thyroid ophthalmopathy, or neuromuscular condition. Mean age of the 47 men and 71 women at the time of surgery was 71 years (range 46 to 93 years). The right eye was operated on in 68 patients. Preoperative visual acuity ranged from 20/20 to hand motions (median 20/50). Patients with a visual acuity of 20/40 or better had significant worsening of acuity with glare testing. Preoperative phoria was present in 10 patients: 6 patients were esophoric at distance; 2 were exophoric at near; 2 were exophoric at distance and near. Preoperative tropia was present in 6 patients. Four patients had an intermittent tropia (exotropia at near, 3; esotropia at distance, 1), 1 patient had a concomitant congenital esotropia, and 1 had a mild abducens nerve palsy subsequently found to be caused by an intracavernous sinus internal carotid artery aneurysm. Intermittent preoperative binocular double vision was present in each of the tropic patients except for the patient with congenital esotropia (Figure 1). None of the 5 patients sought medical attention for the diplopia. Nine patients had constant monocular diplopia. In all patients cataract extraction and IOL implantation were uneventful. Both inferotemporal and su-
Figure 1. (Golnik) Patients with preoperative binocular diplopia; measurements are in prism diopters (E ⫽ esophoria; E(T) ⫽ intermittent esotropia; ET ⫽ esotropia; X ⫽ exophoria; X(T) ⫽ intermittent exotropia; orthoP ⫽ orthophoric).
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perotemporal anesthetic injections were given in 106 patients, 3 of whom required an additional superonasal injection. Twelve patients required only the inferotemporal injection. No patient had a decentered IOL. Follow-up orthoptic evaluation was available for 101 patients (86%) at 1 day, 91 (77%) at 1 week, and 88 (75%) at 1 month (Table 1). One day postoperatively, 22 of 101 patients (22%) developed a change in ocular alignment; most of these (16) had a nonspecific combination of horizontal and vertical misalignment and ophthalmoplegia. At 1 week, 9 of 91 patients (10%) and at 1 month 6 of 88 patients (7%) had a change in alignment from preoperatively. Of the 6 patients with a change in ocular misalignment at 1 month (Figure 2), 5 were phoric and asymptomatic. The sixth patient (patient 1, Figure 2) had a preoperative esophoria that became a symptomatic esotropia at distance only. Although formal motility examination at 1 month was not done by us in 30 of the 118 patients, they were examined by the referring physician; none of the 30 had diplopia. Thus, 0.85% (1 of 118) developed a change in alignment resulting in diplopia. Dipolpia resolved in each of the 9 patients with preoperative monocular diplopia.
Discussion Although there are numerous reports of patients who develop diplopia after cataract surgery, these studies are all retrospective and hampered by referral bias and the lack of thorough preoperative assessment of ocular motility. Our study is the first to prospectively evaluate patients having cataract extraction to determine the incidence of preoperative and postoperative ocular misalignment and diplopia.
Sixteen of our 118 patients had preoperative ocular misalignment. Five of the 16 experienced symptoms of intermittent diplopia: 3 had intermittent exotropia, 1 had intermittent esotropia, and 1 had abducens nerve palsy caused by an intracavernous sinus internal carotid artery aneurysm. None of the 5 patients sought medical attention for the diplopia. Only 1 of 16 patients with preoperative misalignment developed a persistent change in alignment postoperatively. She had an intermittent divergenceinsufficiency-type esotropia (patient 1, Figures 1 and 2). Preoperative visual acuity was 20/50 in both eyes with ⫹0.75 ⫹0.75 ⫻ 140 in the right eye and ⫹1.00 ⫹0.75 ⫻ 180 in the left eye. Five days postoperatively, uncorrected visual acuity was 20/25; a correction of – 0.50 diopters provided 20/20 acuity. Perhaps this patient’s asymmetric postoperative visual acuity precipitated the loss of alignment control. The other cataract was removed 2 months later; however, fusion was not regained. One day postoperatively, acquired ocular misalignment was common (22%). Ophthalmoplegia with nonspecific combined vertical and horizontal misalignment was most frequently observed; for example, an ipsilateral hypertropia worse on down-gaze, exotropia in adduction, and esotropia in abduction, indicating weakness of the inferior, medial, and lateral recti, respectively. These deviations had mostly resolved by 1 week postoperatively. We believe the pattern of misalignment and ophthalmoplegia with subsequent rapid resolution is most consistent with prolonged anesthetic action. Occurrence of postoperative diplopia at 1 day was not uncommon in a study comparing the efficacy of 2 retrobulbar anesthetic mixtures.15 It is possible that a slightly decentered IOL could have been responsible for some of the
Table 1. Acquired postoperative misalignment. Number of Patients Phoric
Tropic
Postoperative
Eso-
Exo-
Hyper-
Combo
Eso-
Exo-
Hyper-
Combo
1 day (n ⫽ 101)
—
—
—
—
4
—
2
16
1 week (n ⫽ 91)
4
3
—
—
—
—
1
1
1 month (n ⫽ 88)
2
3
—
—
1
—
—
—
Combo ⫽ combined vertical/horizontal misalignment
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Figure 2. (Golnik) Summary of 6 patients with acquired misalignment at 1 month; measurements are in prism diopters (orthoP ⫽ orthophoric; X ⫽ exophoria; E ⫽ esophoria; E(T) ⫽ intermittent esotropia; ET ⫽ esotropia; int ⫽ intermittent).
small postoperative misalignments; however, we did not observe a decentered IOL in any eye. We did not perform patch testing before surgery. Thus, it is possible that a patient could have lost control of a previously well-controlled phoria. By 1 month, 6 patients had misalignment not present preoperatively; 5 had developed asymptomatic horizontal phorias. The sixth patient had preoperative intermittent diplopia at distance only with a divergenceinsufficiency-pattern esophoria. After surgery, this patient became persistently diplopic as a result of complete loss of control of this pre-existing phoria. No patient developed persistent, vertical misalignment. Except for a pre-existing esophoria in 1 patient, we could not identify any factor that predisposed these 6 patients to misalignment. Thus, in our small series, the incidence of acquired, persistent, postoperative binocular diplopia was 0.85% (1 of 118). Ocular misalignment after cataract surgery can occur by a variety of mechanisms. The strabismus may or may not be concomitant. Preoperative misalignment and breakdown of a pre-existing phoria can be ruled out by careful preoperative motility evaluation. Postoperative ocular misalignment may be caused by extraocular muscle paresis, restriction, or overaction related to bridle suture placement2; nerve or muscle damage 1208
by the anesthetic needle5; or anesthetic or antibiotic myotoxicity.1,12,16 –18 Postoperative diplopia associated with concomitant ocular misalignment most often results when the patient is unable to regain control of a preoperative sensory tropia that occurred because of the cataract.4,9,19 Occasionally, these patients have disruption of central fusion and cannot be successfully treated with a prism or surgery.4 To our knowledge, breakdown of a preoperative divergence-insufficiency-type intermittent esotropia has not been reported as a sequela of cataract surgery. This patient did have intermittent diplopia at distance before surgery. Thus, this symptom should alert the physician to the potential for persistent postoperative diplopia. In summary, preoperative diplopia (monocular or binocular) and ocular misalignment were not uncommon. Transient ocular misalignment occurred frequently after cataract surgery. Symptomatic, persistent ocular misalignment only occurred in 1 patient (0.85%) who had breakdown of a pre-existing divergence-insufficiency-type intermittent esotropia.
References 1. Rainin EA, Carlson BM. Postoperative diplopia and ptosis; a clinical hypothesis based on the myotoxicity of local anesthetics. Arch Ophthalmol 1985; 103:1337–1339
J CATARACT REFRACT SURG—VOL 26, AUGUST 2000
OCULAR MISALIGNMENT AND DIPLOPIA AFTER CATARACT SURGERY
2. Catalano RA, Nelson LB, Calhoun JH, et al. Persistent strabismus presenting after cataract surgery. Ophthalmology 1987; 94:491– 494 3. Hamed LM, Helveston EM, Ellis FD. Persistent binocular diplopia after cataract surgery. Am J Ophthalmol 1987; 103:741–744 4. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol 1989; 107:23–26 5. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology 1991; 98:247–252 6. Grimmett MR, Lambert SR. Superior rectus muscle overaction after cataract extraction. Am J Ophthalmol 1992; 114:72– 80 7. Hamilton SM, Elsas FJ, Dawson TL. A cluster of patients with inferior rectus restriction following local anesthesia for cataract surgery. J Pediatr Ophthalmol Strabismus 1993; 30:288 –291 8. Esswein MB, von Noorden GK. Paresis of a vertical rectus muscle after cataract surgery. Am J Ophthalmol 1993; 116:424 – 430 9. Sharkey JA, Sellar PW. Acquired central fusion disruption following cataract extraction. J Pediatr Ophthalmol Strabismus 1994; 31:391–393 10. Wylie J, Henderson M, Doyle M, Hickey-Dwyer M. Persistent binocular diplopia following cataract surgery: aetiology and management. Eye 1994; 8:543–546 11. Hunter DG, Lam GC, Guyton DL. Inferior oblique muscle injury from local anesthesia for cataract surgery. Ophthalmology 1995; 102:501–509
12. Capo´ H, Guyton DL. Ipsilateral hypertropia after cataract surgery. Ophthalmology 1996; 103:721–730 13. Capo´ H, Roth E, Johnson T, et al. Vertical strabismus after cataract surgery. Ophthalmology 1996; 103:918 – 921; discussion by DL Guyton, 921 14. Erie JC. Acquired Brown’s syndrome after peribulbar injection. Am J Ophthalmol 1990; 109:349 –350 15. Sarvela PJ, Paloheimo MPJ, Nikki PH. Comparison of pH-adjusted bupivacaine 0.75% and a mixture of bupivacaine 0.75% and lidocaine 2%, both with hyaluronidase, in day-case cataract surgery under regional anesthesia. Anesth Analg 1994; 79:35–39 16. Carlson BM, Emerick S, Komorowski TE, et al. Extraocular muscle regeneration in primates; local anestheticinduced lesions. Ophthalmology 1992; 99:582–589 17. Kushner BJ. Ocular muscle fibrosis following cataract extraction. Arch Ophthalmol 1988; 106:18 –19 18. Chapman JM, Abdelatif OMA, Cheeks L, Green K. Subconjunctival gentamicin induction of extraocular muscle myopathy. Ophthalmic Res 1992; 24:189 –196 19. Brent P. Cataract patients: pre-operative assessment for fusion potential. Am Orthopt J 1986; 36:135–139 From The Cincinnati Eye Institute (Golnik, Kaye, Corcoran, Cionni), the Departments of Ophthalmology & Neurosurgery, University of Cincinnati (Golnik), and Childrens Hospital Medical Center (West), Cincinnati, Ohio, USA. Presented in part as a poster at the annual meeting of the American Academy of Ophthalmology, San Francisco, California, USA, October 1997.
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