Seminars in Ophthalmology
ISSN: 0882-0538 (Print) 1744-5205 (Online) Journal homepage: http://www.tandfonline.com/loi/isio20
Diplopia after Cataract Extraction Marc A. Bouffard & Dean M. Cestari To cite this article: Marc A. Bouffard & Dean M. Cestari (2017): Diplopia after Cataract Extraction, Seminars in Ophthalmology, DOI: 10.1080/08820538.2017.1353806 To link to this article: http://dx.doi.org/10.1080/08820538.2017.1353806
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Date: 13 October 2017, At: 01:03
Seminars in Ophthalmology, Early Online, 1–6, 2017 © Taylor & Francis ISSN: 0882-0538 print / 1744-5205 online DOI: https://doi.org/10.1080/08820538.2017.1353806
Diplopia after Cataract Extraction Marc A. Bouffard and Dean M. Cestari
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Neuro-Ophthalmology service, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA
ABSTRACT Diplopia after cataract extraction is an unexpected outcome for the patient and often a source of confusion for the physician, owing to its relative infrequency. This article reviews the pertinent literature on the subject. Mechanisms include anesthetic myotoxicity, surgical trauma, optical aberrations, cortical disorders in patients with congenital strabismus, and the unmasking of previously unnoticed ocular misalignment. As the population continues to age and cataract extraction is performed in increasing volume, familiarity with this uncommon but important outcome may help to clarify and effectively treat post-cataract-extraction diplopia. Keywords: Adverse events, cataract surgery, double vision, strabismus, surgical complication
INTRODUCTION
procedural complications such as anesthetic-induced myotoxicity, nerve or muscle trauma with the anesthetic needle, and muscle trauma with stay sutures. Less intuitive binocular etiologies include disorders of cortical maladaption such as fixation-switch diplopia and central disruption of fusion, the unmasking of ocular misalignments which were present but unappreciated prior to cataract extraction owing to poor acuity, the concomitant development of causally unrelated diplopia and, rarely, macular processes such as cystoid macular edema. Monocular etiologies, such as lens decentration or retained lens fragments, are less frequent and often less perplexing than the aforementioned causes and will not be discussed in depth here (Table 1). The relative frequencies of the these etiologies were described by Nayak et al., who conducted a retrospective analysis of 150 cases of diplopia following cataract extraction; the most common etiology identified was decompensation of previous strabismus, seen in 54 patients (34%), followed by extraocular muscle dysfunction (41 patients, 25%), refractive disorders (14 patients, 8.5%), concurrent onset of systemic disease (8 patients, 5%), disruption of central fusion (8 patients, 5%), and monocular etiologies (4 patients, 2.5%). No cause could clearly be isolated in 32 patients (20%).3 Even a careful history and examination may be fruitless if some of the key details related to the previous etiologies are unfamiliar.
Developing diplopia after cataract extraction is an unexpected event for the patient and often a source of confusion for the physician. New-onset diplopia after cataract extraction is uncommon. Most large series describe an incidence of diplopia after cataract extraction of between 0.17% and 0.75%.1–3 Owing to the relative infrequency and myriad causes of diplopia after cataract surgery, the individual cataract surgeon may lack experience in the evaluation of post-cataract-extraction diplopia. There are a number of particular details about the surgical approach, anesthesia, prior alignment, current refraction, and other postoperative complications which must be kept in mind during the evaluation of a diplopic patient after cataract extraction. The goal of this review is to present a cogent overview of the causes of diplopia after cataract extraction to aid in the prompt and accurate diagnosis of the underlying process, especially in areas where neuro-ophthalmic consultation is not readily available. Binocular diplopia is due to an ocular misalignment and it resolves when the patient covers either eye. Monocular diplopia is present when viewing through one eye only. Both binocular and monocular etiologies of post-cataract-extraction diplopia exist, and differentiating the two is the first step in the appropriate workup of these patients. Binocular etiologies may relate to
Correspondence: Marc A. Bouffard, M.D. Fellow in Neuro-Ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA. E-mail: [email protected]
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TABLE 1. Etiologies of diplopia particular to cataract extraction. Surgical etiologies Anesthetic myotoxicity - Segmental toxicity with muscle overaction - Diffuse toxicity with muscle underaction Bridle sutures Nerve injury
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Cortical etiologies Fixation-switch diplopia Loss of central fusion Postoperative Optics Binocular Static aniseikonia Dynamic aniseikonia Cystoid macular edema Monocular Corneal edema
DIPLOPIA RELATED TO ANESTHESIA AND TRAUMA Cataract extraction is commonly performed with the aid of a retrobulbar or peribulbar block. Retrobulbar blocks are accomplished by passing a 3-cm-long, 22–27 gauge needle into the retrobulbar space, either via a transcutaneous or transconjunctival approach. The needle is inserted inferotemporal to the globe and is guided towards the orbital apex. Peribulbar blocks are accomplished by passage of a shorter needle into the extraconal space. Commonly employed anesthetics include 2% lidocaine and 0.5% to 0.75% bupivacaine. These agents are sodium channel blockers and thus serve to disrupt sodium-dependent depolarization of nerves. Though typically considered in the context of disrupting sensory afferent input, adequate quantities also achieve paralysis of the globe intraoperatively.4 While direct trauma to an extraocular muscle or cranial nerve is perhaps the most intuitive method of injury by which the passage of an anesthetic needle into the orbit might result in diplopia, anesthesiainduced myotoxicity is likely a more common cause. A good deal of literature on the subject of anesthetic myotoxicity has emerged since its proposal in 1985.5,6 Carlson et al. performed retrobulbar blocks on primates employing either 0.75% bupivacaine, 2.0% mepivacaine, or 2.0% lidocaine plus 1:100,000 epinephrine. The typical result was the superficial degeneration and regeneration of nearby extra-ocular muscles, but on occasion diffuse myotoxicity was seen. Diffuse myotoxicity was common in both primate and human extraocular muscles after direct infiltration of the muscle with local anesthetic.7 The use of hyaluronidase may decrease the potential for myotoxicity from infiltrational anesthesia. Hyaluronidase has been employed with local anesthesia in ophthalmic procedures since at least 19498; its function as a digestive agent may potentiate anesthetic
dispersal through tissue.9 In doing so, hyaluronidase may prevent myotoxic local anesthetics from accumulating in one area and damaging nearby muscles. Hamada et al. compared the frequency of diplopia after cataract extraction in 7,205 patients who received peribulbar anesthesia, 3,582 of whom also received admixed hyaluronidase. No patients in the hyaluronidase group developed diplopia; 27 of the 3,634 patients (0.75%) in the hyaluronidase-free peribulbar anesthetic group developed diplopia.2 In a series presented by Brown et al., 11 of the patients who developed diplopia after cataract surgery using peribulbar or retrobulbar blocks during a period of hyaluronidase shortage were operated on by surgeons who, in their 4–11 years or practice (encompassing approximately 6,900 cataract extractions), had never had a case of postoperative diplopia.10 Differentiating between anesthetic myotoxicity and traumatic myopathies or neuropathies may be difficult if not impossible but, regardless of the exact etiology, the examiner should generally expect to detect a vertical misalignment. Nayak et al. demonstrated that 98% of perioperatively acquired strabismus was vertical.3 The development of a postoperative hypertropia, given the inferotemporal approach of peribulbar and retrobulbar blocks described earlier, should be unsurprising; the inferior rectus and the inferior division of the third nerve which supplies it lie in close proximity to the needle’s path and, if injured, paresis should result in underaction and a hypertropia. However, approximately half of the patients in Nayak’s series with vertical diplopia after cataract extraction presented with hypotropias ipsilateral to the side of cataract extraction, despite a near-identical anesthetic approach. The mixture of postoperative hypertropias and hypotropias may be explained by an initial paresis of the inferior rectus muscle that manifests as a hypertropia followed by muscle sclerosis that results in a chronic hypotropia. Additional explanations include segmental muscle injury resulting in seemingly paradoxical overaction and variable needle trajectory. The nature of the ocular misalignment may evolve over time; a hypertropia may evolve into a hypotropia and vice versa. Capo and Guyton reported this phenomenon in humans in 1996; two patients with postoperative hypertropias and superior rectus muscle overaction later became hypotropic.11 Of the four patients in Nayak’s series who were examined within two weeks of cataract extraction, two initially presented with a hypertropia ipsilateral to cataract extraction only to convert to a hypotropia with time.3 The putative explanation in this case is an initial paretic phase, either from nerve/muscle puncture or anesthesia followed by sclerosis and subsequent restriction. Though initial bupivacaine-induced myotoxicity may begin within minutes,12 Porter et al. demonstrated in a primate model that the maximal myotoxicity of Seminars in Ophthalmology
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Diplopia after Cataract Extraction commonly employed anesthetics, including bupivicaine, did not occur in extraocular muscles until 14 days after retrobulbar blocks.13 Damage to a muscle may potentially result in either underaction or overaction, depending on whether the damage is diffuse or segmental, respectively. Capo and Guyton (1996) hypothesized that changes in the length-tension curve for the affected muscle due to segmental sclerosis might produce a result akin to a resection performed in strabismus surgery.11 This is an appealing hypothesis to explain patterns of deviation wherein the ocular misalignment is greatest when gaze is directed towards the affected muscle. The putative explanation for iatrogenic overaction is segmental sclerosis with resulting elongation of the non-sclerosed segment of muscle. In primary position, this weakens the actin and myosin interdigitations. When directing the eye in the direction of action of the affected muscle, interdigitation may be greater than normal, resulting in overaction. The pattern of overactivity of the affected muscle seems to be quite common; in one case series of 28 patients with ocular misalignment after cataract extraction, 14 (50%) of the 28 of muscles were overactive, 12 (39%) restricted, and 2 (11%) paretic.14 In addition to delayed myotoxicity and segmental sclerosis of the inferior rectus muscle, some cases of post-anesthetic hypotropia may be accounted for by damage to the superior rectus muscle. Peribulbar blocks are 4.8 times more likely to damage the inferior rectus muscle rather than the superior rectus muscle, but may uncommonly affect the latter. Retrobulbar blocks employ a longer needle than employed for peribulbar blocks; cadaveric studies have shown that these can easily allow injury to the superior rectus muscle directly.13 The frequency with which strabismus surgery was required to eliminate postoperative diplopia varied substantially across series.2,10 Strabismus surgery is a highly efficacious treatment for ocular misalignments after cataract extraction. In Capo and Guyton’s series,11 13 patients underwent strabismus surgery. Five had preoperative misalignments measuring greater than 30 PD. Only the affected muscle was operated on in 11 of the 13. All patients experienced positive outcomes and none required further strabismus surgery. It is important to consider that myotoxicity or traumatic myopathies are frequently dynamic processes, as discussed earlier. Therefore, it is important to only perform strabismus surgery once measurements stabilize, typically requiring several months at the minimum. It may be difficult to tell whether there is an advantage in the choice of retrobulbar or peribulbar block as a means to mitigate the chance of postoperative diplopia. Capo, Roth, and Johnson found no difference in the frequency of postoperative diplopia between patients anesthetized with retrobulbar versus peribulbar blocks among 19 patients.14 Conversely, seven of © 2017 Taylor & Francis
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the nine patients in Esswein and von Noorden’s smaller series of patients with postoperative diplopia received peribulbar blocks.15 Given the longer needle length and trajectory required to administer a retrobulbar block, one might assume a resultant increase in the probability of injuring either the cranial nerves or the extraocular muscles. It might also be assumed that the shorter needle and extraconal target of a peribulbar block might confer less risk of direct trauma or anesthetic-related myotoxicity. However, peribulbar blocks typically require a larger volume of anesthetic than is used in retrobulbar blocks to achieve adequate analgesia, thus anesthetic myotoxicity may be just as potent. It is important to note that injury to cranial nerves or extraocular muscles is possible, even under circumstances of correct technical performance. Topical anesthesia may be employed to circumvent the need for retrobulbar and peribulbar blocks. The advantages of such an approach are obvious; there is neither a needle to injure muscle or nerve nor is anesthesia injected. Thus, the risk of developing diplopia as a result of the procedure is minimal. Gomez-Arnau studied postoperative diplopia in 3,587 patients who underwent cataract extraction; none of the 1,420 patients who had topical anesthesia developed postoperative diplopia.1 Despite this benefit, topical anesthesia may not be plausible in every patient. The disadvantage of topical anesthesia is that there is no resultant ophthalmoparesis and the patient must therefore be relied upon to keep the eye still. There is stability conferred to the globe by the instruments used in the cataract extraction itself, but this may be inadequate in an anxious patient. The use of superior rectus muscle stay sutures to stabilize the globe is rare nowadays, but their use to some extent defeats the purpose of topical anesthesia, as stay sutures may cause a vertical misalignment as well.3 Sub-Tenon’s anesthesia might provide a good compromise between the increased risks of peribulbar or retrobulbar blocks and the lack of ophthalmoparesis with the use of topical anesthetics.4 The sub-Tenon’s approach involves exposure of the lateral conjunctiva and passage of a catheter posteriorly along the surface of the globe. Once the catheter has crossed the equator of the globe, anesthetic can be injected. Smaller doses yield anesthesia and larger doses may be employed in order to yield ophthalmoparesis as well. The potential for anestheticinduced myotoxicity and prolonged nerve block exists when doses high enough to yield ophthalmoparesis are employed, though the risk is likely lower than when the muscle itself is inadvertently infiltrated with anesthetic.
DIPLOPIA FROM PRE-EXISTING PROCESSES UNMASKED AFTER CATARACT EXTRACTION Given the temporal association between the patient’s cataract extraction and report of postoperative
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M. A. Bouffard and D. M. Cestari
diplopia, it is often assumed that the former has a causative relationship with the latter, and this is frequently untrue. Recognition of pre-existing misalignments was the most commonly identified cause of diplopia after cataract surgery in Nayak’s series, surpassing even anesthetic-induced myotoxicity.3 Particular caution should be employed in the evaluation of a diplopic patient after cataract extraction with a vertical misalignment; the discussion on the subject of anesthetic myotoxicity (which almost invariably causes a vertical misalignment) does not obviate the need to consider skew deviations, fourth nerve palsies, myasthenia gravis, and other etiologies of a vertical misalignment. Except in cases of secondary cataract formation (e.g., in the setting of corticosteroids or in postvitrectomy cataract formation), cataract development is typically an insidious and bilateral process progressing over many years. The long duration of subnormal vision which some patients may endure can mask even marked and long-term misalignment. After cataract extraction, many patients are able to appreciate a misalignment which was previously present but asymptomatic owing to poor acuity. This is true of any sort of ocular misalignment, related to the cataract (e.g., sensory exotropia due to cataract-mediated low vision) or otherwise (e.g., vergence deficits, orbital connective tissue degeneration, cranial neuropathies, and myopathies).
DIPLOPIA RELATED TO CORTICAL MALADAPTATION There are two disorders which fall into this category, the first of which is fixation-switch diplopia.16 This is an uncommon phenomenon seen when patients with a longstanding strabismus are forced to take up fixation with their non-dominant (typically amblyopic/suppressed) eye. Given the sudden and often dramatic improvement in acuity that results from the extraction of a dense cataract, patients with bilateral cataracts may be forced to fixate with the non-dominant eye if its cataract is extracted first. This switch from fixating with the dominant to the previously suppressed nondominant eye can be problematic in patients with long-term strabismus, resulting in intractable central diplopia until the fellow eye is operated on and the patient may again fixate with the dominant eye. The neural mechanism underpinning monocular suppression in strabismus is poorly understood; in cases of fixation-switch diplopia after cataract extraction, it is presumably the drive to fixate with the eye of greater acuity that forces the abandonment of long-maintained suppression and thus the emergence of diplopia. Baseline strabismus is present in 1–2% of the population and cataracts are highly prevalent in the elderly. Thus, patients prone to fixation switch diplopia are not
exceedingly rare and the lack of awareness of this condition among physicians may propagate the problem. A questionnaire sent to cataract surgeons in Wales demonstrated that only 56% would first operate on the non-amblyopic eye of a patient with bilateral cataracts.17 As such, neuro-ophthalmologists may encounter cases from time to time and awareness of an uncommon phenomenon may allow for a prompt diagnosis and expedited surgery on the fellow eye. The second diagnosis in this category is impairment of central fusion. Reports exist in the literature of previously normal patients who sustained monocular cataracts (typically traumatic in etiology) and spent several years with marked ametropia, due to a combination of delayed cataract extraction and abandoned postoperative refraction.18 These patients invariably developed what seems to be a sensory exotropia—in one series, each patient demonstrated an exotropia with a slight hypotropia and excyclotorsion in one eye. When these patients resumed proper correction in the fellow eye, they suffered from intractable diplopia—even when the misalignment was corrected with prisms. Patients described the second image as “bobbing.” Correspondingly, the examiners noted that the deviation varied constantly during the examination, particularly in the vertical plane. This is thought to arise from central disruption of fusion after prolonged periods of ametropia; with restoration emmetropia, the deficit in fusion becomes apparent. The exact mechanism by which central fusion is lost remains unclear. The presence of similar deficits of central fusion without any report of bobbing eye movements suggests that the abnormal eye movements in these patients might not be the cause of the failure to fuse.19 The abnormal eye bobbing described by Pratt-Johnson is phenomenologically similar to the Heimann-Bielschowsky phenomenon.20–22 Though the abnormal eye movements described by Pratt-Johnson were recognized after restoration of emmetropia, it is possible that these patients developed the Heimann-Bielschowsky phenomenon during their period of ametropia with subsequent lack of recovery.
DIPLOPIA RELATED TO POSTOPERATIVE OPTICS A variety of refractive issues or maculopathies arising from cataract extraction may lead to diplopia. This category includes etiologies such as corneal edema, lens decentration, aniseikonia, and cystoid macular edema. Of the monocular etiologies, lens decentration is perhaps the most straightforward.23 Other refractive issues, such as pseudophakic corneal edema, should be considered as well. Static and dynamic aniseikonia may cause binocular diplopia in the pseudophakic patient, providing a source of confusion. Seminars in Ophthalmology
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Diplopia after Cataract Extraction Static aniseikonia may be accounted for either by differences in lens strength between eyes or by macular edema, both of which are potential considerations in the pseudophake. Cystoid macular edema is a potential complication of cataract extraction, possibly involving macular prostacyclin release as a downstream effect of anterior chamber manipulation.24 Edema of the macula results in increased spatial dispersion between photoreceptors. The rays of light deflected from a target of fixation will therefore be sensed by fewer photoreceptors in an eye with macular edema than in the fellow eye without edema where the photoreceptors are normally arranged. The result is micropsia and, if the size of the image perceived from an edematous macula is small enough, the brain will be unable to fuse it with the image of normal size perceived by the non-edematous macula in the fellow eye. Patients may report this as diplopia, which is technically correct, though the larger and smaller images are superimposed. Closure of either eye results in the resolution of this discrepancy and, thus, the diplopia is binocular. However, these patients will typically have metamorphopsia on Amsler grid testing. Static aniseikonia may also arise in cases of marked asymmetry in lens strength between eyes; minus (concave) lenses generate a diminutive false image and plus (convex) lenses generate a magnified false image. Understanding dynamic aniseikonia is predicated upon an understanding of the prismatic properties of any lens. The thicker the lens, the more prismatic effect is applied to rays of light not passing through the optical center of the lens. For example, a concave/minus lens is thinner at its center than at its periphery and thus acts as a base-out prism on each side of the pupil. Therefore, a patient with an intraocular lens in one eye and a concave spectacle lens of high strength in the fellow eye will experience discrepant prismatic effect between eyes in eccentric gaze (thus, the term dynamic aniseikonia, for it implies eye movement), and rays of light originating from the same target will hit different retinal coordinates in each eye as a result. Like static aniseikonia, dynamic aniseikonia results in binocular diplopia. Unlike static aniseikonia, dynamic aniseikonia only results in diplopia in eccentric gaze.
DISCUSSION Diplopia after cataract extraction is an uncommon but alarming complaint. Its causes are protean and its rarity inherently engenders unfamiliarity with the evaluation, which can have implications for proper identification of underlying disease processes as well as medical-legal issues. The co-occurrence of cataract extraction and report of diplopia may imply that the two are causally related. However, restoration of sight after cataract extraction may allow for the perception of a longstanding ocular misalignment. This may be an © 2017 Taylor & Francis
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even more common cause of diplopia after cataract extraction than surgical or anesthetic iatrogenesis. Certain details in the history and examination may provide critical clues as to the etiology, such as a transition from a hypertropia to a hypotropia over time, muscle overaction, horizontal deviations (which are unlikely to occur as a result of the procedure), the type of anesthesia employed, the approach, the use of hyaluronidase, and preoperative strabismus. It is of prime importance to conduct a thorough assessment of the patient’s efferent visual system prior to cataract extraction, both by history and examination. Documentation of preoperative strabismus is not only helpful should postoperative diplopia arise, but also in the decision to operate on the dominant eye first to prevent fixation-switch diplopia (all other factors being equal). Eliciting a history of childhood patching or surgery can be tremendously helpful, and patients rarely volunteer this unless specifically queried. Intraoperative modifications, such as the addition of hyaluronidase to retrobulbar and peribulbar blocks, the selection of topical or Sub-Tenon’s ansthesia, or avoidance of a bridle suture can further reduce the risk of postoperative diplopia. It is of the utmost importance to include these details in the operative report and anesthesia record for both the good of the patient and the examining physician, should postoperative diplopia occur.
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.
REFERENCES 1. Gomez-Arnau JI, Yanguela J, Gonzales A, et al. Anesthesiarelated diplopia after cataract surgery. Br J Anaesth. 2003;90:189–193. doi:10.1093/bja/aeg029. 2. Hamada S, Devys JM, Xuan TH, et al. Role of hyaluronidase in diplopia after peribulbar anesthesia for cataract surgery. Ophthalmology. 2005;112:879–882. doi:10.1016/j. ophtha.2004.11.059. 3. Nayak H, Kersey JP, Oystreck DT, Cline RA, Lyons CJ. Diplopia following cataract sugery: A review of 150 patients. Eye. 2008;22:1057–1064. doi:10.1038/sj. eye.6702847. 4. Hamilton RC. Techniques of orbital regional anaesthesia. Br J Anesth. 1995;75:88–92. doi:10.1093/bja/75.1.88. 5. Carlson BM, Rainin EA. Rat extraocular muscle regeneration: Repair of local anesthetic-induced damage. Arch Ophthalmol. 1985;103:1372–1377. doi:10.1001/ archopht.1985.01050090125046. 6. Rainin EA, Carlson BM. Post-operative diplopia and ptosis: A clinical hypothesis based on the myotoxicity of anesthetics. Arch Ophthalmol. 1985;103:1337–1339. doi:10.1001/ archopht.1985.01050090089038. 7. Carlson BM, Emerick S, Komorowski TE, Rainin EA, Shepard BM. Extraocular muscle regeneration in primates:
6
8.
9.
10.
11.
Downloaded by [UNIVERSITY OF ADELAIDE LIBRARIES] at 01:03 13 October 2017
12.
13.
14.
15.
M. A. Bouffard and D. M. Cestari Local anesthetic-induced lesions. Ophthalmology. 1992;99:582–589. doi:10.1016/S0161-6420(92)31930-X. Atkinson WS. Use of hyaluronidase with local anesthesia in ophthalmology: Preliminary report. Arch Ophthalmol. 1949;42:628–633. doi:10.1001/archopht.1949.00900050638012. Dempsey GA, Barrett PJ, Kirby IJ. Hyaluronidase and peribulbar block. Br J Anesthes. 1997;78:671–674. doi:10.1093/ bja/78.6.671. Brown SM, Brooks SE, Mazow ML, et al. Cluster of diplopia after periocular anesthesia without hyaluronidase. J Cataract Refract Surg. 1999;25:1245–1249. doi:10.1016/S0886-3350(99) 00151-0. Capo H, Guyton DL. Ipsilateral hypertropia following cataract surgery. Ophthalmology. 1996;103:918–921. doi:10.1016/S0161-6420(96)30623-4. Hall-Graggs ECB. Early ultrastructural changes in skeletal muscle exposed to the local anesthetic bupivacaine (Marcaine). Br J Exp Pathol. 1980;61:139–149. Porter JD, Edney DP, McMahon EJ, Burns LA. Extraocular myotoxicity of the retrobulbar anesthetic bupivicaine hydrochloride. Invest Ophthalmol Vis Sci. 1988;29:162–174. Capo H, Roth E, Johnson T, Munoz M, Siatkowski RM. Vertical strabismus after cataract surgery. Ophthalmology. 1996;103:918–921. doi:10.1016/S0161-6420(96)30587-3. Esswein MD, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J Ophthalmol. 1993;116:424–430. doi:10.1016/S0002-9394(14)71399-6.
16. Boyd TA, Karas Y, Budd GE, Wyatt HT. Fixation switch diplopia. Can J Ophthalmol. 1974;9(3):310–315. 17. Samuel Williams G, Radwan M, Menon J. Cataract surgery planning in amblyopic patients—which eye first? Awareness of the potential for post-operative diplopia amongst consultant ophthalmic surgeons in Wales. Ulster Med J. 2013;82(2):82–84. 18. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol. 1989;107:23–26. doi:10.1016/0002-9394(89)90809-X. 19. Pratt-Johnson JA, Tillson G. Acquired central disruption of fusional amplitude. Ophthalmology. 1979;86(12):2140–2142. doi:10.1016/S0161-6420(79)35292-7. 20. Heimann E. Einseitiger nystagmus. Klin Monatsblat Augenheilkd. 1902;49:99–105. 21. Bielschowsky A. Die enseitigen und gegensinnigen (dissoziierten): Vertikalbewegungen der augent. Graefe’s Arch Ophthalmol. 1931;125:493–553. doi:10.1007/BF01853623. 22. Leigh RJ, Thurston SE, Tomsak RL, Grossman GE, Lanska DJ. Effect of monocular vision loss upon stability of gaze. Invest Ophthalmol Vis Sci. 1989;30:288–292. 23. Bloom PA, Laidlaw A, Adams D. Subjective and objective diplopia caused by intraocular lens decentration. J Cataract Refr Surg. 1992;4(4):266–268. 24. Hudes GR, Li WY, Rockey JH, White P. Prostacyclin is the major prostaglandin synthesized by bovine retinal capillary pericytes in culture. Invest Ophthalmol Vis Sci. 1988;29 (10):1511–1516.
Seminars in Ophthalmology
ISSN: 0882-0538 (Print) 1744-5205 (Online) Journal homepage: http://www.tandfonline.com/loi/isio20
Diplopia after Cataract Extraction Marc A. Bouffard & Dean M. Cestari To cite this article: Marc A. Bouffard & Dean M. Cestari (2017): Diplopia after Cataract Extraction, Seminars in Ophthalmology, DOI: 10.1080/08820538.2017.1353806 To link to this article: http://dx.doi.org/10.1080/08820538.2017.1353806
Published online: 09 Oct 2017.
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Article views: 1
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=isio20 Download by: [UNIVERSITY OF ADELAIDE LIBRARIES]
Date: 13 October 2017, At: 01:03
Seminars in Ophthalmology, Early Online, 1–6, 2017 © Taylor & Francis ISSN: 0882-0538 print / 1744-5205 online DOI: https://doi.org/10.1080/08820538.2017.1353806
Diplopia after Cataract Extraction Marc A. Bouffard and Dean M. Cestari
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Neuro-Ophthalmology service, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA
ABSTRACT Diplopia after cataract extraction is an unexpected outcome for the patient and often a source of confusion for the physician, owing to its relative infrequency. This article reviews the pertinent literature on the subject. Mechanisms include anesthetic myotoxicity, surgical trauma, optical aberrations, cortical disorders in patients with congenital strabismus, and the unmasking of previously unnoticed ocular misalignment. As the population continues to age and cataract extraction is performed in increasing volume, familiarity with this uncommon but important outcome may help to clarify and effectively treat post-cataract-extraction diplopia. Keywords: Adverse events, cataract surgery, double vision, strabismus, surgical complication
INTRODUCTION
procedural complications such as anesthetic-induced myotoxicity, nerve or muscle trauma with the anesthetic needle, and muscle trauma with stay sutures. Less intuitive binocular etiologies include disorders of cortical maladaption such as fixation-switch diplopia and central disruption of fusion, the unmasking of ocular misalignments which were present but unappreciated prior to cataract extraction owing to poor acuity, the concomitant development of causally unrelated diplopia and, rarely, macular processes such as cystoid macular edema. Monocular etiologies, such as lens decentration or retained lens fragments, are less frequent and often less perplexing than the aforementioned causes and will not be discussed in depth here (Table 1). The relative frequencies of the these etiologies were described by Nayak et al., who conducted a retrospective analysis of 150 cases of diplopia following cataract extraction; the most common etiology identified was decompensation of previous strabismus, seen in 54 patients (34%), followed by extraocular muscle dysfunction (41 patients, 25%), refractive disorders (14 patients, 8.5%), concurrent onset of systemic disease (8 patients, 5%), disruption of central fusion (8 patients, 5%), and monocular etiologies (4 patients, 2.5%). No cause could clearly be isolated in 32 patients (20%).3 Even a careful history and examination may be fruitless if some of the key details related to the previous etiologies are unfamiliar.
Developing diplopia after cataract extraction is an unexpected event for the patient and often a source of confusion for the physician. New-onset diplopia after cataract extraction is uncommon. Most large series describe an incidence of diplopia after cataract extraction of between 0.17% and 0.75%.1–3 Owing to the relative infrequency and myriad causes of diplopia after cataract surgery, the individual cataract surgeon may lack experience in the evaluation of post-cataract-extraction diplopia. There are a number of particular details about the surgical approach, anesthesia, prior alignment, current refraction, and other postoperative complications which must be kept in mind during the evaluation of a diplopic patient after cataract extraction. The goal of this review is to present a cogent overview of the causes of diplopia after cataract extraction to aid in the prompt and accurate diagnosis of the underlying process, especially in areas where neuro-ophthalmic consultation is not readily available. Binocular diplopia is due to an ocular misalignment and it resolves when the patient covers either eye. Monocular diplopia is present when viewing through one eye only. Both binocular and monocular etiologies of post-cataract-extraction diplopia exist, and differentiating the two is the first step in the appropriate workup of these patients. Binocular etiologies may relate to
Correspondence: Marc A. Bouffard, M.D. Fellow in Neuro-Ophthalmology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA. E-mail: [email protected]
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TABLE 1. Etiologies of diplopia particular to cataract extraction. Surgical etiologies Anesthetic myotoxicity - Segmental toxicity with muscle overaction - Diffuse toxicity with muscle underaction Bridle sutures Nerve injury
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Cortical etiologies Fixation-switch diplopia Loss of central fusion Postoperative Optics Binocular Static aniseikonia Dynamic aniseikonia Cystoid macular edema Monocular Corneal edema
DIPLOPIA RELATED TO ANESTHESIA AND TRAUMA Cataract extraction is commonly performed with the aid of a retrobulbar or peribulbar block. Retrobulbar blocks are accomplished by passing a 3-cm-long, 22–27 gauge needle into the retrobulbar space, either via a transcutaneous or transconjunctival approach. The needle is inserted inferotemporal to the globe and is guided towards the orbital apex. Peribulbar blocks are accomplished by passage of a shorter needle into the extraconal space. Commonly employed anesthetics include 2% lidocaine and 0.5% to 0.75% bupivacaine. These agents are sodium channel blockers and thus serve to disrupt sodium-dependent depolarization of nerves. Though typically considered in the context of disrupting sensory afferent input, adequate quantities also achieve paralysis of the globe intraoperatively.4 While direct trauma to an extraocular muscle or cranial nerve is perhaps the most intuitive method of injury by which the passage of an anesthetic needle into the orbit might result in diplopia, anesthesiainduced myotoxicity is likely a more common cause. A good deal of literature on the subject of anesthetic myotoxicity has emerged since its proposal in 1985.5,6 Carlson et al. performed retrobulbar blocks on primates employing either 0.75% bupivacaine, 2.0% mepivacaine, or 2.0% lidocaine plus 1:100,000 epinephrine. The typical result was the superficial degeneration and regeneration of nearby extra-ocular muscles, but on occasion diffuse myotoxicity was seen. Diffuse myotoxicity was common in both primate and human extraocular muscles after direct infiltration of the muscle with local anesthetic.7 The use of hyaluronidase may decrease the potential for myotoxicity from infiltrational anesthesia. Hyaluronidase has been employed with local anesthesia in ophthalmic procedures since at least 19498; its function as a digestive agent may potentiate anesthetic
dispersal through tissue.9 In doing so, hyaluronidase may prevent myotoxic local anesthetics from accumulating in one area and damaging nearby muscles. Hamada et al. compared the frequency of diplopia after cataract extraction in 7,205 patients who received peribulbar anesthesia, 3,582 of whom also received admixed hyaluronidase. No patients in the hyaluronidase group developed diplopia; 27 of the 3,634 patients (0.75%) in the hyaluronidase-free peribulbar anesthetic group developed diplopia.2 In a series presented by Brown et al., 11 of the patients who developed diplopia after cataract surgery using peribulbar or retrobulbar blocks during a period of hyaluronidase shortage were operated on by surgeons who, in their 4–11 years or practice (encompassing approximately 6,900 cataract extractions), had never had a case of postoperative diplopia.10 Differentiating between anesthetic myotoxicity and traumatic myopathies or neuropathies may be difficult if not impossible but, regardless of the exact etiology, the examiner should generally expect to detect a vertical misalignment. Nayak et al. demonstrated that 98% of perioperatively acquired strabismus was vertical.3 The development of a postoperative hypertropia, given the inferotemporal approach of peribulbar and retrobulbar blocks described earlier, should be unsurprising; the inferior rectus and the inferior division of the third nerve which supplies it lie in close proximity to the needle’s path and, if injured, paresis should result in underaction and a hypertropia. However, approximately half of the patients in Nayak’s series with vertical diplopia after cataract extraction presented with hypotropias ipsilateral to the side of cataract extraction, despite a near-identical anesthetic approach. The mixture of postoperative hypertropias and hypotropias may be explained by an initial paresis of the inferior rectus muscle that manifests as a hypertropia followed by muscle sclerosis that results in a chronic hypotropia. Additional explanations include segmental muscle injury resulting in seemingly paradoxical overaction and variable needle trajectory. The nature of the ocular misalignment may evolve over time; a hypertropia may evolve into a hypotropia and vice versa. Capo and Guyton reported this phenomenon in humans in 1996; two patients with postoperative hypertropias and superior rectus muscle overaction later became hypotropic.11 Of the four patients in Nayak’s series who were examined within two weeks of cataract extraction, two initially presented with a hypertropia ipsilateral to cataract extraction only to convert to a hypotropia with time.3 The putative explanation in this case is an initial paretic phase, either from nerve/muscle puncture or anesthesia followed by sclerosis and subsequent restriction. Though initial bupivacaine-induced myotoxicity may begin within minutes,12 Porter et al. demonstrated in a primate model that the maximal myotoxicity of Seminars in Ophthalmology
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Diplopia after Cataract Extraction commonly employed anesthetics, including bupivicaine, did not occur in extraocular muscles until 14 days after retrobulbar blocks.13 Damage to a muscle may potentially result in either underaction or overaction, depending on whether the damage is diffuse or segmental, respectively. Capo and Guyton (1996) hypothesized that changes in the length-tension curve for the affected muscle due to segmental sclerosis might produce a result akin to a resection performed in strabismus surgery.11 This is an appealing hypothesis to explain patterns of deviation wherein the ocular misalignment is greatest when gaze is directed towards the affected muscle. The putative explanation for iatrogenic overaction is segmental sclerosis with resulting elongation of the non-sclerosed segment of muscle. In primary position, this weakens the actin and myosin interdigitations. When directing the eye in the direction of action of the affected muscle, interdigitation may be greater than normal, resulting in overaction. The pattern of overactivity of the affected muscle seems to be quite common; in one case series of 28 patients with ocular misalignment after cataract extraction, 14 (50%) of the 28 of muscles were overactive, 12 (39%) restricted, and 2 (11%) paretic.14 In addition to delayed myotoxicity and segmental sclerosis of the inferior rectus muscle, some cases of post-anesthetic hypotropia may be accounted for by damage to the superior rectus muscle. Peribulbar blocks are 4.8 times more likely to damage the inferior rectus muscle rather than the superior rectus muscle, but may uncommonly affect the latter. Retrobulbar blocks employ a longer needle than employed for peribulbar blocks; cadaveric studies have shown that these can easily allow injury to the superior rectus muscle directly.13 The frequency with which strabismus surgery was required to eliminate postoperative diplopia varied substantially across series.2,10 Strabismus surgery is a highly efficacious treatment for ocular misalignments after cataract extraction. In Capo and Guyton’s series,11 13 patients underwent strabismus surgery. Five had preoperative misalignments measuring greater than 30 PD. Only the affected muscle was operated on in 11 of the 13. All patients experienced positive outcomes and none required further strabismus surgery. It is important to consider that myotoxicity or traumatic myopathies are frequently dynamic processes, as discussed earlier. Therefore, it is important to only perform strabismus surgery once measurements stabilize, typically requiring several months at the minimum. It may be difficult to tell whether there is an advantage in the choice of retrobulbar or peribulbar block as a means to mitigate the chance of postoperative diplopia. Capo, Roth, and Johnson found no difference in the frequency of postoperative diplopia between patients anesthetized with retrobulbar versus peribulbar blocks among 19 patients.14 Conversely, seven of © 2017 Taylor & Francis
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the nine patients in Esswein and von Noorden’s smaller series of patients with postoperative diplopia received peribulbar blocks.15 Given the longer needle length and trajectory required to administer a retrobulbar block, one might assume a resultant increase in the probability of injuring either the cranial nerves or the extraocular muscles. It might also be assumed that the shorter needle and extraconal target of a peribulbar block might confer less risk of direct trauma or anesthetic-related myotoxicity. However, peribulbar blocks typically require a larger volume of anesthetic than is used in retrobulbar blocks to achieve adequate analgesia, thus anesthetic myotoxicity may be just as potent. It is important to note that injury to cranial nerves or extraocular muscles is possible, even under circumstances of correct technical performance. Topical anesthesia may be employed to circumvent the need for retrobulbar and peribulbar blocks. The advantages of such an approach are obvious; there is neither a needle to injure muscle or nerve nor is anesthesia injected. Thus, the risk of developing diplopia as a result of the procedure is minimal. Gomez-Arnau studied postoperative diplopia in 3,587 patients who underwent cataract extraction; none of the 1,420 patients who had topical anesthesia developed postoperative diplopia.1 Despite this benefit, topical anesthesia may not be plausible in every patient. The disadvantage of topical anesthesia is that there is no resultant ophthalmoparesis and the patient must therefore be relied upon to keep the eye still. There is stability conferred to the globe by the instruments used in the cataract extraction itself, but this may be inadequate in an anxious patient. The use of superior rectus muscle stay sutures to stabilize the globe is rare nowadays, but their use to some extent defeats the purpose of topical anesthesia, as stay sutures may cause a vertical misalignment as well.3 Sub-Tenon’s anesthesia might provide a good compromise between the increased risks of peribulbar or retrobulbar blocks and the lack of ophthalmoparesis with the use of topical anesthetics.4 The sub-Tenon’s approach involves exposure of the lateral conjunctiva and passage of a catheter posteriorly along the surface of the globe. Once the catheter has crossed the equator of the globe, anesthetic can be injected. Smaller doses yield anesthesia and larger doses may be employed in order to yield ophthalmoparesis as well. The potential for anestheticinduced myotoxicity and prolonged nerve block exists when doses high enough to yield ophthalmoparesis are employed, though the risk is likely lower than when the muscle itself is inadvertently infiltrated with anesthetic.
DIPLOPIA FROM PRE-EXISTING PROCESSES UNMASKED AFTER CATARACT EXTRACTION Given the temporal association between the patient’s cataract extraction and report of postoperative
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diplopia, it is often assumed that the former has a causative relationship with the latter, and this is frequently untrue. Recognition of pre-existing misalignments was the most commonly identified cause of diplopia after cataract surgery in Nayak’s series, surpassing even anesthetic-induced myotoxicity.3 Particular caution should be employed in the evaluation of a diplopic patient after cataract extraction with a vertical misalignment; the discussion on the subject of anesthetic myotoxicity (which almost invariably causes a vertical misalignment) does not obviate the need to consider skew deviations, fourth nerve palsies, myasthenia gravis, and other etiologies of a vertical misalignment. Except in cases of secondary cataract formation (e.g., in the setting of corticosteroids or in postvitrectomy cataract formation), cataract development is typically an insidious and bilateral process progressing over many years. The long duration of subnormal vision which some patients may endure can mask even marked and long-term misalignment. After cataract extraction, many patients are able to appreciate a misalignment which was previously present but asymptomatic owing to poor acuity. This is true of any sort of ocular misalignment, related to the cataract (e.g., sensory exotropia due to cataract-mediated low vision) or otherwise (e.g., vergence deficits, orbital connective tissue degeneration, cranial neuropathies, and myopathies).
DIPLOPIA RELATED TO CORTICAL MALADAPTATION There are two disorders which fall into this category, the first of which is fixation-switch diplopia.16 This is an uncommon phenomenon seen when patients with a longstanding strabismus are forced to take up fixation with their non-dominant (typically amblyopic/suppressed) eye. Given the sudden and often dramatic improvement in acuity that results from the extraction of a dense cataract, patients with bilateral cataracts may be forced to fixate with the non-dominant eye if its cataract is extracted first. This switch from fixating with the dominant to the previously suppressed nondominant eye can be problematic in patients with long-term strabismus, resulting in intractable central diplopia until the fellow eye is operated on and the patient may again fixate with the dominant eye. The neural mechanism underpinning monocular suppression in strabismus is poorly understood; in cases of fixation-switch diplopia after cataract extraction, it is presumably the drive to fixate with the eye of greater acuity that forces the abandonment of long-maintained suppression and thus the emergence of diplopia. Baseline strabismus is present in 1–2% of the population and cataracts are highly prevalent in the elderly. Thus, patients prone to fixation switch diplopia are not
exceedingly rare and the lack of awareness of this condition among physicians may propagate the problem. A questionnaire sent to cataract surgeons in Wales demonstrated that only 56% would first operate on the non-amblyopic eye of a patient with bilateral cataracts.17 As such, neuro-ophthalmologists may encounter cases from time to time and awareness of an uncommon phenomenon may allow for a prompt diagnosis and expedited surgery on the fellow eye. The second diagnosis in this category is impairment of central fusion. Reports exist in the literature of previously normal patients who sustained monocular cataracts (typically traumatic in etiology) and spent several years with marked ametropia, due to a combination of delayed cataract extraction and abandoned postoperative refraction.18 These patients invariably developed what seems to be a sensory exotropia—in one series, each patient demonstrated an exotropia with a slight hypotropia and excyclotorsion in one eye. When these patients resumed proper correction in the fellow eye, they suffered from intractable diplopia—even when the misalignment was corrected with prisms. Patients described the second image as “bobbing.” Correspondingly, the examiners noted that the deviation varied constantly during the examination, particularly in the vertical plane. This is thought to arise from central disruption of fusion after prolonged periods of ametropia; with restoration emmetropia, the deficit in fusion becomes apparent. The exact mechanism by which central fusion is lost remains unclear. The presence of similar deficits of central fusion without any report of bobbing eye movements suggests that the abnormal eye movements in these patients might not be the cause of the failure to fuse.19 The abnormal eye bobbing described by Pratt-Johnson is phenomenologically similar to the Heimann-Bielschowsky phenomenon.20–22 Though the abnormal eye movements described by Pratt-Johnson were recognized after restoration of emmetropia, it is possible that these patients developed the Heimann-Bielschowsky phenomenon during their period of ametropia with subsequent lack of recovery.
DIPLOPIA RELATED TO POSTOPERATIVE OPTICS A variety of refractive issues or maculopathies arising from cataract extraction may lead to diplopia. This category includes etiologies such as corneal edema, lens decentration, aniseikonia, and cystoid macular edema. Of the monocular etiologies, lens decentration is perhaps the most straightforward.23 Other refractive issues, such as pseudophakic corneal edema, should be considered as well. Static and dynamic aniseikonia may cause binocular diplopia in the pseudophakic patient, providing a source of confusion. Seminars in Ophthalmology
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Diplopia after Cataract Extraction Static aniseikonia may be accounted for either by differences in lens strength between eyes or by macular edema, both of which are potential considerations in the pseudophake. Cystoid macular edema is a potential complication of cataract extraction, possibly involving macular prostacyclin release as a downstream effect of anterior chamber manipulation.24 Edema of the macula results in increased spatial dispersion between photoreceptors. The rays of light deflected from a target of fixation will therefore be sensed by fewer photoreceptors in an eye with macular edema than in the fellow eye without edema where the photoreceptors are normally arranged. The result is micropsia and, if the size of the image perceived from an edematous macula is small enough, the brain will be unable to fuse it with the image of normal size perceived by the non-edematous macula in the fellow eye. Patients may report this as diplopia, which is technically correct, though the larger and smaller images are superimposed. Closure of either eye results in the resolution of this discrepancy and, thus, the diplopia is binocular. However, these patients will typically have metamorphopsia on Amsler grid testing. Static aniseikonia may also arise in cases of marked asymmetry in lens strength between eyes; minus (concave) lenses generate a diminutive false image and plus (convex) lenses generate a magnified false image. Understanding dynamic aniseikonia is predicated upon an understanding of the prismatic properties of any lens. The thicker the lens, the more prismatic effect is applied to rays of light not passing through the optical center of the lens. For example, a concave/minus lens is thinner at its center than at its periphery and thus acts as a base-out prism on each side of the pupil. Therefore, a patient with an intraocular lens in one eye and a concave spectacle lens of high strength in the fellow eye will experience discrepant prismatic effect between eyes in eccentric gaze (thus, the term dynamic aniseikonia, for it implies eye movement), and rays of light originating from the same target will hit different retinal coordinates in each eye as a result. Like static aniseikonia, dynamic aniseikonia results in binocular diplopia. Unlike static aniseikonia, dynamic aniseikonia only results in diplopia in eccentric gaze.
DISCUSSION Diplopia after cataract extraction is an uncommon but alarming complaint. Its causes are protean and its rarity inherently engenders unfamiliarity with the evaluation, which can have implications for proper identification of underlying disease processes as well as medical-legal issues. The co-occurrence of cataract extraction and report of diplopia may imply that the two are causally related. However, restoration of sight after cataract extraction may allow for the perception of a longstanding ocular misalignment. This may be an © 2017 Taylor & Francis
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even more common cause of diplopia after cataract extraction than surgical or anesthetic iatrogenesis. Certain details in the history and examination may provide critical clues as to the etiology, such as a transition from a hypertropia to a hypotropia over time, muscle overaction, horizontal deviations (which are unlikely to occur as a result of the procedure), the type of anesthesia employed, the approach, the use of hyaluronidase, and preoperative strabismus. It is of prime importance to conduct a thorough assessment of the patient’s efferent visual system prior to cataract extraction, both by history and examination. Documentation of preoperative strabismus is not only helpful should postoperative diplopia arise, but also in the decision to operate on the dominant eye first to prevent fixation-switch diplopia (all other factors being equal). Eliciting a history of childhood patching or surgery can be tremendously helpful, and patients rarely volunteer this unless specifically queried. Intraoperative modifications, such as the addition of hyaluronidase to retrobulbar and peribulbar blocks, the selection of topical or Sub-Tenon’s ansthesia, or avoidance of a bridle suture can further reduce the risk of postoperative diplopia. It is of the utmost importance to include these details in the operative report and anesthesia record for both the good of the patient and the examining physician, should postoperative diplopia occur.
DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.
REFERENCES 1. Gomez-Arnau JI, Yanguela J, Gonzales A, et al. Anesthesiarelated diplopia after cataract surgery. Br J Anaesth. 2003;90:189–193. doi:10.1093/bja/aeg029. 2. Hamada S, Devys JM, Xuan TH, et al. Role of hyaluronidase in diplopia after peribulbar anesthesia for cataract surgery. Ophthalmology. 2005;112:879–882. doi:10.1016/j. ophtha.2004.11.059. 3. Nayak H, Kersey JP, Oystreck DT, Cline RA, Lyons CJ. Diplopia following cataract sugery: A review of 150 patients. Eye. 2008;22:1057–1064. doi:10.1038/sj. eye.6702847. 4. Hamilton RC. Techniques of orbital regional anaesthesia. Br J Anesth. 1995;75:88–92. doi:10.1093/bja/75.1.88. 5. Carlson BM, Rainin EA. Rat extraocular muscle regeneration: Repair of local anesthetic-induced damage. Arch Ophthalmol. 1985;103:1372–1377. doi:10.1001/ archopht.1985.01050090125046. 6. Rainin EA, Carlson BM. Post-operative diplopia and ptosis: A clinical hypothesis based on the myotoxicity of anesthetics. Arch Ophthalmol. 1985;103:1337–1339. doi:10.1001/ archopht.1985.01050090089038. 7. Carlson BM, Emerick S, Komorowski TE, Rainin EA, Shepard BM. Extraocular muscle regeneration in primates:
6
8.
9.
10.
11.
Downloaded by [UNIVERSITY OF ADELAIDE LIBRARIES] at 01:03 13 October 2017
12.
13.
14.
15.
M. A. Bouffard and D. M. Cestari Local anesthetic-induced lesions. Ophthalmology. 1992;99:582–589. doi:10.1016/S0161-6420(92)31930-X. Atkinson WS. Use of hyaluronidase with local anesthesia in ophthalmology: Preliminary report. Arch Ophthalmol. 1949;42:628–633. doi:10.1001/archopht.1949.00900050638012. Dempsey GA, Barrett PJ, Kirby IJ. Hyaluronidase and peribulbar block. Br J Anesthes. 1997;78:671–674. doi:10.1093/ bja/78.6.671. Brown SM, Brooks SE, Mazow ML, et al. Cluster of diplopia after periocular anesthesia without hyaluronidase. J Cataract Refract Surg. 1999;25:1245–1249. doi:10.1016/S0886-3350(99) 00151-0. Capo H, Guyton DL. Ipsilateral hypertropia following cataract surgery. Ophthalmology. 1996;103:918–921. doi:10.1016/S0161-6420(96)30623-4. Hall-Graggs ECB. Early ultrastructural changes in skeletal muscle exposed to the local anesthetic bupivacaine (Marcaine). Br J Exp Pathol. 1980;61:139–149. Porter JD, Edney DP, McMahon EJ, Burns LA. Extraocular myotoxicity of the retrobulbar anesthetic bupivicaine hydrochloride. Invest Ophthalmol Vis Sci. 1988;29:162–174. Capo H, Roth E, Johnson T, Munoz M, Siatkowski RM. Vertical strabismus after cataract surgery. Ophthalmology. 1996;103:918–921. doi:10.1016/S0161-6420(96)30587-3. Esswein MD, von Noorden GK. Paresis of a vertical rectus muscle after cataract extraction. Am J Ophthalmol. 1993;116:424–430. doi:10.1016/S0002-9394(14)71399-6.
16. Boyd TA, Karas Y, Budd GE, Wyatt HT. Fixation switch diplopia. Can J Ophthalmol. 1974;9(3):310–315. 17. Samuel Williams G, Radwan M, Menon J. Cataract surgery planning in amblyopic patients—which eye first? Awareness of the potential for post-operative diplopia amongst consultant ophthalmic surgeons in Wales. Ulster Med J. 2013;82(2):82–84. 18. Pratt-Johnson JA, Tillson G. Intractable diplopia after vision restoration in unilateral cataract. Am J Ophthalmol. 1989;107:23–26. doi:10.1016/0002-9394(89)90809-X. 19. Pratt-Johnson JA, Tillson G. Acquired central disruption of fusional amplitude. Ophthalmology. 1979;86(12):2140–2142. doi:10.1016/S0161-6420(79)35292-7. 20. Heimann E. Einseitiger nystagmus. Klin Monatsblat Augenheilkd. 1902;49:99–105. 21. Bielschowsky A. Die enseitigen und gegensinnigen (dissoziierten): Vertikalbewegungen der augent. Graefe’s Arch Ophthalmol. 1931;125:493–553. doi:10.1007/BF01853623. 22. Leigh RJ, Thurston SE, Tomsak RL, Grossman GE, Lanska DJ. Effect of monocular vision loss upon stability of gaze. Invest Ophthalmol Vis Sci. 1989;30:288–292. 23. Bloom PA, Laidlaw A, Adams D. Subjective and objective diplopia caused by intraocular lens decentration. J Cataract Refr Surg. 1992;4(4):266–268. 24. Hudes GR, Li WY, Rockey JH, White P. Prostacyclin is the major prostaglandin synthesized by bovine retinal capillary pericytes in culture. Invest Ophthalmol Vis Sci. 1988;29 (10):1511–1516.
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