Diplopia can be a debilitating complication of many types of eye surgery. In eyelid and conjunctival surgery, the muscles can be directly injured or can become scarred to the surrounding connective tissue. In cataract surgery, anesthetic agents can injure the muscles. At times, improving vision with cataract extraction can unmask preexisting strabismus from a fourth nerve palsy, thyroid eye disease, or loss of fusion secondary to long-standing poor vision in one eye. Refractive surgery can cause diplopia, especially when monovision is produced or in those with weak preoperative binocularity. Glaucoma drainage devices can create a mass effect on the globe or muscles, causing alterations in the alignment. These devices can also cause scarring issues similar to those created in conjunctival surgery. Retinal surgery may cause diplopia through effects of the buckle elements on the extraocular muscles or visual changes that can severely affect binocularity. Muscle or globe displacement may result after orbital surgery, leading to the development or exacerbation of diplopia.
Surgeons should be aware of the potential for motility disturbances after ocular surgery and the mechanisms by which they occur to prevent these issues and treat them when necessary. This review discusses the incidence of diplopia after each of these procedures and the mechanisms and treatments involved.
The authors conducted a literature search using the National Library of Medicine's PubMed database for all English language papers published through March 2016 with the main search terms (diplopia or strabismus) in addition to one or more of the following terms: surgery, complication, association, cataract, tube shunt, glaucoma drainage device, orbital decompression, keratomileusis, keratectomy, keratoplasty, keratotomy, refractive, scleral buckle, retinal, oculoplastic, blepharoplasty, trabeculoplasty, trabeculectomy, and glaucoma. Articles were then collected and identified based on relevance. Relevant references within these identified articles were also reviewed. Only studies written in English and published in peer-reviewed journals were included. To avoid redundancy, not all studies were ultimately used as citations.
Eyelid and Conjunctival Surgery
Diplopia can occur after blepharoplasty,1–12 but it is rare; 1 review of 920 cases revealed 3 patients with postoperative diplopia.4 With upper eyelid blepharoplasty, the trochlea or superior oblique muscle or tendon can be injured, causing paresis or, less commonly, Brown syndrome.8,11,12 Lower eyelid blepharoplasty can cause inferior rectus muscle paresis plus mechanical restriction to upward rotation of the globe.11 The inferior oblique, lateral rectus,2 and medial rectus7 muscles can also be injured or scarred.2
Several mechanisms have been proposed to explain postoperative diplopia. Surgery can cause intramuscular hemorrhage and edema, cicatricial changes within the muscle, or accidental incorporation of the muscle in the orbital septum.2 Excessive use of cautery12 or “overzealous dissection”3 may be the culprit. Another theory proposes a Volkmann-like ischemic contracture in which a compartment-like syndrome is created by the increased pressure from edema and hemorrhage in the perimuscular tissue, causing neuromuscular ischemia and muscle paresis.4 A novel mechanism was recently described in which scar formation hinders the anteroposterior travel of the inferior rectus muscle pulley system, causing restrictive hypotropia.10
Prior to surgical correction of diplopia, patients should be observed for several months because some patients improve 8 or 15 months2,4 after eyelid surgery. In most cases, prisms do not work well because the deviation is incomitant.2 Persistent diplopia after blepharoplasty is difficult to treat, often requiring more than one surgery and permanently limiting the field of singular binocular vision.11
Surgical planning depends on the muscles involved and the mechanism of injury. In-office forced duction testing may help differentiate restrictive from paretic causes.11 Imaging with magnetic resonance imaging10 or ultrasound1 may help delineate the injury. Surgical exploration may be necessary to determine the muscles involved, such as distinguishing fat adherence to the inferior rectus muscle from damage to the inferior oblique muscle.5 If the inferior rectus muscle or its pulley is scarred, the scar tissue must be released10 and the muscle may need to be recessed.5 Scarring and fat at the medial rectus muscle should be approached in the same way.7 If the inferior rectus muscle is injured, the proximal segment should be located and reattached to the globe.11 If this is not possible, transposition of the ipsilateral medial and lateral rectus muscles inferiorly in addition to recession of the superior rectus muscle may be necessary.1 Superior oblique muscle weakness can be addressed by recession of the contralateral inferior rectus muscle.12
Diplopia is also an uncommon complication after conjunctivodacryocystorhinostomy. Two case series of 40 patients both had 1 patient with diplopia.13,14 Another series of 42 patients found 2 patients with diplopia only on extreme lateral gaze.15 Diplopia may be caused by restriction from conjunctival scarring16 or fibrosis surrounding the tube.17
Some cases resolve after lysis of conjunctival bands with or without mitomycin C,16,18 although results are inconsistent.16 At times, the tube must be removed to restore normal eye movements and relieve diplopia.17
Conjunctival Lesions and Pterygia
Pterygium surgery can result in diplopia, most commonly by direct trauma to the medial rectus muscle causing exotropia19 or scarring of the muscle and perimuscular connective tissue complex causing esotropia.20
In all cases of diplopia after removal of pterygia or other conjunctival lesions, surgical planning depends on whether the limitation is in the field of the affected muscle or in the opposite field, and on careful forced duction and generation testing.21 Inadvertently detached medial rectus muscles may reattach posterior to their original insertion, causing significant exotropia. These muscles can be difficult to identify because of surrounding fibrous tissue. Although these cases are typically done under general anesthesia, using topical anesthesia may be helpful because the “suspicious tissue” can be held and the patient asked to move the eye in that direction. The movement will clarify whether the tissue is in fact muscle.22 When the muscle cannot be located, a transposition procedure may be required.21
Regarding esotropia management, scar tissue removal alone may be sufficient for patients who have diplopia only with attempted abduction of the affected eye. Medial rectus recession is usually also necessary for patients with diplopia in primary position.20 Corticosteroids, amniotic membranes, and motor exercises may be useful adjunctive treatments.21 Another option for esotropia is a lateral rectus resection, which avoids the scarred area entirely.23 Because diplopia is an uncommon occurrence resulting from pterygium surgery, these treatments have not been compared in trials to determine which is best.
Rates of diplopia after cataract surgery range from 0.1% to 1.4%.24–32 In a study of 150 patients with postoperative diplopia, six etiologies were defined: decompensation of preexisting strabismus (34%), extraocular muscle restriction or paresis (25%), concurrent onset of systemic disease (5%), central fusion disruption (5%), monocular diplopia (2.5%), and refractive causes (0.5%). The remaining patients could not be categorized.33 In a smaller study of 39 cases, diplopia related to cataract extraction resulted from surgical trauma (74%), preexisting conditions (18%), aniseikonia or anisometropia (5%), and macular pathology (2.5%).34 Although not mentioned in these two series, monovision can also cause diplopia, which is discussed in detail in the refractive surgery section.
Although the rates differ, both of these studies attributed many of their cases to surgical trauma, typically from local anesthesia. Direct injection of anesthesia into an extraocular muscle leads to transient paresis followed by segmental contracture of the muscle.35 The superior and inferior rectus muscles are the most vulnerable to injury, although superior36 and inferior oblique37,38 muscle injuries have also been reported. A cadaver study showed that the superior and inferior rectus muscles can both be reached with a 1.5-inch retrobulbar needle, whereas peribulbar injections are more likely to injure the inferior rectus muscle.39 Bupivacaine injection into extraocular muscles increases the muscle volume and maximum cross-sectional area,40 creating dense fibrous connective tissue without viable muscle cells.41 Imaging shows segmental thickening of these muscles.42–45
Diplopia secondary to retrobulbar or peribulbar injections appears to be more common in left eyes due to the more awkward positioning required for a right-handed surgeon or anesthesiologist.25,46 It is also more common without the use of hyaluronidase,29,47–50 possibly because without hyaluronidase, anesthetic agents loculate around the muscles for a longer duration, thereby damaging the tissue.47
Although much less common, sub-Tenon's administration of anesthesia with a cannula has also been shown to cause diplopia, with several case reports describing restriction and fibrosis of the inferior rectus muscle51–53 and one describing superior oblique muscle paresis after injection to the superotemporal quadrant.54 Diplopia after topical anesthesia is much less common, with two studies showing no cases.28,30 In a large study of 1,420 cases performed under topical anesthesia, 3 patients had diplopia, with each case attributed to refractive error or intraocular lens luxation.32 A prospective study showed that 5% of patients had an acquired misalignment of the eyes 2 months after cataract surgery using topical anesthesia, but none had diplopia.55
Several less common etiologies of strabismus after cataract surgery have been reported. Decompensation of a preexisting superior oblique muscle palsy can cause postoperative diplopia,56–58 as could decompensation of other vertical or horizontal phorias. In one study, 32% of patients with diplopia after cataract extraction had unrecognized preoperative sensory strabismus.59 Another issue is previously unsuspected thyroid eye disease. In one study, 8 of 58 patients with diplopia after cataract extraction had incomitant strabismus in addition to radiologic evidence of thyroid eye disease.60 In another study, 4 of 11 patients with vertical rectus overaction had abnormal thyroid blood work.61 Subconjunctival gentamicin injections have also been implicated as a cause of strabismus.62,63 Finally, patients with long-standing poor vision in one eye can lose central fusion, resulting in diplopia after vision is restored.64,65
Most studies on the treatment of diplopia after cataract surgery focus on cases of inferior rectus muscle restriction, reporting inferior rectus recession on an adjustable or non-adjustable suture.66,67 Some authors recommend waiting 4 to 6 months before surgical correction to ensure stability.66 In contrast, one study suggests surgery after only 1 month of stable measurements because delaying surgery may allow patients to develop additional horizontal diplopia.25 Rarely, spontaneous recovery of fusion has been reported.68
The efficacy of inferior rectus recession in these cases ranges widely. It is typically a good option for patients with less than 12 degrees of deviation, but may not be sufficient for larger deviations.69 Adjustable sutures may improve success rates,67,70 with one study reporting 75% success with surgery alone.67 Another study using non-adjustable sutures reported 50% success after initial surgery.69
It is important for patients to be informed of the possibility of developing diplopia after surgery, especially those with long-standing unilateral cataracts who may have a higher risk.71
Refractive surgery has been recognized as a cause of diplopia and strabismus since the era of radial keratotomy, when patients were reported to have esotropia related to accommodative effort after correction of myopia.72,73 More recently, Kushner and Kowal74 identified five mechanisms for diplopia after refractive procedures: technical issues, prior need of prisms, aniseikonia, iatrogenic monovision, and improper control of accommodation in patients with strabismus.
Strabismus from iatrogenic monovision has received the most attention in the literature. Although most patients do well with monovision,75 it causes reduced stereoacuity and an absence of foveal fusion.76 Patients with monovision can have a decompensation of a preexisting deviation such as a fourth nerve palsy or other vertical or horizontal phoria.77,78 Patients with monovision can also develop fixation-switch diplopia, in which the monovision forces fixation with the eye that was previously suppressed, resulting in constant diplopia due to an inability to suppress their previously dominant eye.74 Patients with strabismus are sometimes able to regain fusion by correcting their monovision with glasses, contact lenses, or further refractive surgery, but some patients require strabismus surgery to reestablish motor or sensory control.79 A preoperative trial with contact lenses is warranted if monovision is planned.80
Technical issues may come into play when a flap is decentered, with the corrected area producing a prismatic effect on the cornea.81 Preoperatively, patients' glasses must be checked for the presence of prism because patients may be unaware that they are wearing prisms.74 When aniseikonia is greater than 3% to 5%, moving the corrective power from the spectacle to the corneal plane can cause intractable diplopia.74 Progressive anisometropia that was not fully corrected preoperatively may cause defective fusion due to both poor optical quality and aniseikonia.82 Finally, outcomes of refractive surgery may be targeted incorrectly in patients in whom spectacle correction was helping control the alignment.74
As such, Kowal et al.83,84 determined minimum screening criteria for patients undergoing refractive surgery: history including prior strabismus, episodes of diplopia, bifocals, and eye exercises; checking glasses for prism; cover–uncover and alternate cover testing for distance and near with habitual correction and targeted correction; refraction, including manifest and cycloplegic; and stereoacuity testing. The Worth 4-dot test of fusion may also be useful.
Patients can then be stratified into “no risk,” “moderate risk,” and “high risk” groups. The no-risk patients have myopia with less than 4.00 diopters (D) of anisometropia, no history of strabismus or diplopia, no prism, and minimal to no phoria. Current spectacles, manifest refraction, and cycloplegic refraction must be within 0.50 D. All other patients should be considered to have at least moderate risk and should undergo further testing in addition to counseling concerning the risks. Patients may need to be excluded from surgery if binocularity is weak.85
Strabismus and diplopia occur after glaucoma drainage device placement,86,87 with reported incidence varying widely by study, implant design, and operative location.87–95 In 2005, a systematic review showed significantly higher diplopia rates with Baerveldt implants (9%) compared to Molento (2%) and Ahmed valve (3%) implants, with no statistical difference compared with Krupin valves (7%).96 A recent prospective multi-centered randomized clinical trial calculated the incidence of persistent diplopia after the implantation of Ahmed valve and Baerveldt implants to be statistically equivalent, with rates close to 12%.87
Increasing age and previous eye surgery are risk factors for the development of postoperative motility disturbances or diplopia,86,92 although preoperative motility disturbances do not necessarily worsen after surgery.92 Superior placement is preferable to inferior because the superior orbit has more room to accommodate blebs and cysts.97 Additionally, motility-related symptoms tend to be more disabling with inferiorly placed implants because the diplopia will more often occur in the reading position.98 Temporal placement is preferred over nasal because of more space, better exposure, and avoidance of the oblique muscles.90,97,99
Several different mechanisms cause diplopia after glaucoma drainage device placement.98–109 Large and highly elevated blebs may cause diplopia by mass effect on the muscles, especially when plates are placed directly beneath the muscles.94,107 Formation of Tenon's cysts can cause significant mass effect on the globe.108 Muscle incorporation within the fibrous capsule,89,110,111 breach of the posterior Tenon's capsule causing fat adherence syndrome,89,97,105 or temporary muscle paresis due to direct trauma or edema89 may also cause motility disturbance. Implantation of a glaucoma drainage device in the superonasal quadrant may cause an acquired pseudo-Brown's syndrome86,99,102,103,107,109 if the volume of the plate and bleb cause a mechanical restriction to elevation in adduction by effectively shortening the superior oblique tendon.103 Scarring between muscle and sclera or fibrous replacement of muscle may cause an effect similar to a posterior fixation suture.89,98,104 Rarely, the implant may simply be too large to allow rotation of the eye within the orbit.102
When patients develop diplopia, nonsurgical treatment should be attempted first. Observation is an option because some postoperative motility disturbances may resolve in the first 6 to 12 months after surgery.89 Prisms may be used,86,88,92,103 although treatment with prisms is limited because these are often large, incomitant deviations.95,100,101,104,111 Surgical management is challenging111 because it may be complicated by difficult intraocular pressure control, large implant bulk, and involvement of two extraocular muscles if a Krupin or Baerveldt implant was used.97 Removal of the implant,86 scar tissue, and fibrous capsule around the implant may be required.111 Muscle recession is preferred over resection because the latter may increase restriction.97 If strabismus is comitant and mild in nature, surgery on the contralateral eye may have a role in management, offering the advantages of an easier, more predictable operation and the ability to leave the drainage implant in place.111 Surgical management of strabismus secondary to glaucoma drainage device implantation is a complicated endeavor and requires careful planning, management, and consultation with a glaucoma surgeon.
Diplopia after retinal detachment repair is common, with one prospective study reporting 61% of patients developing diplopia after placement of a scleral buckle.112 Fortunately, most cases resolve within 6 months.113 Most studies found persistent diplopia in 3% to 5% of patients,114–119 although two studies reported higher rates of 14%120 and 23%.121 Interestingly, one study comparing vitrectomy and scleral buckle found similar rates of diplopia, suggesting that changes in vision may play a major role in the disruption of binocularity.122
Many mechanisms have been implicated in muscle imbalance after retinal detachment repair with a scleral buckle. Restrictive abnormalities can be caused by anterior displacement of the superior oblique tendon, leash and reverse leash types of restrictions, myoscleral adhesions posterior to explants, and stretching of muscles induced by large underlying explants.123,124 Several case reports have shown that scleral buckles can migrate through the muscle, with muscle reattachment posterior to the buckle.125–129 Interference between a myopic staphyloma and a scleral buckle can cause motility issues.130 Hydrogel buckles, which are no longer placed, can cause motility issues many years after placement of the buckle.131–133 Even cryotherapy without other manipulation can potentially damage the extraocular muscles.134 As in cataract surgery, myotoxic reactions from injection of local anesthetics directly into muscles can cause strabismus.135
Several factors have been shown to influence the rates of diplopia. The risk of strabismus is 2.5 times higher if the buckle is placed under a rectus muscle.112 One study showed an increased rate of diplopia from 10.7% to 35.3% for patients who required reoperation for their retinal detachment.120 The location and size of the silicone material is also a highly significant factor.120 Diplopia is more likely to follow mobilization of the vertical muscles. In a series of 750 patients, 30 developed muscle imbalance attributed to the scleral buckle. Twenty-five of those patients had a rectus muscle mobilized, with 19 of 21 patients who had vertical rectus muscle mobilization developing diplopia and 4 of 5 patients who had lateral rectus muscle mobilization developing diplopia. The authors concluded that if a muscle must be removed, it should be reattached at its original insertion.116
Treatment is typically stepwise with prisms, then removal of the buckle, and finally surgical intervention on the muscles.114 Some authors suggest that removal of the buckle may not be helpful.136,137 Published rates of success in restoring binocularity vary widely.123,138 A recent study of surgical intervention showed that 72% of patients achieved motor success, defined as horizontal deviation less than 10 prism diopters (PD) and vertical deviation less than 4 PD, but only 62% were free of diplopia in primary position. Patients with horizontal deviations less than 10 PD and minimal restriction on forced duction testing are more likely to have motor success after the first surgery.137 Botulinum toxin chemodenervation may be successful in some cases, with rates ranging from 36% to 85%.139–141
When surgery is performed, excision of scar tissue in addition to recession of a rectus muscle is typically required.123 A cul-de-sac approach involving suture placement at the original insertion, hang-back sutures, and adjustable sutures has been proposed to simplify the dissection and preserve the protective role of the capsule around the exoplant.142 Although most cases are due to restrictive etiology, deviations may also occur due to direct muscle injury,143 for which resection or advancement of the muscle to the posterior edge of the buckle may be performed.142 Surgery on the superior oblique or inferior oblique muscles is sometimes required for cyclodeviations.143 Of note, the standard tables used to determine the amount of muscle movement may not be applicable.143 This issue can be mitigated by the use of adjustable sutures, which allow for fine-tuning of the alignment in the early postoperative period.123,143 If possible, removal of the buckling exoplant should be avoided due to the risk of redetachment. However, removal may be necessary, especially when the exoplant is the direct cause of the motility disturbance.143
Postoperative diplopia is the most common complication after any type of orbital decompression.144,145 Although some patients may have improvement in their motility issues after decompression,146 particularly with a transpalpebral route or lateral wall approach,144 it is more common to develop new or worsened diplopia.147 In a systematic review by Leong et al.,147 incidence of post-decompression diplopia was highest after either transantral (23%) or combined endoscopic-lateral canthotomy (19.9%) approaches, and lowest after decompression performed with eyelid crease incisions, with some studies suggesting up to 41% improvement in preexisting diplopia with this approach. Patients with more serious Graves orbitopathy and preoperative restrictive myopathy are more likely to develop postoperative diplopia, with rates as high as 61%.145,148
The mechanism of motility disturbances and diplopia after decompression is primarily mechanical. The muscles are often fibrotic and restricted prior to decompression as a result of thyroid disease.149 During surgery, the displacement of muscles alters their motility and ocular alignment. The muscles in closest proximity to the osteotomy exhibit the most displacement; the inferior rectus muscle is displaced by translid surgery and the medial rectus muscle is displaced by the coronal approach.150 In an orbital floor decompression, displacement of the entire globe inferiorly may contribute to vertical muscle imbalance.151 A posterior decompression may destabilize the muscle cone at the orbital apex.152 When the inferior oblique muscle must be disinserted for better operative exposure, reattachment may be suboptimal and may impair muscle function, causing postoperative torsional diplopia.153 Muscle incarceration into bone may also occur during the decompression.149 To minimize the risk of diplopia, most studies recommend a multiwall, combined, or balanced approach,144,146,154–161 particularly with preservation of the medial orbital bony strut.157,162,163
When required, strabismus surgery should be delayed until the condition is stable,164 typically at least 6 months after decompression.164,165 Prisms may be used during this time, although they are most helpful when the deviation is small.164 Recent studies indicate that botulinum toxin injection may be helpful in maintaining binocularity.164,166 Although one study suggests correcting strabismus once stability is demonstrated on imaging,164 such an approach is not widespread in the literature. Even with a 6-month delay, many patients will experience continued change in angle deviation that will require reoperation.165
Surgical procedures are similar to standard surgery on patients with thyroid eye disease, with recession preferred over resection.149,167,168 Some surgeons use fixed suture techniques,169 whereas others use adjustable sutures.149,168,170 Neither preoperative motility nor muscle thickness seems to correlate with surgical effect.171 Some studies show that outcomes are similar in patients who have had prior decompression compared with those who have not,168,169 whereas others show lower172 and higher173 rates of success in this population. After decompression, patients may require surgery on more muscles172 and may require more reoperations.170,174 Iatrogenic torsional diplopia may be particularly difficult to treat.153 Although variable and likely dependent on the decompression technique, preoperative morbidity, and disease severity, several studies show favorable outcomes, with operative success rates ranging from 53% up to 94% and improved outcomes on reoperation.167–170,172–175
Strabismus can occur after many types of ocular surgery from direct injury to extraocular muscles, scarring of the muscle complex or conjunctiva, alteration of the muscle pulley system, mass effect from implants, and muscle displacement. The resulting diplopia can be debilitating for patients. Diplopia should be discussed as a risk of surgery during the preoperative informed consent discussion. Prevention of motility disturbances is best whenever possible because treatment can be challenging.
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