Journal of Pediatric Ophthalmology and Strabismus

Review Article 

Strabismus After Ocular Surgery

Ethan K. Sobol, MD; Jamie B. Rosenberg, MD


Many types of ocular surgery can cause diplopia, including eyelid, conjunctival, cataract, refractive, glaucoma, retinal, and orbital surgery. Mechanisms include direct injury to the extraocular muscles from surgery or anesthesia, scarring of the muscle complex and/or conjunctiva, alteration of the muscle pulley system, mass effects from implants, and muscle displacement. Diplopia can also result from a loss of fusion secondary to long-standing poor vision in one eye or from a decompensation of preexisting strabismus that was not recognized preoperatively. Treatment, which typically begins with prisms and is followed by surgery when necessary, can be challenging. In this review, the incidence, mechanisms, and treatments involved in diplopia after various ocular surgeries are discussed. [J Pediatr Ophthalmol Strabismus. 2017;54(5):272–281.]


Many types of ocular surgery can cause diplopia, including eyelid, conjunctival, cataract, refractive, glaucoma, retinal, and orbital surgery. Mechanisms include direct injury to the extraocular muscles from surgery or anesthesia, scarring of the muscle complex and/or conjunctiva, alteration of the muscle pulley system, mass effects from implants, and muscle displacement. Diplopia can also result from a loss of fusion secondary to long-standing poor vision in one eye or from a decompensation of preexisting strabismus that was not recognized preoperatively. Treatment, which typically begins with prisms and is followed by surgery when necessary, can be challenging. In this review, the incidence, mechanisms, and treatments involved in diplopia after various ocular surgeries are discussed. [J Pediatr Ophthalmol Strabismus. 2017;54(5):272–281.]


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.

Literature Search

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.

Cataract Surgery

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

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

Glaucoma Surgery

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.

Retina Surgery

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

Decompressive Orbitotomy

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.


  1. Alfonso E, Levada AJ, Flynn JT. Inferior rectus paresis after secondary blepharoplasty. Br J Ophthalmol. 1984;68:535–537. doi:10.1136/bjo.68.8.535 [CrossRef]
  2. Ghabrial R, Lisman RD, Kane MA, Milite J, Richards R. Diplopia following transconjunctival blepharoplasty. Plast Reconstr Surg. 1998;102:1219–1225. doi:10.1097/00006534-199809020-00049 [CrossRef]
  3. Harley RD, Nelson LB, Flanagan JC, Calhoun JH. Ocular motility disturbances following cosmetic blepharoplasty. Arch Ophthalmol. 1986;104:542–544. doi:10.1001/archopht.1986.01050160098021 [CrossRef]
  4. Hayworth RS, Lisman RD, Muchnick RS, Smith B. Diplopia following blepharoplasty. Ann Ophthalmol. 1984;16:448–451.
  5. Jameson NA, Good WV, Hoyt CS. Fat adherence simulating inferior oblique palsy following blepharoplasty. Arch Ophthalmol. 1992;110:1369. doi:10.1001/archopht.1992.01080220031011 [CrossRef]
  6. Levine MR, Boynton J, Tenzel RR, Miller GR. Complications of blepharoplasty. Ophthalmic Surg. 1975;6:53–57.
  7. Mazow ML, Avilla CW, Morales HJ. Restrictive horizontal strabismus following blepharoplasty. Am J Ophthalmol. 2006;141:773–774. doi:10.1016/j.ajo.2005.11.045 [CrossRef]
  8. Neely KA, Ernest JT, Mottier M. Combined superior oblique paresis and Brown's syndrome after blepharoplasty. Am J Ophthalmol. 1990;109:347–349. doi:10.1016/S0002-9394(14)74565-9 [CrossRef]
  9. Ortiz-Basso T, Vigo R, Prémoli EJ. Horizontal diplopia following upper blepharoplasty. Case Rep Ophthalmol. 2014;5:289–291. doi:10.1159/000367964 [CrossRef]
  10. Pirouzian A, Goldberg RA, Demer JL. Inferior rectus pulley hindrance: a mechanism of restrictive hypertropia following lower lid surgery. J AAPOS. 2004;8:338–344. doi:10.1016/j.jaapos.2004.03.005 [CrossRef]
  11. Syniuta LA, Goldberg RA, Thacker NM, Rosenbaum AL. Acquired strabismus following cosmetic blepharoplasty. Plast Reconstr Surg. 2003;111:2053–2059. doi:10.1097/01.PRS.0000056840.61348.35 [CrossRef]
  12. Wesley RE, Pollard ZF, McCord CD Jr., Superior oblique paresis after blepharoplasty. Plast Reconstr Surg. 1980;66:283–286. doi:10.1097/00006534-198008000-00020 [CrossRef]
  13. Hurwitz JJ, Howcroft MJ. Use of Lester Jones tubes: a review of 40 cases. Can J Ophthalmol. 1981;16:176–177.
  14. Lamping K, Levine MR. Jones' tubes: how good are they?Arch Ophthalmol. 1983;101:260–261. doi:10.1001/archopht.1983.01040010262016 [CrossRef]
  15. Lim C, Martin P, Benger R, Kourt G, Ghabrial R. Lacrimal canalicular bypass surgery with the Lester Jones tube. Am J Ophthalmol. 2004;137:101–108. doi:10.1016/j.ajo.2003.08.002 [CrossRef]
  16. Ashenhurst M, Hill VE, Keyhani K. Restrictive strabismus following Jones tube insertion: a case series of 8 patients. Can J Ophthalmol. 2007;42:613–616. doi:10.3129/i07-104 [CrossRef]
  17. Shin DH, Kim YD, Lee CH, Johnson ON 3rd, Woo KI. Restrictive strabismus and diplopia 2 years after conjunctivodacryocystorhinostomy with medpor-coated tear drain. Ophthal Plast Reconstr Surg. 2015;31:e159–e162. doi:10.1097/IOP.0000000000000183 [CrossRef]
  18. Skov CM, Mazow ML. Diplopia following Jones tube placement. Ophthalmic Surg. 1984;15:932–933.
  19. Raab EL, Metz HS, Ellis FD. Medial rectus injury after pterygium excision. Arch Ophthalmol. 1989;107:1428. doi:10.1001/archopht.1989.01070020502018 [CrossRef]
  20. Ela-Dalman N, Velez FG, Rosenbaum AL. Incomitant esotropia following pterygium excision surgery. Arch Ophthalmol. 2007;125:369–373. doi:10.1001/archopht.125.3.369 [CrossRef]
  21. Laria C, Shokida F, Tatarchuck P, Pinero DP, Gonzalez X. New diplopic restrictive strabismus as a sequela after conjunctival surgery for conjunctival lesions: a series of 3 cases, management and outcome. Binocul Vis Strabolog Q Simms Romano. 2012;27:113–121.
  22. Ugrin MC, Molinari A. Disinsertion of the medial rectus following pterygium surgery: signs and management. Strabismus. 1999;7:147–152. doi:10.1076/stra. [CrossRef]
  23. Jenkins PF, Stavis MI, Jenkins DE 3rd, . Esotropia following pterygium surgery. Binocul Vis Strabismus Q. 2002;17:227–228.
  24. Cadera W. Diplopia after peribulbar anesthesia for cataract surgery. J Pediatr Ophthalmol Strabismus. 1998;35:240–241.
  25. Corboy JM, Jiang X. Postanesthetic hypotropia: a unique syndrome in left eyes. J Cataract Refract Surg. 1997;23:1394–1398. doi:10.1016/S0886-3350(97)80121-6 [CrossRef]
  26. Costa PG, Debert I, Passos LB, Polati M. Persistent diplopia and strabismus after cataract surgery under local anesthesia. Binocul Vis Strabismus Q. 2006;21:155–158.
  27. Golnik KC, West CE, Kaye E, Corcoran KT, Cionni RJ. Incidence of ocular misalignment and diplopia after uneventful cataract surgery. J Cataract Refract Surg. 2000;26:1205–1209. doi:10.1016/S0886-3350(00)00330-8 [CrossRef]
  28. Gómez-Arnau JI, Yangüela J, González A, et al. Anaesthesia-related diplopia after cataract surgery. Br J Anaesth. 2003;90:189–193. doi:10.1093/bja/aeg029 [CrossRef]
  29. 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 [CrossRef]
  30. Johnson DA. Persistent vertical binocular diplopia after cataract surgery. Am J Ophthalmol. 2001;132:831–835. doi:10.1016/S0002-9394(01)01233-8 [CrossRef]
  31. MacDonald IM, Reed GF, Wakeman BJ. Strabismus after regional anesthesia for cataract surgery. Can J Ophthalmol. 2004;39:267–271. doi:10.1016/S0008-4182(04)80124-8 [CrossRef]
  32. Yangüela J, Gómez-Arnau JI, Martín-Rodrigo JC, et al. Diplopia after cataract surgery: comparative results after topical or regional injection anesthesia. Ophthalmology. 2004;111:686–692. doi:10.1016/j.ophtha.2003.11.002 [CrossRef]
  33. Nayak H, Kersey JP, Oystreck DT, Cline RA, Lyons CJ. Diplopia following cataract surgery: a review of 150 patients. Eye (Lond). 2008;22:1057–1064. doi:10.1038/sj.eye.6702847 [CrossRef]
  34. Karagiannis D, Chatzistefanou K, Damanakis A. Prevalence of diplopia related to cataract surgery among cases of diplopia. Eur J Ophthalmol. 2007;17:914–918.
  35. Capó H, Guyton DL. Ipsilateral hypertropia after cataract surgery. Ophthalmology. 1996;103:721–730. doi:10.1016/S0161-6420(96)30623-4 [CrossRef]
  36. Erie JC. Acquired Brown's syndrome after peribulbar anesthesia. Am J Ophthalmol. 1990;109:349–350. doi:10.1016/S0002-9394(14)74566-0 [CrossRef]
  37. Bleik JH, Zaatari GS, Cherfan GM. Inferior oblique muscle injury after peribulbar anesthesia presenting as ipsilateral superior oblique palsy: a clinicopathologic report. J AAPOS. 2006;10:178–179. doi:10.1016/j.jaapos.2005.11.018 [CrossRef]
  38. Hunter DG, Lam GC, Guyton DL. Inferior oblique muscle injury from local anesthesia for cataract surgery. Ophthalmology. 1995;102:501–509. doi:10.1016/S0161-6420(95)30994-3 [CrossRef]
  39. Capó H, Roth E, Johnson T, Muñoz M, Siatkowski RM. Vertical strabismus after cataract surgery. Ophthalmology. 1996;103:918–921. doi:10.1016/S0161-6420(96)30587-3 [CrossRef]
  40. Miller JM, Scott AB, Danh KK, Strasser D, Sane M. Bupivacaine injection remodels extraocular muscles and corrects comitant strabismus. Ophthalmology. 2013;120:2733–2740. doi:10.1016/j.ophtha.2013.06.003 [CrossRef]
  41. Kim CH, Kim US. Large exotropia after retrobulbar anesthesia. Indian J Ophthalmol. 2016;64:91–92. doi:10.4103/0301-4738.178148 [CrossRef]
  42. Ando K, Oohira A, Takao M. Restrictive strabismus after retrobulbar anesthesia. Jpn J Ophthalmol. 1997;41:23–26. doi:10.1016/S0021-5155(96)00003-2 [CrossRef]
  43. Hamed LM, Mancuso A. Inferior rectus muscle contracture syndrome after retrobulbar anesthesia. Ophthalmology. 1991;98:1506–1512. doi:10.1016/S0161-6420(91)32097-9 [CrossRef]
  44. 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.
  45. Kim JH, Hwang JM. Imaging of the superior rectus in superior rectus overaction after retrobulbar anesthesia. Ophthalmology. 2006;113:1681–1684. doi:10.1016/j.ophtha.2006.03.049 [CrossRef]
  46. Pearce IA, McCready PM, Watson MP, Taylor RH. Vertical diplopia following local anaesthetic cataract surgery: predominantly a left eye problem?Eye (Lond). 2000;14:180–184. doi:10.1038/eye.2000.50 [CrossRef]
  47. Brown SM, Brooks SE, Mazow ML, et al. Cluster of diplopia cases after periocular anesthesia without hyaluronidase. J Cataract Refract Surg. 1999;25:1245–1249. doi:10.1016/S0886-3350(99)00151-0 [CrossRef]
  48. Brown SM, Coats DK, Collins ML, Underdahl JP. Second cluster of strabismus cases after periocular anesthesia without hyaluronidase. J Cataract Refract Surg. 2001;27:1872–1875. doi:10.1016/S0886-3350(01)01068-9 [CrossRef]
  49. Jehan FS, Hagan JC 3rd, Whittaker TJ, Subramanian M. Diplopia and ptosis following injection of local anesthesia without hyaluronidase. J Cataract Refract Surg. 2001;27:1876–1879. doi:10.1016/S0886-3350(01)01099-9 [CrossRef]
  50. Strouthidis NG, Sobha S, Lanigan L, Hammond CJ. Vertical diplopia following peribulbar anesthesia: the role of hyaluronidase. J Pediatr Ophthalmol Strabismus. 2004;41:25–30.
  51. Adams W, Morgan SJ. Diplopia following sub-Tenon's infiltration of local anesthesia. J Cataract Refract Surg. 2002;28:1694–1697. doi:10.1016/S0886-3350(01)01280-9 [CrossRef]
  52. Blum RA, Lim LT, Weir CR. Diplopia following sub-tenon's anaesthesia: an unusual complication. Int Ophthalmol. 2012;32:191–193. doi:10.1007/s10792-012-9535-3 [CrossRef]
  53. Jaycock PD, Mather CM, Ferris JD, Kirkpatrick JN. Rectus muscle trauma complicating sub-Tenon's local anaesthesia. Eye (Lond). 2001;15:583–586. doi:10.1038/eye.2001.189 [CrossRef]
  54. Spierer A, Schwalb E. Superior oblique muscle paresis after sub-Tenon's anesthesia for cataract surgery. J Cataract Refract Surg. 1999;25:144–145. doi:10.1016/S0886-3350(99)80025-X [CrossRef]
  55. Chung SA, Kim CY, Chang JH, et al. Change in ocular alignment after topical anesthetic cataract surgery. Graefes Arch Clin Exp Ophthalmol. 2009;247:1269–1272. doi:10.1007/s00417-009-1084-8 [CrossRef]
  56. Catalano RA, Nelson LB, Calhoun JH, Schatz NJ, Harley RD. Persistent strabismus presenting after cataract surgery. Ophthalmology. 1987;94:491–494. doi:10.1016/S0161-6420(87)33419-0 [CrossRef]
  57. D'Haens M, Evens PA, Tassignon MJ. Diplopia as an uncommon complication of cataract surgery. Bull Soc Belge Ophtalmol. 1995;257:43–48.
  58. Kim JH, Hwang JM. Usefulness of magnetic resonance imaging in a patient with diplopia after cataract surgery. Graefes Arch Clin Exp Ophthalmol. 2012;250:151–153. doi:10.1007/s00417-010-1580-x [CrossRef]
  59. Han SK, Kim JH, Hwang JM. Persistent diplopia after retrobulbar anesthesia. J Cataract Refract Surg. 2004;30:1248–1253. doi:10.1016/j.jcrs.2003.09.064 [CrossRef]
  60. Hamed LM, Lingua RW. Thyroid eye disease presenting after cataract surgery. J Pediatr Ophthalmol Strabismus. 1990;27:10–15.
  61. Han SK, Hwang JM. Thyroid disease and vertical rectus muscle overaction after retrobulbar anesthesia. J Cataract Refract Surg. 2003;29:78–84. doi:10.1016/S0886-3350(02)01437-2 [CrossRef]
  62. Chapman JM, Abdelatif OM, Cheeks L, Green K. Subconjunctival gentamicin induction of extraocular toxic muscle myopathy. Ophthalmic Res. 1992;24:189–196. doi:10.1159/000267167 [CrossRef]
  63. Kushner BJ. Case report: ocular muscle fibrosis following cataract extraction. Arch Ophthalmol. 1988;106:18–19. doi:10.1001/archopht.1988.01060130020012 [CrossRef]
  64. 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 [CrossRef]
  65. Sharkey JA, Sellar PW. Acquired central fusion disruption following cataract extraction. J Pediatr Ophthalmol Strabismus. 1994;31:391–393.
  66. Burns CL, Seigel LA. Inferior rectus recession for vertical tropia after cataract surgery. Ophthalmology. 1988;95:1120–1124. doi:10.1016/S0161-6420(88)33050-2 [CrossRef]
  67. Poland PJ, Hiatt RL. The correction of diplopia after cataract extraction. Ann Ophthalmol. 1993;25:110–118.
  68. Sutherland S, Kowal L. Spontaneous recovery from inferior rectus contracture (consecutive hypotropia) following local anesthetic injury. Binocul Vis Strabismus Q. 2003;18:99–100.
  69. Schild AM, Fricke J, Neugebauer A. Inferior rectus muscle recession as a treatment for vertical diplopia following cataract extraction. Graefes Arch Clin Exp Ophthalmol. 2013;251:189–194. doi:10.1007/s00417-012-1996-6 [CrossRef]
  70. Ong-Tone L, Pearce WG. Inferior rectus muscle restriction after retrobulbar anesthesia for cataract extraction. Can J Ophthalmol. 1989;24:162–165.
  71. Rosenbaum AL. Strabismus following uncomplicated cataract surgery. Arch Ophthalmol. 1997;115:253. doi:10.1001/archopht.1997.01100150255018 [CrossRef]
  72. John ME, Howard C. Esotropia following radial keratotomy. J Cataract Refract Surg. 1991;17:246–247. doi:10.1016/S0886-3350(13)80267-2 [CrossRef]
  73. Zwaan J. Strabismus induced by radial keratotomy. Mil Med. 1996;161:630–631.
  74. Kushner BJ, Kowal L. Diplopia after refractive surgery: occurrence and prevention. Arch Ophthalmol. 2003;121:315–321. doi:10.1001/archopht.121.3.315 [CrossRef]
  75. Wright KW, Guemes A, Kapadia MS, Wilson SE. Binocular function and patient satisfaction after monovision induced by myopic photorefractive keratectomy. J Cataract Refract Surg. 1999;25:177–182. doi:10.1016/S0886-3350(99)80123-0 [CrossRef]
  76. Fawcett SL, Herman WK, Alfieri CD, Castleberry KA, Parks MM, Birch EE. Stereoacuity and foveal fusion in adults with long-standing surgical monovision. J AAPOS. 2001;5:342–347. doi:10.1067/mpa.2001.119785 [CrossRef]
  77. Mandava N, Donnenfeld ED, Owens PL, Kelly SE, Haight DH. Ocular deviation following excimer laser photorefractive keratectomy. J Cataract Refract Surg. 1996;22:504–505. doi:10.1016/S0886-3350(96)80051-4 [CrossRef]
  78. Schuler E, Silverberg M, Beade P, Moadel K. Decompensated strabismus after laser in situ keratomileusis. J Cataract Refract Surg. 1999;25:1552–1553. doi:10.1016/S0886-3350(99)00208-4 [CrossRef]
  79. Pollard ZF, Greenberg MF, Bordenca M, Elliott J, Hsu V. Strabismus precipitated by monovision. Am J Ophthalmol. 2011;152:479–482. doi:10.1016/j.ajo.2011.02.008 [CrossRef]
  80. Godts D, Tassignon MJ, Gobin L. Binocular vision impairment after refractive surgery. J Cataract Refract Surg. 2004;30:101–109. doi:10.1016/S0886-3350(03)00412-7 [CrossRef]
  81. Yap EY, Kowal L. Diplopia as a complication of laser in situ keratomileusis surgery. Clin Exp Ophthalmol. 2001;29:268–271. doi:10.1046/j.1442-9071.2001.00418.x [CrossRef]
  82. Holland D, Amm M, de Decker W. Persisting diplopia after bilateral laser in situ keratomileusis. J Cataract Refract Surg. 2000;26:1555–1557. doi:10.1016/S0886-3350(00)00452-1 [CrossRef]
  83. Kowal L, Battu R, Kushner B. Refractive surgery and strabismus. Clin Exp Ophthalmol. 2005;33:90–96. doi:10.1111/j.1442-9071.2005.00953.x [CrossRef]
  84. Kowal L. Refractive surgery and diplopia. Clin Exp Ophthalmol. 2000;28:344–346. doi:10.1046/j.1442-9071.2000.0346d.x [CrossRef]
  85. Valente P, Buzzonetti L, Dickmann A, Rebecchi MT, Petrocelli G, Balestrazzi E. Refractive surgery in patients with high myopic anisometropia. J Refract Surg. 2006;22:461–466.
  86. Bailey AK, Sarkisian SR Jr., Complications of tube implants and their management. Curr Opin Ophthalmol. 2014;25:148–153. doi:10.1097/ICU.0000000000000034 [CrossRef]
  87. Budenz DL, Feuer WJ, Barton K, et al. Comparison Study Group. Postoperative complications in the Ahmed Baerveldt comparison study during five years of follow-up. Am J Ophthalmol. 2016;163:75–82. doi:10.1016/j.ajo.2015.11.023 [CrossRef]
  88. Abdelaziz A, Capó H, Banitt MR, et al. Diplopia after glaucoma drainage device implantation. J AAPOS. 2013;17:192–196. doi:10.1016/j.jaapos.2012.11.017 [CrossRef]
  89. Dobler-Dixon AA, Cantor LB, Sondhi N, Ku WS, Hoop J. Prospective evaluation of extraocular motility following double-plate Molteno implantation. Arch Ophthalmol. 1999;117:1155–1160. doi:10.1001/archopht.117.9.1155 [CrossRef]
  90. Frank JW, Perkins TW, Kushner BJ. Ocular motility defects in patients with the Krupin valve implant. Ophthalmic Surg. 1995;26:228–232.
  91. Harbick KH, Sidoti PA, Budenz DL, et al. Outcomes of inferonasal Baerveldt glaucoma drainage implant surgery. J Glaucoma. 2006;15:7–12. doi:10.1097/01.ijg.0000195597.30600.27 [CrossRef]
  92. Rauscher FM, Gedde SJ, Schiffman JC, Feuer WJ, Barton K, Lee RKTube Versus Trabeculectomy Study Group. Motility disturbances in the tube versus trabeculectomy study during the first year of follow-up. Am J Ophthalmol. 2009;147:458–466. doi:10.1016/j.ajo.2008.09.019 [CrossRef]
  93. Smith MF, Doyle JW, Sherwood MB. Comparison of the Baerveldt glaucoma implant with the double-plate Molteno drainage implant. Arch Ophthalmol. 1995;113:444–447. doi:10.1001/archopht.1995.01100040060027 [CrossRef]
  94. Smith SL, Starita RJ, Fellman RL, Lynn JR. Early clinical experience with the Baerveldt 350-mm2 glaucoma implant and associated extraocular muscle imbalance. Ophthalmology. 1993;100:914–918. doi:10.1016/S0161-6420(93)31554-X [CrossRef]
  95. Wilson-Holt N, Franks W, Nourredin B, Hitchings R. Hypertropia following insertion of inferiorly sited double-plate Molteno tubes. Eye (Lond). 1992;6:515–520. doi:10.1038/eye.1992.109 [CrossRef]
  96. Hong CH, Arosemena A, Zurakowski D, Ayyala RS. Glaucoma drainage devices: a systematic literature review and current controversies. Surv Ophthalmol. 2005;50:48–60. doi:10.1016/j.survophthal.2004.10.006 [CrossRef]
  97. Rosenbaum AL, Santiago AP. Strabismus after glaucoma implant procedures. In: Rosenbaum AL, Santiago AP, eds. Clinical Strabismus Management: Principles and Surgical Techniques. Amsterdam, Netherlands; Saunders; 1999:304–307.
  98. Christmann LM, Wilson ME. Motility disturbances after Molteno implants. J Pediatr Ophthalmol Strabismus. 1992;29:44–48.
  99. Ball SF, Ellis GS Jr, Herrington RG, Liang K. Brown's superior oblique tendon syndrome after Baerveldt glaucoma implant. Arch Ophthalmol. 1992;110:1368. doi:10.1001/archopht.1992.01080220030010 [CrossRef]
  100. Cardakli UF, Perkins TW. Recalcitrant diplopia after implantation of a Krupin valve with disc. Ophthalmic Surg. 1994;25:256–258.
  101. Christiansen SP. Diplopia after glaucoma surgery. Am Orthopt J. 2012;62:9–12. doi:10.3368/aoj.62.1.9 [CrossRef]
  102. Coats DK, Paysse EA, Orenga-Nania S. Acquired Pseudo-Brown's syndrome immediately following Ahmed valve glaucoma implant. Ophthalmic Surg Lasers. 1999;30:396–397.
  103. Dobler AA, Sondhi N, Cantor LB, Ku S. Acquired Brown's syndrome after a double-plate Molteno implant. Am J Ophthalmol. 1993;116:641–642. doi:10.1016/S0002-9394(14)73209-X [CrossRef]
  104. Muñoz M, Parrish RK 2nd, . Strabismus following implantation of Baerveldt drainage devices. Arch Ophthalmol. 1993;111:1096–1099. doi:10.1001/archopht.1993.01090080092023 [CrossRef]
  105. Muñoz M, Parrish R. Hypertropia after implantation of a Molteno drainage device. Am J Ophthalmol. 1992;113:98–100. doi:10.1016/S0002-9394(14)75762-9 [CrossRef]
  106. Pandit J, Graham M. Encysted Tenon's bleb over superiorly placed single-plate Molteno implant causing proptosis and strabismus. Eye (Lond). 1995;9:379–381. doi:10.1038/eye.1995.78 [CrossRef]
  107. Prata JA Jr, Minckler DS, Green RL. Pseudo-Brown's syndrome as a complication of glaucoma drainage implant surgery. Ophthalmic Surg. 1993;24:608–611.
  108. Rhee DJ, Casuso LA, Rosa RH Jr, Budenz DL. Motility disturbance due to true Tenon cyst in a child with a Baerveldt glaucoma drainage implant. Arch Ophthalmol. 2001;119:440–442. doi:10.1001/archopht.119.3.440 [CrossRef]
  109. Ventura MP, Vianna RN, Souza Filho JP, Solari HP, Curi RL. Acquired Brown's syndrome secondary to Ahmed valve implant for neovascular glaucoma. Eye (Lond). 2005;19:230–232. doi:10.1038/sj.eye.6701439 [CrossRef]
  110. Sarkisian SR Jr., Tube shunt complications and their prevention. Curr Opin Ophthalmol. 2009;20:126–130. doi:10.1097/ICU.0b013e328323d519 [CrossRef]
  111. Roizen A, Ela-Dalman N, Velez FG, Coleman AL, Rosenbaum AL. Surgical treatment of strabismus secondary to glaucoma drainage device. Arch Ophthalmol. 2008;126:480–486. doi:10.1001/archopht.126.4.480 [CrossRef]
  112. Berk AT, Saatci AO, Kir E, Durak I, Kaynak S. Extraocular muscle imbalance after scleral buckling. Strabismus. 1996;4:69–75. doi:10.3109/09273979609055041 [CrossRef]
  113. Mets MB, Wendell ME, Gieser RG. Ocular deviation after retinal detachment surgery. Am J Ophthalmol. 1985;99:667–672. doi:10.1016/S0002-9394(14)76033-7 [CrossRef]
  114. Fison PN, Chignell AH. Diplopia after retinal detachment surgery. Br J Ophthalmol. 1987;71:521–525. doi:10.1136/bjo.71.7.521 [CrossRef]
  115. Goezinne F, Berendschot TT, van Daal EW, et al. Diplopia was not predictable and not associated with buckle position after scleral buckling surgery for retinal detachment. Retina. 2012;32:1514–1524. doi:10.1097/IAE.0b013e318240a4fe [CrossRef]
  116. Kanski JJ, Elkington AR, Davies MS. Diplopia after retinal detachment surgery. Am J Ophthalmol. 1973;76:38–40. doi:10.1016/0002-9394(73)90007-X [CrossRef]
  117. Maillette de Buy Wenniger-Prick L, van Mourik-Noordenbos A. Diplopia after retinal detachment surgery. Doc Ophthalmol. 1988;70:237–242. doi:10.1007/BF00154460 [CrossRef]
  118. Peduzzi M, Campos EC, Guerrieri F. Disturbances of ocular motility after retinal detachment surgery. Doc Ophthalmol. 1984;58:115–118. doi:10.1007/BF00140908 [CrossRef]
  119. Davies MS, Elkington AR, Kanski JJ. Diplopia following retinal detachment surgery. Mod Probl Ophthalmol. 1974;12:470–475.
  120. Sewell JJ, Knobloch WH, Eifrig DE. Extraocular muscle imbalance after surgical treatment for retinal detachment. Am J Ophthalmol. 1974;78:321–323. doi:10.1016/0002-9394(74)90096-8 [CrossRef]
  121. Smiddy WE, Loupe D, Michels RG, Enger C, Glaser BM, deBustros S. Extraocular muscle imbalance after scleral buckling surgery. Ophthalmology. 1989;96:1485–1489. doi:10.1016/S0161-6420(89)32701-1 [CrossRef]
  122. Wright LA, Cleary M, Barrie T, Hammer HM. Motility and binocularity outcomes in vitrectomy versus scleral buckling in retinal detachment surgery. Graefes Arch Clin Exp Ophthalmol. 1999;237:1028–1032. doi:10.1007/s004170050340 [CrossRef]
  123. Muñoz M, Rosenbaum AL. Long-term strabismus complications following retinal detachment surgery. J Pediatr Ophthalmol Strabismus. 1987;24:309–314.
  124. Hwang JM, Wright KW. Combined study on the causes of strabismus after the retinal surgery. Korean J Ophthalmol. 1994;8:83–91. doi:10.3341/kjo.1994.8.2.83 [CrossRef]
  125. Ashkenazi I, Moisseiev J, Bartov E, Treister G. Preserved action of a rectus muscle after transection by an encircling solid silicone band. Br J Ophthalmol. 1991;75:508–509. doi:10.1136/bjo.75.8.508 [CrossRef]
  126. Hamlet YJ, Goldstein JH, Rosenbaum JD. Dehiscence of lateral rectus muscle following intrascleral buckling procedure. Ann Ophthalmol. 1982;14:694–697.
  127. Macleod JD, Morris RJ. Detached superior rectus following scleral buckling: anatomy and surgical management. Eye (Lond). 1997;11:30–32. doi:10.1038/eye.1997.6 [CrossRef]
  128. Maguire AM, Zarbin MA, Eliott D. Migration of solid silicone encircling element through four rectus muscles. Ophthalmic Surg. 1993;24:604–607.
  129. Marrakchi S, Malek I, Allagui I, et al. Spontaneously detached extraocular rectus muscles following scleral buckling with soft silicone sponges: a report of two cases. Binocul Vis Strabismus Q. 2002;17:223–226.
  130. Wu TE, Rosenbaum AL, Demer JL. Severe strabismus after scleral buckling: multiple mechanisms revealed by high-resolution magnetic resonance imaging. Ophthalmology. 2005;112:327–336. doi:10.1016/j.ophtha.2004.09.015 [CrossRef]
  131. Metz HS, Rose S, Burkat C. Late-onset progressive strabismus associated with a hydrogel scleral buckle. J AAPOS. 2004;8:72–73. doi:10.1016/j.jaapos.2003.09.014 [CrossRef]
  132. Leibovitch I, Crompton J, Selva D. New onset diplopia: 14 years after retinal detachment surgery with a hydrogel scleral buckle. Br J Ophthalmol. 2005;89:640. doi:10.1136/bjo.2004.053868 [CrossRef]
  133. Chen CJ, Kosek K, Benvenutti E. Outcomes and complications of hydrogel scleral explant removal. Ophthalmic Surg Lasers Imaging. 2012;43:383–387. doi:10.3928/15428877-20120531-03 [CrossRef]
  134. Bell FC, Pruett RC. Effects of cryotherapy upon extraocular muscle. Ophthalmic Surg. 1977;8:71–75.
  135. Salama H, Farr AK, Guyton DL. Anesthetic myotoxicity as a cause of restrictive strabismus after scleral buckling surgery. Retina. 2000;20:478–482. doi:10.1097/00006982-200005000-00008 [CrossRef]
  136. Wong V, Kasbekar S, Young J, Stappler T, Marsh IB, Durnian JM. The effect of scleral exoplant removal on strabismus following retinal detachment repair. J AAPOS. 2011;15:331–333. doi:10.1016/j.jaapos.2011.03.016 [CrossRef]
  137. Rabinowitz R, Velez FG, Pineles SL. Risk factors influencing the outcome of strabismus surgery following retinal detachment surgery with scleral buckle. J AAPOS. 2013;17:594–597. doi:10.1016/j.jaapos.2013.08.009 [CrossRef]
  138. Maurino V, Kwan A, Khoo BK, Gair E, Lee JP. Ocular motility disturbances after surgery for retinal detachment. J AAPOS. 1998;2:285–292. doi:10.1016/S1091-8531(98)90085-4 [CrossRef]
  139. Lee J, Page B, Lipton J. Treatment of strabismus after retinal detachment surgery with botulinum neurotoxin A. Eye (Lond). 1991;5:451–455. doi:10.1038/eye.1991.73 [CrossRef]
  140. Petitto VB, Buckley EG. Use of botulinum toxin in strabismus after retinal detachment surgery. Ophthalmology. 1991;98:509–512. doi:10.1016/S0161-6420(91)32264-4 [CrossRef]
  141. Scott AB. Botulinum treatment of strabismus following retinal detachment surgery. Arch Ophthalmol. 1990;108:509–510. doi:10.1001/archopht.1990.01070060057048 [CrossRef]
  142. Mallette RA, Kwon JY, Guyton DL. A technique for repairing strabismus after scleral buckling surgery. Am J Ophthalmol. 1988;106:364–365. doi:10.1016/S0002-9394(14)76639-5 [CrossRef]
  143. Farr AK, Guyton DL. Strabismus after retinal detachment surgery. Curr Opin Ophthalmol. 2000;11:207–210. doi:10.1097/00055735-200006000-00010 [CrossRef]
  144. Leong SC, White PS. Outcomes following surgical decompression for dysthyroid orbitopathy (Graves' disease). Curr Opin Otolaryngol Head Neck Surg. 2010;18:37–43. doi:10.1097/MOO.0b013e328335017c [CrossRef]
  145. Paridaens D, Hans K, van Buitenen S, Mourits MP. The incidence of diplopia following coronal and translid orbital decompression in Graves' orbitopathy. Eye (Lond). 1998;12:800–805. doi:10.1038/eye.1998.207 [CrossRef]
  146. Bailey KL, Tower RN, Dailey RA. Customized, single-incision, three-wall orbital decompression. Ophthal Plast Reconstr Surg. 2005;21:1–9. doi:10.1097/01.IOP.0000150410.30992.C3 [CrossRef]
  147. Leong SC, Karkos PD, Macewen CJ, White PS. A systematic review of outcomes following surgical decompression for dysthyroid orbitopathy. Laryngoscope. 2009;119:1106–1115. doi:10.1002/lary.20213 [CrossRef]
  148. Nunery WR, Nunery CW, Martin RT, Truong TV, Osborn DR. The risk of diplopia following orbital floor and medial wall decompression in subtypes of ophthalmic Graves' disease. Ophthal Plast Reconstr Surg. 1997;13:153–160. doi:10.1097/00002341-199709000-00001 [CrossRef]
  149. Harrad R. Management of strabismus in thyroid eye disease. Eye (Lond). 2015;29:234–237. doi:10.1038/eye.2014.282 [CrossRef]
  150. Abràmoff MD, Kalmann R, de Graaf ME, Stilma JS, Mourits MP. Rectus extraocular muscle paths and decompression surgery for Graves orbitopathy: mechanism of motility disturbances. Invest Ophthalmol Vis Sci. 2002;43:300–307.
  151. Trokel SL, Cooper WC. Symposium: extraocular muscle problems associated with graves' disease. Orbital decompression: effect on motility and globe position. Ophthalmology. 1979;86:2064–2070. doi:10.1016/S0161-6420(79)35288-5 [CrossRef]
  152. McCord CD Jr., Current trends in orbital decompression. Ophthalmology. 1985;92:21–33. doi:10.1016/S0161-6420(85)34079-4 [CrossRef]
  153. Serafino M, Fogagnolo P, Trivedi RH, Saunders RA, Nucci P. Torsional diplopia after orbital decompression and strabismus surgery. Eur J Ophthalmol. 2010;20:437–441.
  154. Pezato R, Pereira MD, Manso PG, Santos Rde P, Ferreira LM. Three-wall decompression technique using transpalpebral and endonasal approach in patients with Graves' ophthalmopathy. Rhinology. 2003;41:231–234.
  155. Roncevic R, Savkovic Z, Roncevic D. Results of diplopia and strabismus in patients with severe thyroid ophthalmopathy after orbital decompression. Indian J Ophthalmol. 2014;62:268–273. doi:10.4103/0301-4738.120206 [CrossRef]
  156. Schaefer SD, Soliemanzadeh P, Della Rocca DA, et al. Endoscopic and transconjunctival orbital decompression for thyroid-related orbital apex compression. Laryngoscope. 2003;113:508–513. doi:10.1097/00005537-200303000-00021 [CrossRef]
  157. Ulualp SO, Massaro BM, Toohill RJ. Course of proptosis in patients with Graves' disease after endoscopic orbital decompression. Laryngoscope. 1999;109:1217–1222. doi:10.1097/00005537-199908000-00006 [CrossRef]
  158. Unal M, Leri F, Konuk O, Hasanreisoğlu B. Balanced orbital decompression combined with fat removal in Graves ophthalmopathy: do we really need to remove the third wall?Ophthal Plast Reconstr Surg. 2003;19:112–118. doi:10.1097/01.IOP.0000056145.71641.F5 [CrossRef]
  159. White WA, White WL, Shapiro PE. Combined endoscopic medial and inferior orbital decompression with transcutaneous lateral orbital decompression in Graves' orbitopathy. Ophthalmology. 2003;110:1827–1832. doi:10.1016/S0161-6420(03)00566-9 [CrossRef]
  160. Graham SM, Carter KD. Combined-approach orbital decompression for thyroid-related orbitopathy. Clin Otolaryngol Allied Sci. 1999;24:109–113. doi:10.1046/j.1365-2273.1999.00219.x [CrossRef]
  161. Kacker A, Kazim M, Murphy M, Trokel S, Close LG. “Balanced” orbital decompression for severe Graves' orbitopathy: technique with treatment algorithm. Otolaryngol Head Neck Surg. 2003;128:228–235. doi:10.1067/mhn.2003.61 [CrossRef]
  162. Goldberg RA, Shorr N, Cohen MS. The medial orbital strut in the prevention of postdecompression dystopia in dysthyroid ophthalmopathy. Ophthal Plast Reconstr Surg. 1992;8:32–34. doi:10.1097/00002341-199203000-00005 [CrossRef]
  163. Wright ED, Davidson J, Codere F, Desrosiers M. Endoscopic orbital decompression with preservation of an inferomedial bony strut: minimization of postoperative diplopia. J Otolaryngol. 1999;28:252–256.
  164. Jackson JL. Nonsurgical management of diplopia after orbital decompression surgery. Am Orthopt J. 2012;62:29–33. doi:10.3368/aoj.62.1.29 [CrossRef]
  165. Lee YH, Oh SY, Hwang JM. Is 6 months of stable angle of strabismus enough to perform surgery in patients with strabismus related to thyroid ophthalmopathy?Br J Ophthalmol. 2010;94:955–956. doi:10.1136/bjo.2008.154195 [CrossRef]
  166. Wutthiphan S. Role of botulinum toxin A in diplopia following orbital decompression. Strabismus. 2008;16:112–115. doi:10.1080/09273970802292552 [CrossRef]
  167. Michel O, Oberländer N, Neugebauer A, Fricke J, Russmann W. Preliminary report: long-term results of transnasal orbital decompression in malignant Graves' ophthalmopathy. Strabismus. 2000;8:113–118. doi:10.1076/0927-3972(200006)8:2;1-2;FT113 [CrossRef]
  168. Kim MH, Park KA, Oh SY. The effect of previous orbital decompression on results of strabismus surgery in patients with Graves' ophthalmopathy. J AAPOS. 2013;17:188–191. doi:10.1016/j.jaapos.2012.10.019 [CrossRef]
  169. Gilbert J, Dailey RA, Christensen LE. Characteristics and outcomes of strabismus surgery after orbital decompression for thyroid eye disease. J AAPOS. 2005;9:26–30. doi:10.1016/j.jaapos.2004.10.004 [CrossRef]
  170. Russo V, Querques G, Primavera V, Delle Noci N. Incidence and treatment of diplopia after three-wall orbital decompression in Graves' ophthalmopathy. J Pediatr Ophthalmol Strabismus. 2004;41:219–225.
  171. Pitz S, Esch A, Müller-Forell WS, Kahaly G, Mann W, Pfeiffer N. Is there a relationship between the degree of preoperative motility impairment or the muscle thickness and the outcome of strabismus surgery in patients with graves' orbitopathy after decompression surgery?Orbit. 2005;24:173–176. doi:10.1080/01676830500182705 [CrossRef]
  172. Ruttum MS. Effect of prior orbital decompression on outcome of strabismus surgery in patients with thyroid ophthalmopathy. J AAPOS. 2000;4:102–105. doi:10.1067/mpa.2000.103872 [CrossRef]
  173. Dal Canto AJ, Crowe S, Perry JD, Traboulsi EI. Intraoperative relaxed muscle positioning technique for strabismus repair in thyroid eye disease. Ophthalmology. 2006;113:2324–2330. doi:10.1016/j.ophtha.2006.04.036 [CrossRef]
  174. Maino AP, Dawson EL, Adams GG, Rose GE, Lee JP. The management of patients with thyroid eye disease after bilateral orbital 3 wall decompression. Strabismus. 2011;19:35–37. doi:10.3109/09273972.2011.575432 [CrossRef]
  175. Michel O, Oberländer N, Neugebauer P, Neugebauer A, Rüssmann W. Follow-up of transnasal orbital decompression in severe Graves' ophthalmopathy. Ophthalmology. 2001;108:400–404. doi:10.1016/S0161-6420(00)00533-9 [CrossRef]

From Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York.

The Department of Ophthalmology and Visual Sciences at Montefiore Medical Center, Albert Einstein College of Medicine is the recipient of an unrestricted grant from Research to Prevent Blindness and the Division of Pediatric Ophthalmology is the recipient of a grant from the Albert Medow Eye Foundation.

The authors have no financial or proprietary interest in the materials presented herein.

Correspondence: Jamie B. Rosenberg, MD, Department of Ophthalmology and Visual Sciences, Montefiore Medical Center, Albert Einstein College of Medicine, 3332 Rochambeau Avenue, Third Floor, Bronx, NY 10467. E-mail:

Received: July 18, 2016
Accepted: April 18, 2017
Posted Online: July 31, 2017


Sign up to receive

Journal E-contents