Ординатура / Офтальмология / Английские материалы / Pediatric Ophthalmology Current Thought and A Practical Guide_Wilson, Saunders, Trivedi_2008

Take Home Pearls

•Obtain a thorough and well-targeted history. The patient usually supplies most of the information needed to manage complex strabismus, provided that you listen.

•Methodically examine motility yourself.

•Keep an open mind about diagnosis and surgical approach until all information has been received and considered. Information gathering also occurs under direct visualization in the OR and surgical plans should remain flexible to allow for unexpected findings.

•Allow extra time for surgery should the unexpected arise. If the complex case is last on the schedule, there will be less time pressure and less chance of having to stop before the job is complete.

•Critical observation and thinking will lead to success in managing complex strabismus.

Nomograms and tables will not help if the diagnosis is incorrect. If an attempted surgical procedure does not produce the expected effect, reconsider the diagnosis.

•There is no greater reward than seeing the disabled patient, wearing a black patch, previously turned away by other specialists, returned to full function with carefully designed and executed strabismus surgery.

•The importance of good history taking cannot be overstressed. This author had the good fortune to learn under a master of diagnosis in clinical neurology. That

“genius” could seemingly pull diagnoses out of thin air after other experts had exhausted all available diagnostic tests and had long since given up. His secret was a patiently extracted and artfully directed patient history. He was such a keen observer and listener that in most cases his diagnosis was suspected even before the exam.Ancillary testing was usually just a confirmation of what he already knew he would find.

11.10.1Absorbable vs NonAbsorbable Sutures

As described previously, non-absorbable sutures are advised to prevent recurrence of stretched scars and in flap-tear repairs [6−9]. They should also be considered in other situations where the muscle tendon will be under great tension, such as any inferior rectus recession or resection, especially since the inferior rectus has the highest incidence of stretched scar. If the suture will be well covered, such as an inferior rectus, braided polyester is excellent. If the suture may be exposed, such as with an anteriorly positioned lateral rectus, clear polypropylene suture (used in tandem

with braided absorbable suture for stability) is needed, as braided polyester can produce an inflammatory response if it is not well covered. Clear polypropylene is well tolerated and non-reactive, but the knots must be tied underneath the muscle to prevent discomfort from cut suture ends. The 6-0 braided polyester and 6-0 clear polypropylene sutures are commercially available with standard strabismus needles.

11.10.2 Intraoperative “Adjustments”

The springback test is useful to estimate balance of forces at the end of a repair [16]. The eye is rotated

into one extreme of gaze and then allowed to spring back. It is then rotated into the opposite direction and that springback is compared with the first. If they appear equally deviated from the midline, the forces are about equal. If there is an obvious imbalance, the muscles and/or tissues may need to be repositioned.

Classic adjustable sutures are not useable with some scar tissue techniques described previously, and are not advised for stretched scar repair, flap tears, or high-tension muscles. In some cases, awakening the patient in the OR allows measurement of alignment. If the deviation is not satisfactory, the patient is then reanesthetized and the muscle repositioned directly to sclera.

11.11 Postoperative Management

Postoperatively, the use of steroids should be carefully considered and not automatic. Patients with scar migration, or stretched scar, should not have their wound healing further retarded by steroids. Overcorrected strabismus after muscle resection may warrant topical steroids to try to induce stretch.

Vitamin C deficiency causes powerful weakening of scar tissue [6]. Stretched scar patients should be advised to maintain good nutrition with special attention to vitamin C.

When motility restriction is corrected with surgery, the patient should exercise motility into extremes of gaze regularly; however, if motility restriction is created deliberately (inferior oblique anterior transposition, Faden), or if stretched scar has been repaired, the patient should avoid rotating the eyes sharply for several months.

Severe motility restriction after trauma may improve with in-office forced duction manipulation of the eye several times weekly in addition to the athome stretching.

When the repair has not fully corrected the alignment, be honest with the patient by saying that more may need to be done.

References

1.Clark RA, Ariyasu R, Demer JL (2004) Medial rectus pulley posterior fixation: a novel technique to augment recession. J AAPOS 8:451−456

2.Demer JL, Clark RA, Kono R et al. (2002) A 12-year, prospective study of extraocular muscle imaging in complex strabismus. J AAPOS 6:337−347

3.Demer JL, Oh SY, Poukens V (2000) Evidence for active control of rectus extraocular muscle pulleys. Invest Ophthalmol Vis Sci 41:1280−1290

4.Greenwald M (1990) Intraoperative muscle loss due to muscle-tendon dehiscence. Proceedings of the 16th annual meeting of the Association for Pediatric Ophthalmology and Strabismus, Bolton Landing, New York

5.Ketchum LD, Martin NL, Kappel DA (1977) Experimental evaluation of factors affecting the strength of tendon repairs. Plast Reconstr Surg 59:708−719

6.Ludwig IH (1999) Scar remodeling after strabismus surgery. Trans Am Ophth Soc 92:583−651

7.Ludwig IH, Brown MS (2001) Strabismus due to flap tear of a rectus muscle. Trans Am Ophth Soc 99:53−63

8.Ludwig IH, Brown MS (2002) Flap tear of rectus muscles. An underlying cause of strabismus after orbital trauma.

Ophthalmic Plast Reconstr Surg 18:443−450

9.Ludwig IH, Chow AY(2000) Scar remodeling after strabismus surgery. J AAPOS 4:326−333

10.Ludwig IH, Smith JF (2004) Presumed sinus-related strabismus. Trans Am Ophth Soc 102:159−167

11.Parks MM (1958) Isolated cyclovertical muscle palsy. Arch Ophthalmol 60:1027

12.Parks MM (1972) A study of the weakening surgical procedure for eliminating overaction of the inferior obliques. Am J Ophthalmol 73:107

13.Parks MM, Bloom JN (1979) The “slipped” muscle. Ophthalmology 86:1389−1396

14.Plager DA, Parks MM (1990) Recognition and repair of the “lost” rectus muscle. Ophthalmology 97:131−137

15.Stager DR (2001) Anatomy and surgery of the inferior oblique muscle: recent findings. J AAPOS 5:203−208

16.Noorden GK von (1996) Binocular vision and motility. Theory and management of strabismus, 5th edn. Mosby,

St. Louis, pp 526−583

Contents

Core Messages

•The dissociated strabismus complex

(DSC) includes dissociated vertical deviation (DVD), dissociated horizontal deviation (DHD), dissociated torsional deviation (DTD), latent nystagmus, and sub-normal binocularity.

•DSC may represent an atavistic resurgence of the dorsal light reflex that emerges when bifixation and high-grade binocularity are absent.

•Although DVD is usually the most clinically significant component of DSC, some patients will manifest a prominent DHD with less noticeable DVD and DTD.

•DVD, when manifest frequently, can be treated surgically by several different approaches including superior rectus muscle recession, inferior oblique muscle anterior transposition, and inferior rectus muscle resection.

•DHD is not treated effectively by DVD surgery alone. When prominent,

DHD requires a specific surgical strategy that usually involves recession of the lateral rectus muscle on the side of the manifest DHD.

12.1 Introduction

Dissociated deviations in strabismus have been observed and reported for more than a century [30].

The most often quoted early descriptions are from

Bielschowsky [2]. E.L. Raab (Mount Sinai School of Medicine, New York University, New York, N.Y.) is credited with popularizing dissociative vertical deviation (or more commonly, dissociated vertical deviation, DVD) as a descriptive label for this intriguing type of strabismus. Many other names, such as alternating sursumduction and dissociated double hypertropia, have faded from use. More recently, dissociated movements and misalignments have been grouped into what is now known as the dissociated strabismus complex (DSC) [15, 34, 36, 38]. It is well known that these dissociated deviations can be vertical, horizontal, or torsional. DSC obviates the semantic confusion that occurs when referring to a dissociated deviation as a DVD when the most prominent movement, in some patients, is horizontal or torsional. Latent nystagmus and sub-normal binocularity should also be included as parts of DSC.

Within the DCS grouping, vertical movements are recorded using the familiar term, dissociated vertical deviation(DVD).Horizontalmovementsarerecorded as dissociated horizontal deviation (DHD) and torsional movements are known as dissociated torsional deviation (DTD). Examiners are encouraged to use a

1+ to 4+ scale to rate each of the DCS components separately. DVD and DHD can be measured or estimated in prism diopters, but variability exists based

Fig. 12.1  Dissociated strabismus complex. The left eye is shown, elevated, abducted, and extorted behind cover

on the attentiveness of the patient. Often the DVD and DHD are larger at times than can be quantitated using alternate prism and cover measurements.

The classic DSC pattern is of a nonfixating eye slowly elevating, extorting, and abducting upon the spontaneous loss of binocular function or with cover testing (Fig. 12.1). A reversal of these movements is seen with recovery and refixation. Vertical movements usually predominate, but horizontal or torsional movements may be the most noticeable manifestation of the complex in some patients. Latent nystagmus is also usually seen during the exam, but macular binocular vision with high-grade stereopsis is never present.

12.2 Etiology

The exact cause of DSC remains unknown, but two recent theories have been published. Guyton has proposed that DSC [13] movements serve to damp latent nystagmus by stabilizing the fixating eye. This

“nystagmus blockage” function, according to Guyton, is a learned response, which helps to prevent a decrease in visual acuity that would otherwise occur with manifest-latent nystagmus. Using eye movement recordings of patients with DCS, Guyton observed a comitant drift of both eyes with the fixating eye adducting, depressing, and intorting, while the nonfixating eye abducts, extorts, and elevates. The horizontal muscles were shown to produce the horizontal component of the drift, while the oblique muscles produced the cyclovertical drift. According to Guyton, these movements produce what we see clinically as the slow phase of latent nystagmus. Comitant saccades then occur that compensate for the drift of the fixating eye. This produces the fast phase of latent nystagmus. In conjunction with the vertical and cyclovertical vergence movements, there is an upward vertical version that is necessary to compensate for the depression of the fixating eye caused by the vergence movement. This version is produced mostly by the inferior oblique muscle of the fixating eye and the superior rectus muscle of the nonfixating eye. Also, the eye movement recordings documented a horizontal version, away from the fixating eye, presumably to compensate for the collective abduction effects of both oblique muscles as they become ac-

tive in the fixating eye. The combined effect of these movements is that the fixating eye stabilizes, but the nonfixating eye is driven into a variable state of elevation, extorsion, and abduction.

Brodsky [6], in contrast, has stated that any horizontal damping of latent nystagmus is likely an epiphenomenon of dissociated esotonus that helps to explain the horizontal portion (DHD) of DSC, rather than the result of a compensatory adaptation to improve visual acuity. The remaining DSC movements, according to Brodsky [4], are the result of an atavistic resurgence of the dorsal light reflex that emerges when macular binocular vision and high-grade stereopsis are absent. In evolution, primitive responses to external stimuli are suppressed by newer reflexes.

When newer systems fail, these retained primitive reflexes can reappear. Nathan [22] believes that in humans the eyes have phylogenetically retained some of their primitive organ-balance functions. When there is absence of macular binocular vision, unequal visual input can induce a central vestibular imbalance in which the internal sense of vertical no longer corresponds to the gravitational vertical. In further support of this theory, Brodsky [5] has shown evidence that, in DSC, a subjective sensation of visual tilt under monocular conditions produces two compensatory eye movements: a vertical divergence movement to realign the eyes relative to an altered internal representation of vertical, and a cycloversion (torsion) movement that rotates the eyes to neutralize a perceived visual tilt. In contrast, the horizontal component of DSC, known as DHD, is more likely related to a dissociation of the esotonus that is needed in humans to overcome the anatomical tendency for the eyes to be divergent [6].

12.3 Incidence and Associations

The DSC is commonly associated with congenital esotropia, but it may also be seen in association with other forms of strabismus [14, 35]. In addition, it can be seen to develop whenever a child suffers from a permanent unilateral vision loss. DVD, the most prominent component of DSC, is one of the most common types of hyperdeviation seen in a strabismus practice.Helveston[14]foundDVDin11.1%of1000 consecutive patients with strabismus or nystagmus.

Among esotropia patients, the incidence was 14%. In exotropia, DVD was found in 8.7%, and in hypertropia, DVD co-existed in 7.2%. Wilson and Parks [35] found DVD in 62% of 98 patients with congenital esotropia who were followed up to, or beyond, 6 years of age. Other investigators have reported the association of DVD and congenital esotropia in up to 92% of patients [23]. Surgery at an earlier age does not decrease the incidence of DVD [23, 35]. Incidence figures for DSC may depend on how carefully subtle findings are sought when examining patients at high risk for DSC, such as those who have a history of congenital esotropia. In addition, some components of DSC may appear to be present during some examinations and absent during others. DHD is often less prominent than DVD; however, DHD prominent enough to require horizontal muscle surgery occurs in 5% or more of patients with congenital esotropia [10]. In addition, Brodsky [6] found evidence of

DHD in 50% of a cohort of patients with consecutive exotropia after surgery for congenital esotropia. DSC also can occur in association with acquired deviations, whether they are esotropia, exotropia, or hypertropia. All conditions have in common an absence of macular binocular vision. DSC is not seen when high-grade stereopsis (bifixation or macular binocular vision) is preserved.

Since both inferior oblique muscle overaction and DSC occur commonly in congenital esotropia patients, the two conditions often coexist. At times, however, DVD can simulate inferior oblique muscle overaction by becoming manifest in adduction as the nose interrupts fixation. Equally confusing is the association of a true hypertropia with DVD or a true esotropia or exotropia with DHD. As stated previously, latent or manifest-latent nystagmus occurs frequently in association with the other components of DSC. Latent nystagmus is rarely seen in the absence of DSC.

12.4 Ocular Manifestations

The DSC is nearly always bilateral but asymmetric

[32]. When a unilateral dissociated deviation is detected initially, careful observation over several examinations usually reveals an asymmetric, bilateral

DSC, rather than a truly unilateral finding. Dissociated deviations may be controlled by binocular fusion

mechanisms and remain latent, or the deviations may manifest spontaneously. When DSC becomes manifest, it does so intermittently, changing as the state of attention of the individual changes. Visual inattention often produces a larger deviation than can be measured by even prolonged alternate cover testing and variability is the rule. Deviations can appear small and well controlled on one visit only to be large and manifest spontaneously a brief time later. Although dissociated horizontal and torsional movements are being recognized with greater frequency, DVD remains the predominant manifestation in most cases of DSC.

Placing base-down prisms before the higher eye or base-up prisms before the lower eye until all refixation movements are neutralized can quantitate a true hypertropia. The alternate cover test reveals these refixation movements to be upward in one eye and downward in the other eye. The absence of upward refixation movements in either eye on alternate cover testing usually distinguishes DVD from true vertical tropia. In addition, the upward deviation is very slow (2−40°/s) in DVD compared with true hypertropia (200−400°/s) [14]. Movements in DSC do not resemble a saccade or pursuit movement but rather a slow divergence of a non-fixating eye. In addition, one or more of the other components of DSC (DTD, DHD, or latent nystagmus) almost invariably can be detected in patients with prominent DVD.

When one is attempting to quantify DVD or DHD, each eye must be measured separately. Prisms are placed before the eye to be measured until it no longer drifts behind cover. A true neutralization is not reached. The endpoint is when the eye measured becomes still. Both eyes will not “neutralize” simultaneously. Measurements of DSC vary day to day − even moment to moment − and tend to increase with prolonged occlusion. For these reasons, a subjective 1+ to 4+ scale is sometimes used instead of an exact prism diopters measurement to describe each component of DSC and the largest deviation seen during the exam is usually the one graded. For a DVD estimated or measured <10 prism diopters (PD), a 1+ designation is often used. Deviations between 10 and

15 PD are labeled as 2+ , 15−20 as 3+ , and >20 PD as 4+. If a true hypertropia and DVD coexist, prism and alternate cover test neutralization of the hypertropia should be made first. The overlying DVD can then be estimated or measured. Use a rapid alternate cover

test to measure the true hypertropia, not allowing the hypotropic eye time to dissociate behind the cover. The true hypertropia and the more marked DVD usually are present on the same side.

The DSC can exist as a prominent DHD with very little DVD, or as a prominent DVD in one eye and a prominent DHD in the other (Fig. 12.2). The DHD is distinguished from intermittent exotropia by the slow speed of the abducting movement, the association of DTD, and the absence of true neutralization with prisms. Close inspection also reveals that the DHD does not begin to drift until the formally covered eye has returned to the primary position and picked up fixation. In contrast, exotropia produces simultaneous movement of one eye (as it is uncovered) toward fixation and the other eye (as it is covered) away from fixation. In addition, many patients with DHD will reveal a micro-esotropia on rapid alternate cover testing, but slow alternate cover testing (allowing the eye with DHD to fully dissociate) reveals the exodeviated posture behind cover.

Asstatedpreviously,DSCcancoexistwithoblique muscle dysfunction. Wilson and Parks [35] found

DVD and inferior oblique muscle overaction (IOOA) occurring together in 45% of patients with congenital esotropia who were observed to at least 6 years of

Fig. 12.2a,b  Dissociated strabismus complex. a DVD most prominent in the right eye. b DHD most prominent in the left eye

age. In addition, it is well known that in adduction the nose may act as an occluder, allowing DVD to simulate IOOA. A true hypertropia present in side gaze but absent in primary gaze is evidence that oblique muscle dysfunction exists. The adducted eye would manifest a hypotropia when superior oblique muscle overaction (SOOA) is present and a hypertropia when IOOA exists. The absence of a true hypertropia in adduction does not, however, exclude IOOA from occurring in conjunction with SOOA. With coexistence of DVD and IOOA, the adducted eye may elevate under cover from either disorder. The abducted eye, when covered, has opposing forces at work. The

DVD causes the eye to float upward while the IOOA drives the abducted eye downward. A true hypertropia is seen only if the IOOA-stimulated hypotropia of the abducting eye overcomes the DVD-stimulated hyperdeviation. This reasoning also can be used to help verify the coexistence of DVD and either IOOA or SOOA. Oblique muscle dysfunction causes the DVD to appear incomitant. The IOOA reduces DVD in abduction, and SOOA reduces DVD in adduction.

In other words, if DVD is evident in primary gaze but much less elevation is present behind cover when either eye is in abduction, bilateral IOOA should be suspected and a V pattern sought to confirm the diagnosis. If elevation behind cover is much less in adduction, SOOA should be suspected and an A pattern sought to verify the diagnosis. Care must be taken to anticipate the effect on DVD when coexisting oblique muscle dysfunction is treated surgically.

Torticollis has been documented in up to 35% of patients with DVD when an ocular fixation preference is present [1]. Patients with alternating fixation are much less likely to manifest a head tilt secondary to DVD. When present, the head tilt usually is toward the side of the nonfixating eye with the larger, more often manifest, DVD; thus, the DVD usually increases with forced tilt away from the eye with the more severe DVD and decreases on tilt toward the eye with more severe DVD. This tilting pattern is opposite from that seen in superior oblique muscle palsy, in which the hypertropia increases on ipsilateral tilt and decreases on contralateral tilt. Exceptions to this pattern occur when patients with DVD maintain a head posture opposite from that predicted and show forced-tilt changes more like those of superior oblique muscle palsy (Fig. 12.3). Brodsky and coworkers [7] report that patients in their series who

tilted toward the side of the nonfixating eye with the larger DVD had earlier strabismus surgery and better stereopsis than those with a head tilt toward the side of the fixating eye. These patients could calibrate their head position to modulate DVD in the two eyes and stabilize binocular fusion, thus keeping the DVD latent. When patients tilt toward the fixating eye, it is likely a compensatory postural adaptation at the central vestibular level to realign the head to a tilted internal representation of vertical. This does not serve to stabilize binocular fusion, and when seen, it is present despite continuing manifest DVD.

Asymmetrical DVD presents the patient with conflicting needs. The head tilted to one side helps the binocular fusion and to the other side helps the central vertical orientation error. In patients with better fusion and stereopsis, the drive to tilt toward the nonfixating eye with the larger DVD wins out. At times, when fusion is poor, the central drive wins out even at the cost of more manifest DVD.

The Bielschowsky phenomenon [2] is unique to

DSC. It can be demonstrated most easily when DVD and amblyopia are present. Downward movement of the elevated occluded nonfixating eye occurs when

Fig. 12.3  a Right head tilt shows manifest DVD in the right eye. b Left head tilt shows manifest DVD in the left eye

filters of increasing density are placed before the fixating eye. The eye behind cover may even come to rest below primary position. A Bagolini graded red filter bar helps elicit the Bielschowsky phenomenon. Alternatively, illumination to the fixating eye can be progressivelyreducedbyrotatingtwopolarizedfilters on one another to create a darkening filter. Increasing illumination to the fixating eye also can produce the

Bielschowsky phenomenon. The phenomenon has also been demonstrated in the horizontal plane when prominent DHD is present [36].

12.5 Treatment

Although DSC does not cause symptomatic diplopia, it does disrupt binocular vision when it is manifest and it can be disfiguring. Even a small DVD can appear prominent as the eye elevates and sclera begins to be visible at the lower eyelid margin. Also, the exodeviation produced by DHD rarely avoids detection and often prompts complaints from parents of affected patients, even when the deviation manifests infrequently. A prominent abnormal head posture also can be an indication for treatment. In some patients who experience alternating fixation, manifest

DVD predominates when one eye deviates and DHD predominates when fixation switches and the fellow eye drifts.

Despite its ability to be disfiguring, most patients with DSC do not need treatment. The condition is often small in magnitude and well controlled. If a DSC drift is seen only rarely, with fatigue, reassurance and observation is the best course of therapy. Available treatments are imperfect and none of them can eliminate DSC totally. Successful treatment merely reduces the frequency and magnitude of spontaneously manifest DSC so that it is rarely seen at home. Despite treatment, dissociated strabismus can almost always still be detected in the office during alternate cover testing. No patient is cured of DSC, and recurrence of manifest deviations is common even after aggressive treatment.

Nonsurgical treatment options to reduce the frequency of manifest DSC have met with only limited success. Because DSC is usually asymmetric, switching the fixation preference to the eye that deviates most often may improve the patient’s control of DSC

and reduce how often the eyes are seen to drift. Optical and pharmacologic penalization techniques designed to blur the eye that has less DSC and switch fixation to the eye with more DSC have been reported [27, 32]. These treatments are used only when the

DSC is markedly asymmetric and they depend on a fixation switch to the previously nonpreferred eye.

The Worth four-dot test and a variety of vectographic tests can be used to verify this fixation switch.

Most cases of symptomatic DVD or DHD are managed surgically. Standard surgical treatments for

DVD have no effect on DHD [33]; therefore, DHD requires specific surgical strategies. The DTD is not treated surgically. Latent nystagmus is often also present and can become manifest in patients with poorly controlled DSC. Treatment that restores DSC control and gross binocularity may also result in a manifestlatent nystagmus converting back to its latent status.

Recession of the superior rectus muscles is the most common treatment for DVD. Surgery is usually performed bilaterally unless the DVD is strictly unilateral or dense amblyopia is present. When performed unilaterally, a moderate superior rectus muscle recession of 5−9 mm is typical [3]. A hypotropia often is produced that lasts days, weeks, or longer. Fewer undercorrections occur when unilateral surgery is performed for DVD; however, manifest DVD in the previously asymptomatic eye is commonly seen after unilateral surgery, even in patients where a switch in fixation preference does not occur. Reports advocating bilateral surgery either symmetrically or asymmetrically for all patients with DVD have appeared in the literature since at least the early 1980s [18].

When performing bilateral superior rectus muscle recessions for DVD, I prefer large (7−10 mm) symmetric recessions, regardless of the asymmetry in DVD severity between the eyes. If a true hypertropia coexists with DVD, however, I perform more superior rectus muscle recession on the hypertropic eye. The hypertropia usually is found in the eye with the larger DVD, further justifying asymmetric recessions for these patients. For surgeons who prefer asymmetric bilateral surgery for DVD, the quantity of surgery is determined by the severity of DVD in each eye.

In the past, posterior fixation sutures on the superior rectus muscles, either alone or in combination with a superior rectus muscle recession, were advocated as an effective treatment for DVD [28]. Esswein and coworkers [11], however, reported that

although the effectiveness of 3- to 5-mm superior rectus muscle recessions combined with posterior fixation sutures was excellent at 6 months postoperatively (87% corrected or improved), a failure rate of 55% was documented 3 years after surgery. In contrast, the success rate of 7- to 9-mm superior rectus muscle recessions diminished only slightly over time, with 86% corrected or improved at 6 months, 80% after 1 year, 77% after 2 years, and 72% after 3 years.

Posterior fixation sutures for the treatment of DVD are not recommended.

Residual or recurrent DVD may still become frequently manifest after superior rectus muscle recession has been performed bilaterally. Re-recession of these muscles is possible if the initial surgery placed the muscle <8−10 mm from the insertion; however, recession beyond 8−10 mm it is not recommended and, in fact, is difficult to accomplish safely. I prefer to secure the recessed muscle directly onto the sclera rather than using the hang-back technique. Even when the frenulum between the superior rectus muscle and the superior oblique muscle is completely severed, hang-back recessions are unlikely to result in >10 mm of retro-placement from the insertion. To achieve easy exposure of the superior sclera 8−10 mm posterior to the superior rectus insertion, remove the lid speculum and place a Desmarres retractor in its place. Instead of lifting up on the upper eye lid and conjunctival tissues, press them down toward the orbital roof and keep the retractor in contact with the sclera.

Inferior rectus muscle resection is an alternative to re-recession of the superior rectus muscle for residual or recurrent DVD. Although rarely done, inferior rectus muscle resections have been shown to be effective in the treatment of residual DVD after superior rectus muscle recessions [24]. My experience has been the same. When needed, this operation is very effective at dosages of 4−6 mm bilaterally. Some surgeons advocate inferior rectus muscle resections as a primary treatment for DVD [28]; however, the lower eyelid elevation, flattening, and fullness that often result after this procedure has limited its popularity as a first-line surgery.

A modified recession procedure of the inferior oblique muscle, known as inferior oblique anterior transposition (IOAT), was developed to treat severe inferior oblique muscle overaction [9]. This procedure is now also used to treat DVD, especially when

inferior oblique muscle overaction and DVD co-exist (as they often do) [8, 16, 20, 21].The IOATprocedure has been shown to be effective for DVD up to about

15 PD [8]. Larger DVDs, of 20 PD or more, are not well treated by IOAT. The operation works by weakening the inferior oblique muscle and also converting it into an antielevator [17]. The term “antielevation” implies that the muscle still contracts on attempted supra-duction, but in its new location, the contraction limits elevation rather than assisting it. The muscle is not converted into an active depressor.

Stager et al. [29] studied the inferior oblique muscle’s neurovascular bundle as a new functional origin after IOAT. Both the new origin and the new insertion of the inferior oblique muscle parallel the inferior rectus muscle. This altered anatomy produces a cocontraction of sorts with the superior rectus muscle. The inferior oblique contracts on attempted elevation and still has a functional origin and insertion parallel to the inferior rectus muscle.

The IOAT procedure is not without its own unique set of possible complications. The altered anatomy mentioned above helps to explain the frequent occurrence of an upgaze deficit when IOAT is used. If the muscle is spread too widely and/or re-attached too far anteriorly, a characteristic Y or T pattern is produced, characterized by elevation deficiency and divergence in upgaze and the false appearance of residual inferior oblique muscle overaction [17]. A trade-off appears to exist in which further anterior placement of the inferior oblique muscle corrects more DVD but also is more likely to cause an up-gaze deficit and a

T pattern. Limiting the new anterior insertion of the inferior oblique to the level of the inferior rectus insertion reduces the incidence of marked upgaze deficit; however, Gonzalez and Klein [12] have reported using inferior oblique muscle resection combined with transposition anterior to the inferior rectus insertion with good control of larger DVD. Severe upgaze deficit is a risk with this procedure, however.

When marked DVD (>15 PD) coexists with inferior oblique muscle overaction, simultaneous recession surgery on the four vertical muscles is often very effective. This approach is controversial because of the uncertain risk of marked upgaze deficiency and resulting upper eyelid retraction. Limiting the superior rectus muscle recessions to 8 mm and the inferior oblique recessions to 10 mm reduces, in my hands, the likelihood that this combined surgery will pro-

duce a functionally important upgaze deficit; however, IOAT has been combined with superior rectus muscle recessions of up to 10 mm without producing severe upgaze deficits in a limited number of patients [26, 31].

The IOAT also has been suggested as a prophylactic surgery for DVD in patients a history of congenital esotropia who have inferior oblique muscle overaction and are at high risk for developing DVD. (The incidence of DVD in congenital esotropia is

60−90%.) Mims and Wood [21] performed IOAT in

61 patients with congenital esotropia with bilateral inferior oblique muscle overaction. They placed the inferior oblique muscle 2 mm anterior to the temporal border of the inferior rectus muscle insertion. With an average follow-up of 27 months, only 1 patient needed surgery for DVD compared with nine in a control group of patients with congenital esotropia who had not undergone inferior oblique muscle surgery. The IOAT procedure has been recommended whenever inferior oblique muscle overaction is present in a patient with mild coexisting DVD or when the patient is at high risk for DVD.

Other procedures have been reported for the treatment of DVD, but they are not in common use today. These procedures include superior oblique tendon

tuck or resection [25], which can result in Brown syndrome, and botulinum toxin injection to the superior rectus muscles [19], which invariably leads to ptosis lasting several weeks.

Surgical treatment for symptomatic DHD usually involves unilateral or bilateral lateral rectus muscle recession [36, 37]. For patients with unilateral or asymmetric DHD measured or estimated at >15 PD, an ipsilateral lateral rectus recession of 7 mm is recommended. The recession is reduced to 5 mm if the DHD measures 15 PD or less. The lateral rectus recession is reduced if the lateral rectus muscle has been previously resected. This last reduction is based on forced duction testing performed at the time of DHD surgery. More reduction is indicated when the resected lateral muscle is tight. Bilateral lateral rectus muscle recessions carry a higher risk of postoperative esotropia unless a true exotropia is also present along with the DHD.

When esotropia >10 PD coexists with DHD, the lateral rectus recession is limited to 5 mm, or the esotropia may be treated concomitantly with the DHD. This may entail bilateral medial rectus muscle recession along with unilateral lateral rectus muscle recession or bilateral medial rectus muscle posterior fixation sutures, in cases of high accommodative con-

Take Home Pearls

•DVD can co-exist with hypertropia or hypotropia. Careful examination can distinguish these components and help determine the appropriate surgical plan.

•DVD is usually treated with bilateral surgery even if the deviation is seen most often in only one eye.

•Large 7- to 10-mm superior rectus muscle recessions are most often utilized for the surgical treatment of DVD. The IOAT is used for small to moderate DVD when IOOA is present. Inferior rectus muscle resections

are less frequently utilized but are often effective for residual manifest DVD.

•DHD can co-exist with esotropia or exotropia.

Most often, DHD and a micro-esotropia associated with monofixation syndrome co-exist. In these patients, unilateral lateral rectus muscle recession usually improves the DHD without worsening the esotropia.

•DHD with exotropia usually requires bilateral surgery as opposed to DHD alone, which

is usually treated with unilateral surgery.

•DSC does not occur in patients with macular binocular vision and high-grade stereopsis.