Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006

TABLE 10-3. Treatment of Double Elevator Palsy (Monocular Elevation Deficit Syndrome).

•Tight inferior rectus muscle: good superior rectus function Recess ipsilateral inferior rectus muscle (5–6 mm)

•Superior rectus palsy

Recess ipsilateral inferior rectus muscle and ipsilateral transposition of half the medial and lateral rectus muscles up to the superior rectus insertion (preferred by author)

or

Knapp procedure: full-tendon transfer up to the superior rectus muscle

double elevator palsy. In these cases, a recession of the ipsilateral inferior rectus will not correct the hypotropia. Treatment of a true double elevator palsy with weak superior rectus muscle is to perform a transposition of the ipsilateral medial and lateral rectus muscles up to the superior rectus muscle. In patients with the superior rectus palsy type of MED, forced ductions are often positive, and the ipsilateral inferior rectus muscle should be recessed. This author prefers the partial tendon transfer (Hummelsheim) instead of the full-tendon transposition (Knapp) to avoid the possible complication of anterior segment ischemia that can occur up to 20 years after strabismus surgery. In severe cases of hypotropia over 15 PD, consider adding a recession of the contralateral superior rectus muscle.

Orbital Floor Fracture

Signs of a blowout fracture include diplopia secondary to restricted vertical eye movement, enophthalmos, and numbness of face below the traumatized orbit and along the upper teeth. Restrictive strabismus with limited elevation in orbital floor fractures is caused by entrapment of fat and the inferior rectus muscle at the fracture site (Fig. 10-8). Repair of the floor fracture in most cases will improve ductions. In addition to limited elevation, there can be limited depression on the side of the fracture, often associated with a posterior fracture.108 The cause of the limited depression could be contributed to scarring of the inferior rectus to the floor, thus preventing the inferior rectus muscle from transmitting its contractual pull to the globe. Adherence of the inferior rectus to the floor would also isolate the muscle anterior to the fracture and cause the anterior muscle to slacken on attempted downgaze, producing pseudoinferior rectus palsy. These patients characteristically have a small

hypertropia in primary position, underaction of the inferior rectus muscle, and a large hypertropia in downgaze.

The key to the diagnosis of a pseudoinferior rectus palsy is normal inferior rectus muscle function and normal saccades when the eye moves from upgaze to primary position, with inferior rectus muscle weakness and slow ocular movements from primary position to downgaze. Treatment of pseudoinferior rectus palsy is to repair the floor fracture. If this does not relieve symptoms, then strabismus surgery is indicated. This author has found that a small (3–4 mm) ipsilateral inferior rectus muscle tightening procedure (Wright plication or resection) helps to eliminate the anterior muscle slack. A contralateral inferior rectus recession works well and produces only a slight limitation of elevation. If the muscle is captured in a trap-door fracture, direct damage to the inferior rectus muscle occurs and can truly weaken the inferior rectus muscles. Small trap-door floor fractures can pinch and strangle the inferior rectus muscle, causing necrosis and muscle damage.11 Because of the potential for permanent damage, some advocate immediate repair within the first few days if there is imaging evidence that the inferior rectus is entrapped.29 Strabismus surgery should be performed after reconstructive orbital surgery. If orbital reconstruction is not indicated, and the patient has persistent diplopia 4 to 8 weeks after the trauma, then strabismus surgery is indicated. The strabismus surgical plan depends on the pattern of the strabismus. Table 10-4 lists patterns of strabismus and their associated treatment.

Myotoxic Effect of Local Anesthetics

Injection of local anesthetics such as lidocaine and marcaine into an extraocular muscle can result in myotoxic damage to the muscle and cause strabismus.19,40,46 Elderly patients are especially susceptible to the myotoxic effects of local anesthetics. Immediately after the injection of a local anesthetic into an extraocular muscle, there is an acute paresis of the muscle that lasts for one to several days. Over the next few weeks, localized segmental intramuscular fibrosis occurs secondary to local myotoxicity of the anesthetic. The fibrosis results in a tight and contracted muscle. What is particularly interesting is that, in some cases, the injected muscle overacts, producing a deviation that increases in the field of action of the injected muscle.8,13 This deviation is in contrast to the restriction pattern usually

C

FIGURE 10-8C. (C) CT scan shows herniation and entrapment of inferior orbital fat into the maxillary antrum. Note that, after removal of the fat and repair of the fracture, the restriction resolved.

expected with a tight muscle, where the deviation is greatest in the gaze opposite to the field of the muscle’s action. The cause of the muscle overaction is thought to be secondary to intramuscular fibrosis, with stretching of the Z-bands and enhancing

TABLE 10-4. Orbital Floor Fracture: Surgical Plans.

Tight inferior rectus muscle (hypotropia)

•Small hypotropia ( 8 PD) in primary position, no deviation in downgaze, and larger hypotropia in upgaze (tight inferior rectus muscle):

Asymmetrical bilateral inferior rectus muscle recessions, with a larger ipsilateral recession

Add a contralateral superior rectus recession for a large hypotropia in upgaze

•Large hypotropia in primary position, worse in upgaze (tight inferior rectus muscle):

Hypotropia 8 to 15 PD: recess ipsilateral inferior rectus muscle (3.5–5.0 mm)

Hypotropia 15 PD: recess ipsilateral inferior rectus muscle (5–6 mm) PLUS a contralateral superior rectus recession (4–6 mm)

Pseudoinferior rectus muscle palsy (hypertropia)

•Hypertropia in primary position increases in downgaze with ipsilateral limited depression; intact saccades from upgaze to primary position:

Plication of the ipsilateral inferior rectus (3 mm) PLUS contralateral inferior rectus recession (4–5 mm)

the action and myosin interaction.19 The fibrosis acts to stretch the muscle fibers that subsequently increases their force, per the Starling’s length tension curve.19 For example, inadvertent injection of the inferior rectus muscle associated with a retrobulbar injection of anesthetic initially results in an ipsilateral hypertropia because of an inferior rectus paresis. Over a few weeks, this changes into an ipsilateral hypotropia with overaction of the inferior rectus muscle, resulting in the hypertropia being greatest in downgaze.

Any of the extraocular muscles can be infiltrated during a retrobulbar or peribulbar injection of local anesthetics, with the superior and inferior rectus muscles most commonly affected. One of the findings is segmental enlargement of the injected muscle seen on orbital imaging. Hamed and Mancuso46 reported on eight patients with an ipsilateral hypotropia after a retrobulbar injection of anesthetic, with three patients showing segmental enlargement of the inferior rectus muscle. The treatment is to recess the tight or overacting muscle. This method has produced excellent results, especially in the cases involving an overacting injected muscle, with the deviation larger in the field of action of the muscle. One can help prevent intramuscular injection injury by injecting into the orbital quadrant away from the extraocular muscles, using a blunt cannula and limiting anesthetic volume. The incidence of strabismus after cataract surgery has diminished dramatically since the widespread use of topical anesthesia during surgery.

Strabismus After Retinal Surgery

Strabismus can occur virtually after every known retinal surgical procedure.38,57,71,72,103,111,114 The strabismus is usually transient; however, persistent strabismus occurs in approximately 7% of scleral buckling procedures.71,117 Common causes of strabismus after retinal detachment surgery include fat adherence and restriction, a lost or slipped muscle, a displaced superior oblique tendon, a large explant under a rectus muscle, and ectopic fovea.38,47,57,85,110 Other causes of strabismus after retinal surgery include patients with preexisting strabismus before the retinal surgery who then experience sensory strabismus secondary to loss of vision.92,130 Of all the causes of persistent restriction after retinal detachment surgery, fat adherence and periocular scarring is by far the most common and most difficult to treat.1,57,134 Fat adherence is difficult to treat because there

is no synthetic substitute to recreate the natural boundary between the orbital fat and the eye and muscle once Tenon’s capsule is violated.

Occasionally, a lost muscle is associated with postretinal surgery, as can occur when the traction sutures around the muscle are pulled to gain posterior exposure during the retinal surgery. In elderly patients, the muscle is relatively weak, and overzealous traction on the rectus muscle can result in a splitting of the muscle; this has been termed pulled-in-two syndrome (PITS). Spontaneous disinsertion and posterior slippage of a rectus muscle behind an encircling buckle can also occur, without removal of the muscle at the time of retinal surgery.47,57 In these cases, the silicone band will cheese-wire through the muscle insertion over several months postoperatively, resulting in late slippage of the muscle behind the buckle and causing an underaction of the slipped muscle. The slipped rectus muscle can almost always be found attached to sclera at the posterior edge of the encircling buckle or connected to sclera by a pseudotendon. Appropriate treatment is to advance the muscle and reattach the muscle with nonabsorbable suture.

Another cause for strabismus after retinal surgery is an oblique muscle that has been displaced anteriorly by an encircling band.57,72 Placement of the band behind the superior oblique tendon pulls the superior oblique tendon anteriorly to the nasal aspect of the superior rectus insertion. The superior oblique tendon now inserts at the nasal side of the superior rectus insertion, anterior to the equator. The new anterior insertion of the superior oblique tendon changes the action of the superior oblique muscle from a depressor to an elevator. These patients typically present with a hypertropia and limitation of depression of the involved eye. Forced ductions, however, show relatively mild restriction to depression as compared to the limitation on ductions and versions. Treatment is to release the entrapped superior oblique tendon from the buckle or, if there is severe scarring, perform a superior oblique tenotomy. If the hypertropia is greater than 5 PD in primary position, also perform a recession of the contralateral inferior rectus muscle (consider adjustable suture). The inferior oblique muscle can also be entrapped by an encircling element.57 In this case, the element is passed behind, or splits, the inferior oblique muscle. When the band is tied in place, the muscle is pulled anteriorly, resulting in a hypotropia and excyclotropia. The hypotropia occurs because the inferior oblique is displaced anteriorly to the

equator, pulling the front of the eye down. The excyclotropia is caused by the increased tension on the inferior oblique muscle. Torsional diplopia after retinal surgery is not always associated with an entrapped oblique muscle.23 Metz and Norris found two of four patients with torsional diplopia after retinal surgery to have no identifiable abnormality of the oblique muscle.72 The complications of oblique muscle entrapments can be diminished by passing the encircling elements anteriorly, just behind the rectus insertions. Extreme posterior passage of the muscle hook may result in inadvertent hooking of an oblique muscle, especially when working on the superior rectus and lateral rectus muscles.

The placement of a retinal explant sponge or buckle is often identified as a primary cause for strabismus after retinal surgery. Transient strabismus after a retinal encircling procedure is frequent, occurring in approximately 20% of cases. In our experience, however, a retinal encircling element by itself rarely causes persistent strabismus. Persistent strabismus after retinal surgery usually results from secondary scarring or a displaced muscle, as stated previously.78 Infrequently, however, a retinal explant may be the primary cause of restriction; this occurs when a large explant is placed directly under a rectus muscle. The explant causes the muscle to deviate from its normal course, thus tightening the muscle. For example, a large retinal sponge placed directly under the medial rectus will cause a tightening of the medial rectus, as the medial rectus courses over the large sponge and produces an esotropia. Low-profile encircling elements, such as 240 bands that indent the sclera, do not interfere with the course of the rectus muscle and, therefore, do not produce strabismus.

Foveal ectopia occurs in association with macular pucker, peeling of the epiretinal membrane, and retinal translocation surgery. Acquired foveal ectopia produces an interesting type of strabismus and diplopia. These patients will observe that objects in the central visual field appear double, with one image being distorted by metamorphosia. Objects in the peripheral field, however, will often be fused, as the peripheral retina may not be involved with the ectopia. Thus, patients who undergo membrane peeling for a macular pucker may experience postoperative diplopia because of foveal ectopia. The image disparities tend to be small with this condition, and prism glasses have been found to be effective in treating this problem.

Retinal translocation surgery can result in severe torsional diplopia that prisms cannot correct. Instead, oblique muscle surgery is required to treat the problem.38 Extorsion is induced from macular inferior translocation, and intorsion is secondary to superior macular translocation. Extorsion can be corrected by a large Harada–Ito procedure, possibly with an inferior oblique weakening procedure, whereas intorsion can be corrected with a weakening surgery of the superior oblique muscle, perhaps with a tuck of the inferior oblique muscle. Vertical offset of the rectus muscle can also change torsion, but one must consider the risk of anterior segment ischemia in this group of patients.

Glaucoma Explants and Strabismus

The incidence of strabismus after glaucoma explant surgery ranges from 10% to 70%, depending on the study.7,90,112 The cause of the strabismus is, for the most part, the large bleb created by the glaucoma explant. Strabismus associated with a large filtering bleb may be caused by the following mechanisms:

(1) orbital mass, which displaces the eye (Fig. 10-9); (2) a mass directly under a muscle or tendon; or (3) scarring or adhesions secondary to the surgical dissection during placement of the glaucoma explant. The old Baerveldt implant had been associated with the highest incidence of strabismus; however, modifications of the Baerveldt implant (fenestrated Baerveldt) have reduced the bleb size and subsequently reduced the incidence of strabismus. Valved implants have also reduced the size of the filtering blebs and have subsequently produced the lowest incidence of strabismus.

A large explant in the superior nasal quadrant may cause a pseudo-Brown’s syndrome with restricted elevation in adduction, as the bleb displaces and tightens the superior oblique tendon.7,90 Placement of glaucoma explants should be superotemporal rather than superonasal to avoid the problem of a secondary Brown’s syndrome. The treatment of a bleb-induced strabismus is to reduce the size of the bleb by suturing the bleb wall to the explant so it cannot expand. Additionally, the old explant can be replaced with a newer valved explant.

An interesting observation of some patients with strabismus and severe glaucoma is that they do not experience diplopia but, instead, have visual confusion.57 Visual confusion is the simultaneous perception of two different foveal images in a patient

with strabismus. These patients see the superimposed images from each fovea. Patients with end-stage glaucoma have tunnel vision and lose their peripheral visual field. If these patients acquire strabismus, they may experience confusion rather than a true diplopia, as they only have central vision and are forced to use the fovea of each eye.

High Myopia and Esotropia

(Myopic Strabismus Fixus)

High myopia, usually greater than 20 diopters, can be associated with an acquired large-angle esotropia along with limited abduction and a hypotropia9,25,50,63,116; this is a form of acquired strabismus fixus and can be either monocular or binocular. Another term for the high myopia esotropia syndrome is heavy eye syndrome, with hypotropia and limited eye movement.116 Restricted abduction is dramatic, and there is limited elevation of the hypotropic eye. Orbital imaging shows an extremely large globe with a posterior staphyloma that fills the orbit, a large inferior displacement of the lateral rectus muscle, and a mild nasal displacement of the superior rectus muscle. The cause of the esotropia and hypotropia is a combination of restriction, because of the massive expansion of the posterior globe against a tight medial rectus muscle, and displaced lateral and superior rectus muscles that change the normal vector forces. Displacement of the lateral rectus muscle inferiorly and superior rectus muscles nasally is most likely caused by the massive expansion of the posterior aspect of the globe into the superior temporal quadrant.64 The lateral rectus muscle shows the most displacement, probably due to the laxity of its pulley system. Slippage of the lateral rectus muscle below the globe weakens the abduction vector and pulls the eye down, thus contributing to the esotropia and hypotropia. The nasally displaced superior rectus muscle also contributes to the esotropia and hypotropia by pulling the eye nasally and diminishing the elevation vector force.

Treatment is aimed at realigning the lateral rectus muscle and releasing the medial rectus muscle, which is inevitably tight. This author prefers a large recession of the medial rectus muscle, at least 7 to 8 mm on a hang-back suture, and a superior transposition of the lateral rectus muscle with a small resection. The posterior sclera is thin in these cases, and access to the posterior globe is difficult because of the large eye. The hangback suture of the medial rectus allows for a large recession