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

FIGURE 11-17. Diagram of superior oblique tendon insertion. The anterior fibers are responsible for intorsion and the posterior fibers for abduction and depression.

Tightening the anterior fibers will induce intorsion without too much change in the depression and abduction functions of the superior oblique muscle; this is the basis of the Harada–Ito procedure, which is used for correcting extorsion. Tightening the full tendon is termed a superior oblique tuck or plication.

Harada–Ito Procedure

The Harada–Ito procedure is commonly used to treat extorsion associated with a partially recovered acquired superior oblique palsy, where the residual strabismus is only extorsion. Tightening the entire tendon will result in depression and abduction and often produces an iatrogenic Brown’s syndrome. Therefore, the Harada–Ito has the advantage of correcting extorsion without causing a significant Brown’s syndrome. Figure 11-18 shows two techniques for tightening the anterior fibers: Figure 11-18A

shows the disinsertion technique and Figure 11-18B shows a classic Harada–Ito procedure. The author prefers the classic Harada–Ito procedure because it is reversible by simply cutting the pullover suture.

Full-Tendon Tuck or Plication

The superior oblique tuck or plication is reserved for severe bilateral superior oblique underaction where the tendon is lax, usually associated with either a congenital or trauma-induced palsy. A full-tendon tuck or plication tightens both anterior and posterior fibers and enhances all three functions of the superior oblique muscle (Fig. 11-19). Tightening of the entire superior oblique tendon may improve its function slightly, but this will consistently cause an iatrogenic Brown’s syndrome or limited elevation in adduction. Care must be taken to balance the superior oblique tightening against the induced Brown’s syndrome by performing intraoperative forced ductions of the superior oblique after tucking or plicating. The amount of tuck or plication should be readjusted appropriately. This author (K.W.W.)

A B

FIGURE 11-18A,B. Harada–Ito procedure: (A) With the disinsertion technique, the anterior fibers of the superior oblique tendon are sutured, then disinserted, and moved anteriorly and laterally to be secured to sclera at a point 8 mm posterior to the superior border of the lateral rectus insertion. Lateralizing the anterior fibers intorts the eye, thus correcting extorsion. (B) In the classic Harada–Ito procedure, the anterior superior oblique tendon fibers are looped with a suture and displaced laterally without disinsertion. The anterior superior oblique tendon fibers are sutured to sclera 8 mm posterior to the superior border of the lateral rectus muscle.

FIGURE 11-19. Superior rectus tuck or plication. Inset—Sutures are placed in the nasal tendon, then passed through sclera at the insertion. The tendon is pulled to plicate the tendon.

reserves the superior oblique plication for those rare cases of congenital superior palsy caused by a lax superior oblique tendon, or severe bilateral traumatic superior oblique palsy with severe extorsion and esotropia in downgaze. Bilateral medial rectus recessions with infraplacement usually accompany the plications.

SUPERIOR OBLIQUE MUSCLE

WEAKENING PROCEDURES

Superior oblique weakening procedures are used in the management of superior oblique overaction and Brown’s syndrome.19 Various weakening procedures have been described including tenotomy, tenectomy, recession, split-tendon lengthening, and Z-lengthening of the superior oblique tendon. The split-tendon lengthening procedure works well but is difficult to perform and has the disadvantage of causing tendon scarring. The superior

temporal fibers are removed from the sclera, they do not retract but, instead, scar down to sclera under the superior rectus muscle. Another disadvantage of the temporal tenotomy is that the tendon is extremely splayed out at its insertion; thus, it is difficult to hook and tenotomize all the posterior superior oblique fibers.

The preferred procedure, developed by Marshall Parks, is to perform the superior oblique tenotomy nasal to the superior rectus muscle through a temporal conjunctival incision. By placing the conjunctival incision temporal to the superior rectus muscle and reflecting the incision nasally, the surgeon can keep the nasal intermuscular septum intact and minimize scleral–tendon scarring. Intact nasal intermuscular septum is vital to maintain the anatomic relationship of the superior oblique tendon and helps reduce the incidence of postoperative superior oblique palsy.

Wright Superior Oblique Tendon Expander

This procedure controls the separation of the ends of the tendon, allowing quantification of tendon separation.16 A segment of a silicone 240 retinal band is inserted between the cut ends of the superior oblique tendon (Fig. 11-21). The length of silicone is determined by the degree of superior oblique overaction, as well as the amount of A-pattern and downshoot. The maximum length of silicone is 7 mm, but most significant Brown’s syndromes can be surgically managed with a segment of 5 to 6 mm.17 Perform the superior oblique expander through a temporal conjunctival incision, even though the silicone is placed in the nasal tendon. By placing the conjunctival incision temporal to the superior rectus muscle, then reflecting the incision nasally, the surgeon can keep the nasal superior oblique tendon capsule floor and intermuscular septum intact and prevent adhesion of the silicone implant to sclera. This maneuver is analogous to cataract surgery and placing an intraocular lens (IOL) in the capsular bag. An intact nasal tendon capsule floor is important to maintain the anatomic relationships of the superior

FIGURE 11-21A,B. Wright superior oblique tendon expander. (A) A segment of 240 silicone retinal band is sutured between the cut ends of the superior oblique tendon. (B) The silicone segment elongates the tendon.

oblique tendon insertion and not create a new insertion site nasal to the superior rectus muscle. Scarring of the silicone to nasal sclera or the nasal aspect of the superior rectus muscle can cause limitation of depression postoperatively.

SLIPPED OR LOST RECTUS MUSCLE

An important complication of strabismus surgery is a slipped or lost muscle. The medial rectus muscle is the muscle most commonly lost or slipped after strabismus surgery and is the most difficult to retrieve, as there are no fascial connections to oblique muscles that keep the muscle from retracting posteriorly. In contrast, the inferior, superior, and the lateral recti have check ligaments that connect to adjacent oblique muscles.

A slipped rectus muscle occurs when a muscle retracts posterior to the intended recession or resection point but there is some tissue still attached to the intended scleral insertion. A slipped muscle after strabismus surgery is caused by inadvertently suturing the muscle capsule or anterior Tenon’s capsule instead of true muscle tendon. Anterior Tenon’s capsule and muscle capsule are then secured to sclera, so the muscle slips posteriorly while a “pseudotendon” of connective tissue remains attached to sclera.

A lost muscle occurs when the muscle retracts posteriorly and there is no connection of the muscle to sclera. Orbital trauma or hemorrhage can also result in a lost or damaged muscle.3 Typical signs of a slipped or lost muscle include decreased muscle function with limited ductions and lid fissure widening in the field of action of the lost muscle. On occasion, the presentation may be subtle, with slight limitation of ductions as the only finding. The key observation is an incomitant deviation with underaction of the slipped muscle. Initial eye alignment during the first postoperative week may be fairly good in primary position, with only a mild limitation of ductions. Over several weeks to months, however, ductions become progressively more limited. This progression probably represents muscle slippage in addition to secondary contracture of the antagonist muscle against a weakened slipped muscle.

Management of a slipped or lost muscle is to find the muscle and surgically advance it to anterior sclera if possible. Fullthickness locking bites through muscle fibers must be obtained, because partial-thickness locking bites may result in slippage of

the posterior tendon fibers. If a lost muscle cannot be retrieved, then a transposition procedure, such as the Hummelsheim, should be performed.

STRETCHED INSERTION SCAR

In contrast to a slipped or lost muscle that results in an immediate overcorrection, there are many cases where an overcorrection occurs 4 to 6 weeks, and some-times years, after muscle surgery (Fig. 11-22). When this overcorrection is associated with minimal underaction of the operated muscle, consider a stretched or elongated scar, with the operated muscle migrating posteriorly. Late overcorrection is particularly common after inferior rectus recession for a hypotropia associated with thyroid disease, as it occurs in approximately 50% of cases.12 There has been much speculation about the cause for this late overcorrection,15 but work by Ludwig probably provides the best explanation.9,10 This theory states that the new insertion scar of the muscle to sclera stretches after the suture dissolves. The 6-0 vicryl suture used by most ophthalmologists lasts about 3 to 6 weeks, thus explaining the timing of the overcorrection. In this author’s (K.W.W.) experience, the use of a nonabsorbable suture reduces the problem of late overcorrection of the inferior rectus muscle. Any rectus muscle can have a stretched scar and a late overcorrection including, in order of frequency, inferior rectus, medial rectus, and superior rectus muscles. The likelihood of stretched scar formation may be inversely related to the length of the muscle’s arc of contact.4

BOTULINUM NEUROTOXIN

Botulinum is a cholinergic blocking agent. Blockage in a muscle occurs by binding sodium at the myoneural junction, causing the loss of acetylcholine activity that paralyzes the muscle. Minimal diffusion occurs through the nerve or the muscle because there is tight binding within the muscle. Injection of botulinum toxin into a rectus muscle results in paralysis that occurs after 24 to 48 h and lasts from 3 to 6 months.

The most common strabismus indication for use of botulinum is sixth nerve palsy. The treatment is to inject the ipsi-

FIGURE 11-22A,B. Late overcorrection (4 weeks after strabismus surgery) after a left inferior rectus recession for thyroid-related, tight inferior rectus muscle. The left inferior rectus muscle was found to be posterior, caused by a stretched scar. (A) Note the left hypertropia and lower lid retraction. (B) Limited depression, left eye.

lateral medial rectus muscle (antagonist of the paretic lateral rectus muscle). The induced weakness of the medial rectus muscle from botulinum injection balances forces against the weak lateral rectus muscle (weakness with weakness), which

theoretically allows the paretic muscle to regain its strength without secondary contracture of the antagonist. The use of botulinum is controversial, as studies have not shown an improvement in recovery rates for sixth nerve palsy (see Chapter 10).

Botulinum has also been used for comitant strabismus. The rationale for using botulinum toxin in nonparalytic strabismus is twofold: to weaken and lengthen the injected muscle and to induce a mild secondary contracture in the injected muscle’s antagonist. Botulinum causes secondary muscle contracture by paralyzing the injected muscle, producing a large consecutive deviation in the opposite direction; this causes shortening and contracture of the antagonist to the injected muscle, theoretically leading to a permanent correction of the strabismus even after the botulinum wears off. In infantile strabismus, it is theorized that the overacting muscle can be injected before the development of contracture. Because of the temporary large overcorrection associated with the initial paralysis and the need for multiple injections to correct strabismus, strabismus surgery is usually preferred for the treatment of comitant strabismus.

References

1.Apt L, Call NB. Inferior oblique muscle recession. Am J Ophthalmol 1978;95:95–100.

1a. Beisner DH. Reduction of ocular torque by medial rectus recession. Arch Ophthalmol 1971;85:13.

2.Berk RN. Tenotomy of the superior oblique for hypertropia. Arch Ophthalmol 1947;38:605.

3.Cates CA, et al. Slipped medial rectus muscle secondary to orbital hemorrhage following strabismus surgery. J Pediatr Ophthalmol Strabismus 2000;37:361–362.

4.Chatzistefanou KI, et al. Magnetic resonance imaging of the arc of contact of extraocular muscles: implications regarding the incidence

of slipped muscles. J Am Assoc Pediatr Ophthalmol Strabismus 2000; 4:84–93.

4a. Elliot L, Nankin J. Anterior transposition of the inferior oblique. J Pediatr Ophthalmol Strabismus 1981;18:35.

5.Eustis HS, Leoni R. Early reoperation after vertical rectus muscle surgery. J Am Assoc Pediatr Ophthalmol Strabismus 2001;5:217–220.

6.Guemes A, Wright KW. Effect of graded anterior transposition of the inferior oblique muscle on versions and vertical deviation in primary position. J Am Assoc Pediatr Ophthalmol Strabismus 1998;2;201– 206.

7.Kushner BJ. Fifteen-year outcome of surgery for the near angle in patients with accommodative esotropia and a high accommodative