Download Strabismus Surgery

11
Strabismus Surgery
Kenneth W. Wright and Pauline Hong
T
his chapter discusses various strabismus surgery procedures
and how they work. When a muscle contracts, it produces
a force that rotates the globe. The rotational force that moves
an eye is directly proportional to the length of the moment arm
(m) (Fig. 11-1A) and the force of the muscle contraction (F) (Fig.
11-1B).
Rotational force m F
where m moment arm and F muscle force.
Strabismus surgery corrects ocular misalignment by at least
four different mechanisms: slackening a muscle (i.e., recession),
tightening a muscle (i.e., resection or plication), reducing the
length of the moment arm (i.e., Faden), or changing the vector
of the muscle force by moving the muscle’s insertion site (i.e.,
transposition).
MUSCLE RECESSION
A muscle recession moves the muscle insertion closer to the
muscle’s origin (Fig. 11-2), creating muscle slack. This muscle
slack reduces muscle strength per Starling’s length–tension
curve but does not significantly change the moment arm when
the eye is in primary position (Fig. 11-3). The arc of contact of
the rectus muscles wrapping around the globe to insert anterior
to the equator of the eye allows for large recessions of the rectus
muscles without significantly changing the moment arm. Figure
11-3 shows a 7.0-mm recession of the medial and lateral rectus
muscles. Note there is no change in the moment arm with these
large recessions. Thus, the effect of a recession on eye position
is determined by the amount of muscle slack created.1a The
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FIGURE 11-1A,B. (A) Diagram of the horizontal rectus muscles shows
the relationship of the moment arm (m) to the muscle axis and center of
rotation. The moment arm intersects the center of rotation and is perpendicular to the muscle axis. The longer the moment arm, the greater
the rotational force. (B) Starling’s length–tension curve. The relationship
of a muscle’s force is proportional to the tension on the muscle. More
tension on a muscle increases muscle force and slackening a muscle
reduces its force. Note that the relationship is exponential, not linear:
toward the end of the curve, a small amount of slackening produces a disproportionately large amount of muscle weakening.
A
B
C
FIGURE 11-2A–C. Drawing of rectus muscle recession (shaded muscle).
The effect of the recession is greatest when the eye rotates toward the
recessed muscle. (A) The eye rotates toward the recessed muscle, causing
the recessed muscle to tighten, therefore reducing muscle slack. (B) A
rectus muscle resection resulting in muscle slack. (C) The eye rotates
toward the recessed muscle, and the muscle and the muscle slack
increase.
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5.5
7.0
m
MR
FIGURE 11-3. Medial rectus muscle recession. Diagram shows normal
insertion at 5.5 mm posterior to the limbus and a 7.0-mm medial rectus
recession. In primary position, the moment arm (m) has not changed, so
the effect of the recession is to create muscle slack rather than to change
the moment arm.
amount of muscle slack is most accurately determined by measuring the recession from the muscle insertion.8
Note the exponential character of the length–tension curve,
as there is a precipitous loss of muscle force at the end of the
curve when muscle slack is increased (see Fig. 11-1B); this is why
even small, inadvertent inaccuracies of large recessions (6–
7 mm) can cause dramatic changes in muscle force and result
in an unfavorable outcome. Technical mistakes, such as allowing central muscle sag and not properly securing the muscle,
can lead to large overcorrections. For example, each 0.5 mm of
bilateral medial rectus recessions up to a recession of 5.5 mm
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will correct approximately 5 prism diopters (PD) of esotropia.
However, for recessions greater than 5.5 mm, each additional
0.5 mm of recession results in 10 prism diopters of correction
(see chart on inside cover). Thus, an overrecession of only
1.0 mm on a planned 6.0-mm bilateral medial rectus recession
would result in a 20-prism diopter overcorrection. Figure 11-4
shows the proper rectus muscle recession, with the muscle well
secured and no central muscle sag. The best way to prevent
central muscle sag is to broadly splay the new insertion so it is
approximately the same width as the original insertion.
A rectus muscle recession has its greatest effect in the field
of action of the muscle. Figure 11-2 shows that muscle slack
increases when the eye rotates toward the recessed muscle, thus
reducing the rotational force on gaze toward the recessed
muscle. In contrast, eye rotation away from the recessed muscle
causes muscle slack to be reduced. In addition, on rotation away
from the recessed muscle, the recessed muscle is inhibited
(Sherrington’s law), minimizing the effect of the recession in
this gaze. For example, a right medial rectus recession will
produce an incomitant strabismus, with an exodeviation in
primary position and a larger exodeviation in leftgaze with very
little exodeviation in rightgaze. Induced incomitance can correct
incomitant strabismus. If a patient has a small esotropia in
primary position and a large esotropia in leftgaze, a right medial
rectus recession would reduce the incomitance. Comitant strabismus, on the other hand, is best treated with bilateral symmetrical surgery.
Recessions are routinely performed on rectus muscles but
can also be performed on oblique muscles. Inferior oblique
muscle recession is a popular procedure for weakening the inferior oblique muscle. Recession of the superior oblique tendon
has also been described. It not only slackens the superior oblique
tendon but also changes the function of the muscle. A recession
of the superior oblique tendon collapses the normally broad
insertion and moves the new insertion nasal and anterior to the
globe’s equator. This alteration changes the function of the superior oblique muscle and can result in unpredictable outcomes,
including postoperative limitation of depression. A more controlled way of slackening the superior oblique tendon without
changing the functional mechanics of the tendon insertion is
a tendon-lengthening procedure, such as the Wright silicone
tendon expander.
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FIGURE 11-4A,B. (A) Drawing of rectus muscle recession with the
muscle secured to sclera at the recession point posterior to the original
insertion. Note that the new insertion is almost as wide as the original
scleral insertion, and the new insertion is parallel to the original insertion. There is no central muscle sag. (B) Companion photograph shows a
rectus muscle recession with no central sag because the new insertion is
splayed as wide as the original insertion.
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Hang-Back Technique
A hang-back recession suspends the muscle back, posterior to
the scleral insertion, with a suture (Fig. 11-5). This technique
has the advantage of excellent exposure and relatively easy
needle passes through the thick anterior sclera. On the other
hand, hang-back recessions are potentially less accurate than a
fixed recession. Small to medium-sized hang-back recessions of
3 to 6 mm tend to result in overcorrections because they have
inherent central muscle sag (Fig. 11.5). On the other hand, large
hang-back recessions, over 6 mm, tend to produce undercorrections because an otherwise normal muscle will not consistently
retract more than 6 to 7 mm posterior to the insertion. The
surgeon experienced with adjustable suture surgery knows it is
difficult to recess a rectus muscle more than 6 mm using an
adjustable hang-back suture. Large hang-back recessions are
FIGURE 11-5. Hang-back recession. The suture is passed through sclera
at the original insertion and the muscle is suspended posteriorly to
achieve the recession. Inset: Note the caliper is measuring the planned
recession; however, the muscle is overrecessed because of central sag.
Central sag occurs because the new insertion is lax and not splayed as
widely as the original insertion.
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possible if the muscle is tight and contracted, as in the case of
thyroid-associated strabismus, congenital fibrosis syndrome, or
a slipped muscle. Indications for hang-back recessions include a
recession over a retinal buckle, recession over an area of scleral
ectasia, or large recessions, of a tight contracted muscle, if
posterior exposure is difficult. However, for routine strabismus
surgery, the author (K.W.W.) prefers the fixed recession so the
muscle is secured at the desired recession point.
Adjustable Suture Technique
Adjustable suture techniques allow movement of the muscle
position after surgery when the patient is fully awake and the
anesthesia has dissipated (Fig. 11-6). Unlike fixed sutures,
the adjustable suture technique allows for fine-tuning of ocular
alignment in the immediate postoperative period. The adjustable suture procedure is usually performed on recessions in
two stages: in the first stage, surgery is performed under either
local or general anesthesia, and the muscle is placed on a suture
in such a way that the muscle position can be adjusted later.
The second stage, or adjustment phase, is performed when the
patient is fully awake or after the local anesthetic has worn off
(5 h for lidocaine) and the muscle function has returned to
normal. In this phase, the muscle is adjusted to properly align
the eyes and then permanently tied in place. The adjustment
procedure must be performed within 24 to 48 h after the initial
surgery while the muscle is still freely mobile. Later adjustments have not been recommended because the muscle rapidly
adheres to the globe. However, successful in-office reoperation
within the first week of surgery has been described.5 The muscle
is sutured like a hang-back recession, but the suture is tied in
a bowknot or secured by a sliding noose so the position of the
FIGURE 11-6A–C. (A) Bow tie adjustable suture technique. After the
sutures have been passed through the scleral insertion, they are tied
together in a single-loop bow tie. This bow tie can be untied postoperatively to adjust the muscle. (B) Noose adjustable suture. Sutures suspend
the muscle posteriorly, and a noose around the sutures slides up and down
to secure the muscle at the desired position. The ocular alignment is finetuned with the patient awake. The muscle placement is finalized by tying
off the pole sutures, then trimming all loose sutures. (C) Companion
photograph of (B) shows adjustable suture through fornix, with scleral
traction suture holding the conjunctiva superiorly and exposing the
adjustable suture.
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muscle can be easily changed (Fig. 11-6A–C). Adjustable sutures
have limitations similar to hang-back recessions, with the
maximum recession approximately 6 to 7 mm. Central sag
occurs but, because the muscle position can be changed after
surgery, this is usually not an issue. Plan on a slight overcorrection, as advancing an over-recessed muscle is easier than
trying to increase the recession, especially if the recession is
greater than 6 to 7 mm.
The most important indication for an adjustable suture is
complicated strabismus, including paralytic strabismus, largeangle strabismus, reoperations, and thyroid myopathy. In these
situations, the standard tables for surgical measurements do not
apply, and results with the fixed-suture technique are unpredictable. In addition to the more complicated strabismus cases,
many surgeons routinely use adjustable sutures on most cooperative adult patients, even those undergoing uncomplicated,
horizontal surgery. Adjustable sutures are usually used with
recession procedures, as adjustable tightening procedures are difficult to perform.
Patient selection is crucial for successful implementation of
the adjustable suture technique. The adjustment procedure is
somewhat uncomfortable and can evoke substantial anxiety.
There is no specific age limitation for the use of adjustable
sutures, but patients younger than 15 years of age are often too
anxious about medical procedures. Unless a child is exceptionally calm and cooperative, adjustable sutures should be limited
to cooperative adult patients. Strong sedatives before adjustment
should be avoided because sedation influences eye position. The
patient should wear full optical correction when ocular alignment is being assessed during the adjustment procedure to
ensure proper image clarity and control of accommodation.
MUSCLE SHORTENING PROCEDURES
Muscle shortening procedures include muscle resections, tucks,
and plications. These procedures tighten the muscle, but they
do not actually strengthen the muscle. For the most part, they
correct strabismus by creating a tight muscle that acts like a
leash or tether. These procedures produce incomitance, as the
tightened muscle restricts rotation away from the shortened
muscle (Fig. 11-7). For example, a right medial rectus shortening procedure limits abduction of the right eye and creates an
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A
B
C
FIGURE 11-7A–C. Effect of a rectus muscle resection (shaded muscle).
The resection has its greatest effect on gaze away from the resection. (A)
The muscle tightens on gaze away from the resected muscle. (B) A
resected rectus muscle. (C) The muscle slackens on gaze to the resected
muscle.
esodeviation shift that increases in rightgaze. Right medial
rectus tightening would be indicated to correct an incomitant
exotropia that is greater in rightgaze. Note that tightening the
medial rectus muscle does not strengthen adduction but instead
limits abduction. Bilateral medial rectus resections limit divergence and induce an esodeviation greater for distance fixation;
therefore, it is not the answer for convergence insufficiency.
Resection
A muscle resection consists of tightening a muscle by removing
the anterior part of the muscle and reattaching the shortened
muscle to the original insertion site. The muscle resection is the
most popular tightening procedure and is performed on rectus
muscles.
Tuck
A muscle tuck shortens the muscle by folding the muscle and
suturing the folded muscle to muscle. The muscle tuck has, for
the most part, fallen out of favor partially because the muscleto-muscle suturing does not hold well and tends to become
cheese-wire loose over time. A superior oblique tendon tuck or
plication, however, is used for some cases of superior oblique
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palsy, either as a full-tendon plication or plication of the anterior tendon fibers (i.e., Harada–Ito procedure).
Wright Plication
The author (K.W.W.) developed a rectus muscle plication procedure that tightens the muscle by folding the muscle and suturing it to sclera (Fig. 11-8).14,18 With the plication, the muscle is
sutured to the scleral insertion, in contrast to a tuck, where
muscle is sutured to muscle. The muscle–scleral attachment of
A
B
FIGURE 11-8A,B. Wright rectus muscle plication. (A) The muscle is
secured with the suture placed posterior to the insertion at the desired
plication point (usually 6 mm or less). Once the posterior muscle is
secured, the suture ends are passed through the scleral insertion. The
drawing shows the suture secured to the posterior muscle and the doublearmed needles being passed at the scleral insertion. (B) The plication is
completed with the posterior muscle advanced to the insertion. There is
a small roll of redundant tendon that will flatten and disappear 3 to 4
weeks after surgery.
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the plication is more secure than the muscle-to-muscle union
of a tuck.
The plication can be used in place of a standard resection.
Because there is a fold of tendon associated with the plication,
a small lump is present immediately after surgery but disappears
within 3 to 4 weeks. Important advantages of the plication procedure over resection include reversibility. A plication can be
removed by simply cutting and removing the suture within 2
days of the surgery, before the muscle heals to sclera. Another
advantage is safety against a lost muscle. Because the muscle is
not disinserted, there is little risk of a lost muscle. The plication procedure also preserves the anterior ciliary vessels and
reduces the risk of anterior segment ischemia. These advantages
have made the Wright plication popular for small or mediumsized rectus muscle tightening surgeries.
RECESSION AND RESECTION
Resections (or plications) of rectus muscles can be teamed with
a recession of the antagonist muscle same eye to correct strabismus. This monocular surgery is called a recession–resection,
or “R & R,” procedure. The effect of the recession–resection of
agonist and antagonist induces incomitance and limits ocular
rotation in one direction. For example, a right lateral rectus
muscle recession reduces ocular rotation to the right, and a
resection of the right medial rectus muscle also restricts rotation to the right. Limited rotations after an R & R procedure may
improve over several months to years, but some residual incomitance often persists. Because the R & R procedure induces
incomitance, it can be used to treat incomitant strabismus. It is
also useful in treating sensory strabismus, allowing monocular
surgery to be performed only on the amblyopic eye and sparing
surgery to the good eye.
FADEN
The Faden procedure is performed by suturing the rectus muscle
to sclera, 12 to 14 mm posterior to the rectus muscle insertion.
This technique pins the rectus muscle to the sclera so, when the
eye rotates toward the fadened muscle, the arc of contact cannot
unravel. As a result, the moment arm shortens, thus reducing
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the rotational force. The Faden, however, does not significantly
change the moment arm when the eye is in primary position,
and it has no effect when the eye is turned away from the muscle
with the Faden (Fig. 11-9). Thus, a Faden reduces ocular rotational force when the eye rotates toward the fadened muscle and
is used to correct incomitant strabismus.
The weakening effect of the Faden operation by itself is relatively small, so the fadened muscle is usually also recessed as
part of the Faden procedure. The Faden operation works best on
the medial rectus muscle because the medial rectus muscle has
the shortest arc of contact (approximately 6 mm), and a 12- to
14-mm Faden significantly changes its arc of contact. Alternately, a Faden of the lateral rectus muscle has little effect
because the arc of contact is 10 mm, and pinning the muscle at
12 mm does not significantly change this naturally long arc of
contact. For the most part, the Faden operation is indicated to
correct incomitant esotropia by enhancing the effect of a medial
rectus recession, such as in the case of sixth nerve paresis or
high AC/A esotropia. The following case is an example where a
A
FIGURE 11-9A. Faden of rectus muscle. (A) In primary position, the
Faden does not significantly change the moment arm (m).
FIGURE 11-9B–C. (B) Ocular rotation toward the Faden results in shortening of the moment arm (m) as the muscle is pinned to sclera. (C) On
rotation away from the Faden, the moment arm (m) is normal and the
faden has no significant effect. Thus, the Faden weakens the muscle on
rotation toward the fadened muscle.
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Faden and recession of the right medial rectus muscle is indicated. One may rightfully argue, however, that a large (5-mm)
right medial rectus muscle recession would also work without
the difficulty of performing the Faden. As you will see, there is
often more than one way to approach a strabismus.
Rightgaze
Orthotropia
Primary position
Leftgaze
E4
ET 10
ET, esotropia. Surgery: recess the right medial rectus muscle 3 mm with a Faden.
Sixth Nerve Paresis
An example where the Faden may be effective is a partial sixth
nerve paresis and good lateral rectus function. The standard
surgery has historically been a recession of the medial rectus
muscle and resection of the lateral rectus muscle of the paretic
eye, which helps correct the esodeviation in primary position
but does not address the large esotropia that occurs with gaze to
the side of the paretic lateral rectus muscle. Incomitance can be
improved with a recession and a Faden operation of the contralateral medial rectus muscle. A Faden to the contralateral
medial rectus muscle helps correct the esotropia that increases
in the side of the paretic lateral rectus muscle by decreasing the
rotational force of the yoke medial rectus, thus matching the
paretic lateral rectus muscle. Matching yoke muscles only
works if there is good lateral rectus function with no more than
1 limitation of abduction.
High AC/A Ratio Esotropia
Theoretically, the Faden operation reduces convergence at near,
thus lowering the AC/A ratio. Experience with this procedure
indicates that most patients still require a bifocal add to obtain
fusion at near. Augmented bilateral medial rectus recessions
probably work just as well.7 The use of a Faden operation with
a medial rectus recession in high AC/A ratio esotropia patients
remains controversial.
MUSCLE TRANSPOSITION PROCEDURES
Transposition surgery is based on changing the location of the
muscle insertion so the muscle pulls the eye in a different direction (i.e., changes the vector of force). Transposition surgeries
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can be used to treat A- and V-patterns, small vertical tropias,
rectus muscle paresis, and torsion.
Horizontal Muscle Transposition for Aand V-Patterns
See Chapter 9: A- and V-Patterns and Oblique Dysfunction.
Transposition for Small Vertical Deviations
Transposition surgery can correct small vertical deviations by
vertically offsetting the horizontal rectus muscles. A patient
with an esotropia and a small right hypertropia, for example, can
be corrected by a recession–resection procedure of the right eye
with inferior infraplacement of the horizontal rectus muscles.
By transposing the horizontal rectus muscles inferiorly, they act
to pull the eye down, thus correcting the hypertropia. Each horizontal muscle is recessed or resected as specified by the magnitude of the horizontal deviation.
There is approximately 1 prism diopter of improvement in
the vertical deviation per 1 mm of displacement; this is true
when two muscles in the same eye are transposed in the same
direction. Vertical muscle displacements as large as 6 to 7 mm
may be readily performed with this technique. It is most useful
when the surgeon is performing monocular recession–resection
surgery in which both muscles are moved in the same direction
(Fig. 11-10). This surgery, however, is not effective if restriction
is present (e.g., thyroid orbitopathy).
FIGURE 11-10. Full-tendon-width inferior transposition of both horizontal rectus muscles. The muscle on the left has been resected and
infraplaced; the muscle on the right has been recessed and infraplaced.
This technique would be used with a recession/resection procedure to
correct a hypertropia and horizontal strabismus.
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Transposition Procedures for Rectus Muscle Palsy
Three transposition procedures used to correct severe rectus
muscle palsies are described here: Knapp, Jensen, and
Hummelsheim. In a right lateral rectus palsy, there is limited
abduction and a large esotropia that increases in rightgaze. If
there is less than 50% lateral rectus function, the treatment
should be a lateral transposition of all or part of the superior and
inferior rectus muscles. Because the vertical muscles do not contract on attempted abduction, the amount of abduction would
relate to the elasticity or tonic contraction of the transposed
muscles, rather than the active contraction of the transposed
muscles.
KNAPP PROCEDURE
A full-tendon transfer, or Knapp procedure, was originally
described for the management of double elevator palsy. This procedure, however, can also be used for a sixth nerve palsy. The
key for successful surgery is symmetrical transposition to avoid
induced vertical or horizontal deviations. A large posterior dissection to free the muscle of the intermuscular septum and
check ligaments is necessary to mobilize the muscle for the
tendon transfer (Fig. 11-11).
JENSEN PROCEDURE
The Jensen procedure is a split-tendon transfer with the adjacent
muscle tied together but not disinserted (Fig. 11-12). This procedure has the advantage of leaving the anterior ciliary arteries
intact, diminishing the risk of anterior segment ischemia. Even
with the Jensen procedure, however, some vascular compromise
occurs, and anterior segment ischemia has been associated with
this procedure.
HUMMELSHEIM PROCEDURE
The Hummelsheim procedure is a split-tendon transposition
technique designed to preserve anterior ciliary artery perfusion.
Half of each of the two rectus muscles adjacent to the weak
muscle is mobilized. The halves are then transposed and
inserted at the insertion of the weak or lost muscle (Fig. 11-13).
In contrast to the Jensen procedure, the Hummelsheim procedure can be used for a lost muscle, as it does not require the
FIGURE 11-11. Knapp procedure. The
medial rectus (MR) and lateral rectus (LR)
muscles are transposed superiorly to the
insertion of the superior rectus (SR) muscle.
FIGURE 11-12. Jensen procedure. Nonabsorbable sutures tie muscle
halves from adjacent muscles. The final result shows the tendon unions
of superior rectus to lateral rectus and inferior rectus to lateral rectus
muscles. The posterior location of the union is important, and sutures
should be at least 12 mm posterior to the insertions. Anterior union
sutures will reduce the effect of the transposition.
FIGURE 11-13. Hummelsheim procedure. Half of each of the superior
and inferior rectus muscles is transposed to the lateral rectus insertion.
Note that the transposed muscle halves touch the lateral rectus insertion,
and the muscles are sutured together 3 mm posterior to the insertion
(Foster modification).
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presence of the weak muscle. The Hummelsheim procedure is
the author’s procedure of choice for a muscle palsy.
MODIFICATION
OF THE
HUMMELSHEIM
Two modifications of the Hummelsheim procedure, which
increase the effect of the transposition, are described here.
Augmented Hummelsheim Brooks of Augusta, Georgia,
has augmented the Hummelsheim by resecting 4 to 6 mm of the
transposed rectus muscle halves. Resecting some of the transposed muscle halves tighten the transposition, increasing the
leash effect.
Muscle Union Modification (Foster modification)
Increased effect of the Hummelsheim has been suggested if the
transposed muscle is sutured to the paretic muscle. The transposed and paretic muscles are sutured together and then to
sclera, 4 mm posterior the insertion.
Complications of Transposition Surgery
Transposition procedures for rectus muscle palsies can induce
unwanted deviations if there is asymmetrical muscle placement.
In split-tendon procedures, it is important to split and transpose
the muscle equally to prevent inadvertent deviations.
Anterior segment ischemia is always an important consideration. Split-tendon procedures such as the Jensen and Hummelsheim lessen the risks, but even these procedures have been
associated with anterior segment ischemia. The best strategy is
to preserve as many anterior ciliary arteries as possible. A limbal
conjunctival incision disrupts local vessels and may increase the
risk of anterior segment ischemia, suggesting that a fornix incision may be preferable.
Rectus Muscle Transposition for Torsion
Torsional strabismus can be improved by moving vertical rectus
muscles nasally or temporally. Nasal placement of the superior
rectus causes extorsion (corrects intorsion) whereas temporal
placement causes intorsion (corrects extorsion). The opposite
is true for the inferior rectus muscle, with nasal transposition
induces intorsion (corrects extorsion) and temporal transposition induces extorsion (corrects intorsion). Transposition of a
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tendon width (approximately 7 mm) will induce about 4° to 5°
of torsion. Most of the torsional effect is seen in the field of
action of the transposed muscle. If the superior rectus muscle is
nasally transposed 7 mm and the inferior rectus muscle temporally transposed 7 mm, a total of 8° to 10° of extorsion would be
induced, thus correcting 8° to 10° of intorsion. Horizontal rectus
muscle transposition will also produce some torsional changes,
but less than vertical rectus muscle transpositions. Supraplacement of the medial rectus muscle induces intorsion; infraplacement induces extorsion. The opposite is true for the lateral
rectus muscle. It is unusual for a vertical transposition of a horizontal muscle to induce significant torsion. Most cases of torsional strabismus are caused by oblique dysfunction and are best
treated with oblique muscle surgery to correct the torsion. For
example, extorsion associated with bilateral superior oblique
paresis is usually best handled with a bilateral Harada–Ito procedure, not a rectus muscle transposition.
INFERIOR OBLIQUE MUSCLE
WEAKENING PROCEDURES
Surgical management of inferior oblique muscle overaction is
based on weakening or changing the function of the inferior
oblique muscle. Techniques include myectomy, recession, and
anterior transposition. Inferior oblique myotomy is not effective
because the cut ends of the muscle inevitably reunite or scar to
sclera; this causes residual inferior oblique overaction and an
unacceptably high reoperation rate. Myectomy weakens the
inferior oblique, as removing a portion of muscle reduces the
chance of local reattachment. A very large myectomy with surgical transection of the neurovascular bundle virtually eliminates inferior oblique overaction and is termed inferior oblique
extirpation–denervation. Extirpation–denervation may be indicated for severe residual inferior oblique overaction after previous inferior oblique surgery. An inferior oblique recession places
the insertion closer to the origin and induces muscle slack, thus
reducing muscle tension (Fig. 11-14). Apt1 and Elliot4 were the
first to describe the inferior oblique anterior transposition. It is
similar to a recession, but the inferior oblique muscle insertion
is moved anterior to its origin, thus changing the function of the
inferior oblique muscle from an elevator to more of a depressor
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FIGURE 11-14. Inferior oblique recession. The muscle is reattached along
the path of the inferior oblique, but closer to its origin, thus slackening
the muscle.
(Fig. 11-15). The more anterior the placement of the inferior
oblique muscle insertion, the more the muscle becomes a
depressor. This procedure has been shown to be very effective
for treating both primary inferior oblique overaction and inferior
oblique overaction secondary to superior oblique palsy.6
One possible complication of the anteriorization procedure
is postoperative limited elevation. Limited elevation usually
occurs from three possible mechanisms: (1) the new insertion is
too anterior (i.e., anterior to the inferior rectus insertion); (2)
resection of too much muscle (3 mm) at the time of securing
FIGURE 11-15. Inferior oblique anterior transposition. The diagram
shows placement of the inferior oblique (IO) muscle in relationship to
the inferior rectus (IR) insertion. The inferior oblique muscle is placed
1 mm posterior to the inferior rectus insertion. Note that the posterior
inferior oblique muscle fibers are placed posterior to the anterior fibers
and parallel to the inferior rectus muscle (no J-deformity).
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and disinserting the inferior oblique muscle; and (3) anterior
placement of the posterior fibers of the inferior oblique muscle.
Stager described this last mechanism as a common cause for
limited elevation after the anterior transposition procedure. The
posterior fibers of the inferior oblique muscle are important,
as the neurovascular bundle of the muscle inserts into these
muscle fibers. Because the neurovascular bundle is inelastic,
large anteriorizations of the posterior muscle fibers will create
a J-deformity of the muscle, with the neurovascular bundle
tethering the inferior oblique muscle and limiting elevation of
the eye (Fig. 11-16).12a
To prevent postoperative limitation of elevation, the author
(K.W.W.) recommends:
FIGURE 11-16. Full anteriorization of the inferior oblique muscle including the posterior fibers with J-deformity. Anteriorization of the posterior
fibers creates the J-deformity, as the neurofibrovascular bundle tethers the
posterior muscle fibers; this can limit elevation of the eye. Because of this
complication, the author (K.W.W.) does not perform the “J” deformity
anteriorization, except if performed bilaterally for severe dissociated vertical deviation (DVD) and inferior oblique overaction.
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1. Keep the new insertion at or behind the inferior rectus
insertion.
2. Secure the muscle close to its insertion to avoid resecting too much muscle (this would shorten the muscle).
3. Avoid the “J” deformity by keeping the posterior muscle
fibers posterior to the anterior muscle fibers and posterior to the
inferior rectus muscle insertion by at least 3 mm.8,14 The full
anteriorization with a “J” deformity has been used for the treatment of bilateral dissociated vertical deviation (DVD) with inferior oblique overaction. If performed, the full anteriorization
with “J” deformity should be performed bilaterally to avoid
asymmetrical elevation of the eyes.
Graded Recession–Anteriorization
The author (K.W.W.) has reported on a graded recession–
anteriorization approach for the management of inferior oblique
overaction.8,14 This procedure tailors the amount of anteriorization according to the amount of inferior oblique overaction. The
basis of the graded anteriorization procedure is that the more
anterior the inferior oblique insertion, the greater the weakening affect. Table 11-1 lists the inferior oblique placement for a
specific amount of inferior oblique overaction and represents
only a guideline for the management of inferior oblique overaction. The final surgical decision must be based on a combination of factors, including the amount of V-pattern and the
presence of a vertical deviation in primary position. Asymmetrical graded anteriorization is indicated if a hypertropia is
present in primary position; otherwise, consider symmetrical
surgery. More anteriorization of the inferior oblique should be
done on the side of the hyperdeviation. A full anteriorization
(without J-deformity) on the side of the hypertropia and 4 mm
anteriorization on the opposite side will correct approximately
6 prism diopters (PD) of hypertropia. In the case of a unilateral
TABLE 11-1. Graded Recession–Anteriorization of Inferior Oblique
Muscle.
Overaction
Inferior oblique placement
1
2
3
4
4 mm posterior and 2 mm lateral to inferior rectus (IR) insertion
3 mm posterior to IR insertion
1–2 mm posterior to IR insertion
At the IR insertion
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inferior oblique overaction (e.g., associated with congenital
superior oblique paresis), a unilateral anteriorization of 1 mm
will correct approximately 8 to 12 PD of hypertropia.
COMPLICATIONS
Limited elevation after inferior oblique anteriorization has been
discussed previously, but another problem of inferior oblique
surgery is persistence or recurrence of the overaction. A
common cause of residual overaction is incomplete isolation
of the inferior oblique muscle, leaving posterior fibers intact.
It is important to explore posteriorly along the globe for bridging muscle fibers that would indicate missed inferior oblique
fibers.
Weakening procedures of the inferior oblique muscle for
primary overaction only rarely produce a postoperative torsional
diplopia. Even so, an adult patient may complain of a transient
excyclodiplopia after weakening of the inferior oblique muscle.
An important anatomic consideration is the proximity of
the inferior oblique muscle insertion to the macula. A misadventure with a stray needle in this area can cause the loss of
central vision. Another consideration is the course of the inferior temporal vortex vein, which lies underneath the inferior
oblique and can be inadvertently traumatized during surgery.
The proximity of extraconal fat to the inferior oblique muscle
is also an important concern, and fat adherence syndrome
should be kept in mind; this may occur when the inferior
oblique muscle is approached blindly and posterior Tenon’s
capsule is violated. Other possible complications of inferior
oblique surgery include orbital hemorrhage, pupillary dilation,
endophthalmitis, and inadvertent surgery or damage to the
lateral rectus muscle.11 Paramount in avoiding these complications is the clear and direct visualization of the inferior oblique
muscle during its isolation. Blind hooking procedures must be
avoided. Meticulous surgical dissection and hemostasis are the
key to proper exposure and visualization of the anatomy.
SUPERIOR OBLIQUE MUSCLE
TIGHTENING PROCEDURES
The superior oblique tendon can be functionally divided into
the anterior third, responsible for intorsion, and posterior twothirds, responsible for depression and abduction (Fig. 11-17).
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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
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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.
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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
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oblique recession also creates a new insertion site nasal to the
superior rectus muscle, changing the superior oblique muscle
function from a depressor to an elevator. Limited depression has
been described as a complication of the recession procedure. The
superior oblique tenotomy has been popular, but it is an uncontrolled procedure and the tendon ends can separate, resulting in
palsy, or grow back together, causing an undercorrection. A
suture bridge has been used to prevent separation of the tendon
ends, but the suture can act as scaffolding, allowing the tendon
to grow back together. The author (K.W.W.) has developed a procedure to lengthen the superior oblique tendon, the Wright superior oblique tendon expander. This procedure has been very
effective in treating superior oblique overaction and especially
treating Brown’s syndrome.17
Superior Oblique Tenotomy
Superior oblique tenotomy should be performed nasal to the
superior rectus muscle (Fig. 11-20). Guyton’s exaggerated forced
ductions should be performed after tenotomy to verify that the
full tendon was found and tenotomized. Temporal tenotomies
usually have minimal effect, as the superior oblique tendon is
sandwiched between the superior rectus and the sclera. When the
FIGURE 11-20. Berk superior oblique tenotomy performed at the nasal
tendon. (From Ref. 2, with permission.)
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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.
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handbook of pediatric strabismus and amblyopia
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
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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-
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handbook of pediatric strabismus and amblyopia
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
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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.
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