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254 19 Thyroid Eye Disease
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•
Upper lid blepharotomy
•
Lower lid retractor recession.
Thyroid eye disease (TED) is a disfiguring and sight impairing autoimmune
condition for which there is currently no cure. It is the commonest cause of gaze
evoked double vision and of unilateral or bilateral lid retraction and/or proptosis.
It can threaten sight through optic nerve compression or severe corneal exposure.
Treatment is dictated by whether the disease is still active.
19.2 Wet or Dry?
Thyroid eye disease begins as an autoimmune inflammation of the eyelids and
orbital contents. During this active phase the periocular tissues are red and swollen,
earning the alternative name of ‘wet TED’. Monitor activity by noting changes
in the classical signs of inflammation [1] (Fig. 19.2). In addition to the visible
signs, active TED usually causes a deep ache in the orbit(s), especially in extreme
positions of gaze.
The inflammatory component, and along with it the ache, subside spontaneously
after several months, leaving behind a widely variable degree of lasting disfigurement and functional impairment. These are the result of fibrosis and hypertrophy
of the eyelid and orbital connective tissue, muscles, and fat. Diagnose inactive
or ‘dry’ phase TED when the clinical signs become stable, and the ache and
inflammatory signs have subsided.
Immunosuppression can modify the active, wet phase, and if given early enough
may even reverse some of the changes. However, because immunosuppression has
TED Activity based on the classical features of inflammation: clinical activity score (CAS) is the sum of
all items present. A CAS ≥ 3/7 indicates active moderate to severe TED
Spontaneous retrobulbar pain
Pain on attempted up- or down gaze
Redness of the eyelids
Redness of the conjunctiva
Swelling of the eyelids
Inflammation of the caruncle and/or plica
Conjunctival oedema
Fig.19.2 Clinical activity score. Scoring of TED severity based on the clinical signs of inflammation
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the potential for serious side effects, reserve it for preventing visual disability
progression (when its benefits outweigh its risks).
Surgery has no place in the management of active wet TED except in rare cases
of sight threatening optic nerve compression unresponsive to systemic immunosuppression. In these patients, urgent surgical decompression of the orbital apex can
prevent blindness. Severe exposure keratopathy may also require urgent surgery.
19.3 Immunosuppression of Active TED
Offer immunosuppression to patients with a Clinical Activity Score [1] (CAS)
≥3. The onset of gaze dependent diplopia is a conservative threshold for starting
immunosuppression. Currently there are four immunosuppression options:
1. Steroids. These are the usual first line agent.
2. Non-steroidal immunosuppressants. Use these as adjunctive, steroid sparing
treatments.
3. Biologics (Monoclonal antibodies). These are still under investigation, expen-
sive, and carry the risk of rare but devastating side effects. Currently they are a
‘last resort’ option, but this is likely to change.
4. Orbital, low dose radiotherapy to limit extraocular muscle fibrosis. Although
this has its strong proponents the evidence base for this modality remains weak.
Sadly not all patients respond to available immunosuppression.
19.3.1 Steroids
The three options for steroids administration are:
1. Weekly high dose Methylprednisolone given intravenously or orally up to a
total cumulative dose of 8 grammes. This is the current European Group
on Graves’ Orbitopathy (EUGOGO) recommendation. Seventy five percent of
patients respond to this regime.
2. Daily oral Prednisolone. Half of patients respond to this, but the systemic
steroid side effects are greater than for weekly methylprednisolone.
3. Two monthly orbital floor depot Triamcinolone injections. This off-label treat-
ment places the steroid directly in the orbit where it is needed. It has the least
risk of systemic side effects as the total body steroid dose is comparatively low.
However, orbital injection carries the added risks of orbital haemorrhage, nee-
dle penetration of the eye and inadvertent intraocular or intravascular injection,
risks that are associated with any periocular injection. Despite these, I have
found it a very effective treatment for moderate TED. It is also a useful test of
clinical activity. The orbital ache of active thyroid eye disease usually improves
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within a couple of days of an orbital triamcinolone injection. Further discussion
of immunosuppression and its risks is beyond the scope of this book.
19.4 Orbital Triamcinolone Injection [2]
19.4.1 Case Selection
Moderate active thyroid eye disease without optic nerve compression.
19.4.2 Protocol
1. Discuss the risk/benefit of this modality with the patient. Emphasise that this is
an off-label use and obtain consent.
2. Administer 40 mg Triamcinolone acetate to the orbital floor.
3. Review in 8 weeks to establish whether there has been any symptomatic
improvement. If there has not, do not repeat. If there has been an improve-
ment, ask whether the symptoms are now returning? If they are, administer
another dose. If not, review again in 8 weeks to make sure that the active phase
is over.
4. Repeat steps 2 and 3 until there is no symptom recurrence on two consecutive
visits.
5. Once the TED is inactive, discuss rehabilitative surgical options if required.
19.4.3 Steps
1. Lie the patient down comfortably in a slight head up position (to reduce orbital
venous congestion). Ask a nurse to hold the patient’s hand for reassurance.
2. Gently shake the bottle of triamcinolone to resuspend the crystals and draw up
the complete 40 mg in 1 ml dose into a 2 ml syringe. Attach a 1” (25 mm)
long 25 G disposable needle and expel the air from the syringe and needle.
3. Ask the patient to gaze at a spot on the ceiling to keep their eyes still.
4. Pull down the lower lid to expose the inferior fornix and slowly insert the
needle, bevel up, at the junction of the lateral 1/3 and medial 2/3. Advance the
needle tangentially to the eye by at least 3/4 of its length until you encounter
the bone of the orbital floor. Look for any needle related eye movement during
needle insertion (the eye should not move). The sharpness of the needle means
that you receive minimal tactile feedback or resistance. Release your pull on
the lower lid.
5. Holding the syringe and needle still, ask the patient to follow small movements
of your other hand to confirm that the eye movements are free and independent
of the needle.
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6. Attempt to withdraw the plunger slightly while keeping the syringe still, to
ensure that the needle tip is not positioned intravascularly. If you obtain blood,
either withdraw the needle slightly and retest or abandon the injection.
7. While holding the syringe steady with one hand slowly inject using the other.
Remind the patient to keep their eye still. Warn them to expect a slight ache
as the injection proceeds. Ask the patient to tell you if their vision becomes
affected during injection (this could be a sign of intraocular injection).
8. Withdraw the needle and immediately apply moderate pressure to the closed
eye for 5 min, to raise the orbital pressure and reduce the chance of orbital
bleeding.
9. Sit the patient up for a few minutes before allowing them to stand (to avoid
postural hypotension). Check whether their vision remains unaffected and warn
them that late bruising may appear. Ensure that they are given a contact number
to report any untoward reaction.
19.4.4 Notes
•
If the lower lid is too tight to pull down easily, administer the injection tran-
scutaneously. To do this place your index and middle fingers on the lateral
1/3 of the lower lid and feel for the orbital rim. Spread your fingers slightly
to stretch the skin between them to ease needle penetration and push the eye
slightly upwards through the lid with your fingertips. Now, with the syringe
needle bevel up and pointing slightly inferiorly, insert it between your two fin-
gers to skim the inferior orbital rim tangentially to the globe. Advance it until
you feel the orbital floor.
•
Give the patient a courtesy phone call two days after injection to check if they
have noticed any symptom improvement, as they may forget this by the time of
their 8-week review.
19.5 Surgical Management of Inactive (Dry) Thyroid Eye
Disease
There is a hierarchy in the surgical management of inactive (‘burnt out’ or ‘dry’)
TED:
(a) Orbital decompression
First consider orbital decompression. This, the highest risk procedure, has the best
chance of restoring a normal appearance. The bone of one or more orbital walls is
removed to allow the orbital contents to prolapse into the extra space so created.
When it is justified, decompression should be performed as the first step of surgical
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rehabilitation as it can affect ocular balance and eyelid position. Orbital surgery is
beyond the remit of this book.
(b) Extraocular muscle recession
TED induced double vision is a consequence of extra ocular muscle fibrosis. A
fibrosed muscle tethers the eye so limiting movement when its antagonist muscle
contracts. At first the diplopia is noticed in the gaze direction opposite to the field
of action of the affected muscle. The inferior rectus is the most commonly affected
muscle causing up-gaze diplopia and often a compensatory ‘chin up’ head posture.
The medial rectus is the second most commonly affected muscle. Any or all of the
extraocular muscles may be affected. The golden rule is only to recess the affected
muscle. Never resect its antagonist. The surgery is as straightforward to carry out
as any squint surgery, but its outcome is less certain.
19.5.1 Tips
The following tips make TED recessions more predictable.
•
Suture the recessed muscle securely to the sclera at the position that it adopts
once separated from its original insertion (with the globe in the primary gaze
position).
•
Suture the muscle directly to the sclera. Do not leave it on a ‘hang-back,
adjustable suture’, as is popular practice. Indirect fixation reduces the likeli-
hood of a strong union at the new insertion site (because of the abnormally
high stresses at a fibrosed muscle’s insertion). A weak reattachment allows late
drift of the muscle insertion when its anchoring suture cuts out or absorbs. This
drift is so prevalent that most strabismus surgeons deliberately under correct
their adjustable sutures in anticipation. By contrast, ‘late drift’ does not occur
if you suture the insertion to the sclera directly.
•
Recessing the inferior rectus increases lower lid retraction because the lower lid
retractor’s origin is the inferior rectus. Separating the retractor origin from the
muscle belly and placing the lower lid on temporary upward traction overnight
prevents this increase in retraction.
19.5.2 Inferior Rectus Recession with Lid Retractor Recession
(Fig. 19.3)
19.5.2.1 Principle
Identify and separate the lower lid retractor origin from the inferior rectus muscle
belly. Pre-place sutures in the existing muscle insertion before detaching it from
the sclera. Suture the muscle back firmly to the sclera in the position it takes up
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a
b
c d
e f
g
Fig.19.3 Inferior rectus recession with lid retractor recession. a Pull the eye upward and incise
the conjunctiva and tenons over the inferior rectus insertion. b Insert a Chavasse squint hook under
the insertion. c Bluntly dissect the inferior rectus muscle sheath from the muscle. d Tear the origin
of the retractor expansion off the muscle. e Pre-place a double armed, 6/0 absorbable suture into the
inferior rectus close to the insertion. f Use double pass, self-locking loops for muscle fixation. g Do
this at either side of the muscle with an additional central bite for security. h Divide the inferior
rectus insertion with Westcott scissors while taking care not to cut the pre-placed sutures. i Insert
both muscle suture needles through partial thickness sclera at the intended recession point and take
further suture bites through the original insertion where the sclera is thicker and stronger. j Make
a second suture pass through the insertion. k Pull the rectus muscle to its new insertion and tie the
suture. l Suture the conjunctiva and tenons closed over the insertion. m Put the lower lid on upward
traction overnight
h
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i j
k l
m
Fig.19.3 (continued)
in primary gaze. Put the lower lid on upward traction overnight so that the lower
lid retractor origin re-inserts itself more anteriorly on the muscle.
19.5.2.2 Case Selection
Dry phase TED patients with a chin up head posture and/or up-gaze diplopia.
19.5.2.3 Steps
1. Pre-place a limbal traction suture at 6 o’clock and pull the eye upward on
traction (Fig. 19.3a).
2. Incise the conjunctiva and tenons horizontally over the inferior rectus insertion
(6–7 mm posterior to the limbus), expose the insertion by blunt dissection and
insert a Chavasse squint hook under the insertion (Fig. 19.3b).
19.5 Surgical Management of Inactive (Dry) Thyroid Eye Disease 261
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3. Bluntly dissect the inferior rectus muscle sheath from the muscle (Fig. 19.3c).
Do this by pushing firmly against the muscle with the flat end of a dry
triangular swab in a posterior direction.
4. Continue the dissection until the sheath appears to be fixed to the muscle
belly itself by interdigitations (roughly at the equator of the globe). These
interdigitations are the origin of the lower lid retractors. They look like the
attachment of the medial check ligament to the medial rectus.
5. Grip these interdigitations with Jayles toothed forceps and tear them off the
muscle in a posterior direction, so separating the origin of the lower lid
retractor expansion from the muscle (Fig. 19.3d).
6. Pre-place a double armed, 6/0 polyglycolic acid, suture with spatulate
1/4 circle needles, into the inferior rectus close to the insertion (Fig. 19.3e).
Use double pass, self-locking loops [1] for each fixation (Fig. 19.3f). Do
this at either side of the muscle with an additional central bite for security
(Fig. 19.3g). Place bulldog clips on the suture ends to retract them from the
operative field.
7. Divide the inferior rectus insertion with Westcott scissors while taking care
not to cut the pre-placed sutures (Fig. 19.3h). Allow the muscle to retract.
8. Temporarily release the limbal traction suture and return the eye to the primary
gaze position. Mark the newly adopted position of the released inferior rectus
on the sclera. This will be between 4 and 8 mm posterior to the original
insertion. Then retighten the limbal traction suture to pull the eye upwards for
ease of access during suturing.
9. Insert both muscle suture needles through partial thickness sclera [2] at the
marked positions (Fig. 19.3i). Check that the scleral bites are strong by slightly
lifting the needle before completing the pass.
Note: The sclera is extremely thin at this point and needle penetration of the eye
is a real risk. Never point a needle towards the eye unless it is your intention
to penetrate the eye! Avoid this risk by placing the needle tip flat (tangential)
against the sclera (Fig. 19.5).
10. Take suture bites through the original insertion where the sclera is thicker and
stronger [3].
11. Take a second bite of the insertion more centrally than the first.
Note: This two-bite configuration introduces friction which makes it easy to
adjust the suture without it slipping.
12. Again, release the limbal traction suture before pulling slowly on the rectus
muscle suture ends to advance the muscle to its new insertion (Fig. 19.3k). Tie
the suture firmly and cut the ends at least 2 mm long to prevent spontaneous
unravelling.
13. Suture the conjunctiva and tenons closed over the insertion to bury the muscle
suture (Fig. 19.3l).
14. Place a tarsal traction suture through the lid margin and put the lower lid on
upward traction overnight. This allows the lid retractor origin to reattach to
the recessed inferior rectus more anteriorly (Fig. 19.3m).
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a b
c d
Fig.19.4 Double locking suture bites. a Take a partial thickness muscle bite over the squint hook.
b With the same suture take a full thickness muscle bite on the posterior slope of the squint hook.
c Loop the first bite suture under the needle tip. d Pull the needle through the loop to lock the suture
19.5.2.4 Notes
1. Double pass, self-locking suture steps:
(a) Take a partial thickness muscle bite over the squint hook. The latter protects
the underlying sclera from the needle tip (Fig. 19.4a).
(b) With the same suture take a full thickness muscle bite on the posterior slope
of the squint hook (Fig. 19.4b).
(c) Before releasing the needle use forceps to loop the first bite suture under
the needle tip (Fig. 19.4c).
Note: Pulling on the loop lifts the needle tip making it easier to regrasp.
(d) Pull the needle through the loop. This magically locks the suture.
2. Scleral suture bites:
(a) Only use a spatulate 1/4 circle needle for suturing to the sclera.
(b) Place the needle tip flat (tangentially) against the sclera (Fig. 19.5a).
(c) Press the flat of the needle tip against the sclera to depress it slightly
(Fig. 19.5b).
(d) Cautiously advance the needle a short distance tangentially through partial
thickness sclera (Fig. 19.5c).
(e) You can check the needle tip’s progress the within the sclera by rotating
the needle slightly to lift the tip (Fig. 19.5d).
(f) Repeat steps c and d as necessary to obtain the length of bite you require.
(g) Rotate the needle out of the sclera when you have achieved the length of
bite that you require (Fig. 19.5e).
(h) Before removing the needle from the sclera, lift it slightly to check the
strength of the bite (Fig. 19.5f).
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a b
c d
e f
Fig.19.5 Scleral suture bites. a Place the needle tip flat (tangentially) against the sclera. b Depress
the sclera slightly with the flat of the needle. c Cautiously advance the needle a short distance tangentially through partial thickness sclera. d Visualize the needle tip within the sclera by rotating
the needle slightly to lift the tip. Repeat steps c and d as necessary to obtain the length of bite you
require. e Rotate the needle out of the sclera when you have achieved the length of bite that you
require. f Before removing the needle from the sclera, lift it slightly to check the strength of the
bite. g Complete the suture pass
g
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