PRACTICE PEARLS
From New Dimensions in Ophthalmology, sponsored by the Washington Academy of Eye Physicians and Surgeons,
and from Pediatric Ophthalmology for Everyone, presented by the Department of Ophthalmology and Vision
Sciences at the Hospital for Sick Children and the University of Toronto
| THYROID EYE DISEASE —David B. Granet, MD, Anne F. Ratner Professor, Departments of Ophthalmology and
Pediatrics, and Director, Abraham Ratner Children’s Eye Center, University of California, San Diego, School of
Medicine
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| Epidemiology of Graves’ ophthalmopathy: present in 10% to 20% of people with thyroid disease (40% concurrently;
30% 6 mo after diagnosis; 10%-20% thereafter); sometimes perceptible to ophthalmologist before patient
aware he or she has thyroid disease
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| Pathophysiology: autoimmune response; unknown which part of immune system involved; fibroblasts target cells;
interleukin (IL)-6, thyrotropin (TSH), and IgF implicated; orbital fibroblasts increase production of glycosaminoglycans,
which are hydrophilic; fibroblasts swell, leading to change in muscle contractility; fibrosis
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| Signs: eyelid retraction, exophthalmos, exposed dry eye, enlarging of extraocular muscles, and optic nerve dysfunction;
patients become disfigured, diplopic, and unhappy; frustrated when told all they can do is wait; usually blame
thyroid for ocular problems (must be educated that problem results from immune dysfunction); “goiter of the eyes”
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| Types: type 1—fibroblasts infiltrate fatty tissue; muscles appear normal; type 2—muscles become enlarged
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| Treatment: 5-step plan; 1) medical and supportive treatment; 2) botulinum toxin (eg, Botox) and prisms as intervention;
3) orbital surgery; 4) strabismus repair (if necessary); 5) eyelid repair (if necessary); pearls—lubricants
increase comfort; restasis unsuccessful; steroids and external beam irradiation do not work well
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| Emotional impact: patients often become depressed; may develop deep glabellar folds (possibly due to similar
process attacking facial muscles); in recent study, patients with moderate-to-severe disease significantly more depressed,
compared to patients with nonophthalmic Graves’ disease; levels of depression and anxiety similar to
those recorded among people with cancer and AIDS; mood changes associated more with disfigurement than diplopia;
psychologic counseling and possibly medication now recommended for people with disfiguring Graves’ ophthalmopathy;
depression resolves after surgery
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| Bony decompression: most common indication reversal of disfigurement; also relieves facial pressure and discomfort;
best results achieved with type 1 (fat removed along with walls); also depends on severity of proptosis
(grade 1, <22 mm; grade 2, 22-25 mm; grade 3, 25 mm); number of walls removed dictates degree of recovery;
patients may appear normal and be within normal range of proptosis, yet seem abnormal to themselves (ask for
old photographs for comparison); new-onset diplopia occurs in 10% of patients
|
 | Complications: lowering of orbit (orbital ptosis; occurs when too much bone removed from floor); unintended
enophthalmos (botulinum toxin can be used adjunctively with orbital decompression; injection of muscles during
surgery prevents them from falling into gaps created by surgery; helps prevent diplopia; sometimes prevents
need for surgery); optic neuropathy (rare; may result from nerve compression); strabismus surgery—evaluate
motility carefully; computed tomography (CT) provides better view of muscles than magnetic resonance imaging
(MRI); multiple examinations over time necessary; operate on inferior recti first, followed by medial, superior,
lateral, and oblique (mnemonic IMSLO [“I’m slow”])
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| Noninvasive treatment: first-line tactic; prisms work well for small deviations, with good patient acceptance; botulinum
toxin more invasive; “not a great cure,” but does provide some relief; consider surgery when patient stable
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| Botulinum toxin: administered before stabilization; use higher dose than for regular strabismus surgery; in study
conducted by speaker, 33% of patients able to avoid surgery; those patients had mildest disease and smallest deviations;
eye may overcorrect (from hypotropic to hypertropic), because fibrosis has not yet occurred (after fibrosis
sets in, muscle able to go only as far as fibrosis allows); also associated with decreased intraocular pressure
(IOP) in upgaze and primary position; untreated, hypotropic patient may experience Bell’s phenomenon, in
which globe rolls up during sleep, with concomitant increase in IOP; patient appears to have glaucoma (10% of
patients in glaucoma clinics actually have undiagnosed thyroid disease); defer surgery until patient completely
stable; avoid muscle recession (resect only tendon whenever possible); warn patients they can be made better but
not perfect
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| Strabismus surgery: operating on only one muscle associated with proptosis; surgery on inferior recti improves
lid retraction (fixation duress; delay any lid surgery until after strabismus repair); associated with refractive
changes (spherical changes >0.5 diopters (D); cylindrical changes of 0.5 to 1.25 D; axis changes >20º (up to 80º;
patients also advised to delay refractive surgery until strabismus repair completed); address oblique as well as rectus
muscles to restore full comitance to gaze; at speaker’s clinic, 33 mo, on average, from diagnosis to completion
of surgery (9 mo from first surgery to completion of case, including orbital repair, strabismus surgery, and lid repair);
radioactive iodine may worsen findings in patient with preexisting eye disease (exacerbates autoimmune attack);
administer steroids at surgery to dampen immune response
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| Clinical challenges: unilateral disease (reason remains mystery); administer steroids at surgery to prevent triggering
response in other eye, which may be affected several years later; action of immunotherapy; disease predictors
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| ADULT STRABISMUS —Dr. Granet
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| Pediatric vs adult treatment goals: with children, goal to establish binocular function; with adults, goal to restore
it; establishing or restoring normal appearance also important
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| Treating adult strabismus: reasons adults delay surgery—never offered or sought care; previous poor experience
with ophthalmologist; told nothing could be done; all educational issues; “almost invariably, we can help the
adult strabismic”
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| Diplopia: in adults, causes of monocular diplopia may be optical (retinal or neuromuscular); specialists usually treat
binocular cases
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| Causes of adult binocular diplopia: paretic strabismus due to cranial nerve palsy; restrictive thyroid disease; decompensated
heterophoria; convergence insufficiency; trauma, eg, fracture of orbital floor; neurologic causes rare but
include myasthenia gravis; scleral buckling after cataract surgery (inadvertent injection of bupivacaine into muscle
causes it to contract into overly restrictive or permissive pattern); cataract surgery may also uncover preexisting
phoria; technical problems after refractive surgery; problem with glasses (high refractive error associated with
higher risk for induced prism)
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| Management: begin with careful evaluation, including contact lens simulation of monovision; counseling; surgery
should come first (may change refractive error); removing scleral buckle may resolve strabismus, with no further
surgery necessary; reviewing patient’s old records may help with management; check glasses; cycloplegic retinoscopy;
check accommodation; prism spectacles, botulinum toxin (if strabismus associated with thyroid disease),
eye exercises, and surgery all helpful
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| Preoperative considerations: check patient on synoptophore to ensure surgery will not induce diplopia; without fusion,
patient will be unable to hold eyes straight; know medications patient taking
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| Surgical considerations: anesthesia (local or general; patient’s tolerance of any anesthesia); operate on untouched
muscles whenever possible (more predictable result), but know when to violate that rule
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| High myope: lateral rectus slides down, making eye turn inward (medial rectus unopposed); treatment involves
raising and shortening lateral rectus, then recessing medial rectus
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| Poor protoplasm: often seen in adults; obtain tissue from elsewhere if necessary, such as from buccal mucosa or
amniotic membrane graft
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| Delaying adjustable sutures: theoretic advantages of waiting 1 wk to adjust include lower risk for infection and for
splinting effect (time allows patient to recover from surgery and sensorimotor system to adjust); absence of patch
improves patient comfort and decreases time in recovery room; in study of nearly 500 patients, speaker and colleagues
showed delay associated with significant improvement in outcomes (26% required adjustment [range
13%-56%]; no significant complications; patient satisfaction high, even among those requiring adjustment)
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| Pearls: “accommodation is king” (remember cycloplegia for adults with strabismus or refractive errors); “fusion is
your friend;” use caution when conferring monovision on patients with preexisting sensorimotor deficit
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| ADNEXAL TRAUMA —Dan D. DeAngelis, MD, Assistant Professor, Department of Ophthalmology and Vision
Sciences, Faculty of Medicine, University of Toronto, ON
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| Overview: most injuries blunt (contusions and hematomas); usually occur anterior to septum, avoiding problems of
motility and vision; >40,000 adnexal injuries occur annually in United States; fireworks important source of injuries
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| Trauma classification: based on severity of injury (superficial, partial, or full-thickness); extent of area; whether
avulsion of medial or lateral canthal tendon; eyelid margin involvement; tear duct structure damaged
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| Questions to consider in patient evaluation: any missing tissue—eyelid has good vascular supply, so if missing
piece found and reattached, chances for success high; status of lacrimal system—eyelid (medial to punctum)
weak (no tarsus) and easily torn by blunt force; any medial damage indicates exploration of lacrimal system; condition
of ancillary structures—levator or canthal tendons; always consider possibility of intracranial damage, even
with seemingly small eyelid wound
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| Eyelid lacerations: management includes copious irrigation with enough sterile water to decrease bacterial load,
then debridement of necrotic tissue; immediate repair ideal, prevents scarring and permits best view of anatomy
(edema develops later); however, can delay repair 3 to 5 days, to allow for resolution of edema and bruising
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| Full-thickness laceration involving lid margin: lower lid—most important step to reapproximate grey line; place
first suture at grey line, tie together, see if wound edges approximate (if not, remove suture, try again); place second
suture at lash line and third (if needed) at posterior mucocutaneous junction (speaker cautions against, as sutures
may rotate internally, rub against eye, and cause corneal abrasion or ulceration); place another suture
through tarsus on spatula needle to anchor tarsus; tie lid margin sutures after orbicularis reapproximated; upper
lid—put sutures in grey line and lash line; keep tarsus suture at partial thickness to avoid Bell’s phenomenon
and corneal abrasion; otherwise, closure technique similar to that for lower lid
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| Lacerations with canalicular involvement: medial lid fragile, easily torn with blunt force; any medial canthal injury
indicates exploration of tear duct system; sometimes can be performed under slit lamp; may see cut end of
canaliculus (white mucosal lining delineates end of canaliculus); finding medial cut end most difficult part of
repair; monocanalicular and bicanalicular intubation available for upper canalicular lacerations; if laceration
not visible, irrigate upper canaliculus and put pressure on sac to express fluid through medial cut end; fluorescein-tinted
viscoelastic (easy to see) can keep system open for intubation; “pigtail” probe not recommended
(may be difficult to remove and can damage entire canalicular system)
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| Intubation: equivalent to placing stent in laceration; monocanalicular intubation (eg, mini Minoka tube) easy to
insert and retrieve if necessary; can also use Ritleng tube (modified probe; avoids trauma associated with placing
hook in patient’s nose); Crawford tubes first choice (gold standard) for treating bicanalicular lacerations;
deep sutures hold lid together in absence of medial tarsus (pass suture through orbicularis); tubes stay in for 3
mo
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Suggested Reading
Dal Canto AJ et al: Intraoperative relaxed muscle positioning technique for strabismus repair in thyroid eye disease.
Ophthalmology 113:2324, 2006; Farid M et al: Psychological disturbance in Graves ophthalmopathy. Arch
Ophthalmol 123:491, 2005; Gomi CF et al: Change in proptosis following extraocular muscle surgery: effects of
muscle recession in thyroid-associated orbitopathy. J AAPOS April 2, 2007 [Epub ahead of print]; Hoerantner R et
al: Model-based improvements in the treatment of patients with strabismus and axial high myopia. Invest Ophthalmol
Vis Sci 48:1133, 2007; Kikkawa DO et al: Botulinum A toxin injection for restrictive myopathy of thyroid-related
orbitopathy: effects on intraocular pressure. Am J Ophthalmol 135:427, 2003; Kikkawa DO et al: Graded
orbital decompression based on severity of proptosis. Ophthalmology 109:1219, 2002; Korn BS et al: Optic neuropathy
associated with botulinum A toxin in thyroid-related orbitopathy. Ophthal Plast Reconstr Surg 23:109, 2007;
Kushner BJ: Perspective on strabismus, 2006. Arch Ophthalmol 124:1321, 2006; Lennerstrand G et al: Magnetic
resonance imaging and ultrasound measurements of extraocular muscles in thyroid-associated ophthalmopathy
at different stages of the disease. Acta Ophthalmol Scand 85:192, 2007; Long J, Tann T: Adnexal trauma. Ophthalmol
Clin North Am 15:179, 2002; Marcocci C et al: A treatment strategy for Graves orbitopathy. Nat Clin
Pract Endocrinol Metab 3:430, 2007; Nunery WR, Tao J: Thyroid orbitopathy. Ophthamology 114:621, 2007;
Scott AB et al: Bupivacaine injection of eye muscles to treat strabismus. Br J Ophthalmol 91:146, 2007; Stemberger
K et al: Update on thyroid eye disease. Compr Ophthalmol Update 7:287, 2006; Wiersinga WM: Management
of Graves ophthalmopathy. Nat Clin Pract Endocrinol Metab 3:430, 2007.
Educational Objectives
The goal of this program is to improve the management of common eye conditions such as thyroid eye disease, adult
strabismus, and adnexal trauma. After hearing and assimilating this program, the clinician will be better able to:
| 1. Discuss the pathophysiology and epidemiology of Graves’ ophthalmopathy.
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| 2. Implement noninvasive and invasive treatment options for Graves’ ophthalmopathy.
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| 3. Identify the most common reasons why adults often delay strabismus treatment.
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| 4. Perform all the major steps involved in managing adult strabismus.
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| 5. Take into account the key consideration for treating patients who have experienced adnexal trauma.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any
identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Dr. Granet spoke at New Dimensions in Ophthalmology, held March 29-30, 2007, in Seattle, WA, and sponsored by
the Washington Academy of Eye Physicians and Surgeons. Dr. DeAngelis gave his presentation at Pediatric Ophthalmology
for Everyone, held April 21, 2006, in Toronto, ON, and sponsored by the Department of Ophthalmology
and Vision Sciences at the Hospital for Sick Children and the University of Toronto. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
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