Transcript document

Case Presentation 12/19
Presenting: clerk 陳豪宏
Instructor: 張丞賢老師
Patient Profile
Name: 謝X莉
 Age: 46 years old
 Gender: female
 Chart number: 24097375
 Date of admission: 2011/12/12
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Chief complaint
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Right eye pain for 1 week.
Present Illness 1
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This 46 years old female suffered from
insidious right eye pain for 1 week. The
accompanying symptoms are red eye,
tearing (od). She had hyperthyroidism s/p
subtotal thyroidectomy on 2011-8-18.
Thyroid orbitopathy with compressive optic
neuropathy was diagnosed this September.
She was admitted to our hospital and
received steroid pulse therapy on
September 5th this year.
Present Illness 2
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After discharge on September 9th. She
came for OPD follow-up on September
14th. Diplopia was still complained. OCT
showed loss of nerve fibrous layer.
She was admitted for operation on
September 20th, during which orbital
decompression (ou) of temporal sides and
muscle recession of inferior rectus were
done.
On December 12th, she was admitted for
steroid pulse therapy and orbital
decompression of nasal sides.
Present Illness Summary
First Decompression
Thyroidectomy
(Temporal Sides)
08/18
09/19~09/23
First Steroid
Therapy
09/05~09/09
Second decompression
12/12~ now(op:12/16)
Past History
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5.
6.
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hyperthyroidism, s/p operation
hypertension(+)
asthma(+)
heart disease(-)
DM(-)
depressive disorder under medical treatment
Operation history:
L-spine s/p operation 1.5 year ago
hyperthyroidism s/p subtotal thyroidectomy on
2011-8-18 at 謝外科
Orbital Decompression on 09/20
Admission history:
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As listed in the Present Illness
Personal History
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6.
7.
Cigarette Smoking : +, 1/2 pack per
day
Alcohol : denied
Occupation history : denied
Contact history : denied
Travel history : denied
Family History: denied family
systemic disease
Allergy History: denied
Nutritional and Mental status
Nutritional Status:
 Weight: 81.6kg; Height: 151.5cm;
BMI: 35.55
 Mental Status:
 Consciousness: alert. Mentality:
normal.
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Current Medicine
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2011-9-13 PSY OPD Dr.葉怡君
EFEXOR速悅XR(Venlafaxine) 1#AM 1#HS
*/PC*28
Estazolam #(Eurodin)管四
#2 QD/HS*
28
Inderal 10mg (Propranolol) #1 BID/PC*
28
Xanax 0.25mg (Alprazolam)管四#1
BID/PC* 28
Zyprexa 5mg (Olanzapine)**** #1
QD/HS* 28
Physical Examination 1
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Vital sign:
BP: 131 / 105 mmHg, PR: 80 bpm, RR: 18 cpm, BT: 37 ℃
<Ophthalmic examination> 2011/12/12
OD
OS
Eyeball
Conjunctiva
Cornea
AC
Iris
Pupil
Light reflex
Lens
25>-----------105------------<24
injection
injection
clear
clear
moderate, clear
moderate-shallow, clear
np
np
4mm
4mm
+/+
+/+
clear
clear
Physical Examination 2
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Fundus
C/D=0.4
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EOM
20
|
35 ---|---45
|
30
C/D=0.7
disc: temporal pale
20
|
45---|---30
|
10
Tonopen: straight: R: 21,22 L: 22,23
Upward: R: 27,28 L: 27,29 Downward: R: 22 L:22
Vod: 0.1x 1/5
Vos: ND/10cm
Orbital CT
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Hypertrophy of extraocular muscles
(all of ou)
Abnormal Lab finding
12/12:
 Hb: 12.0
 MCV: 79.8
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Hct: 35.3
Plt: 502k
Diagnosis
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Thyroid orbitopathy with compressive
optic neuropathy
Plan:
Pulse therapy of Solumedrol 500mg
q12h IV
 Arrange Auto-P, VEP, OCT of disc.
 Orbital decompression under general
anesthesia.
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Progress 12/13
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S: eye pain(-) Red eye ↓
O: EOM:
20
40
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45
20
35
10
35 (od)
10 (os)
Cornea: clear Conjunctival congestion: ↓
Chemosis: ↓ AC: deep, clear
A+P: arrange VEP, OCT of disk today.
Prepare endoscopic decompression
Progress 12/14
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S: eye pain(-)
O: EOM:
20
35
20
45
35 (od)
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35
35
10 (os)
Cornea: clear
Conjunctiva: mild congested
Chemosis: ↓
AC: deep, clear
VEP: delayed potency and amplitude (ou)
A+P: Keep pulse therapy day 2
Progress 12/15
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S: Still blurred vision (ou)
O: EOM:
20
35
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45
20
40
35
35 (od)
20 (os)
Cornea: clear
Conjunctiva: Congestion ↓ ↓
Chemosis: (-)
few SPK in the left lower eye
IOP: 24.7 (os), 20.5 (od).
A+P: Arrange endoscopic orbital decompression
(ou) tomorrow
Operation on 12/16
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Endoscopic orbital decompression done in this morning. (8.00 am)
Procedures taken:
Preparation for anesthesia
Endoscope usage:
Use periosteal elevator to destruct cribriform pyparacea temporally
and posteriorly.
Destruct the ethmoid bone.
Rigid orbital soft tissue with fibrotic membran was noted.
Incision of the fibrotic membrane and let the orbital fat protrude out
from orbital medial wall.
Hemostasis adequately.
The operation was done successfully and the patient returned to the
ward for recovery.
Progress 12/16
S: no obvious pain of wound post-op.
Still blurred vision
 O: Endoscopic wound of the surgery.
Condition fine.
 A+P:
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Discussion
A Brief Introduction of Thyroid Orbitopathy
Thyroid Eye Disease
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Thyroid eye disease has many names:
Thyroid-associated orbitopathy (TAO)
 Thyroid orbitopathy
 Grave's orbitopathy
 Among others
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All these terms mean the same thing:
 inflammation of the tissues around and
behind the eye producing varying amounts
of swelling and scarring.
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Introduction
It is an autoimmune disease.
 There are at least various theories to
explain its cause and development.
 Thyroid eye disease usually occurs in
people with a history of thyroid
problems.
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However, thyroid eye disease can occur
decades before, or decades after, the
development of thyroid gland disease.
Pathogenesis
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The volume of
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GAG secretion by fibroblasts is increased by activated T-cell
cytokines such as tumor necrosis factor (TNF) alpha and
interferon gamma.
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The extraocular
retroorbital connective and adipose tissue
are increased, due to inflammation and the accumulation of
hydrophilic glycosaminoglycans (GAG), principally hyaluronic
acid, in these tissues.
It implies that T-cell activation is an important part of this
immunopathology.
The accumulation of GAG causes a change in osmotic
pressure, which in turn leads to a fluid accumulation and an
increase in pressure within the orbit.
These changes displace the eyeball forward and can also
interfere with the function of the extraocular muscles and
the venous drainage of the orbits.
Pathogenesis (Summary)
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Autoimmune caused Inflammation
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T cell: TNF-a and interferon r
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Fibroblasts: GAG
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Osmotic pressure
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Fluid accumulation and IOP
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Eyeball forward
Venous drainage malfunction
EOM dysfunction
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Risk Factors
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Treatment: Ra-I therapy may be more
likely to lead to the development or
worsening of TO than medication or
subtotal thyroidectomy.
Sex: TO: female > male
According to studies, smoking definitely
makes thyroid eye disease worse.
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increase in the connective tissue volume of
the orbit, but not the extraocular muscle
volumes.
Thyrotropin receptor autoantibodies
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Higher titer -> Higher prevalence and longer
course of TO.
Epidemiology
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Approximately 20 to 25 percent of
patients with Graves' hyperthyroidism
have clinically obvious TO.
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Along with the eye signs of thyroid
hormone excess (lid retraction and
stare), at the time of diagnosis of the
hyperthyroidism.
However, many more patients with
Graves' hyperthyroidism have
evidence of TO in imaging studies.
Clinical Presentations
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proptosis and periorbital edema
Clinical Presentations 2
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The patient may be distressed by the
appearance of his or her eyes.
Possible major symptoms:
sense of irritation
excessive tearing that is often made
worse by exposure to cold air, wind, or
bright lights
eye or retroorbital discomfort or pain
blurred vision
Diplopia
and occasionally loss of vision.
Proptosis
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The degree of proptosis (exophthalmos) is
dependent on the depth of the orbit and
the degree of enlargement of the
retroocular muscles and retroorbital fibrous
and fatty tissue.
The proptosis may be usually symmetric,
but is often asymmetric, and may be
accompanied by a sensation of pressure
behind the eyeballs.
The proptosis may be masked by
periorbital edema, which is a common
accompaniment.
Apparent proptosis
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Many patients with hyperthyroidism have
lid retraction secondary to thyroid hormone
excess.
It leads to stare and lid lag, resulting from
contraction of the levator palpebrae
muscles of the eyelids.
The stare may give the appearance of
proptosis, when none in fact exists
("apparent proptosis").
These signs alone do not indicate the
presence of ophthalmopathy, and subside
when the hyperthyroidism is treated.
Physical Examinations 1
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Inspection of the conjunctivae and
periorbital tissue, looking for chemosis and
periorbital edema.
Determination of the extent to which the
upper and lower lids can be closed.
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Because failure of apposition promotes drying
and ulceration of the cornea.
Assessment of EOM.
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inability to achieve or maintain convergence.
Limitation of upward gaze. It leads to a
characteristic head-back position in order to see
ahead.
double vision.
Physical Examinations 2
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exophthalmometer.
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measurement of the distance between the
lateral angle of the bony orbit and an imaginary
line tangent to the most anterior part of the
cornea.
The upper limit of normal is 20~22 mm.
as high as 30 mm in patients with severe
proptosis.
Visual acuity and color vision should be
assessed by simple reading tests and color
charts, and visual fields should be
evaluated by confrontation.
Assessment of Severity
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NO SPECS by American Thyroid Association
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Class 0 — No symptoms or signs
Class I — Only signs, no symptoms (eg, lid
retraction, stare, lid lag)
Class II — Soft tissue involvement
Class III — Proptosis
Class IV — Extraocular muscle involvement
Class V — Corneal involvement
Class VI — Sight loss (optic nerve involvement)
Differential Diagnosis
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eye signs of thyroid hormone excess
Bilateral eye signs simulating TO:
severe obesity
Cushing's syndrome
orbital myositis
histiocytosis
myasthenia gravis
very rarely: orbital tumors
statin-induced EOM myopathy.
Differential Diagnosis 2
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For possible unilateral TO, space-occupying
lesions of the orbit must be ruled out first.
When necessary, the diagnosis can be
confirmed by ultrasonography and CT.
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It is important not to inject iodinated contrast
material in patients with Graves' disease
especially if radioiodine therapy is
contemplated.
If diagnos is not in doubt, only tests
necessary are:
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serum TSH
Free T4
TSHR antibodies.
Treatment
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treat according to the severity.
Most patients have mild disease and
do not have progression during
follow-up.
The treatment of TO includes
reversal of hyperthyroidism
relief of symptoms
reduction of inflammation in the
periorbital tissues.
Effects of anti-hyperthyroidism
therapies
Subtotal thyroidectomy and
antithyroid drugs do not appear to
have a negative influence on the
course of orbitopathy.
 However, there is increasing evidence
that radioiodine therapy can cause
the development or worsening of
Graves' orbitopathy more often than
antithyroid drug therapy or surgery.
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Symptomatic treatment
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Eye shades
Artificial tears (saline eye drops)
Raising the head of the bed when sleep.
Photophobia and sensitivity to wind or cold
air can be relieved by use of dark glasses.
Glucocorticoids (oral or IV), are the primary
treatment for severe Grave‘s orbitopathy.
Radiation and surgical decompression can
also be used in selected patients.
Therapies for severe TO
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Oral Prednisone:
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Intravenous glucocorticoid pulse
therapy:
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effective treatment for TO. More side
effects. It has been seen to induce liver
failure.
Fewer side effects and better clinical
outcome in
Radiotherapy: benefits controversial
Orbital decompression surgery
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Three major indications:
If glucocorticoid therapy or orbital
irradiation fails to halt progression of TO
If loss of vision is threatened either by
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ulceration or infection of the cornea
changes in the retina or optic nerve
For cosmetic correction of severe
proptosis
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surgery should be avoided for as long as
possible until the disease stabilizes under
corticosteroid suppression
Orbital decompression surgery
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The orbit may be decompressed by
removing the lateral wall, the roof, or the
medial wall and the floor.
Uptodate suggests the last procedure, also
known as transantral decompression.
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the surgeon removes the floor and medial wall
of the orbit to allow decompression.
It does not leave a scar on the face, and avoids
craniotomy.
Result of decompression surgery
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An excellent result can usually be achieved,
with substantial reduction in proptosis and
edema.
However, diplopia usually does not improve
and may worsen, so that eye muscle
surgery is almost always needed later.
Timing of Surgery: Clinical outcome
appears to be better if decompression
surgery is performed after rather than
before glucocorticoid therapy.
Other operations
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Fat decompression surgery:
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Removal of the retroorbital adipose tissue
Bilateral lateral tarsorrhaphy may be
performed to minimize or prevent corneal
damage.
Surgical recession of Muller's muscle and
the levator will correct upper lid
retraction.
However, decompression surgery is
preferable for both of these problems
because it is more effective both
functionally and cosmetically.
Reference
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Uptodate articles:
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2.
Pathogenesis and clinical features of
Graves' ophthalmopathy (orbitopathy)
Treatment of Graves' orbitopathy
(ophthalmopathy)
The End
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Thank you.