6. HISTORY OF PRESENT ILLNESS
• Pt. was in usual state of health 2yrs back when he
gradually developed heaviness and pain in both eyes
with right sided headache in temporal region.After a
couple of weeks he felt bulging of both eyes as well
with bilateral diplopia on side gaze, condition was
progressive in nature , there were no aggrevating &
relieving factors,it was not associated with
redness,discharge,photophobia and change in
vision,he consulted an ophthalmologist at SHIFA
INTERNATIONAL hospital islamabad,where he was
dignosed as a case of proptosis and was prescribed
oral steroids along with topical lubricants
7. HISTORY OF PRESENTING ILLNESS
• He was also reffered to medical specialist to rule
out thyroid disease as he was also complaining
of frequent vomitting,loss of
appetite,palpitations and diarrhea,where he
was examined and investigated properly.He was
dignosed hyperthyroidism,anti thyroid
treatment was started.He took it for 2yrs but left
it one month ago without the advice of
doctor.Now from last 3 to 4 days he is again
complaining of bulging and pain of both eyes
along with diplopia for which he is taking eye
drops.
9. PAST OPHTHALMIC HISTORY
• He is myopic from last few years and he is
using spectacles of 1.5 diopters in both eyes
for myopic correction.
• No other significant past ophthalmic history
was found.
12. • CARDIO VASCULAR SYSTEM:
• PALPITATIONS PRESENT
• NO BREATHLESSNESS, CHEST
PAIN AND EDEMA FEET
13. SYSTEMIC HISTORY
• RESPIRATORY SYSTEM
• No cough, sputum, hemoptysis,
breathlessness, wheezing and chest pain
• ALIMENTARY SYSTEM:
• Vomiting ( containing food particles)
• Diarrhea present
• No nausea, abdominal pain, dysphagia, heart
burn, constipation, hematemesis, melena
and jaundice
14. SYSTEMIC HISTORY
• URINARY SYSTEM:
• No pain in flanks, dysuria, hematuria,
frequency of micturation, polyuria, oliguria,
nocturia, nausea and vomiting
• NERVOUS SYSTEM:
• Right sided headache in temporal region
• Bilateral Diplopia present on side gaze
• No numbness, giddiness, fits, visual loss
15. • ENDOCRINE SYSTEM
•
•
•
•
Heat intolerance present
Weight loss present
Palpitations present
No polyuria, polyphagia, polydypsia
• MUSCULOSKELETAL SYSTEM:
no joint pain, stiffness, swelling and
restriction of movment.
• SKIN
• No Rash, itch, coloured spots
21. FAMILY HISTORY
Father is diabetic for last 20 years
and is taking oral anti diabetic
treatment.
Mother died of heart attack 1 yr
back.
No other family history of Proptosis,
hyper thyriodism, hypertension,
tuberculosis, asthma and cancer
was present.
31. GENERAL PHYSICAL EXAMINATION
• Neck veins
No pulsation
JVP normal
• AXILLA
• GROIN
• FEET
Lymph Nodes
Lymph nodes
Clubbing
koilonychnia
cynosis
loss of hair
Edema
not palpable
not palpable
Not Significant
34. FUNCTIONAL EXAMINATION :VISUAL ACUITY:
6/18 both eyes with
spectacles 6/6 both
eyes
COLOUR VISION:
normal
VISUAL FIELD:
normal
35. PROPTOSIS EXAMINATION
• INSPECTION
• Bilateral bulging of eyes( front & side views)
• SWALLOW TEST: NEGATIVE
• PALPATION
• BILATERAL AXIAL PROPTOSIS
4-5 mm in both eyes
• SUPERFICIAL PALPATION:
• NORMAL ORBITAL RIM WITHOUT TENDERNESS
• DEEP PALPATION:
• NO ORBITAL MASS ON DEEP PALPATION
36. EXAMINATION OF PROPTOSIS
• EXTRA OCULAR
MOVEMENTS
• ABDUCTION & ELEVATION
DEFECIT & DIPLOPIA IN
SIDE GAZE
• RETROPULSION:
POSITIVE IN BOTH EYES
• NO LYMPHYADENOPATHY
IN ADJOINING AREAS
• AUSCULTATION:
• BRUIT: ABSENT
37. PROPTOSIS EXAMINATION
• Signs checked for bilateral buldging of eyes
• Dalrymples Sign:- +ve
(This is stare due to retraction of upper lid )
• Von Graefes Sign:- +ve
(upper lid lags on downward movement of
eyeball )
38. OCULAR EXAMINATION
• EYELID
• Skin :- Normal on both sides
• Lid Margin:- BILATERAL Upper lid retracted
•
Bilateral Lid lag
• Eyelashes:- Normal on both sides
• INTER PALPEBRAL FISSURE WIDTH
• Pateint value :- 13mm
• Normal range :- 9-11mm
• LACRIMAL SYSTEM
• Drainage system :-Normal
• Regurgitation test –ve
40. OCULAR EXAMINATION
• IRIS :-Normal
• PUPIL:Round and reactive to light
Diameter :- 3mm
• Light reflex :- Normal
• Indirect light reflex :- normal
• LENS :- clear no opacities found
• VITREOUS :- red reflex was intact
41. OCULAR EXAMINATION
• RETINA :Slit lamp :- Mild disc
pallor ( both eyes)
MEASUREMENT OF IOP
BY APPLANATION
TONOMETRY
Pateint value :- 16mmHg
both eyes
(Normal 10-21mmHg)
68. Steroid Therapy for ocular soft tissue
inflammation
• Tab. DELTACORTIL 5mg
6- tab in morning
6- tab in evening
For 1 week
69. TREATMENT…. cont..
• Patient took these medications for almost 2
years with tappered dose but he himself
discontinued the therapy 1 year back.
• Now he is using topical lubricants only.
70. FUTURE OPTIONS
• In case, the symptoms persist
, treatment option for future
include:
• IMMUNOSUPPRESENTS
• SURGICAL DECOMPRESSION OF
ORBIT
• RADIATION THERAPY
74. INTRODUCTION--THYROID EYE
DISEASE
• Seen in 25 – 50% cases of graves disease.
• GRAVES DISEASE also known as BASEDOW’S
DISEASE is an autoimmune disorder that
usually presents in 3rd to 4th decade of life,
affects women more than men, characterized
by a triad of features:
• Hyperthyroidism
• Diffuse thyroid enlargement
• Opthalmopathy
75. INTRODUCTION -- TED
• Thyroid eye disease (TED) may occur in the
absence of clinical and biochemical evidence
of thyroid dysfunction.
• The occurrence of signs of graves disease in a
patient who is not clinically hyperthyroid is
referred to as euthyroid or ophthalmic graves
disease.
• Eye disease may be the first presenting sign of
graves disease.
80. PATHOGENESIS
• This involves an organ specific autoimmune
reaction in which a humoral agent (IgG antibody)
produces the following changes:
• INFLAMMATION OF EXTRAOCULAR
MUSCLES
• INFLAMMATORY CELLULAR
INFILTRATION
81. PATHOGENESIS:
INFLAMMATION OF EXTRAOCULAR MUSCLES
• Pleomorphic cellular infiltration, increased secretion
of glycosaminoglycans,osmotic retention of water.
• Muscles become enlarge( 8 times their normal size,
may compress optic nerve).
• Subsequent degeneration of muscle fibers eventually
leads to fibrosis
• Restrictive myopathy and diplopia.
83. PATHOGENESIS:
INFLAMMATORY CELLULAR INFILTRATION
Infiltration with lymphocytes,
plasma cells, macrophages &
mast cells of interstitial fluid,
orbital fat & lacrimal glands
Increase in volume of
orbital contents
Accumulation of
glycosaminoglycans &
retention of fluid.
Secondary elevation
of intraorbital
pressure.
85. CLINICAL MANIFESTATION
5 main clinical manifestations of TED are:
1… SOFT TISSUE
INVOLVEMENT
(PERIORBITAL & LID SWELLING,
CONJUCTIVAL HYPEREMIA.
2...LID RETRACTION
3…PROPTOSIS
(PASSIVE OR MECHANICAL
PROTRUSION OF EYE BALL)
4…OPTIC NEUROPATHY
(SERIOUS COMPLICATION –
COMPRESSION OF OPTIC NERVE
MAY LEAD TO VISUAL
IMPAIREMENT)
5…RESTRICTIVE
MYOPATHY
(OCULAR MOTILTY IS REDUCED
INITIALLY BY INFLAMMATORY
EDEMA & LATER BY FIBROSIS)
96. DIFFERENTIAL DIAGNOSIS
• ORBITAL CELLULITIS: Onset of proptosis is
earlier & patient has other evidence of
infection. (fever)
• IDIOPATHIC ORBITAL INFLAMMATORY
DISEASE: More painful than thyroid eye
disease.
• OTHER CAUSES OF THICKENED
MUSCLES: sarcoidosis, amyloid, acromegaly.
101. GENERAL MANAGMENT
CONTROL OF OCULAR DISCOMFORT
=Artificial tears
=Topical lubricants
=Sunglasses
ADVISE THE PATIENT TO
=Avoid smoking as it worsens the prognosis
=Avoid dust
=Elevate head when sleeping to avoid periorbital
edema
102. MEDICAL MANAGMENT
CONTROL OF HYPERTHYROIDISM
• Iodine and antithyroid drugs
• Radioactive iodine
ORBITAL DECOMPRESSION
Systemic steroids:
• Oral prednisolone: 60-80mg/day (dose should
be tappered after reduction in symptoms)
• I/V methylprednisolone: 0.5g in 200ml isotonic
saline over 30 min(may be repeated after 48 hrs)
103. SURGICAL MANAGMENT
Surgical treatment when there is severe sight
threatening condition or for cosmetic purpose.
ORBITAL DECOMPRESSION:
(for advanced proptosis & optic nerve compression)
STRABISMUS SURGERY:
(to minimize diplopia)
LID LENTHENING SURGERY
104. OTHER MANAGEMENT OPTIONS
RADIOTHERAPY
FUTURE OPTIONS
• ORBITAL RADIOTHERAPY
CAN BE USED TO TREAT
OPHTHALMOPLEGIA BUT
HAS LITTLE EFFECT ON
PROPTOSIS.
• THE RADIATION(1500-2000
Cgy fractioned over 10 days)
IS USUALLY ADMINISTERED
VIA LATERAL FIELDS WITH
POSTERIOR ANGULATION
• ANTI-TNF α
ANTIBODIES(eg infliximab)
108. Prevalence and relative risk of other
autoimmune diseases in subjects with
autoimmune thyroid disease.
109. • Source
• School of Clinical and Experimental Medicine,
College of Medical and Dental Sciences, Institute
of Biomedical Research, University of
Birmingham, Edgbaston, Birmingham, United
Kingdom. k.boelaert@bham.ac.uk
• BACKGROUND:
• Common autoimmune disorders tend to coexist
in the same subjects and to cluster in families.
110. METHODS
• A cross-sectional multicenter study of 3286
Caucasian subjects was performed(2791 with
Graves' disease; 495 with Hashimoto's
thyroiditis) attending UK hospital thyroid clinics
to quantify the prevalence of coexisting
autoimmune disorders. All subjects completed a
structured questionnaire seeking a personal and
parental history of common autoimmune
disorders, as well as a history of
hyperthyroidism or hypothyroidism among
parents.
111. RESULTS
• The frequency of another autoimmune disorder was 9.67%
in Graves' disease and 14.3% in Hashimoto's thyroiditis index
cases . Rheumatoid arthritis was the most common
coexisting autoimmune disorder (found in 3.15% of Graves'
disease and 4.24% of Hashimoto's thyroiditis cases). Relative
risks of almost all other autoimmune diseases in Graves'
disease or Hashimoto's thyroiditis were significantly
increased (>10 for pernicious anemia, systemic lupus
erythematosus, Addison's disease, celiac disease, and
vitiligo). There was relative "clustering" of Graves' disease in
the index case with parental hyperthyroidism and of
Hashimoto's thyroiditis in the index case with parental
hypothyroidism. Relative risks for most other coexisting
autoimmune disorders were markedly increased among
parents of index cases.
112. CONCLUSION:
• This is one of the largest studies to date to
quantify the risk of diagnosis of coexisting
autoimmune diseases in more than 3000 index
cases with well-characterized Graves' disease or
Hashimoto's thyroiditis. These risks highlight the
importance of screening for other autoimmune
diagnoses if subjects with autoimmune thyroid
disease present with new or nonspecific
symptoms.
113. References
•
Tunbridge WM, Evered DC, Hall R, et al. The spectrum of thyroid disease in a
community: the Whickham survey. Clin Endocrinol (Oxf). 1977;7:481–493
•
Barker JM. Clinical review: type 1 diabetes-associated autoimmunity: natural
history, genetic associations, and screening. J Clin Endocrinol
Metab. 2006;91:1210–1217
•
Tait KF, Marshall T, Berman J, et al. Clustering of autoimmune disease in parents
of siblings from the type 1 diabetes Warren repository. Diabet
Med. 2004;21:358–362
•
Laberge G, Mailloux CM, Gowan K, et al. Early disease onset and increased risk of
other autoimmune diseases in familial generalized vitiligo. Pigment Cell
Res. 2005;18:300–305
•
Kasperlik-Zaluska A, Czarnocka B, Czech W. High prevalence of thyroid
autoimmunity in idiopathic Addison's disease.Autoimmunity. 1994;18:213–216
115. prevalence of patients with
thyroid eye disease
presenting with apparent
unilateral proptosis
116. • SOURCE:
• Orbital Unit of the Department of Visual Science of the
University of Naples “Federico II”
• AIMS & OBJECTIVES:
• The purpose of this retrospective follow-up study is to
evaluate the prevalence of patients with thyroid eye
disease presenting with apparent unilateral proptosis
and determine the occurrence of exophthalmos in
contralateral non-proptotic eye over the time.
Associated features with this event were evaluated.
117. Methods
• A cohort of 655 consecutive patients affected
by thyroid eye disease with a minimum
follow-up of 10 years was reviewed.
Exophthalmos was assessed by using both
Hertel exophthalmometer and computed
tomography (CT). The influence of
age, gender, hormonal status and of different
therapies such as
corticosteroids, radiotherapy and surgical
decompression on this disease progression
118. Results
• A total of 89 patients (13.5%) had clinical
evidence of unilateral exophthalmos at the first
visit. Among these, 13 patients (14%)
developed subsequent contralateral
exophthalmos. The increase of protrusion
ranged from 2 to 7 mm (mean of 4.2). The time
of onset varied from 6 months to 7 years (mean
time: 29 months). Smoking status, young age
and surgical decompression are significantly
associated with development of contralateral
proptosis .
119. Conclusions
• Asymmetric thyroid eye disease with the
appearance of unilateral exophthalmos at the
initial examination is a fairly frequent event,
while subsequent contralateral proptosis
occurs less commonly. However, physicians
should be aware that young patients,
particularly if smokers, undergoing orbital
decompression in one eye may need further
surgery on contralateral side over time.
120. • References
•
Burch HB, Wartofsky L: Graves’ ophthalmopathy: current concepts regarding pathogenesis
and management.
•
•
Hales IB, Rundle FF: Ocular changes in Graves' disease: a long-term follow-up study.
Q J Med 1960, 29:113.
•
•
Gerding MN, Terwee CB, Dekker FW: Quality of life in patients with Graves’ ophthalmopathy
is markedly decreased: measurement by the medical outcomes study instrument.
Thyroid 1997, 7:885-889.
•
•
Bahn RS, Heufelder AE: Pathogenesis of Graves’ ophthalmopathy.
N Engl J Med 1993, 329:1468-1475.
•
•
Gorman CA: Pathogenesis of Graves’ ophthalmopathy.
Thyroid 1994, 4:
•
•
Heufelder AE: Pathogenesis of Graves’ ophthalmopathy: recent controversies and progress.
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