This document discusses Graves disease and thyroid associated ophthalmopathy. Graves disease is an autoimmune disease that commonly presents as a triad of thyroid disorder, eye changes, and skin changes. It is caused by antibodies that stimulate the thyroid gland and cause hyperthyroidism. Treatment options include antithyroid medications, radioactive iodine therapy, or surgery. Thyroid eye disease is an inflammatory disorder of the eye muscles and fatty tissue behind the eyes that is associated with Graves disease. The pathogenesis involves infiltration of tissues by immune cells that causes swelling.

1. GRAVES DISEASE AND THYROID
ASSOSIATED OPHTHALMOPATHY
Presented By : Dr. Liju Rajan
Final yr Postgraduate ASRAM
Moderator : Dr MANAS RANJAN ROUT
ASSOSIATE PROFESSOR
DEPT OF ENT AND HEAD AND NECK SURGERY
ASRAM

2. REFERENCES
• Scott Brown otorhinolaryngology and head and neck surgery- 7th
edition
• Cummings Otolaryngology Head & Neck Surgery- 6th Edition
• Diseases of the Sinuses Diagnosis and Management – David W Kennedy
• Sataloff’s Comprehensive Textbook of Otolaryngology Head and Neck
Surgery
• Stell and Maran head and neck surgery and oncology
• Albert and Jocobiecs principles and practice of ophthalmology – 3rd
Edition
• Ryans retina -6th edition
• Basic and clinical course in Orbit eyelids and lacrimal system –
American academy of ophthalmology.
• Noordens neuro-ophthalmology
• Harrisons principles of internal medicine – 19th Edition
• Bailey and loves short practice of surgery – 26th edition

3. Surgical Anatomy of Orbit- Brief review
• The orbits are the bony cavit ies that contain the globes,
extraocular muscles, nerves. fat, and blood vessels.
• Each bony orbit is pear shaped, tapering posteriorly to
the apex and the optic canal. The medial orbital walls
are considered to be approximately parallel.
• The widest dimension of the orbit is approximately 1 cm
behind the anterior orbital rim.

4. • The paranasal sinuses are either rudimentary
or very small at birth, and they increase in size
through adolescence.
• They lie adjacent to the floor, medial wall, and
anterior portion of the orbital roof.
• The orbital walls are composed of 7 bones:
ethmoid, frontal, lacrimal, maxillary, palatine,
sphenoid, and zygomatic

6. Roof of the Orbit
• composed of the frontal bone and the lesser wing of
the sphenoid
Important landmarks:
• The lacrimal gland fossa, which contains the orbital
lobe of the lacrimal gland
• The fossa for the trochlea of the superior oblique
tendon, located 5 mm behind the superior nasal orbital
rim
• Supra orbital notch, or foramen, which transmits the
supraorbital vessels and branch of the frontal nerve
located adjacent to anterior cranial fossa and frontal
sinus

7. Medial Wall of the Orbit

8. • Composed of the ethmoid, lacrimal, maxillary, and
sphenoid bones
Important landmark:
• Anteromedially lies the fossa for the lacrimal sac,
demarcated by anterior and posterior lacrimal crests.
• The frontoethmoidal suture, marking the approximate
level of the cribriform plate, the roof of the ethmoids,
the floor of the anterior cranial fossa, and the entry of
the anterior and posterior ethmoidal arteries into the
orbit

9. • Anterior part of the lacrimal bone forms a
groove in the orbital surface called the
lacrimal groove houses posterior 2/3rd of the
lacrimal sac.
• The groove extends forward into the frontal
process of maxilla which houses anterior 1/3rd
of lacrimal sac.
• located adjacent to the ethmoid and sphenoid
sinuses and nasal cavity
• medial wall of the optic canal forms the lateral
wall of the sphenoid sinus

10. • The thinnest walls of the orbit are the lamina
papyracea, which covers the ethmoid sinuses along
the medial wall, and the maxillary bone, particularly
in its posteromedial portion. These are the bones
most frequently fractured as a result of indirect, or
blowout, fractures
• Infections of the ethmoid sinuses may extend
through the lamina papyracea to cause orbital
cellulitis and proptosis

11. On the medial orbital wall a ‘rule of 24–12–6’ has been
suggested, based respectively on the average distance (in
mm) from the anterior lacrimal crest to the anterior
ethmoidal foramen, from the anterior to posterior
ethmoidal foramen, and from the posterior ethmoidal
foramen to the optic canal.
On lateral wall of nose The AEA is usually larger than the
PEA and enters the nasal cavity < 20 mm (average 14–18
mm) posterior to the nasolacrimal suture line. The PEA
enters about 10 mm (average 9–13 mm) posterior to the
AEA canal, and the optic canal is located about 4–7 mm
posterior to the PEA canal

12. Lateral Wall of the Orbit

13. • composed of the zygomatic bone and the greater wing of the
sphenoid; separated from the lesser wing portion of the
orbital roof by the superior orbital fissure
Important landmarks:
• the lateral orbital tubercle of Whitnall, with multiple
attachments,
including the lateral canthal tendon,
the lateral horn of the levator aponeurosis,
the check ligament of the lateral rectus,
the Lockwood ligament (the suspensory ligament of
the globe), and
the Whitnaliligament;
• the frontozygomatic suture, located 1 em above the tubercle

14. • Lateral wall is
Located adjacent to the middle cranial
fossa and the temporal fossa
Commonly extends anteriorly to the
equator of the globe, helping to protect
the posterior half of the eye while still
allowing wide peripheral vision
Is the thickest and strongest of the orbital
walls

15. Floor of the Orbit

16. • composed of the maxillary, palatine, and
zygomatic bones
• forms the roof of the maxillary sinus;
• does not extend to the orbital apex but
instead ends at the pterygopalatine fossa;
hence, it is the shortest of the orbital walls
• important landmarks:
the infraorbital groove and infraorbital
canal, which transmit the infraorbital
artery and the maxillary division of the
trigeminal nerve

17. Superior orbital Fissure

19. • The superior orbital fissure separates the greater
and lesser wings of the sphenoid and
• transmits cranial nerves III, IV, and VI;
• the first (ophthalmic) division of cranial nerve
• (CN) V;
• sympathetic nerve fibers.
• Most of the venous drainage from the orbit
passes through this fissure by way of the superior
ophthalmic vein to the cavernous sinus

21. TRIGEMINAL NERVE AND BRANCHES

22. Extraocular Muscles and Orbital Fat
The extraocular muscles are responsible for the
movement of the eye and for synchronous
movements of the eyelids.
The 4 rectus muscles originate in the annulus of Zinn
The levator muscle arises above the annulus on the
lesser wing of the sphenoid.
The superior oblique muscle originates slightly medial
to the levator muscle and travels anteriorly through
the trochlea on the superomedial orbital rim, where
it turns posterolaterally toward the eye.

23. • The inferior oblique muscle originates in the anterior
orbital floor
• Lateral to the lacrimal sac and travels posterolaterally
within the lower eyelid retractors to insert inferolateral
to the macula.
• In the anterior portion of the orbit. the rectus muscles
are connected by a membrane known as the
intermuscular septum. When viewed in the coronal
plane. This membrane forms a ring that divides the
orbital fat into the ilntraconal fat (central surgical
space) and the extraconal fat (peripheral surgical
space).

24. Inferior Orbital Fissure
• The inferior orbital fissure is bounded by the
sphenoid, maxillary, and palatine bones and
lies between the lateral orbital wall and the
orbital floor. It transmits the second
(maxillary)
• Division of CN V, including the zygomatic
nerve and inferior orbital nerve, and branches
of the inferior ophthalmic vein leading to the
pterygoid plexus

26. GRAVES DISEASE

27. Graves Disease
• Is an auto immune disease in general popuation
which usually represent with a triad of
a) Thyroid disorder ( diffuse glandular
enlargement and thyrotoxicosis)
b) Thyroid associated orbitopathy
c) Thyroid associated dermatopathy
• Thyrotoxicosis is defined as the state of thyroid
hormone excess and is not synonymous with
hyperthyroidism, which is the result of excessive
thyroid function

28. • Graves’ disease accounts for 60–80% of thyrotoxicosis.
• The prevalence varies among populations, reflecting
genetic factors
• and iodine intake (high iodine intake is associated with
an increased prevalence of Graves’ disease).
• Graves’ disease occurs in up to 2% of women but is
one-tenth as frequent in men.
• The disorder rarely begins before adolescence and
typically occurs between 20 and 50 years of age;
• it also occurs in the elderly

30. Etio-pathogenesis
• As in autoimmune hypothyroidism, a combination of
environmental and genetic factors, including polymorphisms
in HLA-DR, the immunoregulatory genes CTLA-4, CD25,
PTPN22, FCRL3, and CD226, as well as the TSH-R, contribute
to Graves’ disease susceptibility
• The Chances for graves in Monozygotic twins is 20-30% which
is a stong indicator of function of envionmental factors
• Smoking is risk factor (more for orbitopathy)
• Sudden intake of iodine
• Post partum period
• After anti-retroviral therapy

31. • The presence of TSI causes graves. TSI is
evaluated by TBII asseys. The presence of TBII in
patient with thyrotoxicosis implies TSI
• TPO is also positive in 80%
• TSI can cause placenta and cause intrautrine or
neonatal thyrotoxicosis.
• Because the coexisting thyroiditis can also affect
thyroid function,
• There is no direct correlation between the level
of TSI and thyroid hormone levels in Graves’
disease

33. Clinical Manifestations
1) Signs of thyrotoxicosis

34. • The clinical presentation depends on the
severity of thyrotoxicosis, the duration of
disease, individual susceptibility to excess
thyroid hormone, and the patient’s age.
• In the elderly, features of thyrotoxicosis may
be subtle or masked, and patients may
present mainly with fatigue and weight loss, a
condition known as apathetic thyrotoxicosis.

35. • Neurological manifestations
• Other prominent features include hyperactivity,
nervousness, and irritability, ultimately leading to a
sense of easy fatigability in some patients.
• Insomnia and impaired concentration are common;
• Apathetic thyrotoxicosis may be mistaken for
depression in the elderly.
• Fine tremor is a frequent finding.
• Hyperreflexia,
• Muscle wasting
• proximal myopathy without fasciculation.
• Chorea is rare.
• Thyrotoxicosis is sometimes associated with a form
of hypokalemic periodic paralysis

36. Cardiovascular Manifestations
• ST
• SVT
• AF
• Wide pulse pressure
• Bounting pulse
• Aortic systolic murmer
• palpitations
Increased CO and force of
contraction

37. Dermatopathy
• The skin is usually warm and moist
• sweating and heat intolerance, particularly during
warm weather.
• Palmar erythema,
• onycholysis,
• less commonly, pruritus, urticaria,and diffuse
hyperpigmentation may be evident.
• Hair texture may become fine, and a diffuse
alopecia occurs in up to 40% of patients.

38. Dermatopathy specific to graves
• Pretibial myxodemia
• Thyroid achropathy

39. Other Manifestations
• Diarrhoea
• Seatorrhoea
• Oligomenorrhoea or amonorrhoea
• Loss of libido
• Gynacomastia
• Osteoporosis
REDUCED GI TRANSIT TIME

40. • Thyroid gland diffuse enlargement. The
enlargement will be equal in both lobe and
isthumus
• Firm but non nodular mass
• Bruit is present.

41. DIAGNOSIS
• TFT-TSH/FT4 FT3
• Anti TSH ab ->95% sensitivity & specificity for
diagnosis
• Anti TBG ab/ Anti TPO ab found in up to 80% of
Graves’ disease (also 15 % healthy women & 5% of
men)
• Thyroid scintiscanning with Tc 99 /I 131 in doubt
about the nature of the goiter or thyrotoxicosis
without hyperthyroidism is suspected.
• ANA levels are elevated without evidence of SLE or
other ARD’s

44. Treatment
• 3 modalities of treatment is available
a) antithyroid drugs
b) RAI
c) Thyroidectomy.

45. • Main anti thyroid drug include
Propyl thyouracil
Carbimazole
Methimazole
• All inhibit the function of TPO, reducing oxidation
and organification of iodide.
• These drugs also reduce thyroid antibody levels
by mechanisms that remain unclear
• Propylthiouracil inhibits deiodination of T4 → T3.

47. • Because of hepatotoxicity and short half life
PTU usage is limited to
– 1st trimester of pregnancy
– Adverse reaction to methimazole
– In case of thyroid stom

48. • There are many variations of antithyroid drug
regimens. The initial dose of carbimazole or
methimazole is usually 10–20 mg every 8 or
12 h, but once-daily dosing is possible after
euthyroidism is restored.
• Propylthiouracil is given at a dose of 100–200
mg every 6–8 h, and divided doses are usually
given throughout the course

49. TITRATION REGIMEN
• The initial high starting dose (CBZ -40, PTU-
300) of antithyroid drugs can be gradually
reduced as thyrotoxicosis improves
• The dosing continued for 6-18 months with
maintainance dose of 10-15 mg
• First 6 weeks monitor only FT4 and FT3 and
not TSH

50. BLOCK REGIMEN
• High doses of drugs (PTU-300, CBZ-40) is started.
• The TFT are monitored (FT4 and FT3) and
accordingly levothyroxine is started.
Propranolol (20–40 mg every 6 h) or longer-acting
selective β1 receptor blockers such as atenolol
may be helpful to control adrenergic symptoms,
especially in the early stages before antithyroid
drugs take effect

51. RADIOACTIVE IODINE
• Radioiodine causes progressive destruction of thyroid
cells and can be used as initial treatment or for
relapses after a trial of antithyroid drugs.
• There is a small risk of thyrotoxic crisis after
radioiodine, which can be minimized by pretreatment
with antithyroid drugs for at least a month before
treatment
• Carbimazole or methimazole must be stopped 3–5 days
before radioiodine administration to achieve optimum
iodine uptake.
• Propylthiouracil appears to have a prolonged
radioprotective effect and should be stopped for a
longer period before radioiodine is given, or a larger
dose of radioiodine will be necessary.
• Note : RAI some cases worsens orbitopathy

52. • The dose is calculated on base of clinical features
( thyrotoxicosis, Gland swelling and radioactive
iodine uptake).
• Generally dose of 370 – 555 Mbq is preffered.
• Pregnency and lactation are contra-indication.
• Avoid contact with pregnant women for 7 days
• Radiation thyroiditis- 2wks
• 2-3 months of antithyroid drugs after RAI
• 2nd dose if needed.

53. THYROID ASSOSIATED ORBITOPATHY.

54. • Thyroid eye disease (TED; also known as Graves
ophthalmopathy, dysthyroid oph thalmopathy,
thyroid-associated orbitopathy, thyroid
orbitopathy, thyrotoxic exophthalmos, and other
terms) is an autoimmune inflammatory disorder
whose underlying cause continues to be
elucidated
• The clinical signs, however, are characteristic and
include 1 or more of the following: eyelid retract
ion, lid lag, proptos is, restrictive extraocular
myopathy, and compress ive optic neuropathy

55. PATHOGENESIS
• Infiltration of tissues by immunocompetant cells early
in disease process and subsequent volume expansion.
• Infiltrate consists of CD4 T- Lymphosite and mast cells
in EOM, Orbital fat, intestitial space and connective
tissue.
• IFN-Gamma, TNF- Alpha, IL-1 are seen adjacent to it
which signifies cytokine producrion.
• Cytokines secreted by Th lymphocytes activate CD8+
lymphocytes and autoantibody-producing B cells,
which strengthens the immune reaction.
• These cytokines stimulate the synthesis and secretion
of glycosaminoglycans (GAGs) by fibroblasts.

56. • Unlike fibroblasts from other parts of the body, orbital
fibroblasts express CD40 receptors, generally found on B
cells.
• When engaged by T-cell- bound CD 154, several
fibroblast proinflammatory genes are up-regulated,
including interleukin-6 (I L-6), 1 L-8, and prostaglandin E,
(PGE,).
• In turn , synthesis of hyaluronan and glycosaminoglycan
(GAG) is increased.
• The up-regulation of GAG synthesis is known to be
essenti al in the pathology of TED, and it occurs at a rate
that is 100 -fold greater in orbital fibroblasts deri ved
from patients with TED than in abdominal fibroblasts in
the same patients
• Role of TSH-R in Graves is not fully understood but under
study.

57. GAG deposited in orbital tissue
GAG accumulates water and fatty connective
tissue
Increased orbital volume
Proptosis
Compressive optic neuropathyEOM RESTRICTION

58. Clinical Features
• Lacrimation
• Gritting sensation in eye
• Discomfort
• Photophobia
• Eye lid erythema
• Canaliculus and conjunctival
Injection
Conjunctival oedema
Early symptom

61. • Alternating upper and lower eye lid retraction
signifies a active disease
• Lid retraction – staring look called dalrimple
sign
Upper lid retraction It is due to increased
sympathomymetic tone of fibrosis of LPS
Lower lid retraction due to proptosis

62. PROPTOSIS
• Proptosis
Due to fat expansion ( seen in young)
Due to fat expansion and muscle expansion
( seen in old)
This lead to compressive optic neuropathy
Proptosis measured Using hurtles
exopthalmeter
21-24 mm – grade 1
24- 27mm – grade 2
27-30 mm - grade 3
Above 30 - grade 4

63. Inadequate eye closure due to
Lid retraction
Proptosis
Excessive moisture absorbtion
EXPOSURE KERATITIS
Inferior rectus fibrosis
Decreased function of lacrimal gland due to
inflammation
Reduces bells phenominon

65. EOM RESTRICTION
Diplopia and can be tested using maddox rod
Due to proptosis aswell as fibrosis of muscle due
to constant inflammation
EOM affected are IR>MR>SR>LR>SO
Raise in IOP is seen in patients on upgaze due to
pressure exerted on globe by fibrosed IR muscle

66. Visual loss
Compressive optic neuropathy less common in
people with severe proptosis
Patients with bulkey EOM present with Optic
neuropathy.
RAPD – Marcus gunn pupil
Normal optic disc usually ( retrobulbar neuritis)
rarely disc oedema. But late stages present with
optic atrophy
Raised IOP

68. • Colour vision – affected Ischeras chart
• Visual field – May or may not present with
scotomas. Arcuate, subarcuate and para
central scotomas are most common

69. CLINICAL STAGES
• Active inflammatory stage
• Static stage (no clinical improvement but no
progression)
• Quesent stage ( gradual improvement)

71. Diagnosis

72. GRAVES DISEASE AND THYROID ASSOSIATED
OPHTHALMOPATHY – part 2
Presented By : Dr. Liju Rajan
Final yr Postgraduate ASRAM
Moderator : Dr CP DAS
PROFESSOR AND HOD
DEPT OF ENT AND HEAD AND NECK SURGERY
ASRAM

73. Treatment
1. Treatment for the gland – Already mentioned
2. Supportive care
3. Systemic Steroids
IV steroids
Oral steroids
4. Radiation Therapy
5. Surgery

74. TREATMENT PLAN

75. TREATMENT OF OPHTHALMOPATHY:
SUPPORTIVE MEASURES
• Lubricating eye drops- to avoid exposure
keratopathy
• Cool compresses- reduce inflammation
• Head elevation when sleeping- reduce fluid
retension
• Avoid smoking
• Prism Glasses diplopia of small deviation up to 30
digree
• Eye occlusion in cases of large deviation
• Salt restricted diet
• Sunglasses - photophobia

76. TREATMENT OF OPHTHALMOPATHY:
MEDICAL MANAGEMENT
STEROIDS
ORAL – Oral prednisilone preffered 60-100 mg used as a single
dose In the morning.
IV Steroids – Used 1 gm daily dose on 3 times a week. Equally
Effective as oral steroids with less side effects
Peribulbar injection – Triamcelone acetonate is used. 20 mg is
Injected in single dose. Once a week. Less systamic side effect
Other modalities of treatment include treatment with cyclophosphamide,
Ticlopidine and intravenous immunoglobulins

77. TREATMENT OF OPHTHALMOPATHY:
ORBITAL RADIATION THERAPY
• The treatment modality is controversial. There
are studies supporting orbital radiation as a
treament modality as well as studies which
are not supporting.
• Normaly 2000 rads are given over 10 days 200
rads per day on alternate days in eatch orbit.
Anterior structures like eye ball and lacrimal
glands are covered to avoid side effect.

79. TREATMENT OF OPHTHALMOPATHY:
SURGICAL MANAGEMENT
• Surgical treatment of Graves’
• ophthalmopathy includes decompression of
the orbit,
• strabismus surgery, and
• eyelid retraction repair.

80. ORBITAL DECOMPRESSION
• Surgical decompression creates more space for the
swollen tissues by expanding the walls of the orbit
(bony decompression) or by removing excess orbital
fat (fat decompression)

81. INDICATIONS OF ORBITAL DECOMPRESSION
• Optic Neuropathy – to decompress intraorbital
part of optic nerve, avoid ischemia and better
visual field
• Excessive proptosis with exposure keratitis - To
maintain a transparent cornea
• Before strabismus surgery – Release of tight
EOM during surgery worsens proptosis
• Avoid steroid dependence
• Severe pain
• Cosmetic purpose

82. 4 types of decompression
1 wall decompression – 0-4mm reduction in
proptosis
2 wall decompression – 3-7mm reduction in
3 wall decompression - 6-10 mm reduction
4 wall decompression - 10-17 mm reduction

83. • Ethmoid air sinus in medial wall and maxillary
sinus in inferior wall provide maximum space.
• Temporal fossa and deep bony latral orbit also
provide space
• Orbital roof provide least space.

86. Medial wall decompression
• Preferred approach – by most of surgons
• In a patient with optic neuropathy the optic
nerve has to decompressed.
• Only Medial wall decompression will give
sufficient view of orbital apex
4 pproaches- transnasal endoscopic
Trans antral
Trans cutaneous
Trans caruncular

87. Trans-Nasal endoscopic approach
orbital decompression
• Pre op CT for assesment
• Patient in reverse tendelenberg position. Under
GA
• Nasal packing done for decongestion with
coccane or adrenaline

88. Wide MMA
• an endoscopic wide maxillary antrostomy is
performed in the standard fashion
Anteriorly – post border of NLD
Inferiorly – Inferiorly to Inferior turbinate
Posteriorly – Posterior limit of sinus
MMA should be enough for visualisation of infra-
orbital nerve and contents medial to it.
MMA should not get blocked by orbital contents
and result in a sinusitis.

89. Endoscopic ethmoidectomy
• The anterior and posterior ethmoids are exenterated
• Care is taken to remove every air cell superiorly to the
skull base and laterally to lamina
• lamina papyracea that should be completely
skeletonized.
• Fronto – ethmoid recess exposed.
• Mucosa is preserved along Roof and middle turbinate
to avoid later adhesion with orbital contents.

90. Endoscopic sphenoidectomy
• Usually sphenoidectomy is not required but if
a visual imparement is present
sphenoidectomy is done to visualize optic
nerve.
• The sphenoid is opened widely
• The sphenoid cavity should be inspected to
identify the bulge of the optic nerve and the
carotid artery

92. Medial wall decompression
• The infraorbital nerve is visualized with a 30° or
70° endoscope, as it courses from posterior to
anterior along the roof of the maxillary antrum
• a thin spot is chosen anteriorly on the medial
orbital wall to break through the bone
• Often, the orbital wall bulges in a convex fashion
due to the expanding orbital contents
• The periorbita is bluntly dissected off the bone
with a Cottle elevator

94. • Care taken – peri orbita should not be
puntured at this point
• Medial wall removed up to NL sac
• Medial orbital floor up to inferior orbital nerve
removed.
• A small medial orbital strut of bone at the
posterior maxillary-ethmoid junction in an
attempt to minimize inferomedial
displacement of the muscle cone.

95. • We also leave intact some of the orbital bone
just below the frontoethmoid recess so that
the prolapsing orbit will not obstruct the
frontal sinus outflow
• If the orbital bone is bowed medially in such a
way that it obstructs the frontoethmoid
recess, then it is helpful to remove a small
portion of the adjacent middle turbinate.

96. Incision of periorbita

97. Incising periorbita
• Parallel incisions approximately 3 to 4 mm apart
are made through the periorbita from posterior
to anterior
• The inferomedial periorbita is the last to be
incised
• Gradual massaging of the eyes.
• Intraoperatice measurement of proptosis
• Gelatin filim placed between middle turbinate
and orbit to avoid adhersion
• Avoid nasal packing

99. Video

100. Trans antral approach
• Curved Sublabial incision with standard
caldwell-Luc antrastomy and ethmoidectomy
perfomed.
• Mucosa over maxillary sinus roof stripped off
• Inf.orb.N identified.
• Maxillary roof medial to ION removed with
drill or osteotomies.
• Medial wall of orbit fractured and removed

101. • Incision over periorbital fascia from posterior
to anterior.
• Herniation of orbital fat through incision.
• No of incision depends on degree of proptosis
• Plan incomplete reduction because 1-2mm
reduction may be present in post op period.

102. Optic cannal decompression
• In general, surgical decompression should be
contemplated only for those patients with
acuity of 20/40 or worse,
do not improve on megadose steroids
relapse after the steroids are tapered.
Coexisting trauma,
visual field defect.
color vision involvement
poor pupillary response

103. • After sphenoidotomy the angled endoscope
inserted.
• Optic canal bulge and bulge for ICA identified.
• Bone over the optic nerve is drilled of until
thin piece of bone is left over with copious
irrigation
• The thin bone is fractured and elevated
exposing dura of the nerve.
• Optional incision over dura to expose nerve.

104. Orbital fat decompression
• Orbital fat decompression or removal can be
used either in isolation, or in conjunction with
other bony decompression procedures.
• Vital structures and EOM identified.
Intervening fat is cauterized with bipolar
cautery.

105. Latral wall decompression
• lateral orbital wall can be accessed via a hidden
eyelid crease
• Lateral orbital rim can be removed or preserved.
• Advantages to leaving the rim intact include
– decreased surgical time to remove and replace the
bone flap,
– lack of imaging artifact postoperatively,
– preservation of the lateral canthal tendon
attachments,
– ability to measure postoperative proptosis using an
exophthalmometer against the lateral orbital rim.

106. • For cases in which the rim is removed, it can
be secured by wiring or titanium miniplates or
portex implant
• Anterior decompression allows the contents
into infratemporal fossa while the posterior
aspect of lateral wall to be thinned.

107. Three wall decompression
• Include decompression of medial wall, inferior
wall and latral wall
• Medial wall and lateral wall can be
decompressed in 2 different approaches

108. 4 wall decompression
• Very rarely done
• Only if 3 wall decompression is ineffective
• Increased morbidity
• Fronto temporal craniotomy approach

109. Complications

110. Strabismus Surgery

112. Eye lid surgery