1) The document discusses diseases of the orbit including anatomy, causes of proptosis, orbital infections like cellulitis, dysthyroid ophthalmopathy, and orbital inflammatory pseudotumors. 2) Evaluation of proptosis involves taking history of onset and symptoms, examining for signs of inflammation, restricted eye movement, and proptosis measurement. Investigations include imaging and biopsy. 3) Orbital cellulitis is a serious infection behind the orbital septum treated with intravenous antibiotics and possibly surgery. Dysthyroid ophthalmopathy causes eye changes like proptosis and diplopia managed initially with oral steroids.

1. Diseases of the Orbit
for 4th year medical students
2020
Mahmoud Farouk, MD, FRCS
Assistant Professor of Ophthalmology
Sohag University

2. Anatomy
 The orbit is a pear-shaped cavity, the stalk of which is
the optic canal.

3.  4 walls: roof, floor, medial and lateral.

4. ● The medial walls of the two orbits are parallel, and
the lateral walls form an angle of almost 90 degrees
with one another.

5. Orbital Fissures & Foramina
The superior orbital fissure
 Superior and inferior divisions of the oculomotor nerve (3rd)
 Trochlear n. (4th)
 Lacrimal, frontal, nasociliary n. (5th)
 Abducens n. (6th)
 Sympathetic fibers
 superior ophthalmic vein
The inferior orbital fissure
 Maxillary nerve
 Inferior ophthalmic vein
Optic Canal:
 Optic N.
 Ophthalmic A.

6. Proptosis

7. Definition
Anterior displacement (or protrusion) of one or both
globes
■ The normal distance from the lateral orbital rim to the corneal
apex (in adults) is 14 to 21 mm.
■ A distance > 21 mm or a 2mm difference between the two eyes is
generally abnormal.

8. Causes (Etiology)
1) Congenital: Dermoid cyst, Meningio-enchephalocele
2) Traumatic: Hematoma
3) Inflammatory:
a) Acute: Orbital cellulitis - CST
b) Chronic: Idiopatic orbital inflammatory diseases.
4) Neoplastic:
a) 1ry: lacrimal gland tumers – Optic nerve tumers – Rhabdomyosarcoma –
lymphoma – Hemangioma.
b) 2ry: metastatic (breast – lung)
c) Extension from near by structures (cancer maxilla – Retinoplastoma)
5) Vascular: AV shunt – Varices.
6) Endocrine: Dysthyroid ophthalmopathy

9. Clinical evaluation of a
case of proptosis
 History
 Examination
 Investigations

10. (A) History
1) Ocular:
Proptosis: Onset, course, duration
Pain
Diplopia
Visual impairment
2) Trauma
3) ENT - Medical - Neurological

11. Proptosis
Onset, duration & course
 Sudden : hemorrhage
 Acute: Inflammations
 Intermittent:
1. Orbital varices (90 %) increases on bending forward
2. Recurrent hemorrhage (hemophilia)
3. Vascular tumor
 Chronic progressive:
1. Neoplastic
2. Chronic inflammatory

12.  Pain: Inflammatory & Malignant causes.
 Diplopia: caused by limitation of ocular motility:
1. Restrictive myopathy (dysthyroid ophthalmopathy)
2. Neurological lesion
3. Blow-out fracture
4. Optic nerve sheath meningioma
 Visual impairment
1. Optic nerve compression
2. Exposure keratopathy
3. Choroidal folds

13. (B) Examination
1. Exclusion of Pseudo-proptosis
2. Routine ocular examination
3. Specific orbital examination
4. Systemic: ENT – Medical - Neuro

14. 1) Exclusion of Pseudo-proptosis
 Causes:
1. Large ipsilateral globe (high myopia, buphthalmos).
2. Contralateral enophthalmos (contralateral small globe)
3. Asymmetric orbital size (congenital, post-irradiation,
post-surgical)
4. Asymmetric palpebral fissures (usually caused by
ipsilateral eyelid retraction or contralateral ptosis)

17. (2) Routine ocular examination
1. Visual acuity: decrease in exposure keratopathy
and optic nerve compression.
2. Slitlamp : Cornea
3. Pupils: APD in optic nerve compression
4. Ocular motility: may be limited
5. IOP) may increase
6. Fundus : Papilledema – optic atrophy – choroidal
folds

18. (3) Specific orbital examination
 Inspection
 Palpation
 Auscultation
 Compression (Retropulsion)
 Sensation
 Measurement of proptosis
 Forced duction test

19. 1. Inspection
1) Laterality:
 Unilateral: inflammations - tumors.
 Bilateral: Thyroid.
2) Direction of proptosis:
 Axial: Dysthyroid ophthalmopathy - Tumors within the muscle
cone (optic nerve tumors or Cavernous hemangioma)
 Non-axial:
a. Down & out: mucocele of the frontal sinus
b. Down & in: lacrimal gland tumors
c. Upwards: maxillary carcinoma
d. Downwards: brain meningioma
3) Pulsations: C-C fistula
4) Lid and conjunctival signs of inflammations

20. Dysthyroid ophthalmopathy

21. Intraconal tumors (Cavernous hemangioma)

22. Optic nerve tumors

23. 2. Palpation
 Bony erosion or a mass.
 The degree of tenderness (inflammatory)
 Pulsations
3. Auscultation
 The detection of a bruit should suggest a
carotid-cavernous fistula
 It is synchronous with the heart

24. 4. Compression (Retropulsion)
 Increased resistance to retrodisplacement
of the globe (retropulsion), suggests the
presence of a retrobulbar mass, but it
may also occur with dysthyroid
ophthalmopathy.

25. 5. Sensation
 Hypoesthesia of the cheek and lip is a
typical finding in patients with blow-out
fracture because of injury to the
infraorbital nerve as it travels through
its bony canal in the orbital floor.

26. 6. Measurement By:
1) Plastic ruler
2) Exophthalmometer
 The generally accepted normal
value (between the lateral orbital
rim and apex of the cornea) is <
21 mm.
 A difference > 2 mm between the
2 eyes is abnormal (suggests
proptosis).

27. 7. Forced duction test
1. Negative test (no resistance) neurogenic
2. Positive test (Resistance)  restrictive
 It is particularly useful for differentiating
between a medial wall blow-out fracture
with medial rectus entrapment and 6th
cranial nerve palsy.

29. (C) Investigations
1) Laboratory: CBC – Thyroid
2) Radiological:
 Plain X-rays
 CT– MRI
 US
3) Biopsy & Pathology:
 Fine Needle Aspiration Biopsy
 Incisional biopsy
 Excisional Biopsy

46. Treatment of Proptosis
 Medical treatment of the cause: e.g.
dysthyroid orbitopathy, inflammatory
pseudotumor, orbital tumor …etc.
 Surgical excision of the cause (Orbitotomy):
1) Anterior Orbitotomy
2) Lateral Orbitotomy

47. Orbital Infections
 Preseptal Cellulitis
 Orbital Cellulitis

49. 1. Preseptal Cellulitis
 Cause: usually follows a severe lid infection
(e.g. stye), insect bite, or skin laceration.
 Clinical features : acute onset of unilateral
periorbital swelling, erythema, and
tenderness (No proptosis)
 Treatment: Systemic (oral) antibiotics (as
out-patient), and warm compresses over the
inflamed lid.

53. 2. Orbital Cellulitis
 Definition: Orbital cellulitis is an infection of
the soft tissues of the orbit behind the orbital
septum.

54. Etiology: spread of infection from the neighboring sites
and may be of the following types:
1. Sinus-related: ethmoidal
sinusitis is the most common
cause of orbital cellulitis in
children.
2. From other adjacent structures
e.g. dacryocystitis, dental
infection, and mid-facial
infection.
3. Post-traumatic (penetrating
wound)

55. Clinical Picture

56. Clinical Picture
Symptoms:
 General: fever – malais
 Local: Pain – Decreased vision (why ?) – Diplopia
Signs:
1) Lid edema & redness
2) Conj injection and chemosis
3) Proptosis
4) Limitation of ocular motiliy
5) Pupil: APD.

57. ● Complications:
1. Meningitis and
brain abscess
2. Cavernous sinus
thrombosis
3. Subperiosteal
or orbital abscess
4. CRA occlusion

58.  Investigations:
1. White cell count
2. CT scan of the orbit, sinuses, and brain
3. Blood and nasal cultures.
4. Lumbar puncture if meningeal or cerebral
signs develop

59.  Treatment
1. Hospitalization
2. Systemic antibiotic therapy: A broad-spectrum
antiobiotic (3rd or 4th generation cephalosporins).
3. Surgery
◘ Indications:
1. Resistance to antibiotics
2. Decreasing visual acuity
3. Subperiosteal or orbital abscess

60. Dysthyroid ophthalmopathy

61. I. Dysthyroid ophthalmopathy
 Hyperthyroidism occurs in a number of diseases
including Graves’ disease, toxic goitre, and
thyroiditis.
 Graves’ disease is a term used to describe the
commonest variety of hyperthyroidism, which is
known to have an autoimmune basis.
 It is typically affects women between ages of
20 – 45 years, and characterized by goitre,
infiltrative ophthalmopathy, and peritibial
myxoedema.

62.  When the eye signs of Graves’ disease occur in
a patient who is not clinically with
hyperthyroidism (i.e. with normal T3 & T4),
and who gives no past history of thyroid
dysfunction  This condition is referred to as
euthyroid or ophthalmic Graves’ disease.
(OGD).
 In 10 – 25% of cases, thyroid ophthalmopathy
occurs in the absence of both clinical and
biochemical evidence of thyroid dysfunction,
and this is the most common form
encountered by the ophthalmologists.

63.  In general, the ocular features of Graves’
disease and OGD are similar, although they
tend to be more asymmetrical in OGD than
in Graves’ disease.
 Eye manifestations may precede, occur
concurrently, or even follow the treatment of
thyroid disease.

64. Pathogenesis
 Dysthyroid ophthalmopathy is an
organ-specific autoimmune
disorder in which a humoral agent
(IgG antibody) is believed to be
responsible for the following
changes:

65. 1. Hypertrophy of the extraocular muscles.
2. Cellular infiltration of interstitial tissues with
lymphocytes, plasma cells, macrophages, and mast
cells (in active or congestive stage), followed by
degeneration of muscle fibres leads to fibrosis,
resulting in restrictive myopathy.
3. Proliferation of orbital fat with retention of fluid

67.  The previous changes result in
increase of intraorbital pressure 
further fluid retention within the orbit
and so on (vicious circle).

68. Clinical Types
 Non-infiltrative ophthalmopathy
 Infiltrative ophthalmopathy

69. 1. Non-infiltrative
ophthalmopathy
 Occurs in young adults
 Characterized by lid retraction associated
with either mild proptosis or no proptosis.

70. 2. Infiltrative ophthalmopathy
 Clinical features
►The five main clinical manifestations of dysthyroid
ophthalmopathy are:
1. Eyelid retraction
2. Soft tissue changes
3. Proptosis
4. Optic neuropathy
5. Restrictive myopathy

71. (1) Eyelid retraction
 Clinical features:
1. Dalrymple's sign (lid retraction)
2. Kocher's sign (staring look)
3. Von graefe's sign (lid lag on downgaze)
4. Fine tremor on lid closure
5. Infrequent blinking

72. Dalrymple's sign (lid retraction)

73. Kocher's sign (staring look)

76. Von graefe's sign (lid lag)

77. (2) Soft tissue changes
 Lid edema
 Conjunctival injection (especially overlying
horizontal recti tendons)
 Conjunctival chemosis
 Superior limbic keratoconjunctivitis

79. (3) Proptosis
 It is typically axial
 It may be unilateral or bilateral &
asymmetrical
 It is not influenced by treatment of the
hyperthyroidism.
 Unless treated, it may lead to severe
exposure keratopathy, corneal ulceration,
and endophthalmitis.

81. (4) Optic neuropathy
 It is caused by direct compression on the optic
nerve or its blood supply at the orbital apex by
the enlarged extraocular muscles.

82. (5) Restrictive myopathy
 The order of frequency of muscle involvement
is:
1. Inferior rectus leading to defective elevation
2. Medial rectus leading to defective abduction
3. Superior rectus leading to defective depression
4. Lateral rectus leading to defective adduction

85. Management of Dysthyroid
Ophthalmopathy
► Non-specific
► Topical
► Systemic
► Radiotherapy
► Surgery

86. 1. Non-specific treatment
 Head elevation at night to reduce periorbital
edema
 Taping of eyelids at night for exposure
keratopathy

87. 2. Topical treatment
 Lubricants to reduce ocular irritation:
artificial tears during the day and ointment at
night.

88. 3. Systemic treatment
(Systemic steroids )
 Oral prednisolone 80 mg/day is given initially,
and then the dose is tapered gradually.
◘ Indications:
1. Severe proptosis
2. Severe exposure keratopathy
3. Optic neuropathy
◘ Contraindication: as contraindication to
systemic steroid use e.g. peptic ulcer,
tuberculosis …etc.

89. 4. Radiotherapy
 May be an alternative to systemic steroids (i.e.
same indications) in patients who:
 Have contraindication to steroids
 Are unresponsive to steroids despite adequate dose

90. 5. Surgical treatment
 Include the following procedures:
1. Orbital decompression
2. Muscle (Squint) surgery for diplopia
3. Tarsorrhaphy
4. Levator recession
5. Blepharoplasty

91. Orbital decompression
◘ Indications
1. severe exposure keratopathy
2. Optic neuropathy
3. Cosmetically unacceptable proptosis

93. Muscle (Squint) surgery: for diplopia
◘ Indications
1. Diplopia in the primary or reading position of gaze
2. The angle of deviation is stable for at least 6 months
3. No evidence of active disease at the time of surgery.
◘ The goal of surgery: is to achieve binocular single
vision in the primary position of gaze and on reading
(without diplopia).

95. Tarsorrhaphy
 For severe exposure keratopathy

97. Levator recession
 For severe lid retraction

98. Blepharoplasty
 To reduce excessive periorbital fat and
skin.

99. II. Orbital Inflammatory
Pseudotumors
 Definition
Is idiopathic, non-specific, inflammatory
orbital disease, that may involve all or any of the
soft tissue components of the orbit.

100. Clinical features
 Presentation: is during the middle age, usually
with an acute onset of pain, lid edema,
conjunctival chemosis, ophthalmoplegia
(limitation of ocular motility), and proptosis

101. ▪ The clinical course: is variable and follows
one of the following patterns:
1. Spontaneous remission after a few weeks
with no sequelae
2. Prolonged intermittent episodes of activity
with remission.
3. Severe prolonged inflammation leading to
progressive fibrosis of orbital tissues, and in
severe cases, the end result is a "frozen orbit".

102. Treatment
 Systemic steroids: 60-80 mg/day for 2 weeks. If the
response is good, the dose is gradually tapered, and
re-introduced again in cases of recurrence.
 Radiotherapy: Is considered if no improvement after
2 weeks of systemic steroids with adequate dose.
However, a biopsy should be done first to rule out
(R/O) possibility of orbital tumor.
 Cytotoxic drugs e.g. cyclophosphamide may be used
in few cases who showed resistance to both steroids
and radiotherapy.

104. Blow-out Fracture of Orbital Floor
 Mechanism
A blow-out fracture is
caused by a sudden
increase in the orbital
pressure by a striking
object which is larger
than 5 cm in diameter,
such as a fist or a tennis
ball which results in
fracture of the orbital
floor.

105. Clinical features
 Periocular ecchymosis and
edema
 Enophthalmos may be present
initially or it may develop after 10-
14 days as the edema subsides
 Infraorbital nerve anesthesia
involving the lower eyelid, cheek,
side of nose, upper lip, and upper
teeth.
 Diplopia is typically vertical in
both up- and down-gaze (double
diplopia). It is due to tethering of
muscles in the fracture line.
 Positive forced duction test
 Ocular damage is relatively rare

106. Investigations
 Orbital CT scan is essential. It may show
herniation of the orbital fat through a defect in
the orbital floor (tear-drop sign).

107. Treatment
 Small cracks without diplopia require no
treatment
 Fracture of less than 50% of the orbital floor
associated with improving diplopia require no
treatment unless Enophthalmos is more than 2
mm.
 Fractures of over 50% of the floor associated
with persistent diplopia should be repaired
within 2 weeks by freeing the entrapped tissue
and covering the defect with a bone substitute.