A complete unit of the various diseases involving the orbit and the surrounding structures. It involves the unilateral and bilateral proptosis conditions. Also, the various proptosis etiologies involved in adults and children along with various tumors involving the orbit is also dealt with.
1. DISEASES OF THE ORBIT
Mrs. Lavanya Kalikivayi, M.Opt., FLVPEI., FIACLE,
Associate Professor,
Ahalia School of Optometry & Research Centre,
Palakkad.
2. ANATOMY
⢠The orbit is a pear shaped cavity, the stalk of
which is the optic canal.
⢠The intra-orbital portion of the optic nerve is
longer (25mm) than the distance between the
back of the globe and the optic canal (18mm).
⢠This allows for significant forward
displacement of the globe (proptosis) without
excessive stretching of the nerve.
3. ⢠The Roof consists of two bones: the lesser wing of
sphenoid and the orbital plate of the frontal.
⢠It is located subjacent to anterior cranial fossa and
frontal sinus.
⢠A defect in the roof may cause a pulsatile proptosis
as a result of transmission of CSF pulsation to the
orbit.
⢠The Lateral wall of the orbit also consists two bones:
the greater wing of sphenoid and the zygomatic.
⢠The anterior part of the globe is vulnerable to lateral
trauma, as it protrudes beyond the lateral orbital
margin.
4. ⢠The Floor consists of three bones: the zygomatic,
maxillary and the palantine.
⢠The posteriomedial portion of the maxillary is
relatively weak and get involved in âblow outâ
fracture.
⢠The floor of the orbit also forms the roof of the
maxillary sinus so that a maxillary carcinoma
invading the orbit may displace the globe
upwards.
⢠The medial wall consists of four bones: the
maxillary, lacrimal, ethmoid, and sphenoid.
5. ⢠The lamina papyracea, which forms part of the
medial wall, is paper thin and is perforated by
numerous foramina for nerves and blood vessels.
⢠Orbital cellulitis is therefore frequently
secondary to ethmoidal sinusitis.
⢠The Superior orbital fissure is a slit connecting
the cranium and the orbit, between the greater
and lesser wings of sphenoid bone, through
which passes the following structures:
1. The superior portion contains the lacrimal,
frontal and trochlear nerves, and the superior
ophthalmic vein.
6. 2. The inferior portion contains the superior and
inferior divisions of the oculomotor nerve, the
abducens and nasociliary nerves and
sympathetic fibers from cavernous plexus.
3. Inflammation of the superior orbital fissure and
the apex (Tolsa-Hunt syndrome)may therefore
result in a multitude of signs including
ophthalmoplegia and venous outflow
obstruction.
⢠The Inferior orbital fissure lies between the
greater wing of sphenoid and the maxilla,
connectin the orbit to the pteregopalantine and
infratemporal fossae.
7. ⢠Through it runs the maxillary nerve, zygomatic
nerve and branches of the pterygopalantine
ganglion as well as the inferior ophthalmic vein.
8. ⢠Six Pâs: pain, proptosis, progression, palpation,
pulsation, and periorbital changes.
⢠Pain: inflammatory, infection, oribital
hemorrhage, malignant lacnimal gland tumors
and NPC
⢠Proptosis--Hertel exophthalmometer
⢠Axial proptosis-an intraconal space-occupying
lesion,
⢠Eccentric proptosis--- an ant.space-occupying
lesion.
9. Progression
⢠Days to weeksâ
1. Idiopathic orbital
inflammatory dis.,
2. Cellulitis,
3. Hemorrhage,
4. Thrombophlebitis,
5. Thyroid
ophthalmopathy,
6. Neuroblastoma,
7. Metastatic tumors,
8. Rhabdomyosarcoma,
or Granulocytic
sarcoma.
⢠Over months to years-
1. Dermoids,
2. Benign mixed
tumors,
3. Neurogenic tumors,
4. Cavernous
hemangiomas,
5. Lymphoma,
6. Fibrous
histiocytoma, or
Osteomas
10. ⢠Palpation:
⢠Superonasal quadrant---
1. mucoceles,
2. mucopyoceles,
3. encephaloceles,
4. neurofibromas, or
lymphoma.
⢠Superotemporal quadrant-
1. dermoids,
2. prolapsed lacrimal gland,
3. lacrimal gland tumors,
4. lymphoma, or
5. idiopathic orbital
inflammation disease.
⢠Pulsation:
⢠Without bruits-
1. Neurofibromatosis,
2. Meningoencephaloceles,
or
3. Removal of the orbital
roof.
⢠With or without bruits-
1. Carotid cavernous fistulas,
2. Dural arteriovenous
fistulas, and
3. Orbital arteriovenous
fistulas.
11. Clinical evaluation of orbital disease
1. History: (1)pain, (2)mode of onset of
proptosis
2. Exclusion of pseudoproptosis:
(1) Large ipsilateral globe,
(2) Facial asymmetry,
(3) Contralateral enophthalmos (blow-out
fracture)
12. 3. Evaluation of ocular motility:
⢠Restrictive myopathy (thyroid, blow-out
fracture)
4. Visual acuity
5. Dynamic properties â
⢠Valsalva maneuver or jugular
compression,,pulsation, bruit
6. Forced duction test
7. Differential IOP test
13. Laboratory studies
⢠Thyroid function (T3,T4, TSH)
Antithyroglobulin,
⢠Antimicrosomal antibodies(60%-70% of
patients with Graves disease)
⢠Antineutrophil cytoplasmic antibody (ANCAs),
⢠Serum assay, Wegener granulomatosis
14. Common lesions
⢠Proptosis
⢠Exophthalmos- endrocrinal
⢠Enophthalmos
⢠Pseudoproptosis-slight prominence of eyes
like myopia, paralysis of extra ocular muscles,
obese people, mullers stimulation by cocain
2/13/2023 14
15. Proptosis and Exophthalmos
⢠Abnormal protrusion of eye ball is called
proptosis or exophthalmos.
⢠The term exophthalmos is reserved for
prominence of the eye secondary to thyroid
disease
2/13/2023 15
16. Proptosis
⢠Abnormal protrusion of globe
⢠It may be Unilateral or Bilateral
⢠Unilateral â caused by orbital cellulitis, idiopathic
orbital inflammatory disease, thrombosis of orbital
vein, arterio-venous aneurysms, tumors of structures
of orbit , orbital haemorrahge , emphysema.
⢠Bilateral â endocrine exophthalmos , cavernous sinus
thrombosis , symmetrical orbital tumors, oxycephaly
- diminished orbital volume
2/13/2023 16
21. Types of Proptosis
⢠Axial proptosis - eye is pushed directly
forwards â lesions situated in optic nerve
and central space
⢠Non axial- situated elsewhere in orbit
pushes eye in opposite direction
2/13/2023 21
22. Causes of proptosis in different in different
locations
2/13/2023 22
Extra conal lesions Intra conal lesions Muscular disorders
Dermoid cyst Cavernous haemangioma Thyroid
ophthalmopathy
Rhabdomyosarcoma Optic nerve glioma Pseudo tumor
Extension of nasal
/sinus diseases
Meningioma Cysticercosis
A-V malformations Lymphoproliferative
disorder
Rhabdomyosarcoma
23. Clinical presentation
⢠Static- as seen usually in congenital causes
⢠Increasing â fast- as in cases of
Rhabdomyosarcoma, neuroblastoma,
haemopoetic
⢠Gradual- as in cases of meningiomas
⢠Pulsatile- as in cases of carotid cavernous
fistula
⢠Intermittent- as in cases of orbital varicosity
2/13/2023 23
24. Clinical signs
⢠Impaired mobility
⢠Diplopia
⢠Papilloedema
⢠Optic atrophy
⢠Hertel exophthalmometry â measures more
than 18 mm
⢠Difference in two eyes of more than 2 mm is
considered positive
2/13/2023 24
25. Investigations
⢠Careful history recording
⢠Systemic examination
⢠ENT examination
⢠Biochemical and haematological investigations
⢠Imaging of bony structures- plain x ray
⢠Imaging of soft tissues âCT scan, MRI
⢠Vascular study- orbital venography, carotid
angiography, MR angiography, digital subtraction
angiography
2/13/2023 25
26. Orbital cellulitis
⢠Definition: Purulent inflammation of the cellular
tissue of the orbit
⢠Causes of Orbital Cellulitis:
Spread of infection from neighbouring structures
like nasal sinuses, eyelids, eyeball (like in case
of panophthalmitis) etc
Also due to deep penetrating injuries (specially
in cases of retained Foreign body) and
metastatic infection in cases of pyaemia
26
27.
28. Types of Orbital Cellulitis
⢠Two types- pre septal cellulitis and orbital
cellulitis
⢠Pre septal âstructures anterior to orbital
septum, characterized by
⢠Erythema,
⢠Chemosis,
⢠Conjunctival discharge without restriction of
ocular movements and visual impairment
29. Types of Orbital Cellulitis
⢠Orbital â behind orbital septum, characterized
⢠Severe pain,
⢠Fever,
⢠Diminution of vision (due to retrobulbar neuritis or
compression of optic nerve and /or its blood supply),
⢠Massive swelling of lids,
⢠Chemosis,
⢠Proptosis,
⢠Restriction of ocular movements,
⢠Diplopia,
⢠An abscess may form pointing somewhere in the skin
of the lid near the orbital margin or fornix
29
32. Management
⢠Culture and sensitivity of pus, if present and of
blood
⢠Treatment âBroad spectrum Intravenous
antibiotics , and anti inflammatory
⢠If abscess has formed â Incision and Drainage
under cover of antibiotics
32
33. Cavernous sinus thrombosis
⢠Due to extension of thrombosis from various
feeding vessels
⢠Superior and inferior ophthalmic vein enter in
front
⢠Superior and inferior Petrosal sinus leave from
behind
⢠Cavernous sinus communicates with facial
veins, lateral sinus, jugular vein, Mastoid
emmisary vein-lateral sinus- superior petrosal
sinus 33
34. Cavernous sinus thrombosis
⢠Cavernous sinus on one side communicates
with other side through transverse sinus
⢠Because of connection with mastoid through
mastoid emmisary vein, mastoid tenderness
is diagnostic feature of cavernous sinus
thrombosis
35. Source of infection
⢠Orbital veins - as in cases of eryiepelas, septic
lesion of face, orbital cellulitis , infective
condition of face, mouth, nose, sinuses
⢠Furuncle of upper lip â dangerous area of face
⢠Metastatic infection or septic condition
35
36. Symptoms and Signs
⢠Patient may present with symptoms and signs of
Orbital cellulitis, there is sever supra-orbital pain
⢠Systemic features â headache, fever ,altered
sensorium, vomiting and cerebral symptoms
⢠Transference of symptoms and signs to other
eye (bilateral orbital cellulitis with which it may
be confused is very rare clinical condition).
⢠Mastoid edema and tenderness is present.
36
37. Symptoms and Signs
⢠In case of infection spreading to other eye,
the first sign is involvement of lateral
rectus of other eye
⢠Papilloedema
39. Exophthalmos
⢠Endocrine exophthalmos : Graves
Ophthalmopathy (dysthyroid eye disease) is
the commonest cause of uniocular or bilateral
proptosis in age groups between 25 and 50
years
39
40. Graves Disease
⢠Consists of Exophthalmos, and all signs of
thyrotoxicosis (i.e. tachycardia, muscular
tremors and raised BMR)
⢠The five main clinical manifestations are:
1. Soft tissue involvement
2. Lid retraction
3. Proptosis
4. Optic neuropathy
5. Restrictive myopathy.
40
41. Summary of signs in Graves disease
⢠Lid retraction in the primary gaze (DALRYMPLE SIGN)
⢠Lid lag â retarded descent of the upper lid on down gaze (VON
GRAEFE SIGN)
⢠Infrequent blinking and incomplete closure of lid (STELLWAG SIGN)
⢠Lid edema
⢠Staring and frightening appearance of the eyes which particularly
marked on attention fixation (KOCHER SIGN)
⢠Exophthalmos
⢠Conjunctival congestion over the insertion of recti muscles and
chemosis
⢠Convergence insufficiency (MOBIUS SIGN)
⢠Diplopia
⢠Raised intraocular tension may be present
⢠Superior limbic keratopathy
42. Werner classification of signs (NO SPECS)
⢠Grade 0 â No signs or symptom
⢠Grade 1 â Only sign (lid retraction)
⢠Grade 2 â Soft tissue involvement (Chemosis)
⢠Grade 3 â Proptosis (which may be minimum
<23, moderate , marked >28)
⢠Grade 4 â Extraocular muscle involvement
⢠Grade 5 â Corneal involvement
⢠Grade 6 â Sight loss
42
43. Exophthalmic Ophthalmoplegia
⢠Is proptosis with external ophthalmoplegia
⢠Usually seen in middle aged people , it is of
insidious onset, typically assymetrical limiting
upward movement and abduction due to
swollen, pale edematous, infiltrated ocular
muscles .
⢠There is irreducible exophthalmos with risk of
exposure keratitis , globe dislocation mechanical
compression of optic nerve and ophthalmic
vessels
43
44. Exophthalmic Ophthalmoplegia
⢠Disease is self limiting with intermissions and
relapses, usually not affected by any
treatment.
⢠Spontaneous resolution may take place which
rarely is complete.
44
45. Treatment of Exophthalmic
Ophthalmoplegia
⢠Short term oral steroid therapy (with dose of 40-60
mg) with radiotherapy (1000 rad ) are effective in
controlling soft tissue inflammation
⢠Exposed cornea should be protected by doing
tarsorrhaphy in less severe cases , by orbital
decompression in more severe cases.
⢠Lateral tarsorrhaphy may also be needed.
⢠Residual muscle palsy is dealt with muscle
adjustment surgery.
45
46. Types
⢠Type â I : Characterized by symmetrical mild
proptosis with lid retraction usually associated
with thyrotoxicosis
⢠Type â II : Characterized by extreme
exophthalmos, compressive neuropathy and
extraocular muscle involvement.
⢠This form may be associated with any state of
thyroid function, but usually with
hypothyroidism, seen after thyroidectomy.
46
47. Cause of exophthalmos
⢠Due to edema,
⢠lymphocytic infiltration anfibrosis of orbital
contents and extra-ocular muscles
⢠Lid retraction is due to contraction of Muller
muscle
47
48. Orbital pseudotumor
⢠Idiopathic, non-specific, inflammatory, orbital
disease
⢠Presentation--20-50 years of age.
⢠Painful lid edema,
⢠EOM--limitation proptosis.
⢠Children: 1/3 bilateral involvement.
⢠Adult: bilateral--- associated with systemic
disease.
⢠Treatment--observation, systemic steroids,
radiotherapy,
⢠Cytotoxic drugs.
49. Orbital myositis
⢠Unilateral ptosis, diplopia, redness and pain
over the involved muscle.
⢠Examination-pain on attempted gaze into the
field of action of the involved muscle.
⢠CT: fusiform enlargement of the involved
muscle.
⢠Treatment-systemic steroids or NSAID
50. Tolosa-Hunt syndrome
⢠involve the orbital apex, sup. Orbital fissure,
such as inflammation, vascular and traumatic
lesions, and tumuors.
⢠Presentation-ipsilateral periorbital or
hemicranial pain.
⢠Examination--proptosis, ocular cranial nerve
palsies, pupillomotor dysfunction.
⢠Sensory loss of 1 and 2 divisions of V nerve.
⢠Treatment---systemic steroids.
58. ORBITAL VARICES
A. ORBITAL VARICES
BEFORE VALSALVA
B. ORBITAL VARICES WITH
VALSALVA
C. EYELID VARICES
D. CONJUNCTIVAL VARICES
E. CT PICTURE
F. LEFT EYE FAT ATROPHY &
ASSICIATED
ENOPHTHALMOS &
DEEP SULCUS
72. BLOW OUT FRACTURE
⢠Blow out fracture occurs when a blunt object greater in
diameter than the orbital rim such as fist, tennis or cricket
ball strikes the orbital cavity
⢠The mechanisms proposed for blow out fracture are-
⢠Hydraulic theory
⢠Buckling theory
73. PATHOPHYSIOLOGY
Buckling theory or transmission theory or
Indirect injury theory:
⢠External force to inferior orbital rim is
transmitted along the orbital walls causing a
ripple effect leading to fracture at the weakest
point in the posterior medial region of the
floor.
74. PATHOPHYSIOLOGY
Hydraulic theory or Retropulsion theory or Direct
injury theory:
⢠Sudden compression and backward displacement of
globe raises the intra orbital pressure leading to
fracture of orbital floor.
⢠Medial Wall & Floor âThin &
Fragile
⢠Fracture readily â provide
natural compensation
⢠As they fracture â Orbital Size
75. Types
a) Pure blowout fracture:
⢠Fracture of the orbital floor with intact orbital rim
b) Impure blowout fracture:
⢠Associated fracture of the orbital rim
76. Clinical Features
⢠Circumorbital Edema
⢠Subconjunctival Bleeding â due to fracture -
subperiosteal bleeding - escapes in
subconjuctival plane.
⢠Periorbital haematoma: also proptosis of
variable degree seen initially due to orbital
edema and haemorrhage
77. Clinical Features
⢠Enopthalmos - Increase in size of Orbit -
Eyeball sinks
⢠Periorbital Fat Herniates through fractured
walls - âHanging-dropâ Appearance
⢠Unilateral Epistaxis â bleeding into antrum
79. Clinical Features
⢠Paraesthesia - Numbness in area of
distribution of Infraorbital Nerve over
ipsilateral lower lid, cheek and upper lip
Diplopia or Vertical gage â Inferior Rectus or
Inferior Oblique gets entrapped in fracture
⢠inability of eyeball to move in vertical
direction
80. Clinical Features
⢠Also displacement of orbital contents into
maxillary sinus and traction over globe caused
by entrapped tissue leads to posterior and
inferior displacement of globe.
⢠Pseudoptosis occurs due to loss of support.
81. Evaluation
⢠visual acuity at presentation has medico-legal importance in
ocular trauma cases.
⢠If required eyelids can be gently separated to allow patient to read
the chart.
⢠Palpate orbital rim to look for deformity and crepitus
⢠Slit lamp evaluation of cornea and anterior segment should be
performed.
⢠RAPD points towards optic nerve injury.
⢠Fundus evaluation should be done to note for Berlinâs oedema
82. Ocular motility
⢠Hertel exopthalmometer: To document enophthalmos.
⢠With passage of time and absorption of orbital fat over period can lead to
increase in enophthalmos.
⢠Force Duction Test (FDT): FDT is useful in determining whether
dysmotility is restrictive or paralytic.
In blow out fracture with inferior rectus entrapment FDT is âpositiveâ
indicating mechanical cause.
⢠Force Generation Test (FGT): In testing force generation, the muscle
insertion is grasped and the patient is asked to look into the muscleâs
field of action. A paretic muscle will feel weak when compared with the
fellow eye.
⢠Diplopia charting: With red green glass, diplopia charting with streak
light shows diplopia worsening in upgaze
⢠Hess screen or Lee screen test can be done.
83.
84. Imaging
⢠Plain X-rays:. Waterâs view for detecting an orbital floor
fracture .
⢠X ray shows bony discontinuity in orbital floor with
herniation of soft tissue in maxillary antrum seen as
âhanging dropâ sign
⢠CT gives detailed visualization of bony and soft tissue
injury where entrapment of muscle can be appreciated.
⢠Coronal sections are particularly useful .
⢠MRI Can be utilized when there is need for greater soft
tissue evaluation
⢠MRI is insufficient in assessing the bony structures and
therefore needs to be combined with CT.
85. Superior Orbital Fissure Syndrome
Contents of Superior Orbital Fissure :
⢠3 rd Cranial Nerve (Occulomotor)
⢠4 th Cranial Nerve (Trochlear)
⢠6 th Cranial Nerve (Abducent)
⢠5 th Cranial Nerve (Trigeminal) â Opthalmic
Branch
⢠Opthalmic Artery
⢠Opthalmic Vein
87. Superior Orbital Fissure Syndrome
⢠Due to paresis of these nerves all these
extraocular muscles undergo paralysis
eyeball fails to move âExternal
Opthalmoplegiaâ
⢠As affected eye does not move whereas
contralateral normal eyeball moves focal
axis gets disturbed two images - Diplopia
88. Clinical Manifestations
⢠External Opthalmoplegia â Eyeball fails to
move
⢠Diplopia â Two images of one object
⢠Internal Opthalmoplegia â Fixed Dilated
pupils (parasympathetic â III cranial nerve â
Occulomotor )
⢠Ptosis of Upper Eyelid â upper eyelid drops
down like a curtain â parasympathetic supply.
⢠Orbital Apex Syndrome â If Optic Nerve
Involvement is present.
89. BLOW IN FRACTURE
⢠Fragmented bones of the orbital floor are
displaced into the orbit.
⢠Proptosis â Exopthalmos
⢠More commonly seen in fractures of â orbital
roof
91. IMAGING
⢠CT Scan â Orbit - To visualize the fractured
segments
⢠CT Scan â also helps evaluate the Intraorbital
volume.
⢠By using a software to compare the normal
orbital volume to the affected
⢠MRI
92. Management
⢠Restriction in ocular movement and / or diplopia is
caused not only by entrapment of muscle but soft
tissue edema, hemorrhage and motor nerve palsy
can also be the cause.
⢠A better evaluation can be made if time is allowed
for clearing of initial edema and hemorrhage.
⢠It is generally accepted that a 2 week window of
observation can be allowed in absence of urgent
surgical indications
93. Observation
⢠Minimal diplopia (not in primary or downgaze),
⢠Good ocular motility
⢠No significant enophthalmos or hypo-ophthalmos
94. Medical treatment
⢠Consider broad-spectrum oral antibiotics (e.g., cephalexin 250 to 500 mg
p.o. q.i.d.; or erythromycin 250 to 500 mg p.o. q.i.d; or doxycycline 100 mg
po b.i.d.) for 7 days.
⢠Antibiotics may be considered if the patient has a history of chronic
sinusitis, diabetes, or is otherwise immunocompromised.
⢠Prophylactic antibiotics should not be considered mandatory in patients
with orbital fractures.
⢠Patient advised not to blow nose as it can worsen orbital emphysema.
95. ⢠Nasal decongestants (e.g., oxymetazoline nasal spray b.i.d.) for 3
days. Use is limited to 3 days to minimize the chance of rebound
nasal congestion.
⢠Apply q1â2h ice packs for 20 minutes each hour to the eyelids for
the first 24 to 48 hours and 30-degree incline when at rest.
⢠Consider oral corticosteroids (e.g., Medrol dose pack) if extensive
swelling limits examination of ocular motility and globe position.
⢠Neurosurgical consultation is recommended for all fractures
involving the orbital roof, frontal sinus, or cribriform plate, and for
all fractures associated with intracranial hemorrhage.
⢠Otolaryngology or oral maxillofacial surgery consultation may be
useful for frontal sinus, midfacial, and mandibular fractures
96. Follow up
⢠At 1 and 2 weeks after trauma to be evaluated for persistent diplopia and/or
enophthalmos after the acute orbital edema has resolved.
⢠If sinusitis symptoms develop or were present prior to the injury, the patient
should be seen within a few days of the injury.
⢠Fundus examination to assure there is no peripheral retinal damage.
⢠Depending on the level of associated ocular injury, patients should also be
monitored for the development of associated ocular injuries (e.g., orbital cellulitis,
angle-recession glaucoma, and retinal detachment).
⢠Gonioscopy of the AC angle and dilated retinal examination with scleral depression
is performed 3 to 4 weeks after trauma if a hyphema or microhyphema was
present.
⢠Warning symptoms of retinal detachment and orbital cellulitis are explained to the
patient
