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Orbital Pathology/Lacrimal
Pathology
By Prof E. Oghre
Professor of Optometry
The orbit
The orbit is the space bound by orbital
bones
◦ Ethmoid bone
◦ Frontal bone
◦ Lacrimal bone
◦ Maxillary bone
◦ Palatine bone
◦ Sphenoid bone
◦ Zygomatic bone
• Conical with a volume of approximately
27ml
Orbital Wall
Bones
 Superior (roof) = Frontal .
 Lateral wall = Zygoma, Sphenoid
(greater wing).

 Inferior (floor) = Maxilla (medial),
zygoma (lateral), palatine (posterior).
 Medial wall = Maxilla, lacrimal,
ethmoid, sphenoid (anterior to posterior).
.
 The globe is positioned in the anterior portion
of the orbit and constitutes about 20% of the
entire volume of the orbit.
 It is slightly closer to the lateral orbital wall
than the medial wall and is nearer the roof
than the floor of the orbit.
 At its closest distance to the bony orbit the
globe is about 4 mm from the roof, 4.5 mm
from the lateral wall, 6.5 mm from the medial
wall, and 6.8 mm from the floor.
 The lateral orbital rim is considerably
recessed compared with the medial orbit,
which continues anteriorly to end at the nasal
bridge. This leaves approximately one half of
the globe unprotected.
Orbit
What can go wrong?
 – Fractures
 – Infection (Preseptal –Versus-
(Septal) Orbital Cellulitis
 – Proptosis (Thyroid Eye Disease
/Grave’s Oculopathy)
 – Inflammation
 – Foreign Body
 -- Neoplasms
Causes of orbital diseases
Children Adults
Orbital Cellulitis Trauma
Demoid and epidemoid cysts Thyroid Eye Disease
Capiliary haemangioma and
lymphangioma
Idiopathic orbital inflammatory
Disease(pseudotumour)
Neurofibroma Lacrimal gland inflammation
Rhabdosarcoma Capillary haemangioma
Optic nerve glioma Lymphangioma
Lipoma
Meningioma
metastasis
For whatever reason, all of these
either take up space or/and cause
masses
Fractures
 Blowout fracture
◦ Break in floor of orbit (maxillary bone)
◦ Ethmoid fractures
By the end of the lecture the students
should be able to
1. Explain the mechanism of BOF of the
orbit
2. Describe its symptoms & signs
3. Describe the complications
4. Outline the management
Orbital fractures
 The term "blowout fracture" refers specifically
to a fracture of an orbital wall in the presence
of an intact orbital rim.
 A relatively common form of periorbital injury.
 Although any bone surrounding the orbit may
be fractured, the thin bones of the orbital floor
and medial orbital wall are most vulnerable.
 The most common site for a blowout fracture
is the thin part of the maxillary bone (0.5-mm
thick) in the posterior medial aspect of the
floor.
 In addition, the very thin ethmoid bone (0.25-
mm thick) along the medial wall of the orbit
may be involved
 Due to the relative thickness of the orbital
rim, it is often spared in orbital fractures.
BLOW-OUT FRACTURE OF THE
ORBIT
• Secondary to massive blow to the orbit
resulting in fracture of one/ more of its
walls ( mostly medial wall & floor)
• Common in sports & violence related
trauma
• Mechanism involves sudden rise of
intraorbital pressure & fracture of the
bony socket at its weakest points
Clinical presentation
• Symptoms ; history of trauma with double vision,
pain in and around the orbit, visual loss ( not
always)
• Signs; periocular swelling, bruising ( ecchymosis),
subcutaneous emphysema
• Enophthlamos; in large & severe fractures &
increases with time
• Infraorbital nerve hypoesthesia
Clinical presentation
• EOM abnormalities; vertical diplopia, limited
upgaze & downgaze --- floor fractures, limited
adduction & abduction ---medial wall fracture
• Ocular/ associated damage to the eyeball
– Hyphaema
– RD
– Damage to the angle of the anterior chamber—
glaucoma
– Vitreous haemorrhage
– Orbital hematoma
– Damage to the optic nerve
 Muscle entrapment of right eye with
inability to look up
 • Your observations
 ––––
 • History ?
 –
 • Symptoms
 ––––
 Which is affected eye?????
 Remember: always examine patient
with
 all lights on and grossly, initially
 Your observations
 Bruising
◦ Ecchymosis – 1 to 3 cm
◦ Purpura – 3mm to 1 cm
◦ Petechiae – < 3mm
 – EOM restriction
◦ Ophthalmoplegia
 – Conjunctival injection
 -- Oedema
 – (Pseudo)Ptosis
◦ Lid droop NOT caused by
weakening muscle
 • History ?
◦ hit with……….
 • Trauma history
 • Symptoms
◦ Pain
◦ Diplopia
◦ Tearing
◦ Mild blur to vision (If
JUST the blowout
fracture)
 – Crepitus ( Describes
the grating, crackling
or popping sounds and
sensations
experienced)
 Critical signs of recent blow-out
fracture include:
◦ • edema and ecchymosis of the lid tissues
◦ • restriction of ocular motility, especially
with vertical movements
◦ • orbital crepitus (subcutaneous
emphysema)
◦ • hypoesthesia of the ipsilateral cheek,
due to entrapment of the infraorbital nerve
Complications
 EOM problems
 Visual loss
 Cosmetic
 Secondary infection from the sinuses-
orbital cellulitis & spread of the
infected contents of the sinuses to the
vital tissues like the eyeball & the
brain
Investigations/ confirmatory tests
For confirmation of fracture
 CT scan / X ray orbit
For confirmation of muscle entrapment
 CT scan & forced duction test
Management
 Symptomatic/ conservative:
◦ NSAID for relief of pain & reduction of
inflammation
◦ discourage blowing of the nose to prevent
forcing of the infected sinus contents into
the orbit
◦ antibiotics
 If the diplopia persist beyond 2 weeks/
enophthamos is significant then
surgical repair of the fracture with
release of entrapped muscles may be
required
 Blowout fracture is not a common
disorder but is common in sports &
violence related trauma, it can mostly
be managed conservatively but in
case of a large fracture or persistent
EOM problems & enophthalmos may
require surgical repair.
Cellulitis of the eye
 This can be two different types,
◦ Orbital cellulitis - Purulent inflammation of
the cellular tissue of the orbit
◦ Preseptal cellulitis - Purulent inflammation
of the cellular tissue of the eyelid
 Preseptal cellulitis can be regarded purely
as an eyelid problem, but it is treated here
for ease of understanding
 ORBITAL CELLULITIS
By the end of the lecture the students
should be able to
1. Differentiate between preseptal and true
orbital cellulitis
2. Explain why it is considered to be an
ocular emergency
3. Describe the causes,
4. Explain the clinical presentation,
complications & line of management of
orbital cellulitis
ORBITAL CELLULITIS
 Definition: Purulent inflammation of
the cellular tissue of the orbit
 – Infection posterior to the orbital septum
(anywhere in the orbit)
 – Dangerous condition because of the
close proximity to the orbital apex,
cavernous sinus, meninges and brain,
This should be differentiated from
Preseptal cellulitis in which the Infection
is anterior to the orbital septum
Preseptal cellulitis
 Infection of the subcutaneouss tissue
anterior to the orbital septum ( lids)
 Causes:
◦ Trauma; lid laceration/ insect bite
◦ Spread from local infection; stye/
dacrocystitis
◦ Spread from remote infection;
haemotogenous spread from middle ear/
Upper Respiratory Tract
Clinical presentation of Preseptal
cellulitis
 Symptoms;
◦ History of predisposing factor,
◦ pain
◦ swelling of the lid, mild fever
 Signs;
◦ red swollen tender lids sometimes the lids
may be difficult to open.
 Important negative signs are:
 Eye itself is normal or at the most might be mildly
congested
 Visual acuity is normal
 No proptosis
 No ocular motility problem
 Normal pupils
Preseptal cellulitis
Complications
◦True orbital cellulitis
◦Lid abscess
◦Cavernous sinus thrombosis
management
 To prevent the possibly disastrous spread of
infection to the postseptal area, it is crucial to
quickly suppress the infection. Oral therapy is
necessary;
 Topical antibiotics
 Oral antibiotics – amoxicillin – 500mg TID or
 Amoxicillin/clauvenate (Augumentin) 625mg
TID or
 Cefaclor 250-500mg p.o. QID or
 Trimetheprim (320mg)/ sulfemethoxazole
60mg daily in (BD)
ORBITAL CELLULITIS
 Infection of the soft tissues behind the
orbital septum ( deeper to lids)
 Ocular emergency , could be life
threatening
 Most frequent pathogens are; Strept
pneumoniae ,Staph aureus, Strept
pyogenes & Haem influenzae - (under
5 yrs children)
Aetiology
 Commonly caused by the spread of infection
from the neighbouring areas, i.e. ethmoidal
sinusitis, lacrimal abscess, stye or suppurating
chalazion, dental infection, facial infection,
infection of the eyeball (panophthalmitis etc)
 Spread from the sinuses is the most common
cause)
 Rarely direct infection by a penetrating wound,
especially if a foreign body is retained within the
orbit.
 Metastatic infection via the blood stream, e.g. in
cases of pyaemia.
Extension from preseptal cellulitis
 Haemotogenous spread
 Post- traumatic; accidental/ surgical
 Causative agents include
◦ Bacterial – Streptococcus species, Staph
aureus, and Haemophilus influenzae type
B. Pseudomonas, Klebsiella, Eikenella,
and Enterococcus
◦ • Fungal – Mucor and Aspergillus
◦ • Parasitic
Clinical presentation
 Symptoms;
◦ rapid onset painful swelling of the lids
◦ protrusion of the eye,
◦ fever, malaise
◦ visual loss
◦ history of risk factors
 Signs;
◦ moderate to severe swelling of the lids,
reduced visual acuity,
◦ proptosis, red eye
◦ chemosis of the conjunctiva,
◦ abnormal & painful EOM & pupillary
response
The following signs are most
important
 Ocular.—:
(a) Severe pain in the orbit which increases during
ocular movements.
(b) Lid oedema with redness of the skin
(c) Chemosis of the conjunctiva.
(d) Proptosis which is axial and irreducible.
(e) Limitation of ocular movements , diplopia.
(f) Fundus examination may reveal engorged retinal
veins and sometimes papillitis. Abscess formation may
occur. It may burst through the skin of the eyelids near
the orbital margin or in the conjunctival fornix.
 General.—Fever, malaise are common symptoms.
Sometimes
cerebral symptoms supervene
Complications
Ocular; corneal damage( exposure),
raised IOP, vascular occlusions, optic
nerve damage, endophthalmitis,
Panophthalmitis
• In diabetic patients fungal
superinfection may develop
Intracranial; Extension into brain
through meninges , cavernous sinus
thrombosis may develop, meningitis,
brain abscess,
Management
 A swab is taken from the conjunctival
sac for culture and sensitivity test
 Vigorous systemic and local use of
antibiotic drugs to which the causative
micro-organisms are sensitive,
 Local heat by frequent hot bathing is
very beneficial.
 If abscess formation is suspected,
early incision is recommended.
Management
 Culture and sensitivity of pus and of blood
 Treatment
 Symptomatic: Antipyretic, NSAIDS and Anti
inflammatory
 Broad spectrum Intravenous antibiotics
 Specific ; hospitalization & antibiotic therapy
◦ Ceftazidime 1 g tds , I/M
◦ Metronidazole 500mg tds, PO
◦ Vancomycin in case of allergy to the above mentioned
 If abscess has formed – Incision and Drainage
under cover of antibiotics. Surgical intervention in
case of local abscess or unresponsive cases
 Consultation with ENT specialist, neurosurgeon &
paediatrician if required
Summary
 Orbital cellulitis is differentiated from preseptal
cellulitis with the following signs:
 – Pain with eye movements
 – Ophthalmoplegia
 – Proptosis
 – Globe displacement
 – Decreased vision or vision defect.
 Both preseptal and orbital cellulitis may have:
◦ Fever
◦ Eyelid swelling
◦ Pain
◦ Red eye
◦ Child is ill-appearing
Case 1
 A 1 year old child presented to the
Optometry clinic with the complaint of
a swollen right upper lid for the last
two days. On examination the lid was
red, warm & tender to touch. His
visual acuity was normal, the eye had
mild conjunctival redness, the pupil
was normal and the ocular
movements were also normal.
1. Is the condition confined to the lids or
has it involved the eyeball?
2. Why do you think so?
3. What more information would you like
to have before making a diagnosis?
 The child had a history of insect bite
on the lid two days ago, the swelling
increased thereafter. The insect bite
mark was visible
 There was no history of trauma or
symptoms suggestive of sinusitis
 His temperature was 990 F
 What should be the management,
keeping in mind the nature of the
problem?
 Is there any role of health education in
this case?
Let us see an other case……..
Case 2
 A seven year old child was brought the
Optometry clinic with history of swollen left
upper lid for the last 5 days. He also had
fever for the last two days.
 On examination the child had a grossly
swollen lid. The doctor had difficulty in
opening the lid for examination of the eye.
The visual acuity was 6/6 OD & 6/18 OS. The
lid was warm and tender. The eye was
moderately proptosed with conjunctival
chemosis. The pupil was slow to react to light
and the ocular movements were painful &
limited. The temperature was 1010 F & the
child looked generally unwell……..
1. Is the condition confined to the lids or
has it involved inner orbit?
2. What more information should we ask
for to get an idea about the cause of
the problem?
.
 The child had a history of recurrent flu
and upper respiratory tract infections.
He had history of blocked nose and
thick greenish nasal discharge was
noted on examination.
 The child was put on intravenous
antibiotics but didn’t get better
 What should be the management,
keeping in mind the nature of the
problem?
 What is the difference between the
two cases?
 We consider the second case an
ocular emergency, why?
 What other complications could
happen in the second case?
PROPTOSIS
NOT a diagnosis, a SIGN of underlying orbital
disease

Proptosis is a condition in which the eyeball is
passively pushed forwards by a bulbar mass,
haemorrhage, oedema, inflammatory tissue or
neoplasm. However, some cases may give rise to a
false impression of proptosis, called pseudo-
proptosis.
.
• Proptosis : Abnormal protrusion of eye
ball is called proptosis or
exophthalmos
 Exophthalmos: The term exophthalmos
is reserved for prominence of the eye
secondary to thyroid disease
 Pseudoproptosis: slight prominence of
eyes like
◦ myopia,
◦ paralysis of extra ocular muscles,
◦ obese people,
◦ mullers stimulation by cocaine
CAUSES OF PROPTOSIS
 BILATERAL PROPTOSIS
 Dysthyroid eye disease.
Cavernous sinus thrombosis.
Metastatic neuroblastoma.
Orbital myositis (due to causes other than thyroid
dysfunction).
UNILATERAL PROPTOSIS :
 Haemangioma.
 Dermoid cyst.
 Lymphangioma.
 Rhabdomyosarcoma.
 Causes of Pseudo-Proptosis :
1. Unilateral Enlargement of the globe :
(a) Unilateral axial myopia.
(b) Unilateral congenital glaucoma.
(c) Unilateral infantile glaucoma.
(d) Congenital cystic eyeball.
2. Retraction of the Upper lid from any
cause
3. Asymmetry of the face or the bony
orbits
Types of proptosis
Axial VS Non-Axial
Axial proptosis - eye is pushed directly forwards,
lesions situated in optic nerve and central space •
Non axial- situated elsewhere in orbit pushes eye in
opposite direction
Axial Proptosis
◦ • Displaced along the visual axis
◦ • Intraconal pathology
◦ • Dysthyroid eye disease
 Non-Axial
◦ • Displacement off the visual axis
◦ • Extraconal pathology
◦ • Tumours
Clinical presentation
 Static- as seen usually in congenital
causes
 Increasing
◦ Fast- as in cases Rhabdomyosarcoma,
neuroblastoma, haemopoetic
◦ Gradual- as in cases of meningiomas
 Pulsatile- as in cases of carotid
cavernous fistula
 Intermittent- as in cases of orbital
varicosity
“Proptosis” Signs and Symptoms
• Change in appearance
– Unilateral
– Bilateral
– Sclera showing between superior lid and limbus
• Diplopia
– Non-axial proptosis
• Lagophthalmos
– Secondary dry eye issues
• Ophthalmoplegia
– Whole new set of symptoms
• Decreased BCVA
– Optic nerve head compression
Clinical signs
 • Impaired mobility
 • Diplopia
 • Papilloedema
 • Optic atrophy
 • Hertel exophthalmometry –
measures more than 18 mm
 • Difference in two eyes of more than
2 mm is considered positive
Causes of Proptosis in children
 • Dermoid and epidermoid cyst
 • Capillary haemangioma
 • Optic nerve glioma
 • Rhabdomyosarcoma
 • Leukaemias
 • Metastatic neuroblastoma
 • Plexiform neurofibromatosis
 • Lymphomas
Proptosis in adults
 Thyroid-Related Orbitopathy:
 Metastases – (of malignancy) from
breast, lung, GIT lung, GIT
 Cavernous haemangiomas
 Mucocele
 Lymphoid tumors
 Meningiomas
Investigations
 Careful history recording
 Systemic examination
 ENT examination
 Biochemical and haematological
investigations
 Imaging of bony structures- plain x ray
 Imaging of soft tissues –CT scan, MRI
 Vascular study- orbital venography,
carotid angiography, MR angiography,
digital subtraction angiography
Thyroid-Related Orbitopathy:
 Endocrine exophthalmos : Graves
Ophthalmopathy (dysthyroid eye disease) is
the commonest cause of uniocular or bilateral
proptosis in age groups between 25 and 50
years
 Graves Disease Consists of Exophthalmos,
and all signs of thyrotoxicosis (i.e.
tachycardia, muscular tremors and raised
BMR)
 In early stage the presentation may be
unilateral, becomes bilateral. Palpabral
aperture is wide open due to lid retraction.
Upper lid fail to follow downward movement
of eye (von Graefe sign)
Aetiology of Thyroid-Related
Orbitopathy: Grave’s Disease
• An immunological disorder
(autoimmune) that affects the orbital
muscles and fat
• Thyroid gland and orbital tissues
share surface antigens,
• Lymphocytes, mast cells, and finally
fibrosis infiltrate the conjunctiva,
lacrimal glands, intraconal fat, and
classically, the extraocular muscles
Aetiology contn.
 The precise cause is still obscure.
 Thought to arise from a malfunctioning of
the hypothalamic-pituitary-thyroid
hormonal axis.
 Ophthalmopathy of dysthyroid eye
disease may occur in apparently
euthyroid or even hypothyroid patients.
Clinically two distinct types, namely,
◦ the thyrotoxic and
◦ thyrotrophic types.
Thyrotoxic Exophthalmos
(Graves' Disease)
 Graves' disease is characterised by
hyperthyroid and exophthalmos. The
disease occurs often in females
between the ages 25-45 years
Etiology. —Thyrotoxic
exophthalmos was believed to be due
to an adrenaline-enhanced thyroxine
on the alpha receptors situated in the
smooth muscle of Muller leading to lid
retraction
Ocular Clinical Manifestations
 Exophthalmos - probably due to an increase in the bulk
of the orbital tissue, engorgement of the orbit with the
development of oedema,
 Lid retraction. - (contraction of the muscle of Muller and
weakness of the tone of the rectus muscles)
 Upper lid lag on downward gaze (Von Graefe s sign).
 Infrequent blinking (Stellwag's sign).
 Weakness of convergence for near objects (Moebius'
sign).
 Defective eye movements (Ballet's sign).
 Weak lateral gaze fixation (Suker's sign).
 Unequal pupillary dilatation (Knie's sign).
 Jerky pupillary consensual light contraction (Cowen 's
sign).
 Poor forehead wrinkling on upward gaze (Jojfoy's sign).
 Treatment
Local treatment of the ocular changes is extremely important.
 Protection of the exposed cornea is of prime importance. This is
achieved by the instillation of oily antiseptic and lubricants or the
use of a perforated transparent eye-shield.
 Surgical Treatment.
 —Lateral tarsorrhaphy may be indicated in moderate cases.
 For severe and progressive cases, radiotherapy and orbital
decompression, e.g. orbitotomy via maxillary antrum approach
may be indicated.
 Surgical treatment of extra-ocular muscle abnormalities should
usually be performed only after the defective eye movement has
been stable for at least six months.
Laboratory Assessment of Thyroid Function
ORBITAL TUMOURS
 These include tumours of the globe, optic nerve, lacrimal
system, other orbital contents and tumours of orbital walls.
PRIMARY ORBITAL TUMOURS
1. Developmental Tumours, e.g. dermoid cyst.
Dermoid Cyst. —It presents clinically as a cystic swelling at
the outer and less commonly the inner, upper angle orbit. The
cyst is small, freely mobile and contains sebaceous material
and hair follicles. It is often attached to the underlying bone in
which a defect can be demonstrated radiologically.
2. Vascular Tumours,.
Haemangioma of the Orbit. —It occurs in childhood or early
adult life at 9-16 years of age. It produces a slowly
developing, painless proptosis which is compressible,
sometimes pulsatile but never associated with a bruit. It is
usually unassociated with loss of ocular movements. In the
most typical cases, proptosis is increased by all
circumstances which increase venous congestion, e.g. crying,
straining or pressure on the jugular veins.
 3. Mesenchymal Tumours, e.g. fibroma and sarcoma.
4. Muscle Tumours, e.g. rhabdomyoma and
rhabdomyosarcoma.
5. Hemopoietic Tumours, e.g. Lymphoma,
lymphosarcoma, Hodgkin's disease, etc.
6. Nerve Tissue Tumours, e.g. glioma.
Glioma of the Optic Nerve.—The majority of cases
(88%) occurs before the age of 20 years. There is a
very slowly developing painless proptosis. Vision is
affected early and severely. This embryonic tumour is
an astrocytoma. It assumes a fusiform shape and
causes enlargement of the optic foramen which may be
demonstrated radiologically.
7. Epithelial Tumours, e.g. carcinoma and melanoma
of the lids and the conjunctiva.
Orbital Inflammation
 Myositis
◦ – Acute idiopathic inflammation of an
extraocular muscle
 Diffuse idiopathic orbital inflammation
◦ – Orbital pseudotumor
 Thyroid Eye Disease (Grave’s
disease)
Thank you

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2 Orbital Pathology Oghre.pptx

  • 1. Orbital Pathology/Lacrimal Pathology By Prof E. Oghre Professor of Optometry
  • 2. The orbit The orbit is the space bound by orbital bones ◦ Ethmoid bone ◦ Frontal bone ◦ Lacrimal bone ◦ Maxillary bone ◦ Palatine bone ◦ Sphenoid bone ◦ Zygomatic bone • Conical with a volume of approximately 27ml
  • 3.
  • 4. Orbital Wall Bones  Superior (roof) = Frontal .  Lateral wall = Zygoma, Sphenoid (greater wing).   Inferior (floor) = Maxilla (medial), zygoma (lateral), palatine (posterior).  Medial wall = Maxilla, lacrimal, ethmoid, sphenoid (anterior to posterior).
  • 5. .  The globe is positioned in the anterior portion of the orbit and constitutes about 20% of the entire volume of the orbit.  It is slightly closer to the lateral orbital wall than the medial wall and is nearer the roof than the floor of the orbit.  At its closest distance to the bony orbit the globe is about 4 mm from the roof, 4.5 mm from the lateral wall, 6.5 mm from the medial wall, and 6.8 mm from the floor.  The lateral orbital rim is considerably recessed compared with the medial orbit, which continues anteriorly to end at the nasal bridge. This leaves approximately one half of the globe unprotected.
  • 6. Orbit What can go wrong?  – Fractures  – Infection (Preseptal –Versus- (Septal) Orbital Cellulitis  – Proptosis (Thyroid Eye Disease /Grave’s Oculopathy)  – Inflammation  – Foreign Body  -- Neoplasms
  • 7. Causes of orbital diseases Children Adults Orbital Cellulitis Trauma Demoid and epidemoid cysts Thyroid Eye Disease Capiliary haemangioma and lymphangioma Idiopathic orbital inflammatory Disease(pseudotumour) Neurofibroma Lacrimal gland inflammation Rhabdosarcoma Capillary haemangioma Optic nerve glioma Lymphangioma Lipoma Meningioma metastasis For whatever reason, all of these either take up space or/and cause masses
  • 8. Fractures  Blowout fracture ◦ Break in floor of orbit (maxillary bone) ◦ Ethmoid fractures By the end of the lecture the students should be able to 1. Explain the mechanism of BOF of the orbit 2. Describe its symptoms & signs 3. Describe the complications 4. Outline the management
  • 9. Orbital fractures  The term "blowout fracture" refers specifically to a fracture of an orbital wall in the presence of an intact orbital rim.  A relatively common form of periorbital injury.  Although any bone surrounding the orbit may be fractured, the thin bones of the orbital floor and medial orbital wall are most vulnerable.  The most common site for a blowout fracture is the thin part of the maxillary bone (0.5-mm thick) in the posterior medial aspect of the floor.  In addition, the very thin ethmoid bone (0.25- mm thick) along the medial wall of the orbit may be involved  Due to the relative thickness of the orbital rim, it is often spared in orbital fractures.
  • 10. BLOW-OUT FRACTURE OF THE ORBIT • Secondary to massive blow to the orbit resulting in fracture of one/ more of its walls ( mostly medial wall & floor) • Common in sports & violence related trauma • Mechanism involves sudden rise of intraorbital pressure & fracture of the bony socket at its weakest points
  • 11. Clinical presentation • Symptoms ; history of trauma with double vision, pain in and around the orbit, visual loss ( not always) • Signs; periocular swelling, bruising ( ecchymosis), subcutaneous emphysema • Enophthlamos; in large & severe fractures & increases with time • Infraorbital nerve hypoesthesia
  • 12. Clinical presentation • EOM abnormalities; vertical diplopia, limited upgaze & downgaze --- floor fractures, limited adduction & abduction ---medial wall fracture • Ocular/ associated damage to the eyeball – Hyphaema – RD – Damage to the angle of the anterior chamber— glaucoma – Vitreous haemorrhage – Orbital hematoma – Damage to the optic nerve
  • 13.  Muscle entrapment of right eye with inability to look up
  • 14.  • Your observations  ––––  • History ?  –  • Symptoms  ––––  Which is affected eye?????  Remember: always examine patient with  all lights on and grossly, initially
  • 15.  Your observations  Bruising ◦ Ecchymosis – 1 to 3 cm ◦ Purpura – 3mm to 1 cm ◦ Petechiae – < 3mm  – EOM restriction ◦ Ophthalmoplegia  – Conjunctival injection  -- Oedema  – (Pseudo)Ptosis ◦ Lid droop NOT caused by weakening muscle  • History ? ◦ hit with……….  • Trauma history  • Symptoms ◦ Pain ◦ Diplopia ◦ Tearing ◦ Mild blur to vision (If JUST the blowout fracture)  – Crepitus ( Describes the grating, crackling or popping sounds and sensations experienced)
  • 16.  Critical signs of recent blow-out fracture include: ◦ • edema and ecchymosis of the lid tissues ◦ • restriction of ocular motility, especially with vertical movements ◦ • orbital crepitus (subcutaneous emphysema) ◦ • hypoesthesia of the ipsilateral cheek, due to entrapment of the infraorbital nerve
  • 17. Complications  EOM problems  Visual loss  Cosmetic  Secondary infection from the sinuses- orbital cellulitis & spread of the infected contents of the sinuses to the vital tissues like the eyeball & the brain
  • 18. Investigations/ confirmatory tests For confirmation of fracture  CT scan / X ray orbit For confirmation of muscle entrapment  CT scan & forced duction test
  • 19. Management  Symptomatic/ conservative: ◦ NSAID for relief of pain & reduction of inflammation ◦ discourage blowing of the nose to prevent forcing of the infected sinus contents into the orbit ◦ antibiotics  If the diplopia persist beyond 2 weeks/ enophthamos is significant then surgical repair of the fracture with release of entrapped muscles may be required
  • 20.  Blowout fracture is not a common disorder but is common in sports & violence related trauma, it can mostly be managed conservatively but in case of a large fracture or persistent EOM problems & enophthalmos may require surgical repair.
  • 21. Cellulitis of the eye  This can be two different types, ◦ Orbital cellulitis - Purulent inflammation of the cellular tissue of the orbit ◦ Preseptal cellulitis - Purulent inflammation of the cellular tissue of the eyelid  Preseptal cellulitis can be regarded purely as an eyelid problem, but it is treated here for ease of understanding
  • 22.  ORBITAL CELLULITIS By the end of the lecture the students should be able to 1. Differentiate between preseptal and true orbital cellulitis 2. Explain why it is considered to be an ocular emergency 3. Describe the causes, 4. Explain the clinical presentation, complications & line of management of orbital cellulitis
  • 23. ORBITAL CELLULITIS  Definition: Purulent inflammation of the cellular tissue of the orbit  – Infection posterior to the orbital septum (anywhere in the orbit)  – Dangerous condition because of the close proximity to the orbital apex, cavernous sinus, meninges and brain, This should be differentiated from Preseptal cellulitis in which the Infection is anterior to the orbital septum
  • 24. Preseptal cellulitis  Infection of the subcutaneouss tissue anterior to the orbital septum ( lids)  Causes: ◦ Trauma; lid laceration/ insect bite ◦ Spread from local infection; stye/ dacrocystitis ◦ Spread from remote infection; haemotogenous spread from middle ear/ Upper Respiratory Tract
  • 25. Clinical presentation of Preseptal cellulitis  Symptoms; ◦ History of predisposing factor, ◦ pain ◦ swelling of the lid, mild fever  Signs; ◦ red swollen tender lids sometimes the lids may be difficult to open.  Important negative signs are:  Eye itself is normal or at the most might be mildly congested  Visual acuity is normal  No proptosis  No ocular motility problem  Normal pupils
  • 27. Complications ◦True orbital cellulitis ◦Lid abscess ◦Cavernous sinus thrombosis
  • 28. management  To prevent the possibly disastrous spread of infection to the postseptal area, it is crucial to quickly suppress the infection. Oral therapy is necessary;  Topical antibiotics  Oral antibiotics – amoxicillin – 500mg TID or  Amoxicillin/clauvenate (Augumentin) 625mg TID or  Cefaclor 250-500mg p.o. QID or  Trimetheprim (320mg)/ sulfemethoxazole 60mg daily in (BD)
  • 29. ORBITAL CELLULITIS  Infection of the soft tissues behind the orbital septum ( deeper to lids)  Ocular emergency , could be life threatening  Most frequent pathogens are; Strept pneumoniae ,Staph aureus, Strept pyogenes & Haem influenzae - (under 5 yrs children)
  • 30. Aetiology  Commonly caused by the spread of infection from the neighbouring areas, i.e. ethmoidal sinusitis, lacrimal abscess, stye or suppurating chalazion, dental infection, facial infection, infection of the eyeball (panophthalmitis etc)  Spread from the sinuses is the most common cause)  Rarely direct infection by a penetrating wound, especially if a foreign body is retained within the orbit.  Metastatic infection via the blood stream, e.g. in cases of pyaemia. Extension from preseptal cellulitis  Haemotogenous spread  Post- traumatic; accidental/ surgical
  • 31.  Causative agents include ◦ Bacterial – Streptococcus species, Staph aureus, and Haemophilus influenzae type B. Pseudomonas, Klebsiella, Eikenella, and Enterococcus ◦ • Fungal – Mucor and Aspergillus ◦ • Parasitic
  • 32. Clinical presentation  Symptoms; ◦ rapid onset painful swelling of the lids ◦ protrusion of the eye, ◦ fever, malaise ◦ visual loss ◦ history of risk factors  Signs; ◦ moderate to severe swelling of the lids, reduced visual acuity, ◦ proptosis, red eye ◦ chemosis of the conjunctiva, ◦ abnormal & painful EOM & pupillary response
  • 33. The following signs are most important  Ocular.—: (a) Severe pain in the orbit which increases during ocular movements. (b) Lid oedema with redness of the skin (c) Chemosis of the conjunctiva. (d) Proptosis which is axial and irreducible. (e) Limitation of ocular movements , diplopia. (f) Fundus examination may reveal engorged retinal veins and sometimes papillitis. Abscess formation may occur. It may burst through the skin of the eyelids near the orbital margin or in the conjunctival fornix.  General.—Fever, malaise are common symptoms. Sometimes cerebral symptoms supervene
  • 34.
  • 35. Complications Ocular; corneal damage( exposure), raised IOP, vascular occlusions, optic nerve damage, endophthalmitis, Panophthalmitis • In diabetic patients fungal superinfection may develop Intracranial; Extension into brain through meninges , cavernous sinus thrombosis may develop, meningitis, brain abscess,
  • 36. Management  A swab is taken from the conjunctival sac for culture and sensitivity test  Vigorous systemic and local use of antibiotic drugs to which the causative micro-organisms are sensitive,  Local heat by frequent hot bathing is very beneficial.  If abscess formation is suspected, early incision is recommended.
  • 37. Management  Culture and sensitivity of pus and of blood  Treatment  Symptomatic: Antipyretic, NSAIDS and Anti inflammatory  Broad spectrum Intravenous antibiotics  Specific ; hospitalization & antibiotic therapy ◦ Ceftazidime 1 g tds , I/M ◦ Metronidazole 500mg tds, PO ◦ Vancomycin in case of allergy to the above mentioned  If abscess has formed – Incision and Drainage under cover of antibiotics. Surgical intervention in case of local abscess or unresponsive cases  Consultation with ENT specialist, neurosurgeon & paediatrician if required
  • 38. Summary  Orbital cellulitis is differentiated from preseptal cellulitis with the following signs:  – Pain with eye movements  – Ophthalmoplegia  – Proptosis  – Globe displacement  – Decreased vision or vision defect.  Both preseptal and orbital cellulitis may have: ◦ Fever ◦ Eyelid swelling ◦ Pain ◦ Red eye ◦ Child is ill-appearing
  • 39. Case 1  A 1 year old child presented to the Optometry clinic with the complaint of a swollen right upper lid for the last two days. On examination the lid was red, warm & tender to touch. His visual acuity was normal, the eye had mild conjunctival redness, the pupil was normal and the ocular movements were also normal.
  • 40. 1. Is the condition confined to the lids or has it involved the eyeball? 2. Why do you think so? 3. What more information would you like to have before making a diagnosis?
  • 41.  The child had a history of insect bite on the lid two days ago, the swelling increased thereafter. The insect bite mark was visible  There was no history of trauma or symptoms suggestive of sinusitis  His temperature was 990 F
  • 42.  What should be the management, keeping in mind the nature of the problem?  Is there any role of health education in this case? Let us see an other case……..
  • 43. Case 2  A seven year old child was brought the Optometry clinic with history of swollen left upper lid for the last 5 days. He also had fever for the last two days.  On examination the child had a grossly swollen lid. The doctor had difficulty in opening the lid for examination of the eye. The visual acuity was 6/6 OD & 6/18 OS. The lid was warm and tender. The eye was moderately proptosed with conjunctival chemosis. The pupil was slow to react to light and the ocular movements were painful & limited. The temperature was 1010 F & the child looked generally unwell……..
  • 44. 1. Is the condition confined to the lids or has it involved inner orbit? 2. What more information should we ask for to get an idea about the cause of the problem?
  • 45. .  The child had a history of recurrent flu and upper respiratory tract infections. He had history of blocked nose and thick greenish nasal discharge was noted on examination.  The child was put on intravenous antibiotics but didn’t get better
  • 46.  What should be the management, keeping in mind the nature of the problem?  What is the difference between the two cases?  We consider the second case an ocular emergency, why?  What other complications could happen in the second case?
  • 47. PROPTOSIS NOT a diagnosis, a SIGN of underlying orbital disease  Proptosis is a condition in which the eyeball is passively pushed forwards by a bulbar mass, haemorrhage, oedema, inflammatory tissue or neoplasm. However, some cases may give rise to a false impression of proptosis, called pseudo- proptosis. .
  • 48. • Proptosis : Abnormal protrusion of eye ball is called proptosis or exophthalmos  Exophthalmos: The term exophthalmos is reserved for prominence of the eye secondary to thyroid disease  Pseudoproptosis: slight prominence of eyes like ◦ myopia, ◦ paralysis of extra ocular muscles, ◦ obese people, ◦ mullers stimulation by cocaine
  • 49. CAUSES OF PROPTOSIS  BILATERAL PROPTOSIS  Dysthyroid eye disease. Cavernous sinus thrombosis. Metastatic neuroblastoma. Orbital myositis (due to causes other than thyroid dysfunction). UNILATERAL PROPTOSIS :  Haemangioma.  Dermoid cyst.  Lymphangioma.  Rhabdomyosarcoma.
  • 50.  Causes of Pseudo-Proptosis : 1. Unilateral Enlargement of the globe : (a) Unilateral axial myopia. (b) Unilateral congenital glaucoma. (c) Unilateral infantile glaucoma. (d) Congenital cystic eyeball. 2. Retraction of the Upper lid from any cause 3. Asymmetry of the face or the bony orbits
  • 51. Types of proptosis Axial VS Non-Axial Axial proptosis - eye is pushed directly forwards, lesions situated in optic nerve and central space • Non axial- situated elsewhere in orbit pushes eye in opposite direction Axial Proptosis ◦ • Displaced along the visual axis ◦ • Intraconal pathology ◦ • Dysthyroid eye disease  Non-Axial ◦ • Displacement off the visual axis ◦ • Extraconal pathology ◦ • Tumours
  • 52. Clinical presentation  Static- as seen usually in congenital causes  Increasing ◦ Fast- as in cases Rhabdomyosarcoma, neuroblastoma, haemopoetic ◦ Gradual- as in cases of meningiomas  Pulsatile- as in cases of carotid cavernous fistula  Intermittent- as in cases of orbital varicosity
  • 53. “Proptosis” Signs and Symptoms • Change in appearance – Unilateral – Bilateral – Sclera showing between superior lid and limbus • Diplopia – Non-axial proptosis • Lagophthalmos – Secondary dry eye issues • Ophthalmoplegia – Whole new set of symptoms • Decreased BCVA – Optic nerve head compression
  • 54. Clinical signs  • Impaired mobility  • Diplopia  • Papilloedema  • Optic atrophy  • Hertel exophthalmometry – measures more than 18 mm  • Difference in two eyes of more than 2 mm is considered positive
  • 55. Causes of Proptosis in children  • Dermoid and epidermoid cyst  • Capillary haemangioma  • Optic nerve glioma  • Rhabdomyosarcoma  • Leukaemias  • Metastatic neuroblastoma  • Plexiform neurofibromatosis  • Lymphomas
  • 56. Proptosis in adults  Thyroid-Related Orbitopathy:  Metastases – (of malignancy) from breast, lung, GIT lung, GIT  Cavernous haemangiomas  Mucocele  Lymphoid tumors  Meningiomas
  • 57. Investigations  Careful history recording  Systemic examination  ENT examination  Biochemical and haematological investigations  Imaging of bony structures- plain x ray  Imaging of soft tissues –CT scan, MRI  Vascular study- orbital venography, carotid angiography, MR angiography, digital subtraction angiography
  • 58. Thyroid-Related Orbitopathy:  Endocrine exophthalmos : Graves Ophthalmopathy (dysthyroid eye disease) is the commonest cause of uniocular or bilateral proptosis in age groups between 25 and 50 years  Graves Disease Consists of Exophthalmos, and all signs of thyrotoxicosis (i.e. tachycardia, muscular tremors and raised BMR)  In early stage the presentation may be unilateral, becomes bilateral. Palpabral aperture is wide open due to lid retraction. Upper lid fail to follow downward movement of eye (von Graefe sign)
  • 59. Aetiology of Thyroid-Related Orbitopathy: Grave’s Disease • An immunological disorder (autoimmune) that affects the orbital muscles and fat • Thyroid gland and orbital tissues share surface antigens, • Lymphocytes, mast cells, and finally fibrosis infiltrate the conjunctiva, lacrimal glands, intraconal fat, and classically, the extraocular muscles
  • 60. Aetiology contn.  The precise cause is still obscure.  Thought to arise from a malfunctioning of the hypothalamic-pituitary-thyroid hormonal axis.  Ophthalmopathy of dysthyroid eye disease may occur in apparently euthyroid or even hypothyroid patients. Clinically two distinct types, namely, ◦ the thyrotoxic and ◦ thyrotrophic types.
  • 61. Thyrotoxic Exophthalmos (Graves' Disease)  Graves' disease is characterised by hyperthyroid and exophthalmos. The disease occurs often in females between the ages 25-45 years Etiology. —Thyrotoxic exophthalmos was believed to be due to an adrenaline-enhanced thyroxine on the alpha receptors situated in the smooth muscle of Muller leading to lid retraction
  • 62. Ocular Clinical Manifestations  Exophthalmos - probably due to an increase in the bulk of the orbital tissue, engorgement of the orbit with the development of oedema,  Lid retraction. - (contraction of the muscle of Muller and weakness of the tone of the rectus muscles)  Upper lid lag on downward gaze (Von Graefe s sign).  Infrequent blinking (Stellwag's sign).  Weakness of convergence for near objects (Moebius' sign).  Defective eye movements (Ballet's sign).  Weak lateral gaze fixation (Suker's sign).  Unequal pupillary dilatation (Knie's sign).  Jerky pupillary consensual light contraction (Cowen 's sign).  Poor forehead wrinkling on upward gaze (Jojfoy's sign).
  • 63.  Treatment Local treatment of the ocular changes is extremely important.  Protection of the exposed cornea is of prime importance. This is achieved by the instillation of oily antiseptic and lubricants or the use of a perforated transparent eye-shield.  Surgical Treatment.  —Lateral tarsorrhaphy may be indicated in moderate cases.  For severe and progressive cases, radiotherapy and orbital decompression, e.g. orbitotomy via maxillary antrum approach may be indicated.  Surgical treatment of extra-ocular muscle abnormalities should usually be performed only after the defective eye movement has been stable for at least six months. Laboratory Assessment of Thyroid Function
  • 64. ORBITAL TUMOURS  These include tumours of the globe, optic nerve, lacrimal system, other orbital contents and tumours of orbital walls. PRIMARY ORBITAL TUMOURS 1. Developmental Tumours, e.g. dermoid cyst. Dermoid Cyst. —It presents clinically as a cystic swelling at the outer and less commonly the inner, upper angle orbit. The cyst is small, freely mobile and contains sebaceous material and hair follicles. It is often attached to the underlying bone in which a defect can be demonstrated radiologically. 2. Vascular Tumours,. Haemangioma of the Orbit. —It occurs in childhood or early adult life at 9-16 years of age. It produces a slowly developing, painless proptosis which is compressible, sometimes pulsatile but never associated with a bruit. It is usually unassociated with loss of ocular movements. In the most typical cases, proptosis is increased by all circumstances which increase venous congestion, e.g. crying, straining or pressure on the jugular veins.
  • 65.  3. Mesenchymal Tumours, e.g. fibroma and sarcoma. 4. Muscle Tumours, e.g. rhabdomyoma and rhabdomyosarcoma. 5. Hemopoietic Tumours, e.g. Lymphoma, lymphosarcoma, Hodgkin's disease, etc. 6. Nerve Tissue Tumours, e.g. glioma. Glioma of the Optic Nerve.—The majority of cases (88%) occurs before the age of 20 years. There is a very slowly developing painless proptosis. Vision is affected early and severely. This embryonic tumour is an astrocytoma. It assumes a fusiform shape and causes enlargement of the optic foramen which may be demonstrated radiologically. 7. Epithelial Tumours, e.g. carcinoma and melanoma of the lids and the conjunctiva.
  • 66. Orbital Inflammation  Myositis ◦ – Acute idiopathic inflammation of an extraocular muscle  Diffuse idiopathic orbital inflammation ◦ – Orbital pseudotumor  Thyroid Eye Disease (Grave’s disease)