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Duke Elder > Orbit > Flashcards

Orbit Flashcards

1
Q

Optic foramen

A

Found on the lesser wing of the sphenoid bone
Transmits the optic nerve and the ophthalmic artery

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2
Q

Superior orbital fissure

A

Lies between the greater and lesser wings of the sphenoid bone

Contains: Superior ophthalmic vein, lacrimal (CNV1) and frontal nerves (CNV1) and CN4

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3
Q

What structures are found within the superior orbital fissure and the common tendinous ring?

A

CN3, CN6, and nasociliary nerve (CNV1)

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4
Q

Inferior orbital fissure

A

Lies between the maxilla and the greater wing of the sphenoid

Contains: infraorbital(CNV2) and zygomatic nerves(CNV2), and the inferior ophthalmic vein

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5
Q

Retrobulbar anesthesia

A

Affects all the nerves within the common tendinous ring (annulus of Zinn)

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6
Q

Bones of the Orbit

A
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7
Q

Which wall of the orbit is the weakest

A

Medial wall

It has a thin transparent membrane called the lamina papyracea through which infection can easily spread. This is how ethmoid cellulitis can lead to orbital cellulitis.

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8
Q

What is shown below?

A

A Hertel exophthalmometer -used to measure the degree of proptosis.

> > 20mm indicates proptosis and any difference between the eyes should be investigated further

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9
Q

Types of Exophthalmos

A

Axial proptosis (straight out) indicates a lesion within the tendinous ring such as optic nerve glioma and cavernous haemangioma.

Non-axial proptosis (protrusion at an angle) indicates a lesion outside the tendinous ring such as the lacrimal gland

Pseudoproptosis is the false appearance of proptosis and is typically due to facial anatomy.

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10
Q

Enophthalmos

A

Can be congenital as a result of atrophy of the ocular contents

Psuedoenophthalmos can be seen in a small eye (microphthalmos), ptosis or proptosis of the fellow eye.

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11
Q

Compare preseptal vs orbital cellulitis

A
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12
Q

How is orbital vs preseptal cellulitis anatomically demarcated

A

By the orbital septum which is a membrane that extends from the orbital rim and inserts into the eyelids.

CT of the orbit confirms the diagnosis

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13
Q

Most common cause of axial proptosis in adults?

A

Thryoid eye disease

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14
Q

Stages of thyroid eye disease

A

An active inflammatory stage in which the eyes are red and painful

Followed by a fibrotic phase involving the extraocular muscles where there is oedema and fibrosis. This leads to restrictive myopathy, exophthalmos and optic neuropathy

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15
Q

Pathomechanism of thyroid eye disease

A

TSH IgG binds to TSHr on extraocular muscles and fibroblasts → leads to adipogenesis and hyaluronic acid deposition in orbital muscle → leads to swelling of muscles and fat

Lid retraction occurs due to the sympathetic overstimulation of Muller’s muscle

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16
Q

Most important risk factor for thyroid eye disease?

A

Smoking

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17
Q

Presentation of thryoid eye disease

A

Typically hyperthyroid but can be eu/hypothyroid
Axial proptosis
Lid retraction (Dalrymple sign)
Lid lag (Von Graefe sign)
Characteristic staring appearance (Kocher sign)
Restrictive myopathy

Half the patients with superior limbic keratoconjunctivitis also have TED

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18
Q

What causes Lid retraction (Dalrymple sign)

A

occurs due to sympathetic overstimulation of Muller’s muscle, driven by elevated thyroid hormone

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19
Q

What muscle is affected first in thyroid eye disease?

A

Restrictive myopathy typically affects the inferior rectus first

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20
Q

Investigations for thyroid eye disease

A

CT of the orbit characteristically shows thickening of extraocular/levator muscle and sparing of the tendons

Anti-TSHr antibody

(If there are signs of optic neuropathy (dyschromatopsia, RAPD, field and acuity defects) urgent anti-inflammatory treatment is needed to prevent vision loss)

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21
Q

Management of thyroid eye disease

A
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22
Q
A

An MRI of a patient with thyroid eye disease. The arrows point to enlarged extraocular muscles.

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23
Q

List 3 other causes of Orbital Inflammation

A
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24
Q
A

A is an MRI of a patient with optic nerve sheath meningioma. B is an MRI of a patient with optic nerve glioma. The arrows highlight the nerve and the meninges.

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25
Commonest primary childhood orbital malignancy
Rhabdomyosarcoma
26
Rhabdomyosarcoma
27
Childhood Orbital Tumours
28
Adulthood Orbital Tumours
29
Carotid Cavernous Fistula (CCF)
CCF is an AV malformation between the carotid artery and the cavernous sinus. There are 2 types of CCF and an angiogram is used to provide a definitive diagnosis.
30
Compare the two types of CCF
31
Corkscrew epibulbar vessels seen in a patient with indirect carotid-cavernous sinus fistula.
32
Cavernous Sinus Thrombosis
A clot within the cavernous sinus (venous blood sinus) Typically caused by spreading infection.
33
Cavernous sinus thrombosis presentation
Acute onset headache, nausea, proptosis and diplopia Caused by compression of CN3, CN4 and CN6 as they traverse the sinus
34
Investigations for cavernous sinus thrombosis
MRI with MRI venogram is diagnostic.
35
Which CN is affected first in a cavernous sinus thrombosis
CN6 is first affected because it travels within the sinus as opposed to CN3 and CN4 which travel within the walls of the sinus.
36
Management of cavernous sinus thrombosis
Antibiotics Steroids Thrombolytic medications Surgical drainage
37
Orbital Varices
Orbital varices are venous enlargements within the orbit Typically unilateral and medial. Key defining feature is intermittent proptosis Worsened by the Valsalva maneuver.
38
IOFB - Copper
Pure copper is the most ocular toxic heavy metal in common use Alloys of copper can lead to Sunflower cataracts and Kayser-Fleischer rings (the signs of Wilson's disease)
39
Other bodies
Iron deposits in the ocular epithelial tissue and lead to cell death, resulting in glaucoma, cataract and retinal detachment. Glass, plastic, stone, silver, gold, platinum and lead are all inert Aluminium and zinc have mild toxic effects
40
Investigations for Intraocular Foreign Bodies (IOFB)
CT/X-ray should be taken in all cases MRI is contraindicated as some bodies can be magnetised. Visual evoked potential testing will show a reduced b-wave in some cases of chronically retained IOFB.
41
Management of IOFB
If there is a penetrating injury then primary repair of the globe is the priority. Foreign body removal technique depends on the location.
42
A Chemical burn injury that has resulted in ocular surface failure with neovascularization of the cornea and blindness.
43
Pathology of chemical burns to the eye
Alkali injury is significantly worse than acid. Alkalis cause liquefactive necrosis Acids cause coagulative necrosis
44
How is Corneal healing achieved?
Corneal healing is achieved by the migration of limbal stem cells. If the limbus is damaged then healing is hindered.
45
Management of chemical burns
1. Irrigation with copious amounts of water 2. Antibiotics + cycloplegics + lubricants + analgesia 3. Topical steroids 4. Ascorbic acid - aids collagen formation and mops up free radicals. Should not be used in acid burns! 5. Doxycycline - proteinase inhibitor which aids healing
46
Management of prolonged corneal healing problems
Amniotic membrane transplant Limbal stem cell transplant
47
Role of topical sodium citrate
inhibits collagenases and aids healing. However, administration is painful and so it is not in common use.
48
Pathology of Orbital Floor Fractures
Classically caused by ball/fist injury to the eye Soft tissue of the globe is pushed into the maxillary sinus The inferior rectus can be entrapped, causing vertical diplopia and restriction of eye elevation
49
Surgical emphysema in orbital floor fractures?
Surgical emphysema can also occur in orbital floor fractures but is more pronounced in medial wall fractures.
50
Presentation of orbital wall fractures
Periorbital bruising Vertical diplopia and extraocular muscle entrapment Enophthalmos Infraorbital anaesthesia
51
Investigations for orbital wall fractures
CT is diagnostic Hess charts are used in monitoring and follow-up
52
Left orbital floor fracture seen on CT
53
What movements are resticted if extraocular muscles are extrapped?
In extraocular muscle entrapment, the antagonistic movement is restricted. I.e if the superior rectus is trapped, downgaze will be restricted.
54
Management of orbital wall fractures
Surgery does not have to be immediate, if at all necessary Indications for immediate surgery include: oculocardiac reflex and severe facial destruction. If there is only minimal diplopia and enophthalmos, observation can suffice. **Advise patients to avoid blowing their nose
55
Retrobulbar Haemorrhage
The bony orbit is a rigid chamber and intraorbital bleeding/swelling can lead to a sharp rise in pressure. This is an ophthalmic emergency and can result in blindness.
56
Pathology of Retrobulbar Haemorrhage
Trauma causes oedema/bleeding in the orbit and leads to a rise in intraorbital pressure. Rising intraorbital pressure restricts blood flow and causes optic nerve damage. The process can be thought of as orbital compartment syndrome
57
Presentation of Retrobulbar Haemorrhage
Painful loss of vision Rigid proptosis Restricted ocular movements RAPD Elevated intraocular pressure
58
Investigation for Retrobulbar Haemorrhage
Radioimaging can aid diagnostics but treatment should not be delayed
59
Management of Retrobulbar Haemorrhage
Immediate: IV mannitol + IV acetazolamide + IV methylprednisolone No improvement to medications or severe: Lateral canthotomy and cantholysis Still no improvement: Orbital decompression
60
What is Cantholysis?
Cantholysis is the disinsertion of the lateral canthal tendon. This procedure allows the release of intraorbital pressure.
61
Hyphema
Hyphema is blood in the anterior chamber and is most commonly caused by blunt trauma.
62
Hyphema Pathology
Hyphema is a sign of ocular trauma and warrants further investigation Microhyphema is when the erythrocytes are only visible on a slit lamp
63
Hyphema - occupying half of the anterior chamber
64
Hyphema Pathology
Hyphema is a sign of ocular trauma and warrants further investigation Microhyphema is when the erythrocytes are only visible on a slit lamp
65
Investigations for hyphema
Check drug history for anticoagulants Check medical history for coagulative disorders and sickle cell
66
Management of hyphema
Treatment only required in high-risk cases ie. children, rebleeds and risky medical histories 1. Admit for steroids and bedrest 2. Monitor IOP for red cell glaucoma 3. No improvement → AC paracentesis 4. Trabeculectomy - if all else fails

Duke Elder (12 decks)

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