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Duke Elder > Orbit > Flashcards

Orbit Flashcards

1
Q

List the orbital openings.

A
  • Optic foramen.
  • Superior orbital fissure.
  • Inferior orbital fissure.
  • Tendinous ring (Annulus of Zinn)
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2
Q

Where is the optic foramen found?

A

Found on the lesser wing of the sphenoid bone.

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3
Q

What runs through the optic foramen?

A
  • Optic nerve.
  • Ophthalmic artery.
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4
Q

Where is the superior orbital fissure found?

A

Lies between the greater and lesser wings of the sphenoid bone.

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5
Q

What runs through the superior orbital fissure?

A

(LFTs)
- Lacrimal nerve (CNV1).
- Frontal nerve (CNV1).
- Trochlear nerve (CN4).
- Superior ophthalmic vein.

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6
Q

Where is the inferior orbital fissure found?

A

Lies between the maxilla and the greater wing of the sphenoid.

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7
Q

What runs through the inferior orbital fissure?

A
  • Inferior ophthalmic veins.
  • Infraorbital nerve (CNV2).
  • Zygomatic nerve (CNV2).
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8
Q

What runs through the tendinous ring (annulus of Zinn)?

A
  • CN3 upper division.
  • Nasociliary nerve (CN5a).
  • CN3 lower division.
  • CN6.
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9
Q

Which bones make up the roof of the orbit?

A

‘Front S’
- Frontal bone.
- Lesser wing of the sphenoid.

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10
Q

Which bones make up the medial wall of the orbit?

A

‘SMEL’
- Sphenoid.
- Maxillary.
- Ethmoid.
- Lacrimal.

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11
Q

Which bones make up the floor of the orbit?

A

‘My Zipped Pants’
- Maxillary.
- Zygomatic.
- Palatine.

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12
Q

Which bones make up the lateral wall of the orbit?

A

‘Greater Z’
- Greater wing of the sphenoid.
- Zygomatic.

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13
Q

Which aspect of the orbit is weakest? Why?

A
  • Medial wall.
  • 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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14
Q

What is the hallmark of orbital disease?

A

Eyeball sitting abnormally in the socket.

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15
Q

What is a Herten exophthalmometer? What is considered abnormal?

A

Machine used to measure the protrusion of the globe in the orbit.

> 20mm indicates proptosis.

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16
Q

What are the 3 types of exophthalmos?

A
  • Axial proptosis.
  • Non-axial proptosis.
  • Pseudoproptosos.
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17
Q

What is axial proptosis?

A

Straight out.

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18
Q

What does axial proptosis indicate?

A

Lesion within the tendinous ring such as optic nerve glioma and cavernous haemangioma.

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19
Q

What is non-axial proptosis?

A

Protrusion at an angle.

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20
Q

What does non-axial proptosis indicate?

A

Lesion outside the tendinous ring such as the lacrimal gland.

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21
Q

What is pseudoproptosis? Why does this happen?

A
  • False appearance of proptosis.
  • Typically due to facial anatomy.
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22
Q

What is the difference between proptosis and exophthalmos?

A

Proptosis is the protrusion of any organ whereas exophthalmol is proptosis of the eye.

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23
Q

What is enophthalmos?

A

Sunken eyes, opposite of exophthalmos.

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24
Q

What causes enophthalmos?

A

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

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25
Q

When may pseudoenophthalmos be seen?

A

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

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26
Q

What are the two types of cellulitis seen in ophthalmology?

A

Preseptal and orbital.

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27
Q

What is the main difference between preseptal and orbital cellulitis?

A

Orbital cellulitis is severe and preseptal cellulitis is mild.

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28
Q

Where does preseptal cellulitis occur as opposed to orbital cellulitis?

A

Preseptal: anterior to the orbital septum.
Orbital: eye socket behind the orbital septum.

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29
Q

What typically causes preseptal cellulitis as opposed to orbital cellulitis?

A

Preseptal: direct infection from lid trauma (Staph aureus).
Orbital: infection via air sinuses (ethmoid sinus) by Strep pneumoniae or H. influenzae.

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30
Q

How do patients present in preseptal cellulitis as opposed to orbital cellulitis?

A

Preseptal: lid inflammation and low-grade fever, no signs of eye involvement.
Orbital:
- Children.
- Acutely inflamed orbit.
- Proptosis.
- Fever.
- Restricted ocular movements.
- Defects in vision.
- RAPD.

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31
Q

How is preseptal cellulitis treated as opposed to orbital cellulitis?

A

Preseptal: PO antibiotics.
Orbital: IV antibiotics (admit due to risk of progression into brain).

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32
Q

How are preseptal and orbital cellulitis anatomically demarcated?

A

Demarcated by the orbital septum.

This is a membrane that extends from the orbital rim and inserts into the eyelid.

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33
Q

What is the most common cause of axial proptosis in adults?

A

Thyroid eye disease.

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34
Q

What are the stages of thyroid eye disease?

A
  1. Active inflammatory stage - eyes are red and painful.
  2. Fibrotic phase - oedema and fibrosis, leading to restrictive myopathy, exophthalmos and optic neuropathy. Involved extraocular muscles.
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35
Q

What is the pathophysiology 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.

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36
Q

What causes lid retraction in thyroid eye disease?

A

Sympathetic overstimulation of Muller’s muscle.

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37
Q

What is the single biggest risk factor for thyroid eye disease?

A

Smoking.

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38
Q

Which condition is most associated with thyroid eye disease?

A

Superior limbic keratoconjunctivitis.

N.B., around half of these patients will also have thyroid eye disease.

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39
Q

Describe the presentation of thyroid eye disease.

A
  • Hyperthyroid typically (not always).
  • Axial proptosis.
  • Lid retraction (Dalrymple sign).
  • Lid lag (Von Graefe sign).
  • Characteristic staring appearance (Kocher sign).
  • Restrictive myopathy typically affects the inferior rectus first.
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39
Q

What is Kocher sign?

A

Characteristic staring appearance.

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39
Q

What is Von Graefe sign?

A

Lid lag.

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40
Q

What is Dalrymple’s sign?

A

Lid retraction.

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41
Q

Which muscle is affected first and most commonly in thyroid eye disease?

A

Inferior rectus.

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42
Q

Which investigations are used to diagnose thyroid eye disease?

A
  • CT of the orbit > thickening of extraocular/levator muscle and sparing of the tendons.
  • Anti-TSHr antibody.
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43
Q

Describe the management of severe/acute thyroid eye disease.

A
  • IV methylprednisolone followed by oral prednisolone.
  • Orbital radiation if steroids are contraindicated.
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44
Q

Describe the management of mild/chronic thyroid eye disease.

A
  • Lubricants.
  • Taping - to minimise exposure keratopathy.
  • Topical cyclosporine to reduce inflammation.
  • Aim for euthyroid.
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45
Q

Describe the management of the fibrotic phase of thyroid eye disease?

A

Orbital decompression surgery.

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46
Q

When do we initiate management for severe/acute thyroid eye disease?

A

If there are signs of optic neuropathy:
- Dyschromatopsia.
- RAPD.
- Field and acuity defects.

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47
Q

What are three other causes (aside from thyroid eye disease and cellulitis) that can cause orbital inflammation?

A
  • Tolosa-Hunt syndrome.
  • Granulomatosis with polyangiitis (Wegener’s granulomatosis).
  • Sarcoidosis.
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48
Q

What is Tolosa-Hunt syndrome? What is it caused by?

A
  • Syndrome of headache, ophthalmoplegia and periorbital sensory loss.
  • Caused by granulomatous inflammation of the orbit, cavernous sinus or superior orbital fissure.
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49
Q

What is the key feature of Tolosa-Hunt syndrome?

A

Dramatic response to steroids.

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50
Q

What is granulomatosis with polyangiitis (Wegener’s)?

A

Multisystem necrotising vasculitis that typically affects the upper respiratory tract, kidneys and lungs.

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51
Q

What is the key feature of granulomatosis with polyangiitis (Wegener’s)?

A

C-ANCA positive in most cases.

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52
Q

What is sarcoidosis?

A

Multisystem non-caseating granulomatous disorder that manifests in the eye as uveitis.

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53
Q

What is the key feature of sarcoidosis?

A
  • Elevated serum ACE and calcium.
  • Bilateral hilar lymphadenopathy on chest x-ray.
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54
Q

What are the 4 types of childhood orbital tumour?

A
  • Rhabdomyosarcoma.
  • Neuroblastoma.
  • Capillary haemangioma.
  • Optic nerve glioma.
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55
Q

What is a rhabdomyosarcoma?

A

Commonest primary childhood orbital malignancy.

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56
Q

What does a rhabdomyosarcoma affect?

A

Most commonly affects the genitourinary system and the head and neck.

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57
Q

Where does an orbital rhabdomyosarcoma typically present?

A

Superonasal orbit.

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58
Q

How does orbital rhabdomyosarcoma present?

A

Rapidly progressive, painless, unilateral proptosis with down and out displacement of the eyeball.

59
Q

What is a neuroblastoma?

A

Tumour of neural crest cells that can metastasise to the orbit from elsewhere in the body.

60
Q

How can neuroblastoma be identified histologically?

A

Homer-wright rosettes.

61
Q

What is a capillary haemangioma?

A

High flow vascular hamartoma which grows rapidly in infancy.

Completely resolve at around age 8.

62
Q

How does capillary haemangioma present?

A

Blanching, red, unilateral lesion of the upper lid.

63
Q

When should capillary haemangioma be treated? How?

A
  • If small and no risk of affecting the visual axis > observation is sufficient.
  • If there is a risk of amblyopia > propranolol can be used to increase the rate of lesion regression.
64
Q

What is an optic nerve glioma?

A

Tumour of the glial tissue of the optic nerve, associated with NF1.

65
Q

How does optic nerve glioma present?

A

Slowly progressing unilateral proptosis with visual defects and RAPD.

66
Q

What does a CT show in optic nerve glioma?

A

Characteristic fusiform enlargement of the optic nerve.

67
Q

What are the two types of adulthood orbital tumour?

A
  • Optic nerve sheath meningioma.
  • Cavernous haemangioma.
68
Q

What is an optic nerve sheath meningioma?

A

Tumour of the meningeal tissue of the optic nerve.

69
Q

How does optic nerve sheath meningioma present?

A

Presents with triad:
- Painless, unilateral vision loss.
- Optic nerve atrophy.
- Optociliary shunting of vessels.
- Middle-aged woman.

70
Q

Which investigations are used to diagnose optic nerve sheath meningioma? What do they show?

A
  • CT.
  • Shows thick optic nerve sheath and osteoblastic changes.
71
Q

What is a cavernous haemangioma?

A

Low-flow hamartoma within the common tendinous ring.

72
Q

How does cavernous haemangioma present?

A
  • Slowly progressive axial proptosis.
  • Decreased visual acuity.
  • Middle-aged woman.
73
Q

Which investigations are used to diagnose cavernous haemangioma? What do they show?

A
  • CT.
  • Shows defined lesion within the common tendinous ring.
74
Q

What is the cavernous sinus?

A

Venous structure in the brain made up of a network of hollow spaces that drain blood away from the brain.

75
Q

What is a carotid cavernous fistula?

A

An arteriovenous malformation between the carotid artery and the cavernous sinus.

76
Q

What are the 2 types of carotid cavernous fistula? How do we differentiate between them?

A
  • Direct and indirect.
  • Angiogram is done to provide a definitive diagnosis.
77
Q

What is a DIRECT carotid cavernous fistula?

A

High flow direction connection between the internal carotid artery and the cavernous sinus.

78
Q

What is an INDIRECT carotid cavernous fistula?

A

Low flow connection between internal carotid artery and the cavernous sinus VIA meningeal branches.

79
Q

What typically causes DIRECT carotid cavernous fistula?

A

Trauma.

80
Q

What typically causes INDIRECT carotid cavernous fistula? Who does it appear in?

A

Spontaneous in elderly hypertensive women.

81
Q

How does DIRECT carotid cavernous fistula present?

A
  • Ocular bruit - whooshing sound heard by the patient.
  • Raised IOP.
  • Visual defects.
82
Q

How does INDIRECT carotid cavernous fistula present?

A
  • Gradual onset irritated eye.
  • Increased IOP.
  • Corkscrew epibulbar vessels.
83
Q

How is DIRECT carotid cavernous fistula managed?

A

Embolisation.

84
Q

How is INDIRECT carotid cavernous fistula managed?

A

Most cases self-resolve.

85
Q
A
86
Q

Where does the internal carotid travel that makes it so significant in carotid cavernous fistula?

A

Within the cavernous sinus.

87
Q

What is the cavernous sinus in terms of CST?

A

Venous blood sinus that is prone to thrombosis. Lots of important structures travel within this sinus.

88
Q

What is a cavernous sinus thrombosis? What causes it?

A

A clot within the cavernous sinus.

Typically caused by spreading infection.

89
Q

Describe the presentation of cavernous sinus thrombosis.

A
  • Acute onset headache.
  • Nausea.
  • Proptosis.
  • Diplopia.
90
Q

What causes the characteristic symptoms of cavernous sinus thrombosis?

A

Thrombosis causes compression of CN3, CN4 and CN6 as they traverse the sinus.

91
Q

Which investigation is diagnostic for cavernous sinus thrombosis?

A

MRI with MRI venogram.

92
Q

Which cranial nerve is affected (compressed) first in cavernous sinus thrombosis? Why?

A

CN6 - travels within the sinus as opposed to CN3 and CN4 which travel within the walls of the sinus.

93
Q

What is the management of cavernous sinus thrombosis?

A
  • Antibiotics.
  • Steroids.
  • Thrombolytics.
  • Surgical drainage.
94
Q

What are orbital varices?

A

Venous enlargements within the orbit.

95
Q

How do orbital varices present in terms of distribution?

A
  • Unilateral.
  • Medial.
96
Q

What is the key defining feature of orbital varices?

A

Intermittent proptosis.

97
Q

What worsens orbital varices?

A

Valsalva manoeuvre.

98
Q

What are the 5 types of ocular trauma?

A
  • Intraocular foreign bodies (IOFB).
  • Burns.
  • Orbital floor fractures.
  • Retrobulbar haemorrhage.
  • Hyphaema.
99
Q

What is the most ocular toxic metal?

A

Copper.

100
Q

What can be caused by alloys of copper?

A
  • Sunflower cataracts.
  • Kayser-Fleischer rings.
101
Q

What are the effects of iron on the eye?

A

Deposits in the ocular epithelial tissue:
- Cell death > glaucoma, cataract and retinal detachment.

102
Q

What are some inert foreign bodies?

A
  • Glass.
  • Plastic.
  • Stone.
  • Silver.
  • Gold.
  • Platinum.
  • Lead.
103
Q

Which metals have mild toxic effects on the eye?

A
  • Aluminium.
  • Zinc.
104
Q

Which investigations are diagnostic for intraocular foreign bodies?

A
  • CT/x-ray in ALL cases.
  • Visual evokes potential testing > reduced b-wave in some cases of chronicall retained IOFB.
105
Q

Which investigation is contraindicated in intraocular foreign body?

A

MRI as some bodies can be magnetised.

106
Q

What is the priority in terms of management with a penetrating injury?

A

Repair of the globe.

107
Q

What does foreign body removal technique depend on?

A

The location of the foreign body.

108
Q

Which removal technique is used for a foreign body in the cornea?

A

26G needle.

109
Q

Which removal technique is used for a foreign body in the anterior chamber?

A

Fine forceps.

110
Q

Which removal technique is used for a foreign body in the angle of the anterior chamber?

A

Scleral trapdoor approach.

111
Q

Which removal technique is used for a foreign body in the ciliary body?

A

Electromagnetic removal.

112
Q

Which removal technique is used for a foreign body in the posterior segment?

A

Intraocular magnet or vitrectomy forceps.

113
Q

What are the two substances that can cause ocular burns?

A

Alkalis and acids.

114
Q

Which substance causes significantly worse burns?

A

Alkalis.

115
Q

What kind of necrosis is caused by alkalis?

A

Liquefactive necrosis.

116
Q

What kind of necrosis is caused by acids?

A

Coagulative necrosis.

117
Q

What aids corneal healing?

A

Migration of limbal stem cells. If the limbus is damaged then healing is hindered.

118
Q

What are the steps in managing ocular burns?

A
  1. Irrigation with copious amounts of water.
  2. Antibiotics + cycloplegics + lubricants + analgesia.
  3. Topical steroids.
  4. Ascorbic acid (not to be used in acid burns) - aids collagen formation and mops up free radicals.
  5. Doxycycline - proteinase (MMP) inhibitor which aids healing.
119
Q

Which management techniques are used for prolonged corneal healing problems?

A
  • Amniotic membrane transplant.
  • Limbal stem cell transplant.
120
Q

Why is topical sodium citrate useful in healing ocular burns? Why is it not used?

A
  • Inhibits collagenases and aids healing.
  • Administration is painful so not in common use.
121
Q

What is the classic mechanism of orbital floor fractures?

A

Ball/fist injury to the eye.

122
Q

What is the consequence of an orbital floor fracture?

A
  • Soft tissue of the globe is pushed into the maxillary sinus.
  • Inferior rectus can be entrapped, causing vertical diplopia and restriction of eye elevation.
123
Q

When does surgical emphysema occur?

A
  • Orbital floor fractures.
  • More pronounced in medial wall fractures.
124
Q

Describe the presentation of orbital floor fractures.

A
  • Periorbital bruising.
  • Vertical diplopia and extraocular muscle entrapment.
  • Enophthalmos.
  • Infraorbital anaesthesia.
125
Q

Which investigation is diagnostic for orbital floor fractures?

A

CT.

126
Q

What is used in monitoring and follow-up of orbital floor fractures?

A

Hess charts.

127
Q

What is the typical presentation of extraocular muscle entrapment?

A

Antagonistic movement is restricted.

e.g., if the superior rectus is trapped, downgaze is restricted.

128
Q

What are the indications for surgery on orbital floor fractures?

A
  • Oculocardiac reflex.
  • Severe facial destruction.
129
Q

When can observation suffice for orbital floor fractures?

A
  • Minimal diplopia.
  • Minimal enophthalmos.
130
Q

What should patients with orbital floor fractures be advised?

A

To avoid blowing their nose.

131
Q

What is retrobulbar haemorrhage and why is it an emergency?

A
  • Intra-orbital bleeding/swelling.
  • The bony orbit is a rigid chamber so this can lead to a sharp rise in pressure > blindness.
132
Q

What is the pathology of retrobulbar haemorrhage?

A
  • Trauma causes oedema/bleeding in the orbit and leads to a sharp rise in intraorbital pressure.
  • Rising intraorbital pressure restricts blood flow and causes optic nerve damage.
  • Process can be thought of as orbital compartment syndrome.
133
Q

Describe the presentation of retrobulbar haemorrhage.

A
  • Painful loss of vision.
  • Rigid proptosis.
  • Restricted ocular movements.
  • RAPD.
  • Elevated intraocular pressure.
134
Q

Which investigation is diagnostic of retrobulbar haemorrhage?

A

Radioimaging.

However, this should not delay treatment.

135
Q

What is the immediate management of retrobulbar haemorrhage?

A
  • IV mannitol.
  • IV acetazolamide.
  • IV methylprednisolone.
136
Q

If medications fail to work, what is the next management for retrobulbar haemorrhage?

A

Lateral canthotomy and cantholysis.

137
Q

What is cantholysis?

A

Disinsertion (rupture) of the lateral canthal tendon. This procedure allows the release of intraorbital pressure.

138
Q

If canthotomy and cantholysis fail to work, what is the next management for retrobulbar haemorrhage?

A

Orbital decompression.

139
Q

What is hyphaema? What causes it?

A

Blood in the anterior chamber. Most commonly caused by blunt trauma.

140
Q

What is hyphaema a sign of?

A

Ocular trauma.

Warrants investigation.

141
Q

What is microhyphaema?

A

Erythrocytes are only visible on a slit lamp.

142
Q

What are the risk factors for hyphaema (things to check for)?

A
  • Drug history - anticoagulants.
  • PMH - coagulative disorders and sickle cell.
143
Q

When is treatment required for hyphaema?

A

Only required in high risk cases.

144
Q

What is considered a high risk case for hyphaema?

A
  • Children.
  • Rebleeds.
  • Risky medical histories.
145
Q

What is the treatment for hyphaema?

A
  • Admit for steroids and bedrest.
  • Monitor IOP for red cell glaucoma.
146
Q

If medications fail for hyphaema, what can be tried next?

A

Anterior chamber paracentesis.

147
Q

If AC paracentesis fails for hyphaema, what can be tried next?

A

Trabeculectomy.

Duke Elder (11 decks)

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