1. Case 1
56 year old man presents for routine examination and these are the fundus photos . L R L
10- 21mmHg normal range
Subgroup <21 mmHg
Primary open angle glaucoma
IOP in the 20’s to low 30’s
Acute angle closure glaucoma
IOP 40’s to 60’s
When to refer:
IOP greater than 21 mmHg
Difference of IOP of greater than 5 mmHg
C:D greater than 0.5; asymmetry between 2 eyes
Sx of acute angle closure

2. Case 2 65 year old female presents with monocular diplopia
Over 1.4 million cases done per year in the US
Over 70% of those over the age of 75 have cataract

3. Case 3 65 year old smoker male presents blurred vision centrally
Leading cause of visual loss in patients over the age of 50
It is estimated that over 500,000 Canadians have some form of this disease
Dry
No treatment for the dry type except VITAMINS (C,E, zinc, beta carotene)
Wet
Thermal laser photocoagulation of new blood vessels
Only good if new blood vessels are away from the centre of vision (laser also destroys healthy tissue)
Photodynamic therapy with visudyne consists of laser treatment after dye infusion
Closes blood vessels in the centre of vision but requires numerous treatments (5-6 over a 2 year period)
New Treatment Lucentis/Avastin
Intravitreal injections; 95% vision stabilization; 35% improve
Many injections

4. Case 4
65 year old diabetic male presents with blurred vision centrally
One of leading causes of visual loss
Classified as non-proliferative vs. proliferative (presence of new blood vessels on disc or retina)
Main causes of visual loss include: macular edema, vitreous hemorrhage, macular ischemia
Treated with laser, intravitreal injections of anti-VEGF or steroids, and surgery

5. Acute Visual Loss Potential causes: Cornea Anterior chamber Lens
Acute keratitis (bacterial, fungal, viral)
Angle closure glaucoma
Anterior chamber
Hyphema
Lens
Cataract (usually traumatic)
Vitreous
Hemorrhage
Retina
Vascular occlusions
Arterial
Venous
Wet AMD
Retinal detachments
Optic nerve
Optic neuritis
Ischemic optic neuropathy
Giant cell arteritis
Brain
Cerebrovascular accident
trauma

6. Case 1
65 year old male presents with sudden painful loss of vision. States it was preceded by nausea and vomiting.

7. Case 2
23 year old diabetic presents with sudden visual loss following being hit with a softball.

8. Case 3
57 year old man with 30 year history of DM presents with sudden onset of rapidly progressive acute visual loss.

9. Case 4
65 year old make presents with sudden painless loss of vision. Preceded by flashes of light and floaters.

10. Case 5
65 year old make presents with sudden painless loss of vision. No RAPD. Eye appears white.
Amaurosis fugax- precursor to stroke
Central retinal artery occlusion (CRAO)
Box-carring, retinal opacification
Retinal emergency as perfusion may be restored with aggressive techniques
May be related to embolic disease; systemic evaluation consists of carotid doppler and cardiac echo
Think of giant cell arteritis in patient with bilateral CRAO- EMERGENCY to get on steroids

11. Case 6
65 year old male presents with sudden painless loss of vision. No RAPD. Eye appears white. PMHX smoker, HTN and diabetes.

12. Case 7
77 year old make presents with sudden painless loss of vision. No RAPD. Eye appears white. Smoker, HTN (190/110).
Disc swelling, venous congestion and intraretinal hemorrhage
Can predispose to new blood vessels
May require laser surgery
Linked to hypertension, smoking, aging, clotting
Inflow disease (ocular ischemic syndrome)
mid peripheral blood
Most related to near occlusion of internal carotid artery

13. Case 8
77 year old make presents with new distortion. No RAPD. Eye appears white.

14. Case 9
88 year old make presents with sudden loss of vision and says that it hurts when she chews. RAPD present. Eye appears white.
Ischemic optic neuropathy
Swelling of disc and decrease vision in elderly is more likely to be vascular
Pale swollen disc often accompanied with splinter hemorrhages and loss of acuity; field loss in superior or inferior field (altitudinal)
Arteritic versus non-arteritic (diabetes, HTN…)
Rule out giant cell arteritis
High ESR- may need steroids
Biopsy of vessels to confirm diagnosis

15. Case 10
25 year old female with rapid loss of vision and decreased colour vision in the right eye. RAPD present. Eye is white.
Optic neuritis
Inflammation of nerve may or may not be related to MS; usually young
Nerve is hyperemic and swollen
May benefit from steroids (systemic)
May be retrobulbar in nature- so not visible signs
Rule out a mass lesion

16. Causes of a Red Eye Blepharitis/Styes Lid malpositions Cellulitis
Conjunctival/Scleral Causes
Extraocular Causes
Blepharitis/Styes
Lid malpositions
Ectropion
Entropion
7th Nerve Palsy
Cellulitis
Preseptal
Orbital
Conjunctivitis
Viral
Bacterial
Allergic
Subconjunctival hemorrhage
Pinguecula/Pterygium
Episcleritis/Scleritis

17. Causes of a Red Eye Hypopyon Infectious keratitis
Intraocular Causes
Corneal Causes
Hypopyon
Iritis
Post-operative
Endophthalmitis
Acute angle closure glaucoma
Trauma
Hyphema
Infectious keratitis
Viral (HSV)
Bacterial
Fungal
Trauma
Foreign Body
Abrasion
Contact lens issues

18. Case 2

19. Case 3

20. Case 6 Episcleritis – inflammation of the episclera
Scleritis – inflammation of the sclera

21. Case 7
Viral keratitis – HSV – viral infection of the cornea usually in a
characteristic dendritic pattern

22. Case 8 Bacterial keratitis – bacterial infection of the cornea
Fungal keratitis – fungal infection of the cornea

23. Case 9
Corneal Abrasion – loss of the surface epithelium of the
cornea

24. Case 11 Hypopyon – finding on exam
- variety of causes – infection, inflammation
- collection of WBC in the inferior aspect of the
anterior chamber

25. Case12 Endophthalmitis – inflammatory condition of the intraocular
cavities (AC/vitreous) usually caused by
infection

26. Basic Ocular Anatomy Extraocular Muscles - LR6SO4 Inferior Oblique
Up and in
CN III
Superior Rectus
Up and out
CN III
Medial Rectus
Medially
CN III
Lateral Rectus
Laterally
CN VI
Superior Oblique
Down and in
CN IV
Inferior Rectus
Down and out
CN III

27. Diplopia Monocular = refractive or retinal
Dx: disappears when affected eye is covered but persists when unaffected eye is covered
Binocular = ocular misalignment
Dx: cover test reveals strabismus.
Disappears if either eye is covered

28. Diplopia
Monocular
Non-urgent referral
Binocular
Comitant
Incomitant
Restrictive
Paralytic

29. Strabismus - diagnosis
Upper 3 photos show comitant strabismus
Right gaze
Primary gaze
Left gaze
Strabismus - diagnosis
Lower 3 photos show incomitant strabismus

30. Restrictive Strabismus
Orbital fracture - Hx of trauma
Grave’s disease – Hx of hyperthyroidism, proptosis
Orbital inflammation – red eye, proptosis, pain
Orbital tumor – loss of vision, proptosis, usually no pain or redness

31. A 24 year old man complains of vertical diplopia worsening over the past 2-3 years. He notes he can lessen the problem by tipping his head to his left side. Cover test shows a small right hypertropia. The right eye does not depress in adduction as well as the left eye does in abduction. Review motility photos. What is the diagnosis?

32. Superior oblique function in various positions of gaze
Primary position
adduction
abduction

33. Trochlear (4th n.) Palsy Etiology Children – trauma, congenital
Adults – trauma, vascular, (tumor)
What is the time course of the diplopia?
If acute, then more likely vascular
What other problems does patient have?
Trauma, diabetes, BP, headache, vomiting

34. Oculomotor (3rd n.) Palsy

35. Oculomotor (3rd n.) palsy
Without pupil involvement:
Ischemia:
Diabetes, hypertension, migraine, giant cell arteritis
Incomplete palsies:
Tumor, hematoma, aneurysms
Viral
Meningeal infiltration (eg leukemia) 35

36. Oculomotor (3rd n.) palsy
With pupil involvement:
Aneurysms (ICA, PCA, Basilar a.)
Interpeduncular cistern lesions
Cysts
Schwannoma
Angioma
Meningitis
Surgical/accidental trauma
Carotid-cavernous fistula 36

37. Abducens (6th n.) Palsy Etiology
Children – trauma, post-viral, otitis, tumor
Adults – vascular, trauma, tumor, ICP
What is the time course of the diplopia?
If acute, then more likely vascular
What other problems does patient have?
Trauma, diabetes, BP, headache, vomiting

38. Pupils Pupillary Pathways Pupillary Light Reflex Pupillary Size CN II
CN III
Pupillary Size
Sympathetic system - dilation
Parasympathetic system – constriction
Pupillary light reflex

39. Pupil Size Pathways 2 processes take place with iris dilatation
Discussion in groups for 5 minutes
PUPILLARY CONSTRICTION
-Described by pupillary light reflex – previous slide
PUPILLARY DILATATION
2 processes take place with iris dilatation
1. Iris sphincter relaxes
Accomplished by SUPRANUCLEAR inhibition of the Edinger-Westphal nucleus – thereby reducing the parasympathetic output – relaxing the iris sphincter causing dilatation. This inhibition is inactive during with sleep, narcotics, anesthesia resulting in iris sphincter contraction and pupil constriction with these states.
Reduced light decreases the excitatory impulses to the E-W nucleus, resulting in iris sphincter relaxing and dilation.
2. Iris dilator contracts
Increase in output of the sympathetic nervous system which innervates the iris dilator muscle
Think of the sympathetic nervous system as a ‘turbocharger’ for pupillary dilatation – that is parasympathetic inhibition alone can cause dilatation to some extent – but sympathetic stimulation enhances the speed and size of dilatation (some of the drops we use are sympathomimetic at the postganglionic neuron)
Sympathetic pathway – 1st order neuron originates in the hypothalamus and descends through the brain stem into the lateral column of the spinal cord – it synapses with the 2nd order neuron at the level of C7-T2 (ciliospinal centre of Budge) and then leaves the spinal cord, travels over the apical pleura of the lung (why pts with Pancoast’s lung tumours get Horner’s syndrome) and into the neck to synapse at the superior cervical ganglion – the 3rd order neuron (postganglionic neuron) travels along the internal carotid artery (why pts with carotid dissection can get a Horner’s syndrome) into the head to the orbit (via the cavernous sinus)
Pupil Size Pathways

40. Approach to Anisocoria
1st Question?
Which pupil is the abN pupil?
2nd Question?
What tests will I do on exam to figure that out?
Pupil Size in Bright Light
Pupil Size in Dim Light
Pupillary Light Reaction

41. Horner’s Syndrome - DDx
Damage to the sympathetic pathway resulting in a relatively small pupil
Congenital
Acquired
1st order neuron – central lesions (hypothalamospinal pathway)
Stroke, tumour, MS, cervical spinal cord lesions
2 nd order neuron - pre-ganglionic lesions
Adult-Tumour apex of the lung (Pancoast)
Child- Neuroblastoma
3rd order neuron – post-ganglionic (internal carotid)
Internal carotid artery dissection, cavernous sinus thrombosis, prolactinoma

42. Horner’s Syndrome - Ix Generally - neuroimaging CT/MRI brain and neck
CTA or head/neck or Carotid doppler – carotid dissection
CT chest – Pancoast tumour suspected

43. 3rd Nerve Palsy
Parasympathetic fibres are involved when pupil unable to constrict
Pupillary fibres run along the outside of the 3rd CN
Pupil involved +/- oculomotor dysfunction
Compressive lesions are more likely
Aneurysm, tumour, uncal herniation
Motor fibres are more central in 3rd CN
Oculomotor dysfunction of CN III AND pupil spared
Intrinsic lesions are more likely
Ischemic lesions
Seen in DM, GCA

44. 3rd Nerve Palsy - Ix Pupil involved +/- oculomotor dysfunction
Neuroimaging
CTA (CT angiogram)
Angiogram
Oculomotor dysfunction of CN III + pupil spared
Observation
Should resolve in 8-12 weeks
If not completely resolved at that point - neuroimaging

45. Quick Childhood Eye Exam
Fixation (vision)
Alignment
Inspection – asymmetry of lids, globe prominence, pupils, corneas
- redness, discharge, masses
Red Reflex (retina)
= FAIR Exam

46. Bruckner test
The simultaneous comparison of the red reflex from both eyes using ophthalmoscope
(note difference in red reflex between eyes)

47. Amblyopia – diagnosis
In verbal patient – measure acuity using the hardest test the child can do
Allen picture chart (easy), tumbling E chart (harder), Snellen chart (hardest)

48. Amblyopia Definition Prevalence
Amblyopia
Definition
Loss of visual acuity not correctable by glasses in an otherwise healthy eye (generic definition)
A maldevelopment or loss of vision caused by abnormal binocular interaction or form vision deprivation during visual maturation (patho-physiologic definition)
Prevalence
2 – 4 % of population
Causes more visual loss and “legal” blindness (20/200 acuity) under age 45 than all other causes combined

49. 2. Anisometropia / ametropia (glasses) 3. Vision deprivation
Amblyopia – causes
1. Strabismus
2. Anisometropia / ametropia (glasses)
3. Vision deprivation
ptosis, cataract, hemorrhage

50. Amblyopia – treatment
Only works during “sensitive period” (roughly 0 – 6 years)
Success varies inversely with age
Eliminate any causes first (glasses, ptosis repair, etc.)
Occlusion therapy (patching) is the gold standard

51. Strabismus - prevalence
2 – 4% of population (same as amblyopia, since they are so closely related)

52. Strabismus - diagnosis
Cover test is key (gold standard)

53. TROPIA / PHORIA CONSTANT TROPIA: INTERMITTENT TROPIA: PHORIA:
Eye turn present all of the time
Constant esotropia
INTERMITTENT TROPIA:
Eye turn present some of the time
Intermittent exotropia
PHORIA:
Eye turn present only when fusion broken
Esophoria

54. Strabismus - definition
Misalignment of the eyes
Types:
Esotropia
Exotropia
Hyper/hypotropia
ESOTROPIA
HYPERTROPIA

55. Why is leukocoria important?
Need to know about leukocoria – a presenting sign of retinoblastoma
Ambient light reflecting off the tumor appears white or yellow-white within the pupil
Strabismus is a common feature in retinoblastoma

56. 3.1.1 Munoz
Lesion to Optic Nerve 56

57. Optic Chiasm
Crossing of nasal retina, which represents temporal hemifield

58. Lesion to Optic Chiasm

59. Lesions to Optic Tract Includes visual abnormalities RAPD
upper bank of
calcarine fissure
Lower bank of
Includes visual abnormalities
RAPD

60. Lesion of Dorsal Optic Radiation
Lesions in deep parietal lobe
or Occipital lobe- upper bank
Calcarine fissure
upper bank of
calcarine fissure

61. Lesion of Ventral Optic Radiation (Meyer’s Loop)
Lesions in temporal lobe
(classically)
Occipital cortex-lower bank
Calcarine fissure
Lower bank of
calcarine fissure

62. Eye trauma classification -
Non-penetrating eye injuries (usually blunt) (abrasion, corneal FB, contusion, rupture, chemical burn)
Penetrating eye injuries (usually sharp) (laceration, intraocular FB)
Injuries to the eyelids (blunt: contusions, sharp: lacerations, lacrimal)
Orbital trauma (contusion, penetrating injury/FB, fractures, traumatic optic neuropathy,)

63. Rules 5 Golden of eye trauma 1. Check vision 1st
2. Agent-of-injury is King ! consider FB
3. severe hemorrhage ? open eye
4. Stat irrigation for burns
5. Multi-trauma: ! examine globe 1st

64. Eye Trauma – timing of Rx
Immediate: chemical burn *
Urgent (hrs): ruptured globe, intraocular foreign body
Semi-urgent (48h): lid & lacrimal repair
Less urgent (1-2 weeks): orbital fractures

65. Focused history - Bedside eye exam - Details: how, when, where..
Prior vision, eye condition
Tetanus status
Time of last food/drink
Bedside eye exam -

66. Teaching point: Intraocular Foreign Body
May have pain or NO pain
Decreased vision or normal vision (asymptomatic!)
Signs: as ruptured globe or minimal entry wound or none !
Hx: high index of suspicion (! agent-of-injury)
1st Rx: as in ruptured globe
Urgent referral for surgery
NB: always check vision
Consider CT, X-ray

67. Teaching points: Ruptured Globe
CC: trauma (blunt or sharp), pain, decreased vision, ‘agent-of- injury’
Signs: conj swelling, Hb++ (3D), hyphema +/- extruded uvea, irregular pupil…
1st Rx: protect eye with shield, NPO, bedrest, anti-nausea meds
Urgent transfer to ophthalmology
Caution: do not press on lids during exam
( vision –> shield –> refer )

68. What is your management ?
Orders:
shield over Left eye
Bedrest
NPO
anti-nausea medication prn
(antibiotics..)
urgent referral to Ophthalmology

69. Globe contusion/internal disruption
Subconjunctival hemorrhage
Corneal edema, traumatic iritis
Hyphema
Iris tears, traumatic mydriasis, angle recession
Lens subluxation, cataract
Vitreous/retinal hemorrhage
Commotio retinae, retinal detachment
Optic nerve avulsion, disruption

70. Teaching points: Orbital trauma
Proptosis, ecchymosis, diplopia
Orbital fractures: floor (blow out #), medial wall, lateral wall (zygoma), roof, complex
Assoc. injuries: muscle entrapment, orbital Hb, emphysema, traumatic optic neuropathy
Extra-orbital injury !
Rx :
If mild w. no compromise of function: ice, elevation, rest
If severe/compromise of function/fractures: refer

71. * Early signs * Disc elevates * Margin blurs *Hyperemia
Mechanical
* Disc elevates
* Margin blurs
Peripapillary changes
Cup fills
Vascular
*Hyperemia
* Vessels engorge
Hemorrhages
Infarcts
Exudates

72. Causes of Disc Swelling
Bilateral
Papilledema = raised Intracranial Pressure
Space Occupying Lesion
Intracranial Hypertension
Pseudopapillema
Unilateral
Ischemic
Infiltrative
Infectious
Autoimmune
Neoplastic and…
Pseudopapilledema

73. The Normal Optic Disc Normal CD ratio – ~0.4
Temporal peripapillary pigment

74. Slide #10

75. Slide #6

76. Slide #4
Optic disc drusen
Lumpy bumpy appearance
Vessels not obscured

77. Case: Jill’s Headaches
Jill, 35 y.o has had headaches, nausea, and vomiting for the past month
She experiences brief episodes of dimming vision lasting seconds
She also notices a pulsing noise in her head.

78. Jill’s Optic Discs:
Right Eye
Left Eye