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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.

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Presentation on theme: "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."— Presentation transcript:

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)

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

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