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LMCC (anglais) > Ophthalmology > Flashcards

Ophthalmology Flashcards

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1
Q

What should you ask on history for acute vision loss?

A
  • HPI - onset, duration, progression, and location (whether it is monocular or binocular and whether it involves the entire visual field or a specific part and which part)
  • The patient should be asked about eye pain and whether it is constant or occurs only with eye movement.
  • ROS: Jaw or tongue claudication, temporal headache, proximal muscle pain, and stiffness (giant cell arteritis); and headaches (ocular migraine).
  • PMx: Risk factors for eye disorders (eg, contact lens use, severe myopia, recent eye surgery or injury), risk factors for vascular disease (eg, diabetes, hypertension)
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2
Q

What should be performed on the eye examination for acute vision loss?

A
  • Visual acuity
  • Peripheral visual fields (confrontation)
  • Central visual fields are assessed by Amsler grid.
  • Direct and consensual pupillary light reflexes are examined using the swinging flashlight test.
  • Ocular motility is assessed.
  • Color vision is tested with color plates.
  • The eyelids, sclera, and conjunctiva are examined using a slit lamp if possible.
  • The cornea is examined with fluorescein staining.
  • The anterior chamber is examined for cells and flare in patients who have eye pain or conjunctival injection.
  • The lens is checked for cataracts using a direct ophthalmoscope, slit lamp, or both.
  • Intraocular pressure is measured.
  • Ophthalmoscopy after dilating the pupil with a drop of a sympathomimetic; dilation is nearly full after about 20 minutes. The entire fundus, including the retina, macula, fovea, vessels, and optic disk and its margins, is examined.
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3
Q

What is the Ddx for acute vision loss?

A

Cornea/Anterior Segment:

  • Corneal edema
  • Hyphema (blood in anterior chamber)
  • Acute angle-closure glaucoma
  • Trauma/foreign

Vitreous/Retina/Optic Nerve

  • Vitreous hemorrhage (caused by diabetic retinopathy or trauma)
  • RD
  • Retinal artery/vein occlusion
  • Acute macular lesion
  • Optic neuritis
  • Temporal arteritis
  • Anterior ischemic optic neuropathy (AION)

Cortical/Other

  • Occipital infarction/ hemorrhage
  • Cortical blindness
  • Functional (non-organic, diagnosis of exclusion)
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4
Q

Cornea is relatively dry and clear normally and that clarity is maintained by passive resistance of water by _____ and ____

A

Epithelium

Endothelial pump function

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5
Q

How does corneal edema occur?

A

Edema thus results when the pump is not working (trauma, uveitis, infection) or if too much fluid is getting into stroma (epithelial defect or high IOP – acute rise – angle closure glaucoma).

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6
Q

Causes of corneal edema?

A

Causes: angle closure glaucoma, post-op, abrasion, Fuchs’ Dystrophy

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7
Q

What causes corneal opacity?

A

Can be caused by a keratitis (HSV, marginal - hypersensitivity reaction to the death of bacteria or infectious – caused by contact lens use) or corneal scar from HSV treatment

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8
Q

What is the key to diagnosis of corneal opacity?

A

Key to diagnosis – decreased vision, white corneal infiltrate, epithelial defect, with anterior chamber inflamm.

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9
Q

Risk factors of corneal opacity?

A

Risk factors: diabetes, trauma, alcoholics, debilitated/elderly, CL.

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10
Q

Treatment of corneal opacity?

A

Treatment: culture scrapings, admit if >2mm, abx.

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11
Q

What is hyphema?

A

Blood in anterior chamber from blunt trauma or neovascularization

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12
Q

What is vitreous hemorrhage?

A

Blood in vitreous space

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13
Q

Risk factors for vitreous hemorrhage?

A

Risk factors (eg, diabetes, retinal tear, sickle cell anemia, trauma)

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14
Q

Clinical features of retinal detachment (RD)?

A

 Recent increase in floaters, photopsias (flashing lights), or both
 Visual field defect – loss of peripheral vision, retinal folds

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15
Q

What is retinal detachment (RD)?

A

OCULAR EMERGENCY caused by fluid accumulation UNDER retina.

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16
Q

Etiology of retinal detachment (RD)?

A

Exudative (leaks under it)

Rhegmatogenous (enters through a hole, MUCH MORE COMMON).
• These holes happen because of intrinsic weakness causing thinning of retina or traction (vitrous pulls on weak spots and rips retina, usually peripherally cause the retina is attached at optic nerve and peripheral retina).
• Thus most tears occur due to a change in vitreous dynamics. Usually from a posterior vitreous detachment (PVD).

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17
Q

Treatment of retinal detachment (RD)?

A

Treatment: Should be referred ASAP if macula on and 1-2d if macula off

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18
Q

Risk factors of retinal detachment (RD)?

A

Risk factors (eg, trauma, eye surgery, severe myopia; in men, advanced age)

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19
Q

Key to diagnosis of posterior vitreous detachment?

A

Keys to diagnosis: new floater, Decreased vision if tear of retina, photopsia – because of mechanical stimulation of photoreceptors)

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20
Q

Pathogenesis of posterior vitreous detachment?

A

The 360-deg attached vitreous becomes liquefied (syneretic) with age causing intra-vitreous tractional forces that pull at its attachment. Eventually this traction overcomes optic nerve attachment having a plunger effect leading to a PVD. Because the vitreous is more free once the PVD is released, the traction is now exerted more strongly at the ora (on the retina)

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21
Q

PVD vs RD

A
  • A PVD presents with a new floater, flashing lights, and maybe decreased vision. Only 10% have a tear.
  • A RD presents with decreased vision, photopsia, a recent floater, and a field defect
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22
Q

How soon should you treat PVD?

A

For PVD, treat within 1-2d so it does not become an RD!

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23
Q

Leading cause of permanent vision loss in elderly

A

Age-Related Macular Degeneration

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24
Q

What are the 2 types of Age-Related Macular Degeneration?

A
  • Non-Exudative/”Dry” (Non-Neovascular) AMD

- Exudative/”Wet” (Neovascular) AMD

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25
Q

Which type of Age-Related Macular Degeneration is worse and more common

A

Dry (90%): most common

Wet (10% - WORSE)

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26
Q

How does wet Age-Related Macular Degeneration occur?

A
  • Choroidal neovascularization: drusen predisposes to breaks in Bruch’s membrane causing subsequent growth and proliferation of new, fine choroidal vessels
  • May lead to serous detachment of overlying RPE and retina, hemorrhage, and lipid precipitates into the subretinal space
  • Can also lead to an elevated subretinal mass due to fibrous metaplasia of subretinal fibrovascular proliferation progresses to disciform scarring and severe central vision loss
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27
Q

Clinical features of Age-related Macular Degeneration?

A

 Variable degree of progressive central vision loss
 Metamorphopsia (distorted vision characterized by straight parallel lines appearing convergent or wavy) due to macular edema

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28
Q

Treatment of wet Age-Related Macular Degeneration

A
  • Intravitreal injection of anti-VEGF
  • VEGF Inhibitors
  • Photodynamic therapy with verteporfin - IV injection of verteporfin, followed by low-intensity laser to area of choroidal neovascularization
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29
Q

Treatment of dry Age-Related Macular Degeneration

A
  • Monitor, Amsler grid allows patients to check for metamorphopsia
  • Low vision aids (e.g. magnifiers, closed-circuit television)
  • Anti-oxidants, green leafy vegetables (Vit A,E, b-carotene, Zn, Cu)
  • Sunglasses/visors
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30
Q

How does dry Age-Related Macular Degeneration occur?

A
  • Slowly progressive loss of visual function
  • Drusen: yellow-white deposits between the RPE and Bruch’s membrane (area separating inner choroidal vessels from RPE)
  • Geographic RPE atrophy: coalescence of RPE atrophy, clumps of focal hyperpigmentation or hypopigmentation
  • May progress to neovascular AMD
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31
Q

Investigations for Age-Related Macular Degeneration?

A
  • Amsler grid: held at normal reading distance with glasses on, assesses macular function
  • Fluorescein angiography: assess type and location of choroidal neovascularization-pathologic new vessels leak dye
  • OCT retinal imaging: assess the amount of intraretinal and subretinal exudation
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32
Q

How do you differentiate between BRVO and CRVO?

A

You differentiate just by looking on fundoscopy - look very different.

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33
Q

What is Retinal Vascular Occlusion associated with?

A

Associated with HTN (hard artery compresses soft vein)

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34
Q

Clinical presentation of BRVO

A

Only affects part of the retina and usually presents as a loss of peripheral vision. Hx can sound like RD but can be differentiated by no floaters, no photopsia.

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35
Q

Retinal Vascular Occlusion history can sound like retinal detachment but probably won’t talk about _____ or _____

A

Floaters

Flashing lights

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36
Q

Treatment of BRVO?

A

Treatment: HTN mgmt. ± intravitreal anti-VEGF for macular edema ± laser for neovascularization.

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37
Q

Clinical presentation + findings of CRVO?

A

Affects the entire retina – severity can range DRASTICALLY (20/20 to 20/200). Acute but more gradual painless visual loss. Can have 4-quadrant retinal hemorrhage, cotton wool spots (hemorrhage), macular edema.

There are some situations in young patients who can develop CRVO but still have 20/20 vision because they didn’t have the underlying vascular disease - So when you see it young patients, don’t think vascular problem, think of other things

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38
Q

Treatment of CRVO?

A

Treatment: manage risk factors (HTN, diabetes, CAD, glaucoma) and monitor for complications (ischemia leads to neovascularization, vitreous hemorrhage, glaucoma). Similar to BRVO but degree of ischemia is greater.

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39
Q

What is retinal arterial occlusion?

A

An embolus from the internal carotid via the ophthalmic leads to sudden visual loss through ischemic damage to the retina. More sudden than RVO.

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40
Q

Clinical Features of retinal arterial occlusion?

A

Nearly instantaneous onset – painless vision loss, pale retina, cherry-red fovea, sometimes Hollenhorst plaque (refractile object at the site of arterial occlusion)

Described as a curtain dropping and lifting after several minutes.

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41
Q

Treatment of retinal arterial occlusion?

A

NO REAL TREATMENT, prevent another.

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42
Q

Investigations for retinal arterial occlusion?

A 
	ESR, CRP, and platelet count to exclude giant cell arteritis
	Carotid ultrasonography
	Echocardiography
	Consideration of MRI or CT of brain
	ECG
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43
Q

Secondary complications of retinal arterial occlusion?

A

Watch out for secondary complications - Patients may develop ischemia, leading to neovascularization (NV)

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44
Q

What can retrobulbar optic neuritis be associated with?

A

Usually idiopathic, but can be associated with MS!

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45
Q

Investigations for retrobulbar optic neuritis?

A

DO MRI (stratify for MS), NEURO REFERRAL

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46
Q

CRVO is associated with?

A

Associated with HTN, glaucoma, or clotting disorder.

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47
Q

Retinal arterial occlusion is associated with?

A

Associated with CV risk factors

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48
Q

Pathogenesis of cherry-red fovea?

A

All the retina that is edematous reflects light better - you see the healthy choroidal tissue through the relative thin spot and not adjacent because the retina is thicker and swollen there

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49
Q

Treatment of retrobulbar optic neuritis?

A

Consider IV steroids (controversial but much better than oral, which causes recurrence).

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50
Q

What is Retrobulbar Optic Neuritis?

A

Inflamm of nerve leading to axonal dysfunction. Most optic neuritis is RETROBULBAR (meaning no fundoscopic findings).

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51
Q

Physical exam findings of Retrobulbar Optic Neuritis?

A

Physical: Decreased VA, loss of color vision, afferent pupillary defect, visual field defect.

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52
Q

History of Retrobulbar Optic Neuritis?

A

F, unilateral, 20-40yo, pain with eye movements (from inflamm).

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53
Q

Up to 75% of patients with MS get ______! Presenting feature in 25%.

A

Optic neuritis

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54
Q

Main finding of ischemic optic neuropathy?

A

Main finding would be pallor

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55
Q

Clinical features of ischemic optic neuropathy?

A

 Headache, jaw or tongue claudication, temporal artery tenderness or swelling, pale and swollen optic disk with surrounding hemorrhages, occlusion of retinal artery or its branches
 Sometimes proximal myalgias with stiffness (due to polymyalgia rheumatica)
 Sometimes only vision loss

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56
Q

Ischemic optic neuropathy has similar findings to patients with optic neuritis except

A

They are older, have vasculopathic risk factors (DM, HTN), is more often anterior and therefore swelling visible.

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57
Q

Investigations of ischemic optic neuropathy?

A

Investigations: CRP, platelet count, temporal artery biopsy - Do biopsy within 1wk of starting steroids, this is urgent.

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58
Q

Treatment of ischemic optic neuropathy?

A

Treat with high-dose moderate steroids (prednisone)

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59
Q

Risk factors for Age-Related Macular Degeneration?

A
  • Female
  • Increasing age
  • Family history
  • Smoking
  • Caucasian race
  • Blue irides
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60
Q

Definition of Age-Related Macular Degeneration?

A

Leading cause of irreversible blindness in the Western world, associated with increasing age, usually bilateral but asymmetric

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61
Q

Visual Criteria for Driving (Class 5)

A

o 20/50 best-corrected visual acuity (both eyes open)
o 120 deg horizontal and 30 deg vertical visual fields
o No diplopia in central 40 degrees

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62
Q

Etiology of chronic visual disturbance/loss?

A

Cornea/Anterior Segment:

  • Corneal dystrophy/scarring/edema
  • Refractive error
  • Cataract
  • Glaucoma

Vitreous/Retina/Optic Nerve

  • AMD
  • DR
  • Retinal vascular insufficiency
  • Compressive optic neuropathy (intracranial mass, orbital mass)
  • Intraocular neoplasm
  • Retinitis pigmentosa

Cortical/Other

  • Pituitary adenoma
  • Medication- induced (sildenafil, amiodarone)
  • Nutritional deficiency
  • Papilledema
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63
Q

Definition of glaucoma?

A

Progressive, pressure-sensitive, optic neuropathy involving characteristic structural changes to optic nerve head with associated visual field changes

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64
Q

An isolated increase in IOP is termed _______ – should be followed for increased risk of developing glaucoma

A

Ocular hypertension (OHT)

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65
Q

Pressures _____ increase the risk of developing glaucoma

A

> 21 mmHg

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66
Q

Investigations for glaucoma?

A

 VA testing
 Slit-lamp exam to assess anterior chamber depth; gonioscopy to assess angle patency
 Ophthalmoscopy to assess the disc features
 Tonometry to measure IOP
 Visual field testing
 Pachymetry to measure corneal thickness
 OCT of the nerve fibre layer (NFL) at the optic nerve to monitor for loss of NFL
 Follow-up includes optic disc examination, IOP measurement, OCT of the optic nerve and visual field testing to monitor course of disease

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67
Q

Who should undergo screening for glaucoma?

A

Screen those at-risk >40, high IOP, FHx, black, diabetes

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68
Q

Aqueous flows into the posterior chamber and is made from the _____ (goes to anterior through pupil and absorbed by ______)

A

Ciliary body

Trabecular meshwork

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69
Q

There are 3 things we look for in glaucoma

A

IOP, optic nerve, visual field

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70
Q

Normal cup-disc ratio

A

N <0.5.

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71
Q

Due to the way the retinal fibre is oriented, glaucoma respects the _______.

A

Horizontal midline

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72
Q

Most common form of glaucoma?

A

Primary Open Angle Glaucoma

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73
Q

Definition of primary open angle glaucoma?

A
  • Unobstructed open-angle, resistance is within the trabecular meshwork
  • Insidious and asymptomatic, screening is critical for early detection
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74
Q

Major risk factors of primary open angle glaucoma?

A
  • Ocular hypertension (IOP >21mmHg)
  • Age: prevalence at 40 yr is 1-2% and at 80yr is 10%
  • Ethnicity: African descent
  • Familial (2-3x increased risk); polygenic
  • Thin central cornea
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75
Q

Clinical features of open angle glaucoma?

A
  • Asymptomatic initially
  • Insidious, painless, gradual rise in IOP due to restriction of aqueous outflow
  • Earliest signs are optic disc changes – increased C:D ratio (vertical C:D>0.6)
  • Visual field loss
  • Slow, progressive, irreversible loss of peripheral vision
  • Paracentral defects, arcuate scotoma, and nasal step are characteristics
  • Late loss of central vision if untreated
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76
Q

Treatment of open angle glaucoma?

A

Medical treatment:

  • Increase aqueous outflow: topical prostaglandin analogues, topical alpha-adrenergics, topical cholinergics
  • Decrease aqueous production: topical B-blockers, topical and oral carbonic anhydrase inhibitors, topical alpha-adrenergics

Laser trabeculoplasty

Trabeculectomy

Minimally invasive glaucoma surgery (MIGS)

Tube shunt: for advanced stages of glaucoma

Serial optic nerve head examinations, IOP measurements, OCT of optic nerve and visual field testing to monitor disease course

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77
Q

What is Laser trabeculoplasty?

A

Cyclophotocoagulation in order to achieve selective destruction of ciliary body (for refractory cases)

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78
Q

What is Trabeculectomy?

A

Creation of a new outflow tract from anterior chamber to under the conjunctiva forming a bleb

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79
Q

Etiology of secondary open angle glaucoma?

A

Increased IOP secondary to ocular/systemic disorders that obstruct the trabecular meshwork including: steroid-induced glaucoma, traumatic glaucoma, pigmentary dispersion syndrome, pseudoexfoliation syndrome (protein clogs)

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80
Q

Risk factors of primary angle closure glaucoma?

A
  • Hyperopia: small eye, big lens – large lens crowds the angle
  • Age >70yr
  • Female
  • Family history
  • More common in people of Asian and Inuit descent
  • Mature cataracts
  • Shallow anterior chamber
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81
Q

Definition of primary angle closure glaucoma?

A
  • Peripheral iris bows forward obstructing aqueous access to the trabecular meshwork
  • Sudden forward shift of the lens-iris diaphragm causes pupillary block and results in impaired drainage, leading to a sudden rise in IOP
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82
Q

Clinical features of primary angle closure glaucoma?

A
  • Red, painful eye = RED FLAG
  • Unilateral, but other eye at increased risk
  • Headache on same side
  • Decreased visual acuity, vision acutely blurred from corneal edema
  • Halos around lights
  • Nausea and vomiting, abdominal pain
  • Fixed, mid-dilated pupil
  • Marked increase in IOP; may be noticeable even to palpation (>40mmHg)
  • Shallow anterior chamber ± cells in anterior chamber
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83
Q

Complications of primary angle closure glaucoma?

A
  • Irreversible loss of vision within hours to days if untreated
  • Permanent peripheral anterior synechiae, resulting in permanent angle closure
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84
Q

Treatment of primary angle closure glaucoma?

A

• OCULAREMERGENCY: refer to ophthalmologist for acute angle-closure glaucoma
• Medical treatment
o Aqueous suppressants and hyperosmotic agents
o Miotic drops (pilocarpine) to reverse pupillary block
o Multiple topical IOP-lowering agents
o Hypserosmotic agents such as oral glycerine, or IV mannitol
• Laser iridotomy is definitive

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85
Q

Most common cause of reversible blindness worldwide

A

Cataract

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86
Q

3 types of cataract?

A

 Cortical
 Nuclear sclerotic
 Posterior subscapular – type you get when on steroids chronically.

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87
Q

Contributing factors of cataracts?

A

Contributing factors: age, trauma, metabolic/nutrition, meds.

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88
Q

Definition of cataract?

A

Any opacity of the lens, regardless of etiology – only remove if visually significant.

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89
Q

Etiology of cataracts?

A

Acquired
• age-related (over 90% of all cataracts)
• cataract associated with systemic disease (may have juvenile onset)
o DM
o metabolic disorders (e.g. Wilson’s disease, galactosemia, or homocystinuria)
o hypocalcemia
• traumatic (may be rosette-shaped)
• intraocular inflammation (e.g. uveitis)
• toxic (steroids, phenothiazines)
• radiation

Congenital
• high myopia
• present with altered red reflex or leukocoria
• treat promptly to prevent amblyopia

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90
Q

Investigations of cataracts?

A

 Measure acuity, check for afferent pupillary defect, look at red reflex, try to see retina. Refer to optho.
 Slit-lamp exam

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91
Q

Clinical features of cataracts?

A

 Gradual, painless, progressive decrease in VA
 Glare, dimness, halos around lights at night, monocular diplopia
 “second sight” phenomenon: patient is more myopic than previously noted, due to increased refractive power of the lens (in nuclear sclerosis only)
 Patient may read without previously needed reading glasses - prescription changed 3x in last 6 months

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92
Q

Treatment of cataracts?

A
  • Medical: no role for medical management

- Surgical: definitive treatment - Phacoemulsification (phaco=lens) Most commonly used surgical technique

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93
Q

Post-operative complications of phacoemulsification?

A

Post-operative complications: RD, endophthalmitis, dislocated IOL, macular edema, glaucoma, posterior capsular opacification

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94
Q

Indications for surgery for cataracts?

A

o to improve visual function in patients whose vision loss leads to functional impairment - <20/40
o to aid management of other ocular disease (e.g. cataract that prevents adequate retinal exam or laser treatment of DR)
o congenital or traumatic cataracts

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95
Q

What should you ask on history for eye redness?

A

o Onset: redness sudden (ACG, SCH) or progressive (dry eye)
o Any family members have red eyes or have you had a cold recently (viral conjunctivitis)
o Are you using any drops (toxic/irritant conjunctivitis)
o Have you got something into the eye (FB, traumatic irritation)
o Have you recently had eye surgery (irritation, endophthalmitis)
o Do you wear contacts (CL or infectious keratitis)
o Is your vision decreased (iritis, ACG)
o Discharge
o Are you light-sensitive or have pain (iritis)
o Itchy (allergic conjunctivitis)

96
Q

Physical examination for eye redness?

A

o Measure visual acuity
o Look at redness pattern (hemorrhage vs. diffuse vs. ciliary flush, vs. scleral, etc.)
o Look for discharge (purulent = bacterial, scant/filmy = viral)
o Look for corneal opacity (clear, opaque, or translucent)
o Fluorescein Staining (is there loss of epithelium)
o Look at the anterior chamber with a slit lamp (is there hypopyon, hyphema (layered blood) or is it shallow?
o Do pupils react
o Is IOP elevated
o Is there proptosis or limited of extra-ocular movements

97
Q

Etiology of eye redness?

A

o Lids/Orbit/Lacrimal System: Hordeolum/chalazion, Blepharitis, Entropion/ectropion, Foreign body/laceration, Dacryocystitis/dacryoadenitis
o Cornea: Foreign body (including contact lens), Keratitis, Abrasion, laceration, Ulcer
o Conjunctiva/Sclera: Subconjunctival hemorrhage, Conjunctivitis, Dry eyes, Pterygium, Episcleritis/scleritis, Preseptal/orbital cellulitis
o Anterior chamber: Anterior uveitis (iritis, iridocyclitis), Acute glaucoma, Hyphema, Hypopyon

98
Q

Clinical features of dacryocystitis?

A

● Pain, swelling, redness over lacrimal sac at medial canthus
● Epiphora, crusting ± fever
● Digital pressure on the lacrimal sac may extrude pus through the punctum
● In the chronic form, epiphora may be the only symptom

99
Q

Treatment of dacryocystitis?

A

● Warm compresses, nasal decongestants, systemic and topical antibiotics (cephalexin if a febrile; cefazolin if febrile)
● Incision and drainage; if chronic, obtain cultures by aspiration
● Once infection resolves, consider dacryocystorhinostomy

100
Q

Etiology of dacryocystitis?

A
  • Most commonly due to obstruction of the nasolacrimal duct

- Commonly associated with S.aureus, S.pneumoniae, Pseudomonas species

101
Q

What is dacryocystitis?

A

Acute or chronic infection of the lacrimal sac

102
Q

What is dacryoadenitis?

A

Inflammation of the lacrimal gland (outer third of upper eyelid)

103
Q

Dacryoadenitis is most commonly seen in _____ and ______

A

Children

Young adults

104
Q

Acute causes of dacryoadenitis?

A

Acute causes: S.aureus, mumps, EBV, herpes zoster, N.gonorrhoeae

105
Q

Chronic causes of dacryoadenitis?

A

Chronic causes (often bilateral): lymphoma, leukemia, sarcoidosis, tuberculosis, thyroid ophthalmopathy

106
Q

Clinical features of dacryoadenitis?

A

● Pain, swelling, tearing, discharge, redness of the outer region of the upper eyelid
● Chronic form is more common and may present as painless enlargement of the lacrimal gland

107
Q

Treatment of dacryoadenitis?

A

● Supportive: warm compresses, oral NSAIDs
● Systemic antibiotics if bacterial cause
● If chronic, treat underlying disorder

108
Q

Definition of blepharitis?

A

Inflammation of lid margins

109
Q

Clinical features of blepharitis?

A

● Itching, tearing, foreign body sensation

● Thickened, red lid margins, crusting, discharge with pressure on lids (“tooth paste sign”)

110
Q

Management of blepharitis?

A

Lid scrubs for excess scale, washing of lashes (emulsifies oil to remove them), artificial tears, tobradex for severe cases (to kill bacteria and suppress immune reaction)

111
Q

Etiology of anterior blepharitis?

A

Anterior blepharitis

  • Staphylococcal (S. aureus): ulcerative, dry scales
  • Seborrheic: no ulcers, greasy scales
112
Q

Etiology of posterior blepharitis?

A

Posterior blepharitis: Meibomian gland dysfunction

113
Q

Definition of hordeolum (stye)?

A

Acute inflammation of eyelid gland: either Meibomian glands (internal lid), glands of Zeis (modified sebaceous gland in external) or Moll (lid modified sweat gland).

114
Q

Infectious agent of hordeolum (stye)?

A

Infectious agent is usually S.aureus

115
Q

Clinical features of hordeolum (stye)?

A

Painful, red swelling of lid

116
Q

Treatment of hordeolum (stye)?

A

Treatment: Warm compresses, lid care, gentle massage. Topical antibiotics are typically ineffective

117
Q

Definition of chalazion?

A

Chronic granulomatous inflammation of Meibomian gland often preceded by an internal hordeolum. Acute inflammatory signs are usually absent

118
Q

Treatment of chalazion?

A

Treatment: warm compression. If no improvement after 1mo, consider incision and curettage. Chronic recurrent lesion must be biopsied to rule out malignancy

119
Q

Definition of trichiasis?

A

Definition: Eyelashes turned inwards

120
Q

Etiology of trichiasis?

A

May result from entropion, involutional age change, chronic inflammatory lid diseases (e.g.blepharitis), trauma, burns

121
Q

Clinical features of trichiasis?

A
  • Patient complains of red eye, foreign body sensation, significant discomfort, tearing
  • May result in corneal ulceration and scarring
122
Q

Treatment of trichiasis?

A

Topical lubrication, repeat eyelash epilation, electrolysis, and cryotherapy

123
Q

Definition of entropion?

A

Lid margin folds inward towards globe

124
Q

Etiology of entropion?

A

● Involutional(aging)
● Cicatricial (herpes zoster, surgery, trauma, burns)
● Orbicularis oculi muscle spasm
● Congenital

125
Q

Clinical features of entropion?

A

● Tearing, foreign body sensation, and red eye
● Most commonly affects lower lid
● May cause corneal abrasions with secondary corneal scarring

126
Q

Treatment of entropion?

A

Lubricants, evert lid with tape, and surgery

127
Q

Definition of ectropion?

A

Lid margin turns outward from globe

128
Q

Etiology of ectropion?

A 
●	Involutional (aging)
●	Paralytic (CN VII palsy)
●	Cicatricial (burns, trauma, surgery)
●	Mechanical (lid edema, tumour, herniated fat)
●	Congenital
129
Q

Clinical features of ectropion?

A

Tearing and possibly exposure keratitis

130
Q

Treatment of ectropion?

A

Topical lubrication, eyelid taping overnight, and surgery

131
Q

_______ is the most common cause of bacterial conjunctivitis in neonates

A

C.trachomatis

132
Q

Treatment of bacterial conjunctivitis?

A

Management: broad spectrum abx – polysporin, fucithalmic (fusidic acid), pentamycetin – follow-up if not clear in 1 week

133
Q

Symptoms of dry eye?

A

Symptoms: dryness/sandy/scratchy, slight blur in vision correctable with blink, minimal intermittent redness

134
Q

Etiology of conjunctivitis?

A

● Infectious – bacterial, viral, chlamydial, gonococcal, fungal
● Non-infectious – allergic, atopic, seasonal

135
Q

Symptoms of conjunctivitis?

A

Red eye + itching, tearing + foreign body sensation, crusting of eyelids in the morning

136
Q

Signs of conjunctivitis?

A

Conjunctival follicles + preauricular lymph nodes

137
Q

Clinical features of pingueculum?

A

● Associated with sun and wind exposure, aging

● May be irritating due to abnormal tear film formation over the deposits

138
Q

Treatment of pingueculum?

A

● Irritative symptoms may be treated with lubricating drops

● Surgery for cosmesis only

139
Q

Definition of pterygium?

A

Definition: Fibrovascular, triangular, wing-like encroachment of epithelial tissue on to the cornea

140
Q

Pathogenesis of pterygium?

A

Elastic degeneration of conjunctiva that grows onto cornea (thought to be caused by UV exposure), creates a corneal scar/thinning of corneal stroma

141
Q

Treatment of pterygium?

A

Excise if encroaching on visual axis, cosmetically unappealing, causing pain/intolerable FB sensation – if surgery is not indicated then lubricate and wear sunglasses

142
Q

Clinical features of pterygium?

A

Dry eye symptoms, may induce astigmatism, decrease vision

143
Q

Definition of episcleritis

A

Definition: immunologically mediated inflammation of episcleral

144
Q

Clinical features of episcleritis?

A

● May have discomfort and pain associated with red eye (often interpalpebral)
● Night pain, pain with palpation, photophobia, tears, PERL
● Sectoral or diffuse injection of radially-directed vessels, chemosis, small mobile nodules
● Blanches with topical phenylephrine (constricts superficial vessels)

145
Q

Is episcleritis more common in males or females?

A

More frequent in women

146
Q

Etiology of episcleritis?

A

● Mostly idiopathic
● Associated with collagen vascular diseases, infections (herpes zoster, herpes simplex, and syphilis), inflammatory bowel disease, rosacea, and atopy

147
Q

Treatment of episcleritis?

A

Treatment: usually self-limited, generally benign; usually in ages 20-50, topical steroid + oral NSAIDs

148
Q

Scleritis is more common in?

A

More common in women and elderly

149
Q

Clinical features of scleritis?

A

● Severe “deep” or “boring” pain, photophobia, red eye, decreased vision
● Pain is the best indicator of disease progression
● Inflammation of scleral, episcleral, and conjunctival vessels
● May have anterior chamber cells and flare, corneal infiltrate, scleral thinning, scleral edema
● Sclera may have a purple or “violaceous” hue (best seen in natural light), due to thinning of scleral fibres exposing the bluish-coloured uvea
● Failure to blanch with topical phenylephrine

150
Q

Symptoms of anterior scleritis?

A

Anterior scleritis: pain radiating to face, may cause scleral thinning, in some cases necrotizing

151
Q

Symptoms of posterior scleritis?

A

Posterior scleritis: rapidly progressive blindness, may cause exudative RD

152
Q

How do you differentiate episcleritis and scleritis using phenylephrine drops

A

Can differentiate scleritis from episcleritis with phenylephrine drops, causing vasoconstriction – if still deep scleral vessels present – it is scleritis, if most of the redness is gone, it’s episcleritis (don’t investigate)

153
Q

Treatment of scleritis and episcleritis?

A

Ibuprofen 600mg PO QID for 2 weeks; some may require prednisone but wait for NSAID failure first (have 2 weeks to get labs back for collagen vascular disease (RA, Wegener’s SLE), infectious (HSV/HZV, syphilis, Lyme), inflammatory (gout)

154
Q

Management of scleritis?

A

● Vision threatening-needs to be referred to ophthalmology
● Life threatening-indicator of poor systemic disease control with an increased 5yr mortality rate (not from scleritis) without treatment of underlying untreated or unrecognized autoimmune condition
● Systemic NSAIDs, systemic steroid, and systemic immunomodulation

155
Q

Is scleritis more often unilateral or bilateral?

A

Usually unilateral

156
Q

Symptoms of foreign body?

A

Symptoms: Pain, tearing, photophobia, foreign body sensation, red eye

157
Q

Signs of foreign body?

A

Signs: foreign body, conjunctival injection, epithelial defect that stains with fluorescein, corneal edema, anterior chamber cells/flare, ensure to look for the presence of a conjunctival foreign body

158
Q

Treatment of foreign body?

A

Treatment: Remove or refer to ophthalmology for removal under magnification

159
Q

What can trigger herpes simplex keratitis?

A

May be triggered by stress, fever, sun exposure and immunosuppression

160
Q

Common cause of herpes simplex keratitis?

A

Usually HSV type 1

161
Q

Clinical features of herpes simplex keratitis?

A

● Pain, tearing, foreign body sensation, red eye, may have decreased vision, and eyelid edema, usually unilateral
● Corneal hypoesthesia
● Classic form of HSV infectious epithelial keratitis is a dendritic (thin and branching) lesion with terminal end bulbs in epithelium that stains with fluorescein
● HSV may cause other forms of infectious epithelial keratitis, as well as stromal keratitis (which maybe infectious or immune-mediated), and endotheliitis (presumably immune-mediated but possible role of live virus)

162
Q

Management of herpes simplex keratitis?

A

● Topical antiviral such as trifluridine, or systemic antiviral such as acyclovir
● Debridement of dendrite
● No steroids initially – may exacerbate condition
● Ophthalmologist must exercise caution if adding topical steroids for stromal keratitis, endotheliitis or iritis, and patients covered with antiviral prophylaxis

163
Q

Physical exam findings of herpes simplex keratitis?

A

Visual acuity 20/30 to 20/60, depends on how large and how central, PERL (no afferent pupillary defect), decreased corneal sensation over ulcer, fluorescein: linear, branching ulcer + ‘bulbs’

164
Q

Clinical features of corneal ulcer?

A

● Pain, photophobia, tearing, foreign body sensation, decreased VA (if central ulcer)
● Corneal opacity that necroses and forms an excavated ulcer with infiltrative base
● Overlying corneal epithelial defect that stains with fluorescein
● May develop corneal edema, conjunctival injection, anterior chamber cells/flare, hypopyon, corneal hypoesthesia (in viral keratitis)
● Bacterial ulcers may have purulent discharge, viral ulcers may have watery discharge

165
Q

Etiology of corneal ulcer?

A

● Local necrosis of corneal tissue due to infection - Infection is usually bacterial; rarely viral, fungal, or protozoan (Acanthamoeba)
● Secondary to corneal exposure, abrasion, foreign body, contact lens use (50% of ulcers)
● Also associated with conjunctivitis, blepharitis, keratitis, vitamin A deficiency

166
Q

Investigations of corneal ulcer?

A

Seidel test: fluorescein drop on the cornea under cobalt blue filter is used to detect leaking penetrating lesions; any aqueous leakage will dilute the green stain at site of wound

167
Q

Treatment of corneal ulcer?

A

● Urgent referral to ophthalmology
● Culture prior to treatment
● Topical antibiotics every hour

168
Q

Definition of corneal abrasion?

A

Definition: Epithelial defect due to trauma or contact lens

169
Q

Symptoms of corneal abrasion?

A

Symptoms: Pain, redness, tearing, photophobia, foreign body sensation

170
Q

Signs of corneal abrasion?

A

Signs: de-epithelialized area stains with fluorescein dye

171
Q

Treatment of corneal abrasion?

A

Treatment: topical antibiotic, abrasion from organic material should cover for pseudomonas
● Consider topical NSAIDs (caution due to risk of corneal melt with prolonged use), cycloplegic (relieves pain and photophobia by paralyzing ciliary muscle), patch (do not patch non-contact lens wearers as can precipitate infection)
● Most abrasions clear spontaneously within 24-48h

172
Q

What is uveitis/iritis?

A

Iritis refers to anterior inflammation; is an autoimmune reaction, may be associated with collagen vascular disease (Lupus, IBD, RA, Wegener’s, Ankylosing Spondylitis), 90% idiopathic though

173
Q

Symptoms of uveitis/iritis?

A

Painful red eye + blurry vision + photophobia + may have had previous episodes (recognizes feeling)
● Photophobia: light = pupil constriction, inflamed iris, movement = ^inflammatory mediators = pain

174
Q

Physical exam findings of uveitis/iritis?

A

Usually UNILATERAL; visual acuity is almost always less than 20/40 and gets worse with time; pupils (may be irregular, small, and poorly reactive), corneal sensation normal, VF/extraocular movements non-contributory – need the slit lamp exam for anterior chamber cells – “perilimbal haze” is classic
● Fluorescein: no staining

175
Q

Work-up of uveitis/iritis?

A

Perform after 2nd episode, >50% of the time they are negative

CBC + ALT/AST + Mantoux Skin Test + ACE + Lysozyme + ESR/CRP + HLA-B27 + CXR + SI Joint XR + ANA + FTA-ABS (if HLA-B27 positive, indicates more refractory/recurrent uveitis)

176
Q

Management of uveitis/iritis?

A

Predforte Q1H or Durezol QID – Q2H (steroid) + 2% Homatropine BID + Maxidex QHS; sometimes need PO steroids + ophthalmology follow-up; measure IOP for steroid-induced glaucoma and adjust dosing of steroids

177
Q

What is hyphema?

A

Blood in anterior chamber, often due to damage to root of the iris . May occur with blunt trauma

178
Q

What is the definition of binocular diplopia?

A

Binocular Diplopia: Occurs with both eyes open, eliminated with occlusion of either eye

179
Q

What is the definition of monocular diplopia?

A

Monocular Diplopia: Occurs with one eye open, remains with occlusion of unaffected eye

180
Q

What is a duction?

A

Ductions: an eye movement involving only one eye.

181
Q

What is a version?

A

Versions: movements of both eyes in the same direction. dextroversion, sinestroversion (both eyes together).

182
Q

What is a vergence?

A

Vergences: is the simultaneous movement of both eyes in opposite directions (convergence, divergence)

183
Q

Etiology of monocular diplopia?

A
  • Optical factors: Refractive error/astigmatism, corneal scarring
  • Mechanical process: dislocated lens, postoperative sequelae (cataract surgery, peripheral laser iridotomy)
184
Q

Etiology of binocular diplopia?

A
  • Congenital: strabismus syndromes
  • Oculomotor nerve dysfunction: III, IV, VI Nerve Palsy (paralytic)
  • Neuromuscular junction disease: myasthenia gravis, botulism
  • Mechanical process: muscle restriction/entrapment, thyroid ophthalmopathy
  • Supranuclear Causes: INO (multiple sclerosis, brainstem infarct)
  • Orbital inflammation, infection, or tumor
  • Fracture of orbital floor or “blow out”
  • Decompensation of childhood phoria (e.g., squint)
185
Q

Complications of strabismus?

A

Complications: amblyopia, cosmesis

186
Q

Classification of strabismus?

A
  • Comitant

- Incomitant

187
Q

What is comitant strabismus?

A

Comitant (non-paralytic or concomitant): deviation equal in all positions of gaze. Suggests a central mechanism – childhood strabismus

188
Q

What is incomitant strabismus?

A

Incomitant (paralytic or restrictive): deviation worse in certain positions. Generally due to trauma

189
Q

Which is urgent incomitant strabismus or comitant strabismus?

A

Comitant is not urgent, but INCOMITANT IS

190
Q

What is a tropia?

A

Tropia: A tropia is a misalignment of the two eyes when a patient is looking with both eyes uncovered
• Deviation not corrected by the fusion mechanism

191
Q

What is a phoria?

A
  • Deviation corrected in the binocular state by the fusion mechanism
  • A phoria is a misalignment of the eyes that only appears when binocular viewing is broken and the two eyes are no longer looking at the same object.
  • Very common- majority are asymptomatic
192
Q

What can exacerbate a phoria?

A

May be exacerbated or become manifest with asthenopia (eye strain, fatigue)

193
Q

Types of strabismus?

A
  • Exo- (lateral deviation), eso- (medial deviation)

- Hyper- (upward deviation), hypo- (downward deviation)

194
Q

The cover-uncover test differentiates what?

A

Cover-uncover test allows to differentiate between -tropias and -phorias

195
Q

Any movement of the non-occluded eye in a single cover test indicates a

A

Any movement of the non-occluded eye in a single cover test indicates a -tropia, as that eye picks up fixation in the absence of visual input to the dominant eye

196
Q

Any movement of the occluded eye in a cover-uncover test indicates a

A

Any movement of the occluded eye in a cover-uncover test indicates a -phoria

197
Q

How to perform an alternate cover test?

A
  • Alternating the cover between both eyes reveals the total deviation, both latent and manifest - switching the occluder back and forth to occlude the eyes without allowing the patient to fuse in between occlusion.
  • Maintain cover over one eye for 2-3 s before rapidly shifting to other eye
198
Q

What should be asked on history for diplopia?

A

o Onset? Sudden? Constant? If fast and constant, this is more likely to be serious.
o Does it go away if you cover one eye?
o Are the images side-by-side or up and down? This tells you if it’s a horizontal or vertical muscle problem
o Worse if you look right or left? This question is a way to ask the patient about comitance – paralytic problems are incomitant and so should get worse as you move in the direction that the paralyzed muscle is responsible for and improve as you look away

199
Q

> 1 oculomotor nerve involved is a HUGE RED FLAG, especially if

A

If acute/quick or associated with trauma, vasculopathy, headache, N+V. NEED URGENT NEUROIMAGING

200
Q

Clinical findings of 3rd nerve palsy?

A

Ptosis, mydriasis (since parasympa traveling with 3rd nerve are messed), binocular/horizontal diplopia since all muscles except LR and SO are affected (eye is down and out).

Can either have pupil involvement or not. Mydriasis maybe or not.

201
Q

Clinical findings of 6th nerve palsy?

A

Patients cannot move their eye outward. Why? Lateral rectus is damaged so binocular, horizontal diplopia. Patients will have an esotropia – the weak lateral rectus cannot balance the pull of the medial rectus and so eye is adducted; the degree of esotropia increases when one looks toward the side of the palsy. Some patients will have a headturn toward the side of the palsy resulting in abduction of the paretic eye.

202
Q

Vertical Diplopia Assessment

A
  1. Perform cover-uncover test on each eye to determine which eye is hypertropic
  2. Repeat cover-uncover testing on right and left gaze – which side was worse?
  3. Tilt their head right and left, repeating cover-uncover test – which side was worse?
203
Q

Clinical findings of 4th nerve palsy?

A

Binocular/vertical diplopia. We can tolerate horizontal diplopia more than vertical 4th nerve powers the superior oblique, which moves the eye down and out. With the eyes in primary position (ie straight ahead) the SO rotates the eye. When you look toward your nose, the SO is now more aligned with the direction of gaze and depresses the eye (When looking straight ahead, the primary depressor is the inferior rectus. But when looking inwards towards the nose, the primary depressor becomes the SO)

204
Q

Ocular manifestations of multiple sclerosis

A

 Blurred vision and decreased colour vision secondary to optic neuritis
 Central scotoma due to damage to papillomacular bundle of retinal nerve fibres
 Diplopia secondary to INO
 RAPD, ptosis, nystagmus, uveitis, optic atrophy, optic neuritis
 White matter demyelinating lesions of optic nerve on MRI

205
Q

Treatment of optic neuritis in MS?

A
  • IV steroids with taper to oral form for optic neuritis

- DO NOT treat with oral steroids in isolation due to increased risk of developing MS

206
Q

Graves’ ophthalmopathy occurs _____ of thyroid gland status

A

Despite control

207
Q

Treatment of Graves’ ophthalmopathy

A
  • Monitor for corneal exposure and maintain corneal hydration
  • Manage diplopia, proptosis, and compressive optic neuropathy with one or a combination of:
    • steroids (during acute phase)
    • orbital bony decompression
    • external beam radiation of the orbit
  • Consider strabismus and/or eyelid surgical procedures once acute phase subsides
208
Q

Risk factors for infantile strabismus

A

Include family history (1st- or 2nd-degree relative), genetic disorders (Down syndrome and Crouzon syndrome), prenatal drug exposure (including alcohol), prematurity or low birth weight, congenital eye defects, and cerebral palsy.

209
Q

Causes of acquired strabismus

A
  • Refractive error (high hyperopia)
  • Tumors (eg, retinoblastoma)
  • Head trauma
  • Neurologic conditions (eg, cerebral palsy; spina bifida; palsy of the 3rd cranial nerve, 4th cranial nerve, or 6th cranial nerve)
  • Viral infections (eg, encephalitis, meningitis)
  • Acquired eye defects
210
Q

Esotropia is more common ____

A

Commonly infantile.

211
Q

Infantile esotropia is associated with

A

Associated with a large angle deviation, latent nystagmus, a crossfixation pattern of fixation, a normal accommodative convergence to accommodation ratio, and age-appropriate refractive errors

212
Q

When is the onset of infantile esotropia?

A

Onset prior to 6mo of age

213
Q

What percentage of infantile esotropia is associated with CP and hydrocephalus?

A

30%

214
Q

What is accommodative esotropia?

A

It refers to eye crossing that is caused by the focusing efforts of the eyes as they try to see clearly. Starts intermittent and eventually becomes constant.

215
Q

When does accommodative esotropia develop?

A

Develops between 2-4yo

216
Q

Two types of accommodative esotropia?

A 
o	Refractive (high hyperopia). Treat by prescribing full cycloplegic refraction and re-evaluate (GLASSES CAN STRAIGHTEN EYES HERE in refractive). Monitor for signs of fusion
o	Non-refractive - issue with convergence and accommodation. If non-reactive, need bifocals and medical therapy
217
Q

What is sensory esotropia?

A

Occurs when severe visual loss (due to conditions such as cataracts, optic nerve anomalies, or tumors) interferes with the brain’s effort to maintain ocular alignment

218
Q

Causes of incomitant esotropia?

A
  • Sixth nerve palsy
  • MR restriction (thyroid, orbital fracture)
  • Duane syndrome
219
Q

What is Duane syndrome?

A

Duane syndrome - Defect in 4th week of gestation of the 6th nerve. All types feature: retraction in adduction, limited horizontal movement, eyelid fissure narrowing! Affects left more than right. Differentiate from 6th nerve palsy by lid fissure narrowing and degree of ET for degree of abduction deficit.

220
Q

When is the onset and associations of congenital exotropia?

A

Congenital: onset before 6 mo with large angle deviation and associated with craniofacial malformation or neuro impairment. Visual prognosis is poor, needs surgery.

221
Q

Causes of acquired exotropia?

A
  • Intermittent exotropia: usually noticed when ill, tired, stressed, daydreaming. Deviation is usually greater at distance than near. When children with strabismus go outside, they tend to close one eye because one of them has more glare than the other.
  • Sensory exotropia: eye with poorer vision drifts outward (age >2)
  • Consecutive exotropia: develops after strabismus surgery
222
Q

Causes of hypertropia?

A

Hypertropia can be paralytic, caused by 4th (trochlear) cranial nerve palsy that occurs congenitally or after head trauma or, less commonly, as a result of 3rd cranial nerve palsy.

223
Q

Causes of hypotropia?

A

Hypotropia can be restrictive, caused by mechanical restriction of full movement of the globe rather than neurologic interference with eye movement. A blowout fracture of the orbit floor or walls. Less commonly, restrictive hypotropia can be caused by Graves ophthalmopathy (thyroid eye disease) and Brown’s syndrome

224
Q

What is Brown’s syndrome?

A

Brown’s: Superior oblique tendon sheath syndrome – bilateral in 10%. Here the SO cannot move in trochlea well; characteristic restriction of elevation in adduction. Can be congenital (more likely to be constant) or acquired (trauma to trochlea – more likely to be intermittent and resolve spontaneously). Child turns head toward damaged side to minimize SO use.

225
Q

What should be asked on history for strabismus?

A

Family history of amblyopia or strabismus and, if family or caregivers have noticed deviation of gaze, questions about when the deviation began, when or how often it is present, and whether there is a preference for using one eye for fixation

226
Q

Physical exam for strabismus?

A

Assessment of visual acuity, pupil reactivity, and the extent of extraocular movements. Slit-lamp examination is done to detect signs of cataract, and funduscopic examination is done to detect signs of structural defects or pathology of disorders such as retinoblastoma. Neurologic examination, particularly of the cranial nerve

227
Q

Diagnosis of strabismus?

A

 Corneal light reflex test is a good screening test, but it is not very sensitive for detecting small deviations
 Cover test
 Alternate uncover test
 Prisms - used to quantify the deviation and provide a measurement of the magnitude of misalignment of the visual axes.

228
Q

What is pseudostrabismus

A

The appearance of esotropia in a child with good visual acuity in both eyes but a wide nasal bridge or broad epicanthal folds that obscure much of the white sclera nasally when looking laterally. The light reflex and cover tests are normal in a child with pseudostrabismus.

229
Q

Treatment of strabismus?

A

 Measures to encourage use of the amblyopic eye, such as patching the better eye or administering atropine drops into the better eye to provide a visual advantage to the amblyopic eye
 Eyeglasses or contact lenses are sometimes used if the amount of refractive error is significant enough to interfere with fusion, especially in children with accommodative esotropia. Orthoptic eye exercises can help correct intermittent exotropia with convergence insufficiency.
 Surgical repair consists of loosening (recession) and tightening (resection) procedures, most often involving the horizontal rectus muscles, and is most often done bilaterally.

230
Q

Definition of amblyopia?

A

Definition: Decreased vision in an anatomically normal eye due to abnormal binocular interaction or form deprivation

231
Q

Etiology of amblyopia?

A

 Media opacity (impairs the quality of image presented to the cortex. E.g. congenital ptosis, corneal scar)
 Refractive error (anisometropia - when two eyes have unequal refractive power, induced refractive error – pressure from a capillary hemangioma causing astigmatism)
 Strabismus (mainly esotropia)– amblyopia is an adaptive mechanism here – prevents diplopia

232
Q

What is strabismic amblyopia?

A

 Can result even from a small misalignment - It’s hard to ignore the small misalignments because the overlap is so large and the brain perceives that as blur. But with big misalignments, only a small part is overlapping and blurry. So they may not develop amblyopia, but also may not develop stereopsis.
 They actually have an increased field of vision because the eyes are looking so far apart. But not all patients with strabismus get amblyopia (e.g. Exotropia often does not).

233
Q

Diagnosis of amblyopia?

A
  • Holler Test”: young child upset if good eye is covered
  • Quantitative visual acuity by age 3-4 yr using picture charts and/or matching game (Sheridan-Gardiner), testing each eye separately
234
Q

Treatment of amblyopia?

A

 Correct with glasses for accommodative esotropia
 Occlusion therapy: patching the good eye to force the brain to use the non-dominant eye and redevelop its vision with follow-up to prevent occlusion ambylopia
• Cycloplegic drops (e.g.atropine) to impair accommodation and blurvision of the good eye
 Surgery: recession (weakening) by moving muscle insertion further back on the globe or resection
 (strengthening) by shortening the muscle
 Botulinum toxin for single muscle weakening
 After ocular alignment is restored (glasses, surgery, botulinum toxin), patching (2-6 hours/day) is frequently necessary to maintain vision until ~8 yr of age

235
Q

What is anisometropic amblyopia?

A

Anisometropic amblyopia: when each eye has a different refraction usually when difference is 2-3D between eyes. Brain only sees one clear and one blurry image and ignores the blurry one leading to amblyopia.

LMCC (anglais) (23 decks)

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