Ophthalmology Flashcards
What should you ask on history for acute vision loss?
- 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)
What should be performed on the eye examination for acute vision loss?
- 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.
What is the Ddx for acute vision loss?
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)
Cornea is relatively dry and clear normally and that clarity is maintained by passive resistance of water by _____ and ____
Epithelium
Endothelial pump function
How does corneal edema occur?
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).
Causes of corneal edema?
Causes: angle closure glaucoma, post-op, abrasion, Fuchs’ Dystrophy
What causes corneal opacity?
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
What is the key to diagnosis of corneal opacity?
Key to diagnosis – decreased vision, white corneal infiltrate, epithelial defect, with anterior chamber inflamm.
Risk factors of corneal opacity?
Risk factors: diabetes, trauma, alcoholics, debilitated/elderly, CL.
Treatment of corneal opacity?
Treatment: culture scrapings, admit if >2mm, abx.
What is hyphema?
Blood in anterior chamber from blunt trauma or neovascularization
What is vitreous hemorrhage?
Blood in vitreous space
Risk factors for vitreous hemorrhage?
Risk factors (eg, diabetes, retinal tear, sickle cell anemia, trauma)
Clinical features of retinal detachment (RD)?
Recent increase in floaters, photopsias (flashing lights), or both
Visual field defect – loss of peripheral vision, retinal folds
What is retinal detachment (RD)?
OCULAR EMERGENCY caused by fluid accumulation UNDER retina.
Etiology of retinal detachment (RD)?
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).
Treatment of retinal detachment (RD)?
Treatment: Should be referred ASAP if macula on and 1-2d if macula off
Risk factors of retinal detachment (RD)?
Risk factors (eg, trauma, eye surgery, severe myopia; in men, advanced age)
Key to diagnosis of posterior vitreous detachment?
Keys to diagnosis: new floater, Decreased vision if tear of retina, photopsia – because of mechanical stimulation of photoreceptors)
Pathogenesis of posterior vitreous detachment?
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)
PVD vs RD
- 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
How soon should you treat PVD?
For PVD, treat within 1-2d so it does not become an RD!
Leading cause of permanent vision loss in elderly
Age-Related Macular Degeneration
What are the 2 types of Age-Related Macular Degeneration?
- Non-Exudative/”Dry” (Non-Neovascular) AMD
- Exudative/”Wet” (Neovascular) AMD
Which type of Age-Related Macular Degeneration is worse and more common
Dry (90%): most common
Wet (10% - WORSE)
How does wet Age-Related Macular Degeneration occur?
- 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
Clinical features of Age-related Macular Degeneration?
Variable degree of progressive central vision loss
Metamorphopsia (distorted vision characterized by straight parallel lines appearing convergent or wavy) due to macular edema
Treatment of wet Age-Related Macular Degeneration
- 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
Treatment of dry Age-Related Macular Degeneration
- 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
How does dry Age-Related Macular Degeneration occur?
- 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
Investigations for Age-Related Macular Degeneration?
- 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
How do you differentiate between BRVO and CRVO?
You differentiate just by looking on fundoscopy - look very different.
What is Retinal Vascular Occlusion associated with?
Associated with HTN (hard artery compresses soft vein)
Clinical presentation of BRVO
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.
Retinal Vascular Occlusion history can sound like retinal detachment but probably won’t talk about _____ or _____
Floaters
Flashing lights
Treatment of BRVO?
Treatment: HTN mgmt. ± intravitreal anti-VEGF for macular edema ± laser for neovascularization.
Clinical presentation + findings of CRVO?
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
Treatment of CRVO?
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.
What is retinal arterial occlusion?
An embolus from the internal carotid via the ophthalmic leads to sudden visual loss through ischemic damage to the retina. More sudden than RVO.
Clinical Features of retinal arterial occlusion?
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.
Treatment of retinal arterial occlusion?
NO REAL TREATMENT, prevent another.
Investigations for retinal arterial occlusion?
ESR, CRP, and platelet count to exclude giant cell arteritis Carotid ultrasonography Echocardiography Consideration of MRI or CT of brain ECG
Secondary complications of retinal arterial occlusion?
Watch out for secondary complications - Patients may develop ischemia, leading to neovascularization (NV)
What can retrobulbar optic neuritis be associated with?
Usually idiopathic, but can be associated with MS!
Investigations for retrobulbar optic neuritis?
DO MRI (stratify for MS), NEURO REFERRAL
CRVO is associated with?
Associated with HTN, glaucoma, or clotting disorder.
Retinal arterial occlusion is associated with?
Associated with CV risk factors
Pathogenesis of cherry-red fovea?
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
Treatment of retrobulbar optic neuritis?
Consider IV steroids (controversial but much better than oral, which causes recurrence).
What is Retrobulbar Optic Neuritis?
Inflamm of nerve leading to axonal dysfunction. Most optic neuritis is RETROBULBAR (meaning no fundoscopic findings).
Physical exam findings of Retrobulbar Optic Neuritis?
Physical: Decreased VA, loss of color vision, afferent pupillary defect, visual field defect.
History of Retrobulbar Optic Neuritis?
F, unilateral, 20-40yo, pain with eye movements (from inflamm).
Up to 75% of patients with MS get ______! Presenting feature in 25%.
Optic neuritis
Main finding of ischemic optic neuropathy?
Main finding would be pallor
Clinical features of ischemic optic neuropathy?
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
Ischemic optic neuropathy has similar findings to patients with optic neuritis except
They are older, have vasculopathic risk factors (DM, HTN), is more often anterior and therefore swelling visible.
Investigations of ischemic optic neuropathy?
Investigations: CRP, platelet count, temporal artery biopsy - Do biopsy within 1wk of starting steroids, this is urgent.
Treatment of ischemic optic neuropathy?
Treat with high-dose moderate steroids (prednisone)
Risk factors for Age-Related Macular Degeneration?
- Female
- Increasing age
- Family history
- Smoking
- Caucasian race
- Blue irides
Definition of Age-Related Macular Degeneration?
Leading cause of irreversible blindness in the Western world, associated with increasing age, usually bilateral but asymmetric
Visual Criteria for Driving (Class 5)
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
Etiology of chronic visual disturbance/loss?
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
Definition of glaucoma?
Progressive, pressure-sensitive, optic neuropathy involving characteristic structural changes to optic nerve head with associated visual field changes
An isolated increase in IOP is termed _______ – should be followed for increased risk of developing glaucoma
Ocular hypertension (OHT)
Pressures _____ increase the risk of developing glaucoma
> 21 mmHg
Investigations for glaucoma?
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
Who should undergo screening for glaucoma?
Screen those at-risk >40, high IOP, FHx, black, diabetes
Aqueous flows into the posterior chamber and is made from the _____ (goes to anterior through pupil and absorbed by ______)
Ciliary body
Trabecular meshwork
There are 3 things we look for in glaucoma
IOP, optic nerve, visual field
Normal cup-disc ratio
N <0.5.
Due to the way the retinal fibre is oriented, glaucoma respects the _______.
Horizontal midline
Most common form of glaucoma?
Primary Open Angle Glaucoma
Definition of primary open angle glaucoma?
- Unobstructed open-angle, resistance is within the trabecular meshwork
- Insidious and asymptomatic, screening is critical for early detection
Major risk factors of primary open angle glaucoma?
- 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
Clinical features of open angle glaucoma?
- 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
Treatment of open angle glaucoma?
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
What is Laser trabeculoplasty?
Cyclophotocoagulation in order to achieve selective destruction of ciliary body (for refractory cases)
What is Trabeculectomy?
Creation of a new outflow tract from anterior chamber to under the conjunctiva forming a bleb
Etiology of secondary open angle glaucoma?
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)
Risk factors of primary angle closure glaucoma?
- 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
Definition of primary angle closure glaucoma?
- 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
Clinical features of primary angle closure glaucoma?
- 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
Complications of primary angle closure glaucoma?
- Irreversible loss of vision within hours to days if untreated
- Permanent peripheral anterior synechiae, resulting in permanent angle closure
Treatment of primary angle closure glaucoma?
• 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
Most common cause of reversible blindness worldwide
Cataract
3 types of cataract?
Cortical
Nuclear sclerotic
Posterior subscapular – type you get when on steroids chronically.
Contributing factors of cataracts?
Contributing factors: age, trauma, metabolic/nutrition, meds.
Definition of cataract?
Any opacity of the lens, regardless of etiology – only remove if visually significant.
Etiology of cataracts?
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
Investigations of cataracts?
Measure acuity, check for afferent pupillary defect, look at red reflex, try to see retina. Refer to optho.
Slit-lamp exam
Clinical features of cataracts?
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
Treatment of cataracts?
- Medical: no role for medical management
- Surgical: definitive treatment - Phacoemulsification (phaco=lens) Most commonly used surgical technique
Post-operative complications of phacoemulsification?
Post-operative complications: RD, endophthalmitis, dislocated IOL, macular edema, glaucoma, posterior capsular opacification
Indications for surgery for cataracts?
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