vision loss khader m.farwan. objectives review of eye anatomy refine history and examination of the...
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Vision LossVision Loss
KHADER M.FARWAN
ObjectivesObjectives
• Review of eye anatomy
• Refine history and examination of the eye
• Work through emergent causes of sudden monocular vision loss in a case-based format
Spelling ReviewSpelling Review
Ophthalmology
Anatomy ReviewAnatomy Review
Function & transperancy
Anatomy ReviewAnatomy Review
Anatomy ReviewAnatomy Review
• Eyelids
• Tears
• Cornea
• Aqueous
• Lens
• Vitreous
Anatomy ReviewAnatomy Review
• Retina– Fovea / “Macula”– Central retinal artery
supplied by branch of ophthalmic artery (1st major branch of internal carotid)
Anatomy ReviewAnatomy Review
• Optic nerve or retinal lesions do not respect vertical meridian
• Defects that clear or start at vertical midline signify lesion at chiasm or beyond
http://eyesite.ucsd.edu/viewpoint/images/glaucoma.jpg
Vision LossVision Loss
• Categorization– Total or Partial– One or Both eyes– Sudden or Gradual– Painful or Painless
HistoryHistory
• Question Danger Signs– How long ago? Recent– How sudden? Sudden: ischemia or
bleed– Course? Worsening
HistoryHistory
• What do they see?– Flashes or floaters– “Curtain” rising or falling– Central patch or distortion
• Key symptoms– Pain or headache– Nausea / Vomiting
HistoryHistory
• In addition to general Hx/Px:– Usual corrective glasses / contacts? Still in?– Previous transient episodes?– Trauma?
ExaminationExamination
• Visual acuity
• Visual field testing
• Swinging light test
• Direct ophthalmoscopy
• Dilating the eye
• Tonometry
ExaminationExamination
• Visual acuity– Snellen chart
• 20 feet distance• Credit for a line if most letters
correctly identified• If acuity poorer than largest letter
(eg 20/200), measure distance pt can read it (eg 5/200 at 5 feet)
ExaminationExamination
• Visual acuity– Practically, if that poor, acuity described by
• Finger-counting• Hand-motion• Light perception
ExaminationExamination
• Visual acuityTo correct refractive error:
1) Use pin hole
2) Use ophthalmoscope
ExaminationExamination
• Visual field testing– Confrontation– With the patient looking at your nose, ask if
your nose and other facial features are seen clearly
• Inability to clearly see your: Nose => central scotoma Eyes or lips => paracentral scotoma Ears => peripheral visual field
defect
ExaminationExamination
• Swinging light test– Relative Afferent Pupillary Defect (RAPD)
– See http://www.richmondeye.com/apd.htm
– “Marcus-Gunn Pupil”– Significant retinal or optic nerve disease,
in one eye more than the other– Very helpful for Ophtho to know in consult
ExaminationExamination
• Direct ophthalmoscopy– Close as possible
• Remove your glasses
• Switch viewing eye
– Start at zero correction• Or to correct observer refraction (eg – 4 diopters)
• Rotate counter-clockwise for near-sighted pt
Better use of the ophthalmoscope. Luff A, Elkington A.Practitioner. 236(1511): 161-5
ExaminationExamination
• Direct ophthalmoscopy– Red Reflex
• Compare brightness and color at 1-2 feet • Indicates media free of opacity• Not always easy to do, helpful if (N)• “Eight-ball” Vitreous hemorrhage
– Move in along line of red reflex • Aim for opposite mastoid process• Often brings optic disc straight into view
ExaminationExamination
• Direct ophthalmoscopy– Place free hand on forehead
• Prevents facial contact• Resting own forehead on thumb stabilises image• Able to lift upper lid if necessary
– Comfort• Encourage subject to keep breathing during
examination• Sit patient up, avoid hunching
ExaminationExamination
• Direct ophthalmoscopy– Use anti-glare filter– Try red-free filter for better
vessel visualization
ExaminationExamination
• Direct ophthalmoscopy– PanOptic Ophthalmoscope
• Greater field of view
• “5x larger view of fundus”
• USD $400 range
Anatomy ReviewAnatomy Review
Optic disc• Color: Yellow-orange,
central cup whiter• Size: Cup less than half
diameter of disc• Margin: Sharp (may be
less sharp nasally)
imc.gsm.com/integrated/ bcs/heent/page14.html
Anatomy ReviewAnatomy Review
Fovea / “Macula”• Color: Slightly darker,
devoid of retinal vessels• Size: Same as disc• Location: Temporal and
slightly inferior to disc
imc.gsm.com/integrated/ bcs/heent/page14.html
Anatomy ReviewAnatomy Review
Vessels• Size: 3:2 Vein:Artery• Caliber: look for abnormal
tortuosity• 4 main vascular arcades
– Superior- & Inferior-
– Nasal & Temporal
imc.gsm.com/integrated/ bcs/heent/page14.html
Cilioretinal artery
ExaminationExamination
• Direct ophthalmoscopy– Four quadrant scan
– Follow vessels to periphery
(may need to re-focus)
– Get pt to look at the light
to see macula
ExaminationExamination
• Dilating the eye– Especially important for suspected
• Intraocular FB
• Central retinal artery occlusion
• Retinal detachment
– Hesitancy amongst non-ophthalmologists
ExaminationExamination
• Dilating the eyeTropicamide 1%Mydriasis and glaucoma: exploding the myth. A systematic review.
Pandit RJ, Taylor R. Diabet Med. 2000 Oct;17(10):693-9
“Risk of inducing acute glaucoma following … tropicamide alone close is to zero, no case being identified”
Near fatal anticholinergic intoxication after routine fundoscopy.
Brunner GA, et al. Intensive Care Med. 1998 Jul;24(7):730-1.
ExaminationExamination
• Dilating the eyeTropicamide 1%Contraindications:
• Acute head injury/coma
• Acute or intermittent angle-closure glaucoma
(but NOT chronic open-angle glaucoma)
• Probably anyone at high risk for above
(eg. Older asian lady, severely far-sighted person)
ExaminationExamination
• Dilating the eyeTropicamide 1% – Onset 10-15 mins, duration 4-6 h– Side effects: blurred vision, light sensitvity– Safety: must not drive for 6 h
The effect of pupil dilation with tropicamide on vision and driving simulator performance. Potamitis, T., et al. Eye. 2000 Jun;14 (3A):302-6
ExaminationExamination
• TonometryTonopen– Contraindicated if suspected ruptured globe
– Ttono = 10 – 21 mm Hg (N)
– False elevation IOP• Blepharospasm (“squeezers”)
• Avoid pressure on the eye by holding eyelids only against bony orbital rim
Case 1Case 1
SUDDEN, TOTAL LOSS, ONE EYE • 70 yo F with HTN, DM lost vision in one eye over
a few minutes earlier this morning. • No trauma. No eye pain, or N/V• Findings:
– (N) External eye and EOM, red reflex– (N) Acuity on left, only hand motion right– RAPD+– (N) Fundoscopy unaffected eye
Case 1Case 1
• Retina pale
• “Cherry Red Spot” fovea
• Splinter hemorrhage
Clinical Eye Atlas
Case 1Case 1
• Diagnosis?
• Treatment?a) Massage eyeball
b) Timoptic drops
c) Sticking a needle in the eye
Clinical Eye Atlas
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Sudden painless monocular loss of vision
• May have history of previous transient episodes. “Amaurosis fugax”
http://meded.ucsd.edu/isp/1994/im-quiz/images/crao.jpg
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Retina infarction => pallor, edema, less transparency
• Irreversible damage begins at 90 mins
http://meded.ucsd.edu/isp/1994/im-quiz/images/crao.jpg
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Macula, thinnest portion, remains visible
• Cherry red spot may take 24 h to develop
• Visual acuity may be normal if cilioretinal vessel patent
http://www.umanitoba.ca/faculties/medicine/units/ophthalmology/tutorial_folders.html/images/Cra.jpg
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Causes– Embolic (carotid, cardiac)– Thrombosis– Temporal arteritis– Vasculitis (eg. lupus)– Sickle cell disease– Trauma
www.emedicine.com/emerg/ images/521crao1.JPG
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• TreatmentAttempt moving embolus distally:– Digital massage
• Firm steady pressure x 15 seconds, release, repeat
– IOP lowering drugs• Beta-blockers/CAI/alpha-agonists…
– +/- Vasodilation techniques• Rebreathing to increase PaCO2
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Treatment– Consult ophthalmology immediately
• Paracentesis anterior chamber
• ?? HBO, thrombolytics
– Locate source • ESR for temporal arteritis
• ECG for A. fib
• Medicine consult (Carotid doppler, ECHO?…)
How to Tap an EyeHow to Tap an Eye
Anterior chamber paracentesis1. Administer local anesthesia2. Use a 30-gauge needle on a tuberculin
syringe3. Enter the eye at the limbus with bevel up4. Ensure that the needle does not damage
the lens5. Withdraw fluid until the anterior chamber
shallows slightly (0.1-0.2 cc)6. Administer a topical antibiotic post-
procedure
http://www.emedicine.com/oph/topic387.htm
Central Retinal Artery OcclusionCentral Retinal Artery Occlusion
• Complications– Vision loss
• Prognosis poor in most• But up to 10% retain central vision
(acuity improves to 20/50 or better in 80% of those)
– Recurrent thromboemboli• CVA• Further visual loss to same or contralateral eye
– Progression of temporal arteritis
Case 2Case 2
PARTIAL LOSS, ONE EYE • A 60 yo M with HTN and DM complains of progressive
loss of vision in one eye over the last 2 days. • No other symptoms• Painless uniform dulling of vision. • Findings:
– (N) External eye and EOM– Acuity 20/25 OD, 20/200 OS– RAPD+– (N) Fundoscopy unaffected eye
Case 2Case 2
How would you manage
this at 2 AM?
a) Immediate ophtho consult
b) Thrombolytic therapy
c) Decrease the intraocular pressure
d) Globe massage to dissolve clot
e) None of the above
Clinical Eye Atlas
Case 2Case 2
Unmistakable fundoscopy:• “Blood and Thunder” or
“Ketchup fundus”• Dilated tortuous veins• Flame hemorrhages• Disc edema
Clinical Eye Atlas
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
• Key facts– 10 times more common than CRAO– Painless monocular loss of vision over hours
to days– Vision may improve through the day– ? CRV impingement by lamina or
atherosclerosis of CRA
• Ischemic vs. non-ischemic types
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
• Risk Factors– Age > 50– Diabetes– HTN– Hyperviscosity syndromes– Glaucoma– Recurrent amaurosis
fugax
http://www.umanitoba.ca/faculties/medicine/units/ophthalmology/tutorial_folders.html/images/CRV_occlusion
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
Non-ischemic– Good vision– RAPD absent– Fewer retinal
hemorrhages– Cotton-wool spots
• May resolve fully or progress to ischemic type
http://webeye.ophth.uiowa.edu/dept/crvo/fig12.htm
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
Ischemic– Severe visual loss– RAPD+– Extensive retinal
hemorrhage and cotton-wool spots
http://webeye.ophth.uiowa.edu/dept/crvo/fig12.htm
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
• Treatment– No known effective treatment or prevention– Ophthalmology may consider:
• ASA
• Anti-coagulation
• Fibrinolytics
• Corticosteroids
• Anti-inflammatories
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
• Treatment– Medical follow-up to screen for atherosclerosis
and other risk factors– Ophthalmology assessment to follow for late
complications (~ 3 mos)
Central Retinal Vein OcclusionCentral Retinal Vein Occlusion
• Complications– Ocular neovascularization
• Anterior => neovascular glaucoma
• Posterior => vitreous hemorrhage
– Poor vision (20/200 or worse in 90%)
Case 3Case 3
• A 50 yo M presents with a 2 day history of persistent flashing lights and floaters in one eye, as well as a tiny shadow in one corner
• Findings: – (N) External eye and EOM
– (N) Acuity 20/20 bilaterally
– (N) Visual field testing
– RAPD absent
– (N) Fundoscopy unaffected eye
Case 3Case 3
• At 2 AM would you:a) Send home with GP follow-up
b) Instill tropicamide and repeat exam
c) Call ophthalmology immediately
d) Keep the patient overnight for ocular U/S
Retinal DetachmentRetinal Detachment
• Separation of inner sensory layers from underlying RPE – Tear in retina
– Traction
– Subretinal fluid
• Mechanical stimulation of retinal tissue.
http://www.vilegel.com.au/diseases/retinaltear/rt3.jpg
www.avclinic.com/ photodynamic_therapy.htm
Anatomy Review
Potential space with no adhesions between layers
Retinal DetachmentRetinal Detachment
• Risk Factors– Severe myopia (eg. –12 to –15)
– Advanced age– Previous cataract surgery– Blunt trauma– Family history
Retinal DetachmentRetinal Detachment
• History– Shower of black spots or floaters– Flashing lights (photopsia)– From a “shadow” in periphery to “dark curtain”– Wavy distortion of objects (metamorphopsia)
Retinal DetachmentRetinal Detachment
• Beware!– Visual field defects
• Late sign
• Patients less aware of superior field defects
• Most common defect is inferiorly
(hard to detect because of nose)
– Fundoscopy• Dilated eye exam a MUST (maybe not by us)
• Detachments start in periphery, difficult to visualize
Retinal DetachmentRetinal Detachment
• Beware!– Location
• Superior field defect indicates an inferior retinal detachment
• Detachments of the superior retina are far more serious
– May rapidly extend inferiorly to involve the macula and thereby cause the loss of central vision.
Retinal DetachmentRetinal Detachment
http://www.alberta-retina.com/rdinfo.htmhttp://www.vilegel.com.au/diseases/retinaltear/rt3.jpg
Retinal DetachmentRetinal Detachment
• Treatment – Consult ophthalmology
immediately any time of night esp. if “mac on”
– Prevent worsening RD • Bed rest, supine if
superior RD
• Protect eye from trauma (eg. metal eye shield)
http://insight.med.utah.edu/opatharch/images/retina/22078.jpg
Retinal DetachmentRetinal Detachment
• Treatment – Transient floaters not as urgent
• Full exam in clinic likely needed
• Home with ophtho call and follow-up
• WARNING: RT ED if FURTHER flashing lights or floaters, LASTING more than seconds
Case 4Case 4
SUDDEN, TOTAL LOSS, ONE EYE • 60 yo F with a unilateral headache for one week
lost all vision in her right eye over a few minutes. • No trauma, eye pain, or N/V• Findings:
– (N) External eye and EOM– (N) Acuity on left, only hand motion right– RAPD+– Visual field testing normal– (N) Fundoscopy unaffected eye
Case 4
Clinical Eye Atlas
The patient most likely has
a) Papilledema
b) CRAO
c) CRVO
d) Ischemic Optic Neuropathy (ION)
e) Temporal arteritis
Case 4 vs Case 1Case 4 vs Case 1
Clinical Eye Atlas
Pale, swollen
optic disc
Anterior Ischemic Optic Anterior Ischemic Optic Neuropathy (AION)Neuropathy (AION)
• Acute ischemia or infarction optic nerve head– Arteritic – Non-arteritic
http://webeye.ophth.uiowa.edu/dept/AION/fig4.htm
Anterior Ischemic Optic Anterior Ischemic Optic Neuropathy (AION)Neuropathy (AION)
• Sudden unilateral loss of vision– May be altitudinal
• Pallid optic disc swelling– “Chalky white”
http://webeye.ophth.uiowa.edu/dept/AION/fig4.htm
http://webeye.ophth.uiowa.edu/dept/AION/7-AION-features.htm
Arteritic (AAION)Arteritic (AAION)
• Association with Temporal Arteritis
• Suspect if – Age >50– Headache– Jaw pain or fatigue on chewing (claudication)– Scalp tenderness
• Puts other eye at up to 50% risk of same
Arteritic (AAION)Arteritic (AAION)
• Treatment– Send ESR and start steroids if elevated
Prednisone 60-100 mg PO OD– Temporal artery biopsy within 1 week
Non-Arteritic (NAAION)Non-Arteritic (NAAION)
• Presumably atherosclerotic
• Treatment– Follow-up for atherosclerotic risk factors– ASA
Case 5Case 5
SUDDEN, PARTIAL LOSS, ONE EYE • 60 yo M with migraine history complains of
painful blurry vision in one eye over a few minutes.
• No trauma. Unlike past migraines• Significant nausea, vomiting, diaphoresis• Findings
– Red eye – Only hand motion visual acuity one eye– Unable to examine further because of photophobia
Case 5Case 5
SUDDEN, PARTIAL LOSS, ONE EYE
• 60 yo M with migraine history complains of painful blurry vision in one eye over a few minutes.
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Aqueous humor produced in posterior chamber
• Blockage of normal drainage and circulation to anterior chamber
• Increasing IOP worsens outflow as iris pushed forward– Often 40-80 mm Hg
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• History– Sudden onset – Precipitant
• Bending forward
• Dark environment
• Illness or sympathetic overdrive
• Dilating drops
• Anticholinergic med (even benadryl!)
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• History– Pain (eye, head, ear, sinuses, or teeth)
– Photophobia– Vision: blurry, halos or starbursts around lights– Nausea / Vomiting– Diaphoresis
** May mimic migraine, heart, or GI disease because of systemic complaints
www.kocmut.com/assets/ images/glaucoma.JPG
• Exam– Decreased visual acuity
– Red eye
– Pupil
• Sluggish mid-dilated
• Can be irregular
(eg. slightly oval)
– Corneal haziness
– Eyeball firm to palpation
http://www.emguidemaps.homestead.com/files/redeye.html
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Exam – Anterior chamber
• Shallow
• “Shadow sign”
• Cells and flare
www.hypertension-consult.com/Secure/textbookarticles/Primary_Care_Book/126.htmwww.opt.indiana.edu/riley/HomePage/Direct_Oscope/Text_Direct_Oscopt.html
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Treatment– Immediate ophtho consult – Treat pain and nausea– Avoid dilating drops!– Lower IOP
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Treatment– Block aqueous production
• Beta blocker (eg. Timolol 0.5% 1 drop)– Onset 30 mins, peak 1-2 h
– Caution if asthma, heart failure, heart block
• CAI (eg. Acetazolamide 500 mg IV/PO/IM)– Avoid in sulfa allergy, renal insufficiency
• Alpha-2 agonist (eg. Apraclonidine 1 drop)– Additive effect
Topical Eye DropsTopical Eye Drops
1. Nasolacrimal occlusion2. Eyelid closure
– Simple techniques– Decrease systemic absorption (by 60%)– Increases bioavailability
Improving the therapeutic index of topically applied ocular drugs. Zimmerman TJ, et al. Archives of Ophthalmology. 102(4):551-553, 1984.
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Treatment– Reduce vitreous volume
• Hyperosmotic agents (eg. Mannitol 1-2 g/kg IV)
Acute Angle Closure GlaucomaAcute Angle Closure Glaucoma
• Treatment– Improve aqueous outflow
• Supine position – May help iris fall back posteriorly
• +/- Miotic agent (eg. Pilocarpine 1 drop q15 mins)– Often requires IOP < 40 mm Hg before effective
– Beware… WORSENS certain AACG types
Case 6Case 6
ACUTE, PARTIAL LOSS, ONE EYE • 30 yo F with recent URI noticed pain and
decreased vision in one eye over a few days. • No trauma, or N/V• Findings:
– Red eye and painful EOM– RAPD+– (N) Acuity – (N) Fundoscopy
Optic NeuritisOptic Neuritis
• Key Points– Relatively common and important cause of
visual loss– Usually in young adults, esp. caucasian women– Commonly first manifestation of MS– Presumably autoimmune reaction with
demyelinating inflammation of optic nerve
Optic NeuritisOptic Neuritis
• History– May have preceding viral illness, or previous episodes
– Usually monocular
– Pain• Variable degree
• Worse on eye movement
– Vision loss• Exacerbated by heat or exercise (Uhthoff phenomenon)
• Central scotoma or altered color/brightness/depth perception
Optic NeuritisOptic Neuritis
• Exam– Visual acuity variable– RAPD + – Field defects (central scotoma, altitudinal, arcs)– Fundoscopy
• Often normal (retrobulbar in 2/3)
• +/- Pale or swollen disc
Optic NeuritisOptic Neuritis
• Management– Consult ophtho and neurology– Steroids?
Beck RW, Cleary PA, Anderson MM, et al: A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. N Engl J Med 1992;326:581-588.
Optic Neuritis Study Group: The 5-year risk of multiple sclerosis after optic neuritis: experience of the Optic Neuritis Treatment Trial. Neurology 1997;49:1403-1413.
Optic NeuritisOptic Neuritis
• Optic Neuritis Treatment Trial (ONTT)– Vision
• Speeds recovery • No effect on visual outcome at 5 yrs
– AVOID oral steroids due to increased recurrence
– Multiple Sclerosis• IV steroids may help decrease short-term risk of MS• No long term protection
SummarySummaryEye Pain
RAPD Key findings
CRAO No Yes Pale retina, cherry-red spot
CRVO No +/- Blood and thunder / “Ketchup” fundus
RD No +/- May have localized field defect, cloudy veil. But suspect on history
AION No Yes Swollen pale disc, signs of temporal arteritis
Acute Angle Closure Glaucoma
Yes +/- Painful red eye, hazy cornea, irregular pupil, “shadow sign”,
firm globe
Optic Neuritis Yes Yes Painful EOM, young female pt
SummarySummaryUrgency Can wait till AM? ED Treatment
CRAO CALL
IMMEDIATELY
Only if subacute (Many days old)
Orbital massage Lower the IOP
CRVO CALL when convenient
Yes, wait ASA
RD CALL
IMMEDIATELY
At their discretion Bed rest supine
Eye shield
AION CALL if TA, severe sx, uncertain dx, can wait if not TA
Yes, wait Steroids if TA
Acute Angle Closure Glaucoma
CALL IMMEDIATELY
No Lower the IOP
Treat N/V
Optic Neuritis
CALL Yes, for ophtho AVOID oral steroids
THANK YOUTHANK YOU
Traumatic Optic NeuropathyTraumatic Optic Neuropathy
• Mechanism:– Hemorrhage of optic nerve sheath
– Avulsion optic nerve
– Most cases retrobulbar (no external or ophthalmoscopic evidence of injury)
• Difficulties:– Poor correlation between severity of impact and degree
of visual loss.
– Visual deterioration immediately or after several hours
Traumatic Optic NeuropathyTraumatic Optic Neuropathy
• Management:– Controversial– Anecdotal evidence for steroids– Role and timing of surgical tx unclear
(reserved for those who fail to improve, or deteriorate despite steroids?)
Acute visual loss and other disorders of the eyes. Laskowits et al. Neurology Clinics of North America. 16 (2) p. 323-49. May 1998.