Transcript Acute and Chronic visual loss (1 hour) DR. SHEHAH - mcstmf

ACUTE AND CHRONIC VISUAL LOSS
Dr Mahmood Fauzi
ASSIST PROF OPHTHALMOLOGY
AL MAAREFA COLLEGE
OBJECTIVES
Define visual loss
 Differentiate between acute and chronic visual loss
 Formulate differential diagnoses for acute and
chronic visual loss
 Take history and Outline the examination procedure
for case presenting with visual loss
 Recognize the Danger signs while history taking.
 Recognize chief ocular conditions presenting with
visual loss ,understand their systemic associations,
their etiology, clinical presentation and management.
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VISION LOSS
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Categorization
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Total or Partial
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One or Both eyes
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Sudden/ Acute or Gradual / Chronic
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Painful or Painless
DEFINING ACUTE
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In medicine, an acute disease is a disease with a
rapid onset and/or a short course.
minutes up to few weeks
DDX OF ACUTE VISION LOSS
Painful (usually)
Corneal Abrasion
 Corneal ulcer
 Acute angle closure
glaucoma
 Acute uveitis (sometimes
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Painless (usually)
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painless)
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Endophthalmitis
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Hyphema
Vitreous hemorrhage.
Retinal Artery
Occlusion
Retinal Vein Occlusion
Retinal Detachment
Optic Neuritis (can be
associated with ocular pain on eye
movement)
DEFINING CHRONIC
CHRONIC
A chronic condition is a human health
condition or disease that is persistent or
otherwise long – lasting in its effects. The
term chronic is usually applied when the
course of the disease lasts for more than
three months
DDX OF CHRONIC VISION LOSS
1- Amblyopia
2- Corneal opacities
3- Cataract
4- Glaucoma
5- Retinal vascular diseases
6- Macular degeneration
7- Chronic uveitis
8- Refractive error
9-Neglected or persistent cause of acute visual loss
HISTORY
Questions
Danger Signs
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How long ago?
Recent
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How sudden?
Sudden: ischemia or bleed
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Course?
Worsening
HISTORY
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What do they see?
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Flashes or floaters
“Curtain” rising or falling
Central patch or distortion
Key symptoms
Pain or headache
 Nausea / Vomiting
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HISTORY
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In addition to general Hx/Px:
Usual corrective glasses / contacts? Still in?
 Previous transient episodes?
 Trauma?
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EXAMINING A PATIENT WITH LOSS OF VISION
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Visual acuity
Visual field testing
Swinging light test
Direct ophthalmoscopy
Dilating the eye
Tropicamide 1%
Especially important for
suspected
Intraocular FB
Central retinal artery occlusion
Retinal detachment
•
Tonometry
Tonopen
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
CORNEAL ULCER OR MICROBIAL KERATITIS
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History of (trauma, CL wear)
Need urgent referral to ophthalmologist
Need samples for microbiology
Might need hospitalization
Treated with frequent application of
topical broad spectrum antibiotics.
If neglected can lead to corneal perforation
and endophthalmitis
Corneal Epithelial Defect (CED) or
Corneal Abrasion
ACUTE 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 GLAUCOMA
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C/O acute vision loss, pain,
headache, vomiting
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Corneal edema
Mid-dilated non-reactive
pupil
Ciliary injection
High IOP (around 50s)
Optic disc swelling
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Systemic IOP lowering
medications
YAG laser peripheral
iridotomy ASAP
ACUTE ANGLE CLOSURE GLAUCOMA EXAM
Anterior chamber
Shallow
 “Shadow sign”
 Cells and flare

www.opt.indiana.edu/riley/HomePage/Direct_Oscope/Text_Direct_Oscopt.html
www.hypertension-consult.com/Secure/textbookarticles/Primary_Care_Book/126.htm
ACUTE UVEITIS
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Most commonly idiopathic
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can be associated with pain and high IOP
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Characterized by: ciliary injection, keratic
precipitates (KPs), iris nodules, synechia,
vitritis, vasculitis, chorioretinitis and/or
papillitis.
Any type of uveitis (anterior, intermediate and
posterior) can cause acute loss of vision but
usually posterior (toxoplasmosis retinitis)
Rule out infection and malignancy
Treatment is usually with Local or systemic
immunosuppression
ENDOPHTHALMITIS
Painful loss of vision
 Usually Recent
intraocular surgery.
 Usually unilateral
(except septicemia)
 Need urgent referral to
ophthalmologist.
 Need vitreous samples
for microbiology
 Need intravitreal
antibiotic injections
 Might need retina
surgery.
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HYPHEMA
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History of trauma (usually)
Medical illness (DM, HTN)
Painless loss of vision
Rubiosis (NVI) due to CRVO or PDR
High IOP
Treat the cause
Steroids and cycloplegic topical drops.
Might need surgery (AC washout)
VITREOUS HEMORRHAGE
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History of trauma
Medical illness (DM,
HTN)
Painless loss of vision
Rubiosis (NVI) due to
CRVO or PDR
Retinal Hrg, NVD, NVE
Treat the cause
Might need surgery
(PPV)
CENTRAL RETINAL ARTERY OCCLUSION
• Sudden painless monocular loss of vision
• May have history of previous transient episodes.
• “Amaurosis fugax”
Causes
Embolic (carotid, cardiac)
Thrombosis
Temporal arteritis
Vasculitis (eg. lupus)
Sickle cell disease
Trauma
Treatment
Attempt moving embolus distally:
Digital massage
Firm steady pressure x 15 seconds, release, repeat
IOP lowering drugs
Beta-blockers/CAI/alpha-agonists… +/- Vasodilation techniques
Re-breathing to increase PaCO2
RETINAL ARTERY OCCLUSION
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BRAO
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CRAO
CENTRAL RETINAL ARTERY OCCLUSION
• Macula, thinnest portion,
remains visible
• Cherry red spot may take
24 h to develop
• Visual acuity may be
normal if sparing by
cilioretinal vessel patent
RETINAL VEIN OCCLUSION
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BRVO
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CRVO
CENTRAL RETINAL VEIN OCCLUSION
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Key facts
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10 times more common than CRAO
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Painless monocular loss of vision over hours to
days
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Vision may improve through the day
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? CRV impingement by lamina or
atherosclerosis of CRA
Ischemic vs. non-ischemic types
CENTRAL RETINAL VEIN OCCLUSION
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Treatment
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No known effective treatment or prevention
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Ophthalmology may consider:
 ASA
 Anti-coagulation
 Fibrinolytics
 Corticosteroids
 Anti-inflammatories
CRVO
Non-ischemic
Good vision
 RAPD absent
 Fewer retinal
hemorrhages
 Cotton-wool spots
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May resolve fully or
progress to ischemic type
Ischemic
Severe visual loss
 RAPD+
 Extensive retinal
hemorrhage and cottonwool spots
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RETINAL DETACHMENT
 Separation
of
inner sensory
layers from
underlying RPE
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Tear in retina
Traction
Subretinal fluid
 Mechanical
stimulation of
retinal tissue.
RETINAL DETACHMENT
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Risk Factors
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Severe myopia (eg. –12 to –15)
Advanced age
Previous cataract surgery
Blunt trauma
Family history
RETINAL DETACHMENT
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Typical black curtain
complaint
Shower of black spots
or floaters
 Flashing lights
(photopsia)
 From a “shadow” in
periphery to “dark
curtain”
 Wavy distortion of
objects
(metamorphopsia)
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RETINAL DETACHMENT- MANAGEMENT
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Transient floaters not as urgent
 Full exam in clinic likely needed
 Home with ophtho call and follow-up
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WARNING: RT ED if FURTHER flashing
lights or floaters, LASTING more than
seconds
OPTIC NEURITIS
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Key Points
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Relatively common and important cause of visual loss
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Usually in young adults, esp. caucasian women
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Commonly first manifestation of MS
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Examination- Marcus-Gunn Pupil
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Presumably autoimmune reaction with
demyelinating inflammation of optic nerve
OPTIC NEURITIS
RAPD
 Color vision
 VF
 Management
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Consult ophtho and neurology
 Steroids?
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ISCHEMIC OPTIC NEUROPATHY
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Usually painless
– Vascular - embolic or thrombotic
Signs
– Acutely - hyperemic, swollen nerve
sometimes sectoral
– Later - pallid nerve
Treatment
– Little can be done
– Consider:
• Checking carotids
• Checking heart
• +/- Aspirin
OPTIC NERVE EDEMA
Papilledema is a term reserved for optic
nerve edema, usually bilateral, caused by
elevated intracranial pressure
 A definite ophthalmologic or life
emergency
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MACULAR DEGENERATION
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Loss of central vision
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Reading, recognising faces impaired
Peripheral (navigational) vision preserved
 Leading cause of legal blindness in developed
world
 Multifactorial
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Age
 Smoking, vascular disease, UV light, diet, FHx, …
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Atrophic (dry, 90%) or exudative (wet, 10%)
Geographic atrophy – Dry AMD
Macular scarring – Wet AMD
MANAGEMENT
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Dry AMD
Lifestyle
Stop smoking, reduce UV exposure, Zinc & antioxidants
Low vision aids
Legal blindness and driving
Monitoring with Amsler chart
Wet AMD
 Observation
 Laser photocoagulation
 Verteporfin photodynamic therapy (PDT)
 Anti-VEGF
CORNEAL OPACITIES
•
Corneal scars
(Trachoma, old trauma, old
infection, advanced
keratoconus)
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Corneal dystrophies
(macular stromal corneal
dystrophy, congenital hereditary
corneal dystrophy CHED, Fuchs
corneal dystrophy)
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Corneal
degenerations
(band keratopathy, CDK)
TREATMENT OF CORNEAL OPACITIES
Refraction
 Laser (if superficial
opacity)
 Corneal transplant
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ACUTE DISCOVERY OF CHRONIC VISUAL LOSS
 Catract
Can develop or worsen
quickly
 – Usually in association
with trauma
 metabolic Imbalances
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RESOURCES
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http://cme.medcomasia.com/cme_symposium/han
dout.asp?id=433&yr=2006&m=8&d=20
http://www.patient.co.uk/doctor/gradual-loss-ofvision
QUIZ TIME
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http://www.studyblue.com/notes/note/n/02chronic-visual-loss/deck/2322409