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K A I L A M O S M O T H E R LY, O D FA A O
A S A PA C O N F E R E N C E
Patients who need eye exams…
No Financial Disclosures
Course Objectives
Briefly review basic anatomy and physiology of the eye.
Review of ocular findings of the following systemic conditions/therapy:
Hypertension
Sleep Apnea
Trauma
Plaquenil Therapy
How does the eye work?
Basic Steps to Vision Part 1: Light enters the eye.
The light is bent (refracted) primarily by the cornea & secondarily by the lens to focus onto the retina which contains blood vessels.
The majority of the light is focused onto the macula clearest portion of vision.
How does the eye work?
Basic Steps to Vision Part 2: The retina converts the light signal into a neural signal through
special photoreceptor cells.
This neural signal is transmitted to the optic nerve (CN II).
Optic nerve exits the eye and continues through the visual pathway which passes through multiple lobes of the brain to the visual cortex for visual processing.
Hypertension
Hypertension
Why do optometrists care about hypertension?
Beaver Dam Eye Study
Hypertension Retinopathy Retinopathy Blood Pressure
Retinal Occlusions
Glaucoma
Hypertensive Retinopathy
Diabetic Retinopathy
Hypertensive Retinopathy
53 yo Male
CC: “near blur”
BP: 138/68 Dx with HTN one week prior
Poor compliance with meds
Retinal Occlusions
Glaucoma
Hypertensive Retinopathy
Diabetic Retinopathy
Vein Occlusions
Why we care:
Retinal vein occlusions are the second most common cause of vision loss from retinal vascular disease—
following only diabetes.
www.uptodate.com
Pathophysiology
Clinical Manifestations
Patient Presentation
Symptomatic
Central Vision Peripheral
Vision
Asymptomatic
Clinical Manifestations
Scotomas: “Blurred” or “Grey” vision in area corresponding to area of occlusion.
Eye Fun Fact: Our visual field is inverted/reversed
relative to the retina. ST BRVO = IN VF
Clinical Manifestations
Central Vision Macular Edema
Spectral Domain Optical Coherence Tomography
Clinical Manifestations
Central Vision Macular edema—more common in CRVO
Ischemic CRVO
Clinical Manifestations
Risk Factors for Vision Loss: CRVO > BRVO
Ischemic CRVO > Non-Ischemic CRVO
Visual Acuity at Presentation (CRVO Study): ≥20/40
2/3 maintained VA, 10% progressed to VA < 20/200
20/50 – 20/200
½ maintained VA, 1/3 progressed to VA <20/200
< 20/200
20% improved VA >20/200
Clinical Manifestations
Common Complication of Vein Occlusions = Neovascularization Neovascularization Vitreous Hemorrhage, Glaucoma, & Retinal Detachment
Neovascularization
Vitreous Hemorrhage
Tractional Retinal Detachment
Hypertension Summary
Multiple Primary and Secondary Ocular Complications:
Hypertensive Retinopathy
Vein Occlusions
Vitreous Hemorrhage
Neovascular Glaucoma
Macular Edema
Tractional Retinal Detachment
V I S I O N L O S S
Hypertension Take Home
Annual Eye Exams Newly Diagnosed
Urgent If patient has malignant HTN
Request reports from OD or OMD
If sudden monocular vision loss in HTN patient:
Document VA & Urgently Refer
Sleep Apnea
Sleep Apnea
Epidemiology: 30 million Americans
Men > Women
What does optometry have to do with sleep apnea? Link between sleep apnea and normotensive glaucoma (NTG).
Normotensive Glaucoma
Glaucoma:
Most common optic neuropathy
2nd leading cause of blindness worldwide Leading cause of blindness among African-Americans
Glaucoma
Clinical Manifestations
Patient Presentation
Symptomatic
Advanced Disease
Asymptomatic
Clinical Manifestations
http://www.chicagoglaucomaconsultants.com/
Glaucoma Theories
Mechanical (↑ IOP)
Ischemic
NTG ?
Normotensive Glaucoma
Things that go bump in the night…
IOP
BP & O2
Ocular Perfusion Pressure
The optic nerve is susceptible to any type of oxygen deprivation.
Normotensive Glaucoma
Prevalence of NTG in sleep apnea patients: 7.2% (NTG) vs. 2% (General Population)
Prevalence of sleep apnea in NTG patients:
<45 – 0%
45-64 -50%
>65 – 70%
Sleep Apnea
Sleep Apnea Part 2: CPAP Problems
Increase ocular irritation
Increase tear evaporation
Increase squamous metaplasia
Hayirci et al. The effect of continuous positive airway pressure treatment for obstructive sleep apnea syndrome on the ocular surface. Cornea (2012) 6:604-8
Sleep Apnea
Increase Squamous Metaplasia Abnormal epithelial differentiation
De Paiva et al. Dry eye-induced conjunctival epithelial squamous metaplasia is modulated by interferon gamma. Invest Ophthalmol Vis Sci (2007) 48 (6):2553-60
Sleep Apnea Take Home
Sleep apnea patients should be evaluated for NTG
Especially if > 65 yo
OD/OMD may consult the primary care provider for NTG to discuss HTN treatment.
Any patients with complaints of ocular surface irritation with CPAP devices should be referred.
Ocular Trauma
Trauma
Epidemiology: 3 million ocular or orbital injuries/year
20,000 – 68,000 are vision threatening
40,000 sustain vision loss
Beaver Dam Study
~20% of adults experience trauma in lifetime
1/3 of these patients will have repeat trauma
Trauma is the leading cause of unilateral blindness in the US.
Trauma
Cause of injury:
~1/2 of injuries were penetrating (sharp objects)
Frontal airbags during motor vehicle accidents
~1/4 of all injuries are sports related
#1 most dangerous sport for the eye?
#2 most dangerous sport for the eye?
Trauma
Blunt Trauma Pathophysiology Posterior Segment Outer tunic of the eye has three distinct layers with varying
amount of elasticity.
Sclera
Choroid
Retina
When the eye is injured, the equator of the eye expands rapidly which can cause separation in the outer layers.
Patients must have DILATED eye exam to r/o post-segment injury.
Clinical Manifestations
Patient Presentation
Symptomatic
Central Vision Peripheral
Vision
Asymptomatic
Blunt Trauma
Retinal Detachment STAT Referral
Same day if possible.
Blunt Trauma
Choroidal Rupture Urgent Referral
Blunt Trauma
BLUNT FORCE
Corneal Compression
Dis
pla
ced
Aq
ueo
us
Shearing Trauma
Blunt Trauma
Traumatic Glaucoma
Aqueous Outflow
IOP
Blunt Trauma
Traumatic Glaucoma
Many signs of traumatic glaucoma or injury to the angle can not be detected the day of the trauma—these patients need to be monitored 2-3 weeks following the event for evaluation of the angle with a procedure called
gonioscopy.
Blunt Trauma
Blunt Trauma Take Home
Blunt force ocular trauma patients need a DILATED eye exam as soon as possible after injury.
Any signs of a hyphema (blood in the anterior chamber) should be immediately referred.
All blunt force ocular trauma patients should have gonisocopy to examine the anterior chamber angle in the weeks immediately following the injury.
M A N Y O F T H E F O L L O W I N G S L I D E S C O M P L I M E N T S O F W E N D Y H A R R I S O N , O D , P H D , FA A O
Plaquenil Toxicity
Plaquenil Toxicity
Plaquenil Drug commonly prescribed for autoimmune diseases (RA, Lupus, etc.)
Why do optometrists care about this?
Plaquenil can bind to melanin and cause retinal toxicity.
Plaquenil Toxicity
Plaquenil Toxicity
Retinal toxicity was previously thought to be rare. ~1% after a cumulative dose of 1000g.
Enter the age of preventative medicine… 5-7 years to reach this cumulative dose at “normal” dosing
400mg/daily
Clinical Manifestations
Patient Presentation
Symptomatic
Macular Disease
Plaquenil Toxcitiy
Vision loss from plaquenil toxicity is
permanent and progressive.
Plaquenil Toxicity
Newly published guidelines (2011) from American Academy of Ophthalmology.
Patients taking plaquenil should be screened:
Baseline
5 Years
Yearly
Plaquenil Toxicity
Plaquenil screening must include one of the following:
Multifocal Electroretinogram Fundus Autofluorescence
Spectral Domain Optical Coherence Tomographer
mfERG
mfERG
mfERG Plaquenil Patient
Plaquenil Toxicity
Plaquenil Toxicity
Plaquenil Takehome
Any patients on plaquenil therapy need to be evaluated for toxicity. Recommended:
Baseline
5 years
Yearly
Evaluation must include objective test: mfERG*
FAF
SD-OCT
Plaquenil Takehome
Patients at high risk for plaquenil toxicity:
Long term use (5+ years)
High dose/size (>6.5mg/kg/day)
Kidney or liver problems
Macular problems
Age-Related Macular Degeneration
Elderly