kaila m osmotherly, od faao asapa conference › › resource › resmgr › 2014... ·...

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