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Eyecare Review for Primary Care Practitioners PowerPoint Presentation

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Description : This medical presentation titled "Eyecare Review for Primary Care Practitioners" provides information related to eyecare including its anatomy, optics, turned Eyes, lazy eye, external conditions, internal conditions, and diabetic retinopathy.

Tags : eyecare, anatomy, optics, turned Eyes, lazy eye, external conditions, internal conditions, diabetic retinopathy

Published on : Apr 25, 2021 | Views : 2333 | Downloads : 5

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Slide 1-

Eyecare Review— For Primary Care Practitioners
Slide 2-

Primary Care Practitioners See variety of eye problems Discuss treatment options Facilitate referrals Positioned to explain optometry's role as primary eye care providers
Slide 3-

Outline Anatomy Optics Turned Eyes Lazy Eye External Conditions Internal Conditions Diabetic Retinopathy
Slide 4-

ANATOMY
Slide 5-

Basic Anatomy Sclera Cornea Pupil Lens Iris Ciliary Body Choroid Retina Fovea Optic Nerve
Slide 6-

Lashes—protection from foreign material Glands—lubricate anterior surface Meibomian glands Glands of Zeis Glands of Moll Lids
Slide 7-

Thin, transparent, vascular layer lining Backs of eyelids Fornices Anterior sclera Conjunctiva
Slide 8-

Tough outer shell Composed of collagen bundles Protects from penetration Sclera
Slide 9-

Composed of regularly oriented collagen fibers 5 layers Cornea
Slide 10-

Space between cornea and iris Filled with aqueous humor produced by ciliary body Anterior Chamber
Slide 11-

Iris gives eye color 2 muscles: Dilator—opens Sphincter—constricts Iris
Slide 12-

Allows light to enter Enables view to back of eye and eye health evaluation Pupil
Slide 13-

Located behind iris Focuses light on retina Allows for accommodation Normally transparent Where cataracts form Lens
Slide 14-

Primary functions Pulls on lens for accommodation Epithelium secretes aqueous fluid that fills anterior chamber Ciliary Body
Slide 15-

Red Reflex Light reflection off retina Useful for assessing media clarity Affected by any opacity of cornea, lens, vitreous White reflex = leukocoria Refer immediately!
Slide 16-

Vitreous Humor Gel-like fluid that fills back cavity Serves as support structure for blood vessels while eye formed—before birth After birth, just ‘hangs out’ in there Where floaters are located
Slide 17-

Fundus Interior surface of eye Includes Optic nerve Retina Vasculature
Slide 18-

Optic Nerve Head Collection of nerve fibers and blood vessels from retina Transfers info to brain’s visual cortex Slightly yellow-pink when healthy White ‘full moon’ appearance can mean trouble!
Slide 19-

Optic Nerve Head Cup is natural depression in center of nerve Cup size varies between people Very large cup, or change in appearance over time, can indicate glaucoma Physiologic Cup Optic Disc Optic Nerve
Slide 20-

Macula Dense collection of cone photoreceptors Fine detail and color vision Macular degeneration affects this area
Slide 21-

Retinal Vessels Include arteries and veins Only place in body where you can directly visualize blood vessels Excellent indicators of systemic diseases HTN Diabetes High cholesterol Carotid disease
Slide 22-

Peripheral Retina Can only be evaluated with dilated pupil Important to evaluate periodically to fully assess eye health
Slide 23-

OPTICS
Slide 24-

Optics Review Myopia Hyperopia Astigmatism Presbyopia
Slide 25-

Myopia Nearsightedness See well up close but blurry in distance Eye is too long Light focuses in front of retina
Slide 26-

Hyperopia Farsightedness See well in distance Eye is too short Focus point is behind retina
Slide 27-

Hyperopia Blurry image on retina Lens focuses to compensate Hyperopes often asymptomatic much their of lives Can cause headaches or eyestrain with extended reading These problems can get worse after age 40
Slide 28-

Astigmatism Surface of cornea is irregular or misshapen Light focuses at various points causing distorted vision Often combined with nearsightedness and farsightedness
Slide 29-

Presbyopia Normal, age-related change Near vision becomes difficult Mid-40s lens becomes less elastic and loses ability to change focus Time for bifocals…
Slide 30-

MISALIGNED EYES
Slide 31-

Turned Eyes - Strabismus Eye misalignment One or both turn in, out, up or down Caused by muscle imbalance 3 Kinds of Strabismus Esotropia Exotropia Hypertropia
Slide 32-

1. Esotropia Eye turns in towards nose
Slide 33-

3 Types of Esotropia Infantile (congenital) Develops in first 3 months of life Surgery usually recommended— along with vision therapy and glasses Accommodative Usually noted around age 2 Child typically farsighted Focusing to make images clear can cause eyes to turn inward Treated with glasses but vision therapy may also be needed
Slide 34-

3 Types of Esotropia Partially Accommodative Combination of accommodative dysfunction and muscle imbalance Glasses and vision therapy won’t completely correct eye turn Surgery may be required for best binocularity
Slide 35-

If you see Esotropia Refer to pediatric optometrist or ophthalmologist Sooner the better for best chance of good vision
Slide 36-

2. Exotropia Eye turns outward Congenital—present at birth Surgery usually needed to re-align Many exotropias are intermittent May occur when patient is tired or not paying attention Concentration can force eyes to re-align Vision therapy and/or glasses can help
Slide 37-

2. Exotropia When intermittent Brain sometimes receives info from both eyes (binocular) Less chance of amblyopia However, important to be seen by eyecare provider when deviation noted
Slide 38-

3. Hypertropia One eye vertically misaligned Usually from paresis of an extra-ocular muscle Typically much more subtle for patient to describe and provider to diagnose
Slide 39-

2 Types Congenital Most common type Patients can compensate for years by tilting head Can be discovered by looking at childhood photos
Slide 40-

2 Types Acquired Trauma— Extra-ocular muscle ‘trapped’ by orbital fracture Vascular infarct— Systemic diseases that affect blood supply to nerves can cause temporary nerve palsy Diabetes and HTN most common Palsies tend to resolve over weeks or months Neurological— In rare cases a tumor or aneurysm can cause symptoms
Slide 41-

LAZY EYE
Slide 42-

Lazy Eye - Amblyopia Decreased vision uncorrectable by glasses or contacts—not due to eye disease For some reason, brain doesn’t fully acknowledge images seen
Slide 43-

Lazy Eye - Amblyopia 3 Types of Amblyopia Strabismic Anisometropic Stimulus deprivation
Slide 44-

1. Strabismic Amblyopia One eye deviates from other and sends conflicting info to brain Brain doesn’t like to see double—so “turns off” info from deviated eye Results in under developed visual cortex for that eye Can usually be reversed or decreased if treated during first 9 years Need to visit eyecare provider ASAP to determine cause
Slide 45-

Treatment If caught early, treatment can teach brain how to see better Vision therapy/patching Glasses Surgical re-alignment Early vision screenings are critical!
Slide 46-

2. Anisometropic Amblyopia Anisometropia—significant difference in Rx between eyes Commonly one eye more farsighted Farsighted eye works hard to see clearly—and sometimes gives up Brain relies on info from other eye
Slide 47-

2. Anisometropic Amblyopia If not caught, one eye won’t learn to see as well as other Vision therapy and glasses are both beneficial Sooner the better
Slide 48-

3. Deprivational Amblyopia Any opacity in visual pathway can be devastating to developing visual system Congenital cataracts Corneal opacities Ptosis (droopy eyelid) Other media opacities
Slide 49-

EXTERNAL CONDITIONS
Slide 50-

Common External Ocular Conditions Blepharitis Hordeolum—stye Preseptal cellulitis Orbital cellulitis Pterygium Corneal ulcer Conjunctivitis Viral “pink eye” Adenovirus Bacterial Allergic Hyperacute Chlamydial
Slide 51-

Blepharitis Inflammation of eyelids (anterior or posterior) Symptoms Itching Burning Crusting Dry eye sensation Foreign body sensation
Slide 52-

Blepharitis Signs Crusts on lid margins Thickened, reddened eyelids Plugged or inspisated meibomian glands along eyelid Treatment Warm compresses, 10 minutes 1-2 x/day Lid scrubs with diluted baby shampoo Artificial tears Erythromycin ointment at night
Slide 53-

Hordeolum (stye) Abscessed meibomian gland Raised, tender nodule Often gets larger over days to a week
Slide 54-

Hordeolum Signs Raised nodule protruding out from or under lid Red, swollen lid Capped glands at site of infection Treatment Warm compresses, BID-TID for 10 mins Topical meds don’t penetrate abscess Oral antibiotics if no response to traditional treatment
Slide 55-

Preseptal Cellulitis Bacterial infection of eyelid anterior to orbital septum Can arise from concurrent sinus infection penetrating lid trauma dental infection hordeolum insect bite
Slide 56-

Preseptal Cellulitis Signs Painful, swollen lid extending past orbital rim May be unable to open eye No decreased vision, restricted ocular motility or proptosis White conjunctiva Treatment Amoxicillin (augmentin) 500 mg PO TID Treat infection quickly to minimize risk of orbital cellulitis
Slide 57-

Orbital Cellulitis Serious infection of soft tissues behind orbital septum Can be life-threatening Causes Sinus infection Extension of preseptal cellulitis Dental infection Penetrating lid injury After ocular surgery
Slide 58-

Orbital Cellulitis Signs Tender, warm periorbital lid edema Proptosis Painful ophthalmoplegia Decreased vision Severe malaise, fever and pain Treatment Medical emergency Hospitalization with IV antibiotics Consider orbit/head CT to look for abscess Consult pediatrician or infectious disease specialist
Slide 59-

Preseptal vs. Orbital Cellulitis Preseptal Painful, swollen lid extending beyond orbital rim Normal vision Full EOMs White conjunctiva No proptosis No fever Orbital Painful, swollen lid that stops at orbital rim Decreased vision Restricted ocular motilities Proptosis Fever/malaise
Slide 60-

Pterygium Triangular-shaped growth of conjunctival tissue onto cornea Causes UV exposure Dryness Irritants Smoke Dust
Slide 61-

Pterygium Signs Dry eye Irritation Redness Blurred vision Management and Treatment UV tint on glasses Avoid irritating environments Artificial tears Topical vasoconstrictor or mild steroid Surgery
Slide 62-

Corneal Ulcer Infection of cornea Bacterial Fungal Acanthamoeba Causes SCL wearer Trauma Compromised cornea from pre-existing condition
Slide 63-

Corneal Ulcer Signs Pain Photophobia Blurred vision Discharge Hypopyon Treatment: Start immediately Fortified antibiotics Fluoroquinolones Culture may not be necessary if ulcer is small Must be monitored daily!
Slide 64-

Conjunctivitis (red eye) Various Causes Viral/Adenovirus Bacterial Allergic Chlamydial Herpetic Toxic
Slide 65-

Conjunctivitis Signs Irritation Burning/stinging Watering Photophobia Pain or foreign body sensation Itching Discharge Watery Mucoid Mucopurulent Purulent
Slide 66-

1. Viral Conjunctivitis (pink eye) Most viral infections are fairly mild and self-limiting Signs & Symptoms Watering Redness Photophobia Discomfort/foreign body sensation Palpable preauricular node
Slide 67-

1. Viral Conjunctivitis Patients often have recent history of URI Treat symptoms Cool compresses Artificial tears Topical vasoconstrictors or mild anti-inflammatory Frequent handwashing Usually runs course in 1-3 weeks
Slide 68-

2. Adenoviral Conjunctivitis Highly contagious Most common types Pharyngoconjunctival fever (PCF)— can be caused by adenovirus types 3, 4 & 7 Epidemic keratoconjunctivitis (EKC)— caused most commonly by adenovirus types 8 & 19
Slide 69-

2. Adenoviral Conjunctivitis Signs Watering Conjunctival follicles Subconjunctival hemorrhages Chemosis Pseudomembranes Lymphadenopathy Keratitis
Slide 70-

3. Bacterial Conjunctivitis Common, especially in children Usually self-limiting Signs/symptoms Acute redness Burning/grittiness Mucopurulent discharge Lids stuck shut in morning
Slide 71-

3. Bacterial Conjunctivitis Common organisms: S. aureus, S. epidermidis, S. pneumonia, H. influenza (esp. peds) Usually self-limiting But important to use broad-spectrum antibiotic until discharge cleared (5-7 days) Antibiotics Tobramycin Polytrim—polymyxin + trimethoprim Fluoroquinolones like Ocuflox or Ciloxan
Slide 72-

5. Hyperacute Conjunctivitis Cause Sexually transmitted Neisseria gonorrhoeae Signs Swollen, tender lids Copious purulent discharge Significant conjunctival redness and swelling Lymphadenopathy
Slide 73-

5. Hyperacute Conjunctivitis Treatment Lavage Take scrapings for culture and sensitivity testing Patients usually hospitalized and started on IM Ceftriaxone Topical antibiotics not effective
Slide 74-

6. Chlamydial Conjunctivitis Cause Sexually transmitted ocular infection Signs Patients typically have mild but persistent follicular conjunctivitis non respondent to topical antibiotics Any conjunctivitis lasting longer than 3 weeks despite therapy should be suspect
Slide 75-

6. Chlamydial Conjunctivitis Patients can have concomitant genital infection (could be asymptomatic) Refer for work-up if necessary Treatment Oral—Azithromycin 1g, doxycycline 100mg bid x 7 days, erythromycin 500mg qid x 7 days. Also need to tx partners! Topical—erythromycin, tetracycline, or sulfacetamide ung bid-tid x 2-3 weeks
Slide 76-

4. Allergic Conjunctivitis Can be seasonal or acute Signs/symptoms Itching is hallmark Conjunctival redness Chemosis Lid edema Thin, watery discharge No palpable preauricular nodes
Slide 77-

4. Allergic Conjunctivitis Treatment Eliminate offending agent If mild Cool compresses Artificial tears/vasoconstrictors If moderate or severe Topical antihistamine/mast-cell stabilizer (ie. Patanol) Topical NSAID Topical steroid Oral antihistamine
Slide 78-

INTERNAL CONDITIONS
Slide 79-

Internal Ocular Conditions Glaucoma Cataracts Macular Degeneration Retinal detachment
Slide 80-

Glaucoma Progressive loss of Nerve fiber layer at ONH (increased cupping) Can lead to peripheral visual field loss Sometimes caused by elevated intraocular pressure
Slide 81-

Glaucoma Pathophysiology of progression not well understood Increased IOP Damages nerves as they leave eye, causing cell death Reduces blood supply to ONH, indirectly destroying cells by starving them of oxygen and nutrients Abnormal levels of neurotransmitter (glutamate) cause cells to die off
Slide 82-

Glaucoma Monitoring IOP ONH appearance Visual field testing Newer methods include HRT (Heidelberg Retinal Tomograph II) GDx Nerve Fiber Analyzer Genetic testing
Slide 83-

Glaucoma IOP reduction is mainstay of treatment Decrease aqueous production B-blockers Alpha-agonists Carbonic anhydrase inhibitors Increase uveoscleral outflow prostaglandin analogs
Slide 84-

Cataract Clouding of natural lens Patients experience Blurred/dim vision Glare, especially at night Halos around lights Doubling or ghost images of objects
Slide 85-

Etiology Everyone develops them if they live long enough! Types of cataracts Age-related—senile Trauma—blunt or perforating injury Systemic conditions—diabetes Medications—steroids
Slide 86-

Main Types Age-related Nuclear sclerotic Cortical spokes Posterior sub-capsular Mature cataract
Slide 87-

Treatment Surgery When loss of vision interferes with daily activities Driving Reading Hobbies
Slide 88-

Outpatient Surgery 5-10 minutes with skilled surgeon Incision through cornea or sclera under upper lid Circular tear in anterior capsule Lens broken up with ultra sound instrument Fragments suctioned out Lens implant inserted
Slide 89-

Secondary Cataract Cloudiness forms on posterior capsule after cataract surgery 30-50% of patients YAG laser used to create opening Vision quickly restored
Slide 90-

Macular Degeneration #1 cause of blindness in Americans over age 65
Slide 91-

Pathophysiology Causes not well understood Theorized link to UV light exposure subsequent release of free radicals oxidation within retinal tissues Another theory—areas of decreased vascular perfusion in retina, lead to cell death
Slide 92-

Two Types Dry (atrophic) 90% of those diagnosed Wet (exudative) 10% of those diagnosed But accounts for 90% of blindness caused by disease
Slide 93-

Symptoms None Blurred vision Metamorphopsia—straight lines appear wavy or distorted Scotomas—missing areas in vision
Slide 94-

Dry Form Slow, progressive loss of central vision Breakdown of underlying retinal tissues, resulting in mottling or clumping of normal pigment Drusen begin to accumulate Geographic atrophy can also occur
Slide 95-

Wet Form Can quickly degrade central vision Break in underlying tissues allows new blood vessels or fluid to come through New blood vessels are weak so frequently break and bleed
Slide 96-

Treatment for Dry Form Regular eye exams Careful discussion regarding family history Education UV protection Antioxidants AREDS PreserVision Stop smoking
Slide 97-

Treatment for Wet Form Refer to retinal specialist Photocoagulation Photo-dynamic therapy (PDT) Submacular surgery Macular translocation Anti-angiogenic drug therapy
Slide 98-

Retinal Detachment Several types Rhegmatogenous—caused by break in retina Exudative—caused by fluid accumulation beneath retina Tractional—proliferative fibrovascular vitreal strands
Slide 99-

Signs & Symptoms Flashing lights in peripheral vision New floaters—black spots or ‘cobwebs’ Peripheral scotoma—dark shadow or “curtain” blocking vision
Slide 100-

Emergency Patients with these symptoms must see eyecare provider immediately Additional risk factors Highly nearsighted Diabetic Recent trauma/injury
Slide 101-

Treatment Laser photocoagulation or cryotherapy Pneumatic retinopexy—gas bubble to tamponade retina back into place Scleral buckle Silicone oil
Slide 102-

DIABETIC RETINOPATHY
Slide 103-

Diabetic Retinopathy Diabetes affects retinal micro-vasculature One of leading causes of blindness among ages 20-64
Slide 104-

Progression Over time, elevated and fluctuating blood sugar damages vessel walls Vessels leak fluid, lipids or blood into retina New vessels grow to bring more oxygen to retina
Slide 105-

Symptoms Fluctuating vision Blurred vision Distortion Sudden loss of vision
Slide 106-

Treatment Control blood sugar Refer to retinal specialist when vision threatened PRP (pan-retinal photocoagulation) Focal laser Vitrectomy Retinal detachment repair
Slide 107-

Working Together Together we can catch vision threatening conditions earlier Glad to answer questions Always happy to take your calls
Slide 108-

Questions?